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|Haven Of Wiidom > Members' Zones > Grano's hangout|
|Posted by: granobulax Mar 6 2009, 08:06 AM|
| Well, others have their own personal spot so I thought this would be a good oppertunity to keep those interested up to date on some things going on with me.
Feel free to talk about thinks I post as well as ask questions about related topics on this thread. *I know I created the Random thread but I want normal to serious talk on this one*
Now, for those who don't know, I'll take a minute to tell about a normal week for me.
I work on friday, saturday, and sunday nights. One shift lasts 12 1/2 hours from 6:30 PM to 7:00 AM. When I get off of work on monday morning, I get roughly four hours of sleep and then get ready for my microbiology lab. It lasts from 1:00 to 4:00 PM where I then go to my microbiology lecture for another hour and a half. I go home, study/spend time with my family and go to bed. On tuesday, I have my nursing clinical day at the hospital. This is a 12 hour day from 6:30 in the morning until 6:30 at night. I go home and study/spend time with my family. Wednesday, I go to my nursing lab from 12:00 noon until 4:00 PM to practice for my skills checkoffs and then go to my second microbiology lecture for another hour and a half. I then go home and study/spend time with my family. Thursdays are my nursing lecture day from 8:00 AM to noon. After lecture, I go to the lab to practice for my skills checkoffs for another 3-5 hours. Then I go home and study/spend time with my family. Fridays, I go to the lab to practice some more before going to work at 6:30 to start the process all over again.
Whew! I can't wait to get done with school!
|Posted by: granobulax Mar 6 2009, 08:06 AM|
|Oh, I had my second nursing exam today. I scored an 84% which I'm extremely happy with.|
|Posted by: treacherous Mar 6 2009, 02:23 PM|
|Wow, I thought my work week was tough. How do you find the time to even look at this site anymore?|
|Posted by: Jailer411 Mar 6 2009, 03:28 PM|
|Posted by: granobulax Mar 6 2009, 05:19 PM|
That's why you don't see me on for more than 5-10 minutes at a time.
I'm not on nearly as much as I used to be.
|Posted by: Jailer411 Mar 6 2009, 05:21 PM|
|Hey Grano, are you trying to become a doctor?|
|Posted by: granobulax Mar 6 2009, 05:24 PM|
I'm first going for my LPN (Licensed Practical Nurse) this summer and next summer for my RN (Registered Nurse).
Nope, no doctro, but the next best thing in my opinion.
|Posted by: Pseudonym Mar 6 2009, 09:05 PM|
|I was gonna use Thrax %&*$|
|Posted by: Jailer411 Mar 6 2009, 09:06 PM|
Grano beat you to it
|Posted by: Bassetman Mar 6 2009, 09:17 PM|
|Muahaha. Another trend I started.|
|Posted by: granobulax Mar 6 2009, 11:51 PM|
Of all the characters to use, we both were going to use Thrax. What are the chances?
|Posted by: granobulax Mar 6 2009, 11:51 PM|
What trend is that? Personal threads?
|Posted by: Bassetman Mar 7 2009, 12:58 AM|
| Yeah. The whole blog-style member's zone.
|Posted by: Solomon Mar 7 2009, 04:37 AM|
|Do you like music?|
|Posted by: granobulax Mar 7 2009, 05:52 AM|
Yes, I like music. I listen to a wide variety of music,
|Posted by: Solomon Mar 7 2009, 06:08 AM|
|I'm not alone in the realm of music.|
|Posted by: granobulax Mar 7 2009, 09:32 AM|
|I also enjoy classical music.|
|Posted by: MarvelFan15 Mar 7 2009, 03:46 PM|
No kidding? So do I It's just...my computer crshed, and I no longer have ITunes.
|Posted by: Solomon Mar 7 2009, 06:18 PM|
Me too. No joke.
|Posted by: granobulax Mar 7 2009, 06:42 PM|
Here, take a listen to this. It's Russian and modern in the sense of classical music but I really like this piece.
|Posted by: Solomon Mar 7 2009, 06:44 PM|
Creepy as hell. I'm getting chills down my spine. Was that Sean Connery at the beginning?
|Posted by: granobulax Mar 8 2009, 03:56 AM|
Yes, it's Sean Connery. That song was composed for The Hunt for Red October.
And yes, anyone that can play anything Mozart has mad talent.
|Posted by: The Ripper Mar 8 2009, 04:03 AM|
|I love the classical music too! Grano, it seems that we may match in tastes!|
|Posted by: granobulax Mar 9 2009, 01:43 AM|
|I got to give my first injection today. I'm psyched about finally getting to do some good stuff|
|Posted by: Solomon Mar 9 2009, 02:03 AM|
|Posted by: granobulax Mar 9 2009, 02:53 AM|
Why? You scared of needles?
|Posted by: treacherous Mar 9 2009, 03:05 AM|
|You injected what into who?|
|Posted by: The Ripper Mar 9 2009, 03:05 AM|
Kudos for you on your achievement! Oh, and Grano, ignore the nay-sayings.
|Posted by: granobulax Mar 9 2009, 03:08 AM|
Wouldn't you like to know...
Nah, it was insulin for a diabetic.
|Posted by: granobulax Mar 9 2009, 03:08 AM|
Thanks Ripper. I was pretty nervous at first, but when it was done, I thought "Wow, that was easy"
|Posted by: MarvelFan15 Mar 9 2009, 04:15 AM|
I have that movie!
|Posted by: granobulax Mar 9 2009, 04:27 AM|
|Posted by: Solomon Mar 9 2009, 10:19 AM|
No just the thought of you doing the injecting.
|Posted by: granobulax Mar 9 2009, 02:28 PM|
|Posted by: Marvel Man Mar 10 2009, 01:00 AM|
| Grano, what's your opinion on stem cell research?
|Posted by: granobulax Mar 10 2009, 01:06 AM|
I'm for it under the right circumstances. There are stem cells that can be aquired without using dead babies and such.
|Posted by: Solomon Mar 10 2009, 10:19 AM|
| See what happens when you don't vote for bobthe5th.
(if your a vet you'll get it.)
|Posted by: Bassetman Mar 10 2009, 09:11 PM|
|I miss Bob. He was my Wingy.|
|Posted by: Solomon Mar 10 2009, 09:29 PM|
Yeah I miss him too. I really wish he'd come back.
|Posted by: Darkender Mar 10 2009, 09:37 PM|
Was that Sharpshooter?
|Posted by: Jailer411 Mar 10 2009, 09:40 PM|
Sharpshooter was bobthe4th.
|Posted by: Pseudonym Mar 10 2009, 09:45 PM|
Well the way Stem CEll research works, is that you fertilize eggs which grow into stem cells. That's what my Bio teaches me so... I think depending on your definition of babies, you are.
|Posted by: treacherous Mar 10 2009, 10:04 PM|
How do you know that?
Surfer could probably get Shooter or TOAF over here, but they wouldn't stay long. Not unless they were promised another admin war against Nesh.
|Posted by: Jailer411 Mar 11 2009, 12:34 AM|
I try to keep myself from posting things like that. Questions start to come up.
|Posted by: Darkender Mar 11 2009, 01:02 AM|
|Posted by: granobulax Mar 11 2009, 01:03 AM|
Yes, yes they do...
Anyways, I had yet another clinical day today. I was able to do some good patient teaching and refine some of my paperwork. Boring, yet necessary.
|Posted by: granobulax Mar 12 2009, 12:48 AM|
| Take a look at the 3x5 notecard I made for my microbiology test. Keep in mind that I compressed all of this into font 3.5 and brought a magnifying glass to class with me to read.
Ch 11 Mutation A mutation is a heritable change in the base sequence of that genome. Genetic alterations can also be brought about by recombination, the physical exchange of DNA between genetic elements. Entire genes, sets of genes, or even larger segments of DNA can be transferred between chromosomes or other genetic elements. Prokaryotes don¡¦t reproduce sexually so they possess mechanisms of lateral genetic exchange that allow for both gene transfer and recombination. They employ a genetic mark to any gene whose presence is monitored during a genetics experiment. Induced mutation: natural mutation. Aleletarias mutation: harmful/ majority of mutations. Uncommon positive mutations. Genotype: changed but not expressed. Phenotype: Changed and expressed. Wild type strain: A strain isolated from nature. Changes are from wild type. Cystic fibrosis = common = 1 amino acid is incorrect. Selectable mutation confers a clear advantage on the mutant strain under certain environmental conditions, so the progeny of the mutant cell are able to outgrow and replace the parent. A good example of a selectable mutation is drug resistance: an antibiotic-resistant mutant can grow in the presence of antibiotic concentrations that inhibit or kill the parent and is thus selected for under these conditions. Selection is therefore an extremely powerful genetic tool, allowing the isolation of a single mutant from a population containing millions or even billions of parental organisms. Induced mutation:: are those that are made deliberately. Spontaneous mutation: Those that occur without human intervention. Can occur with contact with natural radiation (cosmic rays and so on) that alters the structure of bases in the DNA. Also, oxygen radicals can affect DNA structure by chemically modifying DNA. The bulk of spontaneous mutations result from errors in the pairing of bases during DNA replication. Point modifications: change only one base pair. They¡¦re caused by base-pair substitutions in the DNA or by the loss or gain of a single base pair. As is the case with all mutations, the phenotypic change that results from a point mutation depends on exactly there the mutation occurs in the gene, what the nucleotide change is, and what product the gene encodes. Missense mutation: The information ¡§sense¡¨ (precise sequence of amino acids) in the ensuing polypeptide has changed. Changes in the first or second base of the triplet more often lead to significant changes in the polypeptide. For instance, a single-vase change from UAC to AAC results in an amino acid change within the polypeptide from tyrosine to asparagines at the specific site. TAC/ATG could be AAC/TTG „³ AAC Asparagine codon „³ faulty protein; Missence mutation, TAG/ATC „³ UAG Stop codon „³ incomplete protein; Nonsense mutation, TAT/ATA „³ UAU Tyrosine codon „³ Normal protein; Silent mutation, or TAC/ATG „³ Tyrosine codon „³ Normal protein; Wild type. Nonsense mutations: Results in premature termination of translation, leading to an incomplete polypeptide that would almost certainly not be functional. Frameshift; Insertion adds a base in a codon to shift the code sequence in a gene. Deletion simply takes a base away, effectively shifting the sequence in similar fashion. Spontaneous mutations are from DNA replication. Mutation rate in RNA genomes is about 1,000-fold higher than in DNA genomes. UV radiation = non-ionizing. X-ray and gamma = penetrating radiation (high energy). Transformation: a genetic transfer process by which free DNA is incorporated into a recipient cell and brings about genetic change. Competent bacteria can pick up dead bacteria. Mechanism of transformation in a gram-positive bacterium: a) Binding of double-stranded DNA by a membrane-bound DNA-binding protein. B Passage of one of the two strands into the cell while nuclease activity degrades the other strand. C) The single strand in the cell is bound by specific proteins, and recombination with homologous regions of the bacterial chromosome is mediated by RecA protein. D) Transformed cell. Transduction: A bacterial virus (bacteriophage) transfers DNA from one cell to another. Viruses can transfer host genes in two ways. In the first, called generalized transduction, DNA derived from virtually any portion of the host genome is [packaged inside the mature virion in place of the virus genome. Ch 15 Purple phototropic bacteria: Key genera: Chromatium, ectothiorhodospira, phrodobacter, phodospirillum. Carry out anoxygenic photosynthesis. Unlike cyanobacteria no O2 is released. Contain bacterioclorophylls and carotenoid pigments. These pigments give purple bacteria their purple, red and brown colors. Produce intracytoplasmic photosynthetic membrane systems. Purple sulfur bacteria: Utilize hydrogen sulfide (H2S) as an electron donor for CO2 reduction in photosynthesis. The sulfide is oxidized to elemental sulfur that is stored in globules inside the cells. Usually found in illuminated anoxic zones of lakes and other aquatic habitats where H2S accumulates and also in sulfur springs. Nitrifying Bacteria: Chemolithotropic bacteria are physiologically united by their ability to utilize inorganic electron donors as energy sources gaining energy from the process. Many are also capable of autotrophic growth and share a major physiological trait with phototrophic bacteria and cyanobacteria. Nobody oxidizes both ammonia and nitrates. Nitrifying bacteria are widespread in soil and water. They live in habitats where considerable amounts of ammonia are present such as decomposition and sewage treatment facilities or lakes and streams where sewage dumps into the water. Sulfur andiron-oxidizing bacteria: Able to grow chemolithotrophically on reduced sulfer compounds. Two classes; living at neutral pH and acidic pH. Some grow chemolithotrophically using ferrous iron as an electron donor. Some are acidophilic. Hydrogen Oxidizing bacteria: Grow with H2 as sole electron donor and O2 as electron acceptor using ¡§knallgas¡¨ reaction, the reduction of O2 with H2 as their energy metabolism. Makes water. Most can grow autotrophically using reactions of the Calvin cycle to incorporate CO2. Grow best under microoxic conditions because hydrogenases are typically oxygen sensitive. Nickel must be present in medium because all hydrogenases contain Ni2 as key metal cofactor. Some can grow on carbon monoxide as electron donor. Cooxidizing bacteria called carboxydotrophic bacteria grow autotrophically using the Calvin cycle. CO2 consumption by carboxydotrophic bacteria in nature is a significant ecological process to reduce CO2 in atmosphere. Methanotrophs and Methylotrophs Methane is found in anoxic muds, marches, anoxic zones of lakes, the rumen, and the mammalian intestinal tract. Utilize methane as electron donors. All aerobes available in soil and water. 2 step breakdown process. Common in decomposition one carbon compounds. Widespread in aquatic and terrestrial environments. Methanotrophs are often concentrated in a narrow band at the zone where methane and oxygen meet. Methanotrophs and nitrosifying bacteria: Methanotrophs are able to oxidize ammonia although they cannot grow chemolithotrophically using ammonia as sole electron donor. In addition to methane oxidation, methane monooxytenase also functions to oxidize ammonia. Ammonia is generally toxic to methanotrophs and the preferred nitrogen source is nitrate. Methanotrophic bacteria and certain marine mussels and sponges develop symbiotic relationships. Some marine mussels live in the vicinity of hydrocarbon seeps on the seafloor, places where methane is released in substantial amounts. Isolated mussel gill tissues consume methane at high rates in the presence of O2. The symbionts are bound in vacuoles within animal cells near the gill surface, which probably ensures an effective gas exchange with seawater. Pseudomonas and Pseudomonads: Straight or slightly curved chemoorganotrophic aerobic rods with polar flagella. A plant pathogen that is responsible for a number of necrotic plant lesions and that is characterized by its yellow colored pigments. Characteristics of pseudomonads: very simple nutritional requirements. Striking properties of pseudomonads is their use many different organic compounds as carbon and energy sources. Utilize over 100 different compounds and only a few species utilize fewer than 20. Straight or curved rods but not vibroid; size 0.5-1.0 u.m. by 1.5-4.0 u.m. no spores; gram negative; polar flagella- single or multiple; no sheaths, appendages, or buds; respiratory metabolism, never fermentative, although may produce small amounts of acid from glucose aerobically; use low-molecular weight organic compounds, not polymers; some are chemolithotrophic, using H2 or CO as sole electron donor; some can use nitrate as electron acceptor anaerobically; some can use arginine as energy source anaerobically. Ecologically important organisms in soil and water and are probably responsible for the degradation of many soluble compounds derived from the breakdown of plant and animal materials in oxic habitats. They are also capable of breaking down many xenobiotic (not naturally occurring) compounds, such as pesticides and other toxic chemicals and are thus important agents of bioremediation in the environment. Most pseudomonads metabolize glucose. A number of pseudomonads are pathogenic. Frequently associated with infections of the urinary and respiratory tracts in humans. The organism is an opportunist, initiating infections in individuals whose resistance is low. It can also cause systemic infections, usually in individuals who have experienced extensive skin damage. Other pseudomonads are also human pathogens. Can infect the lungs of patients with cystic fibrosis. Naturally resistant to many widely used antibiotics. Free-living aerobic nitrogen-fixing bacteria: A variety of organisms inhabit soil and are capable of living N2 aerobically. The genus Azotobacter comprises large, gram-negative, obligately aerobic rods capable of fixing N2 nonsymbiotically. Phylogenetically, most free-living nitrogen-fixing bacteria. Azotobacter is able to grow on many different carbohydrates, alcohols, and organic acids. The metabolism of carbon compounds is strictly oxidative, and acids or other fermentation products are rarely produced. All members fix nitrogen but can also grow on simple forms of combined nitrogen; ammonia, urea, and nitrate. Azotobacter can form resting structures called cysts show negligible endogenous respiration and are resistant to desiccation, mechanical disintegration, and ultraviolet and ionizing radiation. Cysts are not especially heat-resistant, and they are not completely dormant because they rapidly oxidize carbon sources if supplied. Enteric bacteria: Comprise a relatively homo generous phylognetic group within the Gammaproteobacteria and consist of facultatively aerobic, gram-negative, nonsporulating rods that are either nonmotile or motile by peritrichous flagella. Enteric bacteria are also oxidase-negative, have relatively simple nutritional requirements, and ferment sugars to a variety of end products. Many species pathogenic to humans, other animals, or plants, as well as other species of industrial importance. Fermentation patterns in Enteric Bacteria: One important taxonomic characteristic separating the various genera of enteric bacteria is the type and proportion of fermentation products produced by anaerobic fermentation of glucose. Salmonella and Escherichia are quite closely related, the two genera. In contrast to most Escherichia, members of the genus Salmonella are usually pathogenic, either to humans or to other warm-blooded animals. Most common diseases caused by salmonellas are typhoid fever and gastroenteritis. Shigellas are also genetically very closely related to Escherichia. Tests for DNA hybridization show that strains of Shigella have 70% or even higher genomic hybridization with E. coli and therefore probably form a single species. Shigella is commonly pathogenic to humans, causing a rather severe gastroenteritis. Shigella dysenteriae is transmitted by food and waterborne routes and is capable of invading intestinal epithelial cells. Proteus is characterized by rapid motility. Frequent cause of urinary tract infections in humans and probably benefits in this regard from its ready ability to degrade urea. Bibrio, Aliivibrio, and Photobacterium: The Vibrio group, family Vibrionaceae, contains gram-negative facultatevely aerobic rods and curved rods that possess a fermentative metabolism. Most vibrios and related bacteria are aquatic, found in marine, brackish, or freshwater habitats. Vibrio cholera is the specific cause of the disease cholera in humans. The organism does not normally cause disease in other hosts. Cholera is one of the most common infectious human diseases in underdeveloped countries. Transmitted almost exclusively via water. Bacterial Bioluminescence, several species of bacteria can emit light. Rickettsias: Are small, gram-negative, coccoid or rod-shaped proteobacteria. They are, with one exception, obligate intracellular parasites and have not yet been cultivate in the absence of host cells. Rickettsias are the causative agents of several human diseases, including typhus (any one of several similar diseases caused by louseborne bacteria), rocky mountain spotted fever, and Q fever. Metabolism and Pathogenesis: They can oxidize only glutamate or glutamine and cannot oxidize glucose or organic acids. Able to synthesize at least some of the small molecules needed for macromolecular synthesis and growth, and they obtain the rest of their nutrients from the host cell. Do not survive long outside their hosts. They must be transmitted from animal to animal by arthropod vectors. Can also be transmitted to the respiratory system by aerosols. C. burnetti is the most resistant of the rickettsias to physicals damage, probably because it produces a resistant, sporelike form. Spirilla are gram-negative, motile, spiral-shaped Proteobacteria that show a wide variety of physiological attributes. Some of the key taxonomic criteria used are cell shape, sixe, number of polar flagellation (single or multiple), relation to oxygen (obligatley aerobic, microaerophilic, facultative), relationship to plans (as symbionts or plant pathogens) or animals (as pathogens), fermentative ability, and certain other physiological characteristics (for example, nitrogen-fixing ability, halophilic nature, thermophilic nature). Magnetic spirilla: highly motile microaeropilic magnetic spirilla have been isolated form freshwater habitats. Within the cells are chains of 5-40 magnetic particles called magnetosomes. Sulfate- and Sulfur- Reducing Proteobacteria: Sulfate and sulfur are electron acceptors for a large group of anaerobic Deltaproteobacteria that utilize organic compounds or H2 as electron donors. Hydrogen sulfide is the product of both sulfate and sulfur reduction. Over 40 genera of these organisms, collectively called the dissimilative sulfate-reducing bacteria and sulfur-reducing bacteria. Use of sulfate or sulfur as electron acceptors in energy generation instead of their assimilation as biosynthetic sources of sulfur. General properties: Utilize lactate, pyruvate, ethanol, or certain fatty acids as electron donors, reducing sulfate to hydrogen sulfide; they are unable to catablolize acetate. Specialize in the oxidation of fatty acids, particularly acetate, reducing sulfate to sulfide. Obligate anaerobes, and strict anoxic techniques must be used in their cultivation. Widespread in aquatic and terrestrial environments that become anoxic as a result of microbial decomposition process. Phylogenetically a member of the gram-positive Bacteria, consists of endospore-forming rods found primarily in soil. Growth and reduction of sulfate by Desulfotomaculum in certain canned foods leads to a type of spoilage called sulfide stinker. The Eplilonproteobacteria, the fifth class of proteobacteria, was initially defined by certain pathogenic bacteria, in particular Campylobacter and Helicobacter. However, environmental studies of marine and terrestrial habitats have shown that a diversity of Epsilonproteobacteria can be found in a variety of habitats in nature, where their numbers and metabolic capabilities suggest they play important ecological roles. Are especially abundant at oxic-anoxic interfaces in sulfur-rich environments, such as around hydrothermal vents, where they catalyze metabolic transformations of sulfur and lice in association with animals that live in these vent areas. Many of these bacteria are autotrophs and use H2, formate, asulfide, or thiosulphate as electron donor, with nitrite, oxygen, or elemental sulfur as electron acceptor, depending on the species. Campylobacter and Helicobacter: Although they represent separate families in this class, campylobacteraceae and Helicobacteraceae, they share a number of characteristics. They are all gram-negative, motile spirilla, and most species are pathogenic to humans or other animals. Campylobacter and Helicobacter species are also microaeropilic an are therefore cultured from clinical specimens in media incubated at low O2 and high CO2. Campylobacter species, over a dozen of which have been described, cause acute enteritis leading to (usually) bloody diarrhea, and pathogenesis is due to several factors, including an enterotoxin that is related to cholera toxin. Helicobacter pylori, also a pathogen, causes both chronic and acute gastritis, leading to the formation of peptic ulcers. Ch 16 Nonsporulating Gram-positive Bacteria: Called the Firmicutes and is composed of the lactic acid bacteria, which are classical nonsporulating gram-positive rods and cocci. Staphylococcus and Micrococcus: Both aerobic organisms with a typical respiratory metabolism. They are catalase-positive. Relatively resistant to reduced water potential and tolerate drying and high salt fairly well. Many species are pigmented. Micrococcus is and obligate aerobe and produces acid from glucose only under aerobic conditions, whereas Staphylococcus is a facultative aerobe and produces acid from glucose both aerobically and anaerobically, Staphylococcus also typically forms cell clusters. Staph are common commensals and parasites of humans and animals, and they occasionally cause serious infections. In humans, there are two major species, Staphylococcus epidermidis, a nonpigmented, nonpathogenic organism usually found on the skin or mucous membranes, and Staphylococcus aureus, a yellow pigmented species that is most commonly associated with pathological conditions, including boils, pimples, pneumonia, osteomyelitis, meningitis, and arthritis. The lactic acid Bacteria are gram-positive rods and cocci that produce lactic acid as a major or sole fermentation product. Members of this group lack porphyrins and cytochromes, do not carry out oxidative phosphorylation, and hence obtain energy only by substrate level phosphorylation. Grow anaerobically. Not sensitive to O2 and can grow in its presence. Thus called aerotolerant anaerobes. Obtain energy only from the metabolism of sugars. Limited biosynthetic abilities. Complex nutritional requirements include needs for amino acids, vitamins, purines, and pyrimidines. Streptococcus and other Cocci: quite distinct habitats and activities. Some species are pathogenic to humans and animals. Important roles in the production of buttermilk, silage, and other fermented products. Two genera are recognized. The genus Lactococcus contains those streptococci of dairy significance, whereas the genus Enterococcus includes streptococci that are primary of fecal origin. Lactobacillus: Rod-shaped, varying from long and slender to short, bent rods. Most species are homofermentative, but some are heterofermentative. Common in dairy products, and some strains are used in the preparation fo fermented milk products. Acidophilus mild, yogurt, sauerkraut, silage and pickles. More resistant to acidic conditions that are the other lactic acid bacteria. Able to grow well at pH values as low as 4. Acid resistance enables them to continue growing during natural lactic fermentations, even when the pH value has dropped too low for other lactic acid bacteria to grow. Responsible for the final stages of most lactic acid fermentations. They are rarely, ff ever, pathogenic. Listeria: requires microoxic or fully oxic conditions for growth and produces catalase. Causes a foodborne illness. Transmitted in contaminated, usually read-to-eat, foods. Can cause anything from a mild illness to a fatal form of meningitis. Endospore-forming Gram-Positive Bacteria: Bacillus, species of which are aerobic or facultatively aerobic. Bacillus: produce extracellular hydrolytic enzymes. Produce antibiotics, including bacitracin, polymyxin, tyroxidin, gramicidin, and circulin. Antibiotics are released during sporulation. Produce insect larvicides. Causes a fetal condition called milky disease in Japanese beetle larvae and larvae of closely related beetles. Causes a fatal disease of larvae of many different groups of insects, although individual strains are specific as to the host affected. Endospore preparations derived are commercially available as biological insecticides. Clostridium: lack a respiratory chain. Obtain ATP only by substrate level phosphorylation. Many anaerobic energy yielding mechanisms are known. Separation of the genus into subgroups is based primarily on these properties and on the fermentable substrate used. Main habitat is soil, where they live primarily in anoxic ¡§pockets,¡¨ made anoxic by facultative organisms metabolizing organic compounds. Inhabit the anoxic environment of the mammalian intestinal tract. Capable of causing severe disease in humans under specialized conditions. Both sugar and amino acid fermenters. Produce specific toxins or in those causing gas gangrene, a group of toxins. Can also cause gastroenteritis in humans and domestic animals. A major unsolved ecological problem is what role these extremely powerful toxins play in soil, the natural habitat of the organism. Cell Wall-less Gram-positive Bacteria: the Mycoplamas: they lack cell walls and are one of the smallest organisms capable of autonomous growth. Properties of Mycoplasmas: more resistant to osmotic lysis. Able to survive conditions under which protoplasts lyse. The presence of sterols. Plasmic membranes of mycoplasmas more stable than that of other bacteria. Growth of Mycoplasmas: Cells are small and pleomorphic. Small coccoid elements, larger, swollen forms, and filamentous forms of variable lengths, often highly branched. The minimum reproductive unit of 0.2-0.3 um probably represents the smallest free-living cell. The genomes of mycoplasmas are also smaller than those of most bacteria, between 500 and 1,100 kbp of DNA in most cases. This is comparable to the genome size of the obligately parasitic Chlamydia and rickettsia and about one-fifth or one-fourth that of Escherichia coli. Corynebacteria: Gram-positive, aerobic, non-motile, rod-shaped. Forming irregular-shaped, club-shaped, or V-shaped cell arrangements during normal growth. V-shaped cell groups arise as a result o snapping division. The genus Corynebacterium consists of an extremely diverse group of bacteria, including animal and plant pathogens and saprophytes. Some species are pathogenic. Characteristics of Mycobacteria: Somewhat pleomorphic and may undergo branching or filamentous growth. Become fragmented into rods or coccoid elements upon slight disturbance. Can be separated into two major groups, slow growers and fast growers. Form tight, compact, often wrinkled colonies. Hydrophobic nature of the cell surface that make cells stick together. Simple nutritional requirements. Growth in cords reflects the presence of a characteristic glycolipid, the cord factor, on the cell surface. Filamentous Actinobacteria: Streptomyces and relatives- Filamentous, gram-positive Bacteria that form branching filaments. Form spores. Spore-forming habit is of both phylogenetic and taxonomic importance. Over 500 species of Streptomyces are recognized. Are of indefinite length and often lack cross-walls in the vegetative phase. Grow at the tips of the filaments. Vegetative phase consists of complex, tightly woven matrix. As colony ages, sporophores are formed, which project above the surface of the colony and give rise to spores. Differences in the shape and arrangement of aerial filaments are used in classifying the streptomyces species. Ecology and isolation of streptomyces: a few can be found in aquatic habitats, mostly in soil. Earthy odor caused by metabolites called geosmins. Alkaline to neutral soils are favorable over acid soils. More are found in well drained soil such as sandy loams or soils covering limestone where conditions are more likely to be aerobic. Antibiotics of streptomyces: Adjacent colonies of other bacteria show zones of inhibition on agar plates. Over 500 distinct antibiotics made. Many genes are required to encode the enzymes for antibiotic synthesis. The genomes of streptomyces are quite large. Cyanobacteria and prochlorophytes: Cyanobacteria comprise a large morphologically and ecologically heterogeneous group of phototrophic bacteria. Are oxygenic phototrophs. Represent one of the major phyla of bacteria. Shows a distinct relationship to gram-positive bacteria. First oxygen evolving phototrophic organisms on earth. Responsible for the conversion of the atmosphere of the earth fro anoxic to oxic. Structure: Both unicellular and filamentous forms are known. Can be divided into five morphological groups; unicellular, dividing by binary fission. Unicellular, deciding by multiple fission. Filamentous, containing differentiated cells that function in nitrogen fixation. Filamentous nonheterocystous forms, and branching filamentous species. Cell wall similar to gram-negative bacteria and peptidoglycan is present in the walls. Many produce sheaths that bind groups together. The photosynthetic membrane system is complex and multilayered. All have phycobilins accessory pigments in photosynthesis. Can produce a blue-green color or red and brown.. Structural variations; gas vesicles and heterocysts- Common in species that live in open waters. The function of gas vesicles is to regulate cell buoyancy to remain in optimum photosynthesis. Some form heterocysts which are rounded and usually enlarged cells distributed regularly along a filament. Heterocysts arise from differentiation of vegetative cells . Sole sites of nitrogen fixation in heterocystous cyanobacteria. Heterocysts have intercellular connections with adjacent vegative cells to heterocysts. Lack photosystem II. Fixed carbon imported to the heterocysts for an adjacent vegetative cell solves the problem. Surrounded by a thickened cell wall. Contains large amounts of glycolipid. Maintains an anoxic environment. Ecology: Widely distributed in terrestrial, freshwater, and marine habitats. More tolerant of environmental extremes. Often the dominant or sole oxygenic phototrophic organisms in hot springs, saline lakes, and other extreme environments. Found on the surfaces of rocks or soil and occasionally even within rocks. Desert soils they form extensive crusts during most of the year and growing during the winter and spring rains. Shallow marine bays where warm seawater temperatures they create mats of considerable thickness. Freshwater lakes they develop blooms. Chlamydia: obligatetly parasitic bacteria with poor metabolic capacities. Chlamydophila psittaci, the causative agent of the disease psittacosis. Chlamydia trachomatis, the causative agent of trachoma. Chlamydophila pneumonia, the cause of respiratory syndromes. Molecular and metabolic properties: Chlamydias are intriguing because of the biological, evolutionary and metabolic problems they pose. Gram-negative-type cell walls, have both DNA and RNA. Dividing by binary fission. Biosynthetic capacities of the chlamydias are much more limited than even the rickettsias. Green sulfur bacteria are a phylognetically distinct group of nonmotile anoxygenic phototrophic bacteria that contain only obligately anaerobic and phototrophic species among cultured isolates. Morphologically restricted and includes short to long rods. Spirochetes are gram-negative, motile, tightly coiled bacteria. Slender and flexuous in shape. Morphologically unique. Widespread in aquatic environments and in animals. Some cause diseases, including syphilis. Made up of a protoplasmic cylinder, consisting of the regions enclosed by the cell wall and cytoplasmic membrane. Motility is conferred by single to many flagella the emerge from each pose. Flagella fold back from each pole on to the protoplasmic cylinder and remain located in the periplasm of the cell. Have also been called endoflagella. Surrounded by a multilayered but flexible membrane called the outer sheath. Motility: endoflagellum anchored at one end and extends about two-thirds of the length of the cell. The protoplasmic cylinder rotates in the opposite direction, placing torsion on the cell. Move by flexing or lashing motions due to torque exerted at the ends of the protoplasmic cylinder. Treponema: anaerobic host-associated spirochetes. Treponoma pallidum, the causal agent of syphilis is the best known species of Treponema. It differs in morphology form other spirochetes as it¡¦s flat and wavy. T. pallidum cell is remarkably thin. T. pallidum appears restricted to humans. Are microaerophiles. Treponema denticola is a major oral treponeme, ferments amino acids. Borrelia: majority of Borrelia are animal or human pathogens. Borrelia reurrentis is the causative agent of relapsing fever in humans, transmitted via an insect vector by the human body louse. Sensitive to tetracycline. Other species case diseases in cattle, sheep, horses, and birds. Most transmitted by ticks. Borrelia burgdorferi is the causative agent, tickborne disease called Lyme disease. B burgdorferi, one of the few known bacteria the has a linear chromosome. Leptospira and leptonema: strictly aerobic spirochetes that use long chain fatty acids as electron donor and carbon sources. Only substrates utilized by leptospiras for growth. Leptospira cells is thin, finely coiled, and usually bent at each end into a semicircular hook. Major species are Leptospira interrogans and Leptospira biflexa. L. interrigans are parasitic for humans and animals. In humans the most common leptospiral syndrome is leptosirosis. Leptospiras ordinarily enter the body through the mucous membranes or through breaks in the skin. Ch 17 Phylogenetic overview of archaea: A phylogenetic tree of Archaea based on sequence of 16S rRNA genes, reveals a major evolutionary split of Archaea into two groups. The Crenarchaeota and the Euryarchaeota. Crenarchaeota: contain mostly hyperthermophiles whose growth temperature optimum is greater than 80 degrees C ¡V including those able to grow at the highest temperatures of all known organisms. Several nonthermophilic a. Many hyperthermophiles are chemolithotrophic autotrophs. Are the sole primary producers in these habitats. Crenarchaeota tend to cluster closely together. Cold dwelling relatives have been identified by community analysis of rRNA genes. Euryarchaeota: Physiologically diverse group. Many inhabit extreme environments of one kind or the other. Includes methanogens and several extremely halophilic archaea, the ¡§halobacteria¡¨. Methanogens are the strictest of anaerobes while extreme halophile are obligate aerobes. Other groups include hyperthermophiles Thermococcus and Pyrococcus and the methanogen Methanopyrus and the cell wall-less Thermoplasma (similar to mycoplasmas). A large group yet uncultured euryarchaeotes exists in the marine environment. Many euryarchaeotes inhabit freshwater and terrestrial habitats. Energy conservation and autotrophy in Archaea: Energy metabolism in methanogens is unlike that of any other microbial group. Chemoorganotrophy and chemolithotrophy in Archaea: Several Archaea are chemoorganotrophic and thus use organic compounds as electron donors for energy metabolism. Catabolism of glucose in Archaea proceeds via slight modifications of Entner-Doudoroff or glycolytic pathways. Oxidation of acetate to CO2 in Archaea proceeds through the citric acid cycle or by the acetyl-CoA pathway. There are electron transport chains including cytochromes of the a, b, and c types in some archaea. Employing these and other electron carriers, chemoorganotrophic metabolism in most Archaea proceeds by introduction of electrons from organic electron donors into an electron transport chain, leading o the reduction of O2,S, or some other electron acceptor. Electron-transport reactions drive thy synthesis of a proton motive force that couples to ATP synthesis through membrane bound ATVases. Chemolithotrophy is also well established in the Archaea. Autotrophy in Archaea: Autotrophy is widespread in the Archaea and proceeds by several different pathways. Many of the catabolic and anabolic pathways in the Achaea are similar to those in bacteria. Extremely halophilic Archaea: sometimes called haloarchaea, are a diverse group of prokaryotes. Inhabits natural environments high in salt, such as solar salt evaporation ponds and salt lakes, or artificial saline habitats such as the surfaces of heavily salted foods. Salt habitats are called hypersaline. Extreme halophile is used to indicate that these organisms are not only halophilic, but that their requirements for salt is very high. Considered an extreme halophile if it requires at least 1.5 M NaCl for growth. Most require 2-4 M NaCl for optimal growth. Hypersaline environments: Chemistry and productivity: Extremely hypersaline habitats are rare. soda lakes are highly alkaline hypersaline environments. The diverse chemistries of hypersaline habitats has selected for a large diversity of halophilic microorganisms. Marine salterns are also habitats for extreme halophiles. Marine salterns are small, enclosed basins filled with seawater that are left to evaporate, yielding solar sea salt. Taxonomy and physiology: Stain gram-negatively, reproduce by binary fission, and do not form resting stages or spores. Most halobacteria are nonmotile. Plasmids from extreme halophiles are among the largest naturally occurring plasmids known and might actually be small chromosomes. Most species of extremely halophilic Archaea are obligate aerobes. Water balance in extreme Halophiles: Require large amounts of sodium for growth, typically supplied as Na Cl. Compatible solutes counteract the tendency of the cell to become dehydrated under conditions of high osmotic strength by placing the cell in positive water balance with its surroundings. Bacteriorhodopsin and light-mediated ATP synthesis in halobacteria: Certain species of haloarchaea can carry out a light driven synthesis of ATP. This occurs without chlorophyll pigments, so it is not photosynthesis. Other light-sensitive pigments are present, including red and orange carotenoids¡Xprimarily C50 pigments called bacterioruberins¡Xand inducible pigments involved in energy conservation. Methane producing Archaea: Methanogens- produce methane (CH4) as an integral part of their energy metabolism. Methane production is called methanogenesis. Diversity and physiology: Show a variety of morphologies. Taxonomy is based on both phenotypic and phylogenetic analyses, with several taxonomic orders being recognized. Substrates: Eleven substrates can be converted to methane by pure culture of methanogens. Do not include such common compounds as glucose and organic or fatty acids. Glucose can be converted to methane, but only in reactions in which methanogens and other anaerobic bacteria cooperate. With the right mixture of organisms, virtually any organic compound, even hydrocarbons, can be converted to methane plus CO2. Thermoplasmatales: a phylogenetically distinct line of Archaea contains thermophilic and extremely acidophilic genera: Thermoplasma, Ferroplasma, and Picrophilus. Among the most acidophilic of all known microorganisms with picrophilus being capable of growth even below pH 0. Archaea lacking cell walls: To survive the osmotic stresses of life without a cell wall and to withstand the dual environmental extremes of low pH and high temperature, Thermoplasma has evolved a unique cytoplasmic membrane structure. The membrane contains a lipopolysaccharide-like material called lipoglycan. This substance consists of a tetraether lipid monolayer membrane with mannose and glucose. Nanoarchaeum and aciduliprofundum: Nanoarchaeum equitans is one of the smallest cellular organisms with one of the smallest genomes of any cell, it lives as an obligate symbiont of the crenarchaeote Ignicoccus. They cannot grow in pure culture and replicate only when attached to the surface of Ignicoccus cells in the densities up to 10 or more cells per Ignicoccus cell. Whether Nanoarchaeum cells act as a parasite of it¡¦s host is not yet known. N. equitans and its host Ignicoccus were first isolated from a submarine hydrothermal vent off the coast of Iceland. The metabolism of Nanoarchaeum is not yet well understood but it appears to depend on its host for many of its metabolic functions; Ignicoccus is an autotroph that uses H2 as electron donor and S as electron acceptor. Habitats and energy metabolism of Crenarchaeota: Most hyperthermophilic archaea have been isolated from geothermally heated soils or waters containing elemental sulfur and sulfides and most species metabolize sulfur in one way or another. Mildly to extreme acidic owing to the production of sulfuric acid. Got sulfur rich environments called solfataras, are found throughout the world. Solfataras can be mildly acidic to slightly alkaline or extremely acidic with pH values below 1. Hyperthermophilic crenarchaeotes have been obtained from both acidic and alkaline environments, but the majority of these organisms inhabit neutral or mildly acidic hot habitats. Hyperthermophilic Crenarchaeota also inhabit hydrothermal vents. All hyperthermophiles with growth temperature optima above 100 degrees C have come from submarine sources. Deep hydrothermal vents are the hottest habitants so far known to yield prokaryotes. Energy metabolism: hyperthermophilic Crenarchaota are obligate anaerobes. Their energy-yielding metabolism is either chemoorganotrophic or chemolithotrophic and is dependent of diverse electron donors and acceptors, Fermentation sin rare, and most bioenergetic strategies involve anaerobic respirations. Electron transfer within the cytoplasmic membrane leading to the formation of a proton motive force from which ATP is made by way of proton translocating ATPases. Grow chemolithotrophically under anoxic conditions. Hyperthermophiles from terrestrial volcanic habitats: Terrestrial volcanic habitats can have temperatures are high as 100 degrees C and are thus suitable for hyperthermophilic archaea. Hyperthermophiles from submarine volcanic habitats: We now turn to the microbiology of submarine volcanic habitats, homes to the most thermophilic of all known Archaea. Nonthermophilic Crenarchaeota: have been identified from community sampling of SSU rRNA genes from many cool or cold marine and terrestrial environments. Microbiologists have found crenarchaeotes in oxic marine waters worldwide. Marine crenarchaeotes thrive even in frigid waters and sea ice, such as those near Antarctica. These organisms are planktonic and presents in significant numbers in waters that are both nutrient poor and very cold. Marine crenarchaeotes can account for up to 40% of the prokaryotes of deep ocean waters. They contain ether-linked lipids, the hallmark of the Archaea. Crenarchaeota play a major role in the global carbon cycle. Nonthermophilic species of Euryarchaeota are also present in marine environments. Nitrification in archaea: a crenarchaeota named Nirosopumilus maritimus was isolated from a saltwater aquarium and shown to grow chemolithotrophically by aerobically oxidizing ammonia to nitrate, the first demonstration of nitrification in Archaea. Stability of Monomers: at temperatures as low as 120 degrees C, some important small molecules are destroyed at significant rates. ATP and NAD hydrolyse rapidly at these temperatures; the half-life of ATP or NAD in vitro is less than 30 minutes at 120 degrees C and shortens dramatically at temperatures above this. The high concentrations of cytoplasmic solutes, such as salts, sugars, and other small molecules, likely have a protective effect on ATP and other key molecules. More heat-stable molecules might replace the function of certain of these compounds. Protein folding and thermostability: Most proteins denature at high temperatures. For increased levels of amino acids that form alpha helices, which may help stabilize these proteins. Enzymes from hyperthermophiles contain the same major structural features; as their heat labile counterparts form mesophilic bacteria. Thermostable proteins typically do display some structural features that improve their thermostability. These include highly hydrophobic cores, which decrease the tendency of the protein to unfold in an ionic environment. More ionic interactions on the protein surfaces, which also help hold the proteins together and work against unfolding. It is the folding of the protein that most affects its heat stability and noncovalent, ionic bonds called salt bridges on a proteins surface likely play a major role in maintaining the biologically active structure. Chaperonins: assisting proteins to remain in their native state- chaperonins function to refold partially denatured proteins. Hyperthermophilic Archaea produce special classes of chaperonins that function only at the highest growth temperatures. In cells of Pyrodictium abyssi, a major chaperonin is the protein complex called thermosome. This complex is thought to keep the cells other proteins properly folded and functional at high temperature and help cells survive. DNA Stability at high temperatures: solutes and reverse gyrase- One mechanism increases cellular solute levels, as ions, particularly potassium, and compatible organic solutes affect DNA stability. The cytoplasm of the hyperthermophilic methanogen Methanopyrus contains molar levels of potassium cyclic 2,3-diphosphoglycerate. This solute prevents chemical damage to DNA, such as depurination of depyrimidization from high temperatures. These chemical changes can lead to mutation. Potassium di-myo-mositrol phosphate that protect against osmotic stress. A unique protein found only in hyperthermophiles is the reverse DNA gyrase. Reverse gyrase introduces positive supercoils into DNA. Positive supercoiling stabilizes DNA to heat and thereby prevents the DNA helix from denaturing. DNA stability: DNA binding proteins- a small heat stable DNA-binding protein present in cells of Sulfolobus binds to the minor groove of DNA in a nonspecific manner and increases its melting temperature by some 40 degrees C. This protein called Sac7d, sharply kinks the DNA and thus may also be involved in gene regulation. Lipid stability: Virtually all hyperthermophilic Archaea synthesize lipids of the dibiphytanyl tetraether type. dibiphytanyl tetraether lipids are naturally head resistant because the covalent bond between phytanyl units forms a lipid monolayer membrane structure instead of the normal lipid bilayer. This structure, supported by covalent bonds, resists the tendency of heat to pull apart a lipid bilayer constructed of fatty acids.
|Posted by: Pseudonym Mar 12 2009, 12:56 AM|
|Impressive. How were your hands after writing that?|
|Posted by: granobulax Mar 12 2009, 01:00 AM|
They were fine. It took me the better part of three days to look up the information and type it out. Whew, I'm glad that's over.
|Posted by: Leo Sanders Mar 12 2009, 01:58 AM|
|I would be like screw that Im going home...|
|Posted by: granobulax Mar 12 2009, 02:20 AM|
It's what ya got to do when you go to college.
|Posted by: treacherous Mar 12 2009, 03:34 PM|
That's nothing like what I did in college. Nothing at all.
|Posted by: granobulax Mar 12 2009, 04:18 PM|
What did you do in college?
|Posted by: Solomon Mar 12 2009, 07:11 PM|
| I'll give you a hint:
|Posted by: treacherous Mar 12 2009, 08:10 PM|
|Posted by: Solomon Mar 12 2009, 08:59 PM|
|Posted by: granobulax Mar 12 2009, 09:00 PM|
|I hear ya. I've been in college three years now and with my wife for two years if ya catch my drift.|
|Posted by: Jailer411 Mar 12 2009, 09:02 PM|
|Posted by: granobulax Mar 12 2009, 09:45 PM|
| So, I go to lab tomorrow to check off on phlebotomy, IV insertion, hep lock, solution change, IV dressing change, and central line catheter care.
Wish me luck!
|Posted by: treacherous Mar 12 2009, 09:45 PM|
Took him a minute.
|Posted by: granobulax Mar 12 2009, 09:46 PM|
|Posted by: Bloody_Freak Mar 27 2009, 11:26 AM|
|Why doesn't the drug Percocet work for me in the slightest? Figured you might be able to help....|
|Posted by: granobulax Mar 27 2009, 06:40 PM|
One of the side effects of percocet is tolorance. You may be tolorant to the medication. You should notify your physician and possibly get a non-opioid analgesic.
You see, most narcotics will bind to opiate receptors in the central nervous system. That process may not work correctly with you.
Hope that helps!
|Posted by: Bloody_Freak Mar 27 2009, 09:32 PM|
Ya, I took three of them like three-four hours ago and I still haven't had an effect...
Thanks for the help man.
|Posted by: granobulax Mar 27 2009, 09:42 PM|
What dosage do you take?
|Posted by: Bloody_Freak Mar 27 2009, 09:53 PM|
Huh? I dunno...
|Posted by: Solomon Mar 27 2009, 10:13 PM|
| I remember I used to get real bad migraines as a kid. My parents would have to take me to the hospital, and they'd inject me with all sorts of drugs. There was one where I became very irritable. I'd been fine and then the next minute I'd just start yelling and cussing everybody.
Doctor: How are you feeling?
Me: F*** you! My head hurts what the hell kinda doctor are you?! Asking me how I feel? I think you to shut the f*** up and actually do something!
... They never gave me that again.
|Posted by: granobulax Mar 27 2009, 10:47 PM|
It was probably Ritalin
|Posted by: Solomon Mar 27 2009, 10:49 PM|
Maybe. See what you get to do after med school grano?! It'll be great.
|Posted by: granobulax Mar 27 2009, 10:56 PM|
There's no way I'm doing Pediatrics.
|Posted by: Solomon Mar 27 2009, 11:10 PM|
| Just imagine a grown adult like that.
Maybe I should come visit you, and repay you for all those hugs.
|Posted by: Bloody_Freak Mar 28 2009, 12:24 AM|
OMG! I said the almost exact same thing when they took me to the hospital the first time I dislocated my knee. xD
|Posted by: granobulax Mar 28 2009, 12:56 AM|
|Posted by: Solomon Mar 28 2009, 03:30 PM|
Hey man, I know exactly how you feel.
|Posted by: Darkender Mar 28 2009, 04:41 PM|
|What a shame. Some people are just so angry inside...|
|Posted by: treacherous Mar 28 2009, 04:59 PM|
Solomon is an angry little man trapped in an unknown aged man's body.
|Posted by: Pseudonym Mar 28 2009, 05:12 PM|
|Posted by: Solomon Mar 28 2009, 08:59 PM|
That pretty much sums it up.
|Posted by: granobulax Mar 31 2009, 03:14 AM|
| Well, here's this semester's care plan I had to do for my Nursing II class. It kinda gives an Idea of the stuff I have to do. The patients name has been omitted for privacy and legal issues. If anyone bothers to read some of it, you'll learn what's entailed in being a nurse.
MOHAVE COMMUNITY COLLEGE
NURSING CARE PLAN
Clinical date for care plan: 3/10/2009
Student: Granobulax S.N. MCC
A. ADMISSION DATA
Date of admission: 2/19/2009
Medical diagnosis: Acute Respiratory Distress
Age: 63 (Client appears older than stated age) Sex: Male Marital Status: Divorced in 1990
Ethnicity: Caucasian Religion: Nondenominational
Physician Specialty: Internal Medicine
Vital signs upon admission:
B/P: 80/54 P: 65 R: 16 T: 98.0 Ht: 5’10” Wt: 86.5 Kg (192 lbs)
Allergies: No known allergies
B. HEALTH-ILLNESS TRANSITION
History of present illness: History of COPD. No previous experiences with ARDS. Pneumonia suspected but not confirmed. Client states, “I’ve been pretty healthy all my life. Only in this last year have I had any major problems.” Client also stated, “There was no ‘attack’, just a gradual decline in my breathing. It started just over a year ago when my breathing just got worse and worse. I finally had to come in to the hospital because I couldn’t take it any more.” (Client data)
Significant client health history (include family history): The client has a history of hyperkalemia, pneumonia, chronic obstructive pulmonary disease, hypertension, deep vein thrombosis, and post traumatic stress disorder (Chart data). Client states, “My father committed suicide, my sister committed suicide, and my mother died of Alzheimer’s disease.” There is noted occurrence of admitting diagnosis within family history, however possible psychological damage associated with traumatic family deaths noted (Client data).
Pathophysiology of primary diagnosis (definition, etiology, signs and
symptoms. Underline behavior exhibited by this client. Cite reference.)
Acute Respiratory Distress Syndrome: The basic changes in the lungs result from injury to the alveolar wall and capillary membrane, leading to release of chemical mediators, increased permeability of alveolar capillary membranes, increased fluid and protein in the interstitial area and alveoli, and damage to the surfactant-producing cells. These events result in decreased diffusion of oxygen, reduced blood flow to the lungs, difficulty in expanding the lungs, and diffuse atelectasis. Reductions in tidal volume and vital capacity occur. Damage to lung tissue progresses as increased numbers of neutrophils migrate to the lungs, releasing proteases and other mediators. Hyaline membranes form from protein-rich fluid in the alveoli, and platelet aggregation and micro thrombi develop in the pulmonary circulation, causing stiffness and decreased compliance. If the patient survives, diffuse necrosis and fibrosis are apparent throughout the lungs.
Excess fluid in the lungs predisposes to pneumonia as a complication. Congestive heart failure may develop.
Etiology: Severe or prolonged shock may cause ARDS because of ischemic damage to the lung tissue. Inflammation in the lungs arises directly from such events as inhalation of toxic chemicals or smoke; excessive oxygen concentration in inspired air; severe viral infections in the lungs; toxins from systemic infection, particularly by gram-negative organisms; fat emboli; explosions; aspiration of highly acidic gastric contents; or long trauma. Other causes include disseminated intravascular coagulation, cancer, acute pancreatitis, and uremia.
Signs and symptoms: Early signs may be masked by the effects of the primary problem. Onset is usually marked by dyspnea, restlessness, rapid, shallow respirations, and increased heart rate. Arterial blood has measurements indicate a significant decrease in PO2. As lung congestion increases, the accessory muscles are used, rales can be heard, productive cough with frothy sputum may be evident, and cyanosis and lethargy with confusion develop. A combination of respiratory and metabolic acidosis evolves as diffusion is impaired and anaerobic metabolism is required. (Gould, 2002, p. 414-415)
4. Holistic assessment
a. Physiological integrity
System Subjective Data Objective Data
Client states he has never experienced any problems with his heart or blood vessels. History of hyperkalemia with abnormal heart rhythms. Heart rate low normal upon admission and has maintained normal range cardiovascular function throughout hospital stay.
Client states he has episodes of panic and anxiety. He worries about what he eats and drinks for fear of increasing his cough. When he has difficulty breathing, he compares it to the feeling of drowning, where he cannot get air. Admitted with acute respiratory distress syndrome with possible pneumonia. Arterial blood gas levels indicate respiratory acidosis. Wheezing and crackles present with diminished lung sounds. Pulse oxemetry at 95% with O2 nasal canula at 3 L. O2 stats dropped to 89% upon exertion with O2 at three litters with nasal canula. Audible wheezes noted at time of exertion.
Client stated frustration with needing assistance to use the restroom. Client prefers the bedpan to needed assistance with ambulation to restroom. Clients bowel sounds present in all four quadrants. Previous bowel movement 3/9/2009
Client states no problems. Urine straw colored and clear. Odorless with lab results confirming no urinary tract infection. Specific gravity of 1.0150, within normal limits.
Client states no problems. Client sight assisted with the aid of glasses. Hears voices without asking to repeat. Has tactile use of hands as evidenced by client stating his lunch was hot upon touching food. No neuro/sensory dysfunction observed.
Client complains of weakness and fatigue. Client after transfer from bed to chair and again upon transfer from chair to bed, respirations were exaggerated as evidenced by respirations increased to 28 and shallow.
Client states reoccurring dull to sharp pain on a scale of 2/10 to 5/10 from Agent Orange he received during Vietnam War. Client states “I know that it itches, but I know not to scratch it because it gets worse.” Visible erythema on anterior portion of forearms. Dry skin covering whole body with wrinkling skin attributed to aging. No open or bleeding areas noted.
b. Psychosocial integrity
Client’s perception of effect of illness/surgery on self-concept: The client stated, “My military training has lead me to lead a very independent life. I have always been able to depend on myself while still being able to help my friends and family.” Now, since he’s been sick with COPD and this recent outbreak of respiratory distress, the client states that he feels the loss of his independence. “The simple things seem to be the worst. Like going to the bathroom without help. It’s embarrassing.” Client has a potential for ineffective coping related to statements of independence and embarrassment. The client has stated a real difficulty with having to rely on any help at all. Client’s affect: The client exhibited subtle affect. He spoke in a monotone voice and his demeanor appeared calm. His tone was more ‘matter of fact’ than sad or depressed.
c. Cultural considerations
Role: marital status, children, parents, etc.: Divorced in 1990 from his wife of over thirty years. He has one son, age 30 and one daughter, age 29. Client states that, “My son and I hadn’t been on speaking terms in 16 years but over this last year that I’ve been having these breathing problems, he’s been talking to me.” Client then goes on to say, “After I get better, I’m moving to Missouri with my son. He’s going to help me whenever I need help.” Client recognizes this as a positive aspect of his health illness. The Client mother died of Alzheimer’s disease and both his father and only sister committed suicide. Client declined to speak further on the suicides other than to say, “It happens.” He then states that his military training has helped to numb him from things like suicide. Client has potential for self-harm related to statements of family suicides and statement of “My military training has numbed me to things like that.”
2. Client’s preferences unique to culture: hygiene, diet support: Client states bathing no more than once a week for fear of asking for help with bathing. He states embarrassment when asking friends or family for help with ADL’s. Client states he has a bad diet. He eats once a day or every other day. He states he eats a lot of fast food because he does not want to have to cook.
3. Compliance with health care plan: Since hospitalization, Client has been compliant with his health care plan as evidenced by participation in all treatments, respiratory therapy, physical therapy, and dietary. Client states understanding of care plan and states necessity of changes in medical and physical needs to able him to lead a productive life with minimal health risk. Client states “Now that I know more about my disease, I can do what it takes to feel more comfortable with my problems. That’s why I’m moving to Missouri with my son to have the help I need.” The client is due to be transferred to the Gardens rehab facility as has been suggested by his physician for strengthening needed to reach ultimate level of functioning with ADL’s and maintain as much independence as possible.
d. Spiritual state
Client’s statements that reflect joy/purpose of living vs. hopelessness
2. Client’s inner strength/weaknesses: Client identified his strengths to be independence, self reliance, and a good decision maker. Client expressed a reliance on others and a lack of trust in others as his weaknesses. By showing trust in his son, the client has reached one of his goals of showing trust in others.
(including blood work,
x-rays, scans, etc.) Results
(abnormals in red) Indicate possible reasons for abnormal results
Complete Blood Count
10.2 (4.8-10.8 k/cmm)
3.97 L (4.70-6.10 Mil/cmm)
11.9 L (13.1-17.1 gm/dl)
34.2 L (42.0-52.0%)
86.2 (80.0-94.0 fl)
29.9 (27.0-34.0 pg)
34.7 (33.0-37.0 gm/dl)
232 (150-450 k/cmm)
7.1 L (7.4-10.4 fl)
89 H (50-70%)
7 L (20-45%)
9.1 H (2.0-7.3 k/cmm)
0.7 L (1.0-4.8 k/cmm)
0.00 L (0.04- 0.44 k/cmm)
13.1 (11.1-14.5 Sec.)
136 (135-145 mEq/l)
3.9 (3.5-5.0 mEq/l)
97 L (100-108 mEq/l)
29 (21-32 mEq/l)
107 (70-110 mg/dl)
27 H (6-20 mg/dl)
20 (6-20 ratio)
6.6 (6.0-8.2 gm/dl)
3.0 L (3.4-5.0 gm/dl)
3.6 (2.0-4.0 mg/dl)
0.8 L (1.0-3.0 ratio)
278 (275-286 mOs/kg)
31 (15-37 u/l)
166 H (30-65 u/l)
79 (50-138 mg/dl)
0.71 (0.20-1.00 mg/dl)
0.26 (0-0.30 mg/dl)
0.5 (0.2-0.8 mg/dl)
244 H (140-199 mg/dl)
128 (35-150 mg/dl)
1.8 (1.8-2.4 mg/dl)
Anemia, bone marrow failure, erythropoietin deficiency, hemorrhage, malnutrition, over hydration, nutritional deficiencies of; iron, copper, folate, vitamin B-12, vitamin B-6. (RBC Count, 2009)
Anemia, erythropoietin deficiency, malnutrition, nutritional deficiencies of; iron, folate, vitamin B-12, vitamin B-6. Over hydration. (Hemoglobin, 2009)
Blood loss, anemia, bone marrow failure, destruction of red blood cells, malnutrition or specific diet deficiencies, (Hematocrit (HCT), 2009)
Disseminated intravascular coagulation, hemolytic anemia, hypersplenism, idiopathic thrombocytopenic purpura. (Platelet Count, 2009)
Bacterial infection, many inflammatory processes, during physical stress (Differential, 2006)
Sepsis (Blood Differential, 2009)
Bacterial infection, many inflammatory processes, during physical stress (Differential, 2006)
Sepsis (Blood Differential, 2009)
Alcohol intoxification, over production of certain steroids in the body (such as cortisol) (Eosinophil Count – Absolute, 2009)
Client is on Lovenox prophylacticly. There’s not enough information to support reasons for a low PTT/INR.
Certain kidney disorders, chronic compensated respiratory acidosis, congestive heart failure, excessive sweating, gastric suctioning, metabolic alkalosis, overhydration, syndrome of inappropriate ADH secretion, vomiting. (Serum Chloride, 2009)
Congestive heart failure, excessive protein levels, gastrointestinal bleeding, hypovolemia, kidney disease, kidney failure, shock. (BUN, 2009)
Ascites, glomerulonephritis, liver disease, malabsorbtion, malnutrition. (Albumin – Serum, 2009)
Overproduction of globulins, underproduction of albumins, selective loss of albumin in the circulation. (Total Protein and A/G Ration, 2009)
Celiac disease, Cirrhosis, hepatitis, hereditary hemochromatosis, liver ischemia, liver tumor, use of drugs that are poisonous to the liver. (ALT, 2009)
Biliary cirrhosis, high fat diet, nephrotic syndrome. (Cholesterol – Test, 2009)
(up to 5) Purpose for this client Nursing implications/
Amlodipine 5mg tab PO
ASA/Aspirin 81mg tab PO
Enoxaparin 40mg Sub Q Injection
Fentanyl 50mcg /hr Transdermal
Potassium Chloride 20 mEq PO Systemic vasodilatation resulting in decreased blood pressure.
Decreased platelet aggregation.
Prevention of deep vein thrombosis.
Moderate to severe chronic pain requiring continuous opioid analgesic therapy for an extended time.
Replacement. Prevention of deficiency. Assessment:
Monitor blood pressure and pulse before therapy, during dose titration, and periodically during therapy. Monitor intake and output ratios and daily weight. Assess for signs of CHF (peripheral edema, rales/crackles, dyspnea, weight gain, jugular venous distention.
Advise client to take medications as directed, even if feeling well. Take missed doses as soon as possible unless almost time for next dose; do not double doses. May need to be discontinued gradually. Instruct client on correct technique for monitoring pulse. Instruct client to contact health care professional if heart rate is <50 bpm. Caution client to change positions slowly to minimize orthostatic hypotension. May cause drowsiness or dizziness. Instruct the client on the importance of maintaining good dental hygiene and seeing dentists frequently for teeth cleaning to prevent tenderness, bleeding, and gingival hyperplasia. Instruct client to avoid concurrent use of alcohol or OTC medications, especially cold preparations, without consulting a health care professional. Advise client to notify health care professional if irregular heartbeats, dyspnea, swelling of hands and feet, pronounced dizziness, nausea, constipation, or hypotension occurs or if headache is severe or persistent. Caution client to wear protective clothing and use sunscreen to prevent photosensitivity reactions. Advise client to inform health care professional of medication regiment before treatment or surgery. Encourage client to comply with other interventions for hypertension (weight reduction, low sodium diet, smoking cessation, moderation of alcohol consumption, regular exercise, and stress management.) Medication controls, but not cures hypertension. Instruct client and family in proper technique for monitoring blood pressure. Advise client to take blood pressure weekly and to report significant changes to health care professional.*
May cause elevated serum ALT, AST, and alkaline phosphatase. May return to normal despite continued use. If severe abnormalities or active liver disease occurs, discontinue and use with caution in the future. May alter results of serum uric acid, urine vanillylmandelic acid, protirilin induced thyroid stimulating hormone, urine hydroxyindoleacetic acid determinations, and radionuclide thyroid imaging. May lower serum potassium and cholesterol concentrations. Prolongs bleeding time for 4-7 days. Monitor patient for tinnitus, headache, hyperventilation, agitation, mental confusion, lethargy, diarrhea, and sweating. If these symptoms appear, withhold medication and notify physician or other health care professional immediately.
Instruct patient to take salicylates with a full glass of water and to remain in an upright position for 15-30 min after administration. Advise patient to report tinnitus, unusual bleeding of gums, bruising, black tarry stools, or fever lasting longer than 3 days. Caution patient to avoid concurrent use of alcohol with this medication to minimize possible gastric irritation; 3 or more glasses of alcohol per day may increase the risk of GI bleeding. Caution patient to avoid taking concurrently with acetaminophen or NSAIDs for more than a few days, unless directed by health care professional to prevent analgesic nephropathy. Tablets with an acetic (vinegar-like) odor should be discarded. Advise patients receiving aspirin prophylactically to take nly prescribed dose. Increasing the dose has not been found to provide additional benefits.*
Assess for signs of bleeding and hemorrhage (Bleeding gums; nosebleeds; unusual bruising; black, tarry stools; hematuria; fall in hematocrit or blood pressure; guaiac-positive stools). Notify physician if these occur. Assess for evidence of additional or increased thrombosis. Symptoms depend on area of involvement. Monitor neurological status frequently for signs of neurological impairment. May require urgent treatment. Monitor for hypersensitivity reactions (chills, fever, urticaria). Report signs to physician. Observe injection sites for hematomas, ecchymosis, or inflammation. Monitor CBC platelet count, and stools for occult blood periodically during theapy. If thrombocytopenia occurs, monitor closely. If hematocrit decreases unexpectedly, assess the patient for potential bleeding sites. May caus increase in AST and ALT levels. For overdose, protamine sulfate 1mg for each mg of enoxaparin should be administered by slow IV injection.
Advise patient to report any symptoms of unusual bleeding or bruising, dizziness, itching, rash, fever, swelling, or difficulty breathing to health care professional immediately.*
Assess type, location, and intensity of pain before and 24 hours after application and periodically during therapy. Monitor pain frequently during initiation of therapy and dose changes to assess need for supplementary analgesics for breakthrough pain. Assess blood pressure, pulse, and respirations before and periodically during administration. If respiratory rate is <10/min, assess level of sedation. Physical stimulation may be sufficient to prevent significant hypoventilation. Dose may need to be decreased by 25-50%. Initial drowsiness will diminish with continued use. Prolonged use may lead to physical and psychological dependence and tolerance. This should not prevent patient from receiving adequate analgesia. Most patients who receive opioid analgesics for pain do not develop psychological dependence. Progressively higher doses may be required to relieve pain with long-term therapy. It may take up to 6 days after increasing doses to reach equilibrium, so patients should wear higher dose through 2 applications before increasing dose again. Assess bowel function routinely. Prevent constipaiion with increased intake of fluids and bulk, and laxatives to minimize constipating effects. May increase plasma amylase and lipase levels. If an opioid antagonist s required to reverse respiratory depression or coma, naloxone (narcan) is the antidote.
Instruct patient in how and when to ask for pain medication. Instruct patient in correct method for application and disposal of dransdermal system. Tatalities have occurred from children having access to improperly discarded patches. May be worn while bathing, showering, or swimming. May cause drowsiness or dizziness. Caution patient to call for assistance when ambulating or smoking and to avoid driving or other activities requiring alertness until response to medication is known. Advise patient to change positions slowly to minimize dizziness. Caution patient to avoid concurrent use of alcohol or other CNS depressants with this medication. Advise patient that fever electric blankets, heating pads, saunas, hot tubs and heated water beds increase the release of fentanyl from the patch. Advise patient that good oral hygiene, frequent mouth rinses and sugarless gum or candy may decrease dry mouth.*
Assess for signs and symptoms of hypokalemia (weakness, fatigue U wave on ECG, arrhythmias, polyuria, polydipsia) and toxicity (hyperkalemia; slow, irregular heartbeat; fatigue; muscle weakness; paresthesia; confusion; dyspnea; peaked T waves; depressed ST segments; prolonged QT segments; widened QRS complexes; loss of P waves; and cardiac arrhythmias) Treatment of toxicity includes discontinuation of potassium, and administration of sodium bicarbonate to correct acidosis, dextrose and insulin to facilitate passage of potassium into cells. Monitor serum potassium before and periodically during therapy. Monitor renal function, serum bicarbonate, and pH. Hypomagnesemia should be corrected to facilitate effectiveness of potassium replacement. Monitor serum chloride because of hypochloremia may occur if replacing potassium without concurrent chloride.
Explain to patient purpose of the medication and the need to take as directed, especially when concurrent digoxin or diuretics are taken. A missed dose sould be taken as soon as remembered within 2 hr; if not, return to regular dose schedule. Do not double dose. Emphasize correct method of administration. Instruct patient to avoid salt substitutes or low-salt milk or food unless approved by health care professional. Patient should be advised to read all labels to prevent excess potassium intake. Advise patient regarding sources of dietary potassium. Encourage compliance with recommended diet. Instruct patient to report dark, tarry, or bloody stools; weakness; unusual fatigue; or tingling of extremities. Notify health care professional if nausea, vomiting, diarrhea, or stomach discomfort persists. Dosage may require adjustment. Emphasize the importance of regular follow-up exams to monitor serum levels and progress.*
*(Davis’s Drug Guide for Nurses 10th Edition, 2005)
C. Developmental Transitions: The client is having difficulty with dealing with his deteriorating lungs. He states a sense of panic when he has difficulty breathing. Client teaching should assist with this transition to latter stages of his COPD. The client states acceptance to all other issues attributed to aging.
Erikson’s Developmental Stage/Task: The client is struggling between integrity and despair. Client states his integrity is from years of military training. Despite all that has happened to him over the last year, he prides himself on his independence to this point. He states he is fighting off despair as the realization of his waning independence is leading to a role of dependence.
Role changes: The client is having difficulty transitioning from a provider to being cared for. With the reconciliation with his son, the client has decided to move to allow for assistance from his son. The client has stated difficulty with this because of his independence and lack of trust in others.
D. Situational Transitions (divorce, work changes, relocation, hospitalization): The clients hospitalization for acute respiratory distress syndrome has made the client aware that he will be in need of constant assistance for the first time in his life. The client also had difficulty with transitioning from his divorce 19 years ago. His wife left him and his son refused to speak to him for 18 years after the divorce.
E. Organizational Transitions (access to/movement within the healthcare system) : Client states no difficulty with access to or movement within the healthcare system.
7.Significance of Assessment Findings: Shortness of breath and diminished lung sounds throughout all lobes suggests that the client will be in need of long term assistance, whether with family as the primary care provider or through a long term care facility. Psychological therapy would be beneficial for the patient to deal with his post traumatic stress disorder as well as possible psychological problems associated with tragic family deaths.
II. NURSING DIAGNOSES
A. List all relevant nursing diagnoses for this client
B. Top 2 Priority Nursing Diagnoses according to Maslow as applied to this client.
III. Plan of Safe Effective Care
Using the two diagnoses that are the highest priorities, make a short and a long-term
goal, interventions, outcomes and rationales for each.
Impaired gas exchange r/t altered oxygen supply m/b reduced tolerance for activity*
GOALS (expected outcome):
Short term: Client will keep an O2 level of > 94% by 1600 today.
Long term: Client will remain free of symptoms of respiratory distress.*
Assess respiratory rate, depth. Note use of accessory muscles, pursed lip breathing, and inability to speak / converse.
Elevate head of bed, assist client to assume position to ease work of breathing. Include periods of time in prone position as tolerated. Encourage deep-slow or pursed-lip breathing as individually needed / tolerated.
Assess / routinely monitor skin and mucous membrane color.
Auscultate breath sounds, noting areas of decreased air-flow and / or adventitious sounds.
Palpate for fremitus.
Monitor level of consciousness / mental status. Investigate changes.
Evaluate level of activity tolerance. Provide calm quiet environment. Limit client’s activity or encourage bed / chair rest during acute phase. Have client resume activity gradually and increase as individually tolerated.
Nonitor vital signs and cardiac rhythm.
Monitor / graph serial ABG’s and pulse oximetry.
Administer supplemental oxygen judiciously, using appropriate delivery method and titrate as indicated by ABG results and client tolerance.
Administer antianxiety, sedative, or narcotic agents with caution.
Prepare for additional referrals / interventions; e.g., pulmonary specialist, pulmonary rehabilitation program.* Useful in evaluating the degree of respiratory distress and / or chronicity of the disease process.
Oxygen delibery may be improvd by upright position and breathing exercises to decrease airway collape, dyspnea, and work of breathing. Recent research supports use of prone position to increase PaO2.
Cyanosis may be peripheral or central. Duskiness and central cyanosis indicate advanced hypoxemia.
Breath sounds may be faint because of decreased airflow or areas of consolidation. Presence of wheezes may indicate bronchospasm / retained secretions. Scattered moist crackles may indicate interstitial fluid / cardiac decompensation.
Decrease of vibratory tremors suggests flid collection or air trapping.
Restlessness and anxiety are common manifestations of hypoxia. Worsening ABG’s accompanied by confusion / somnolence are indicative of cerebral dysfunction due to hypoxemia.
During severe / acute / refractory respiratory distress, client may be totally unable to perform basic self-care activities because of hypoxemia and dyspnea. Rest interspersed with care activities remains an important part of treatment regimen. An exercise program is aimed at improving aerobic capacity and functional performance, increasing endurance and strength without causing severe dyspnea and can enhance sense of well-being.
Tachycardia, dysrhythmias, and changes in blood pressure can reflect effect of systemic hypoxemia on cardiac function.
PaCO2 usually elevated, and PaO2 is generally decreased, so that hypoxia is present in a greater or lesser degree.
Used to correct / prevent worsening of hypoxemia improve survival, and quality of life. Supplemental oxygen can be provided during exacerbations only, or as a long-term therapy.
May be used to reduce dyspnea by controlling anxiety and restlessness, which increases oxygen consumption / demand exacerbating dyspnea. Must be monitored closely because depressive effect may lead to respiratory failure.
May be indicated to confirm diagnosis and optimize appropriate treatment. A multidisciplinary approach including education and exercise treaining may be helpful in improving client function and quality of life.*
*(Nursing Care Plans, 2006)
A. Short term goal (met, partially met, not met)
Client maintained an O2 level of 95% throughout shift.
B. Long term goal (met, partially met, not met)
Unable to assess at this time.
Imbalanced Nutrition: less than body requirements r/t fatigue m/b Reported altered taste sensation, aversion to eating, lack of interest in food*
GOALS (expected outcome):
Short term: Client will eat 90% of breakfast and lunch by 1600 today.
Long term: Demonstrates lifestyle changes to maintain appropriate weight.*
Assess dietary habits, recent food intake. Note degree of difficulty with eating. Evaluate weight and body size.
Auscultate bowel sounds.
Give frequent oral care, remove expectorated secretions promptly, provide specific container for disposal of secretions and tissues.
Encourage a rest period of 1 hr before and after meals. Provide frequent small feedings.
Avoid gas-producing foods and carbonated beverages.
Avoid very hot or very cold foods.
Weigh as indicated.
Consult dietitian / nutritional support team to provide easily digested, nutritionally balanced meals by appropriate means.
Review laboratory studies; e.g., serum albumin / prealbumin, transferring, amino acid profile, iron, nitrogen blance studies, glucose, liver function studies, electrolytes.
Administer supplemental oxygen during meals as indicated.* Client in acute respiratory distress is often anorectic because of dyspnea, sputum production, and medication effects. In addition many COPD clients habitually ead poorly even though respiratory insufficiency creates a hypermetabolic state with increased caloric needs. As a result, client often is admitted with some degree of malnutrition. People who have emphysema are often thin with wasted musculature.
Diminished / hypoactive bowel sounds may reflect decreased gastric motility and constipation related to limited fluid intake, poor food choices, decreased activity, and hypoxemia.
Noxious tastes, smells, and sights are prime deterrents to appetite and can produce nausea and vomiting with increased respiratory difficulty.
Helps reduce fatigue during mealtime, and provides opportunity to increase total calorie intake.
Can produce abdominal distention, which hampers abdominal breathing and diaphragmatic movement and can increase dyspnea.
Extremes in temperature can precipitate / aggravate coughing spasms.
Useful in determining caloric needs, setting weight goal, and evaluating adequacy of nutritional plan.
Needs to provide maximal nutrients with minimal client effort.
Evaluates / treats deficits and monitors effectiveness of nutritional therapy.
Decreases dyspnea and increases energy for eating, enhancing intake.*
*(Nursing Care Plans, 2006)
A. Short term goal (met, partially met, not met)
Client ate 100% of his breakfast but only 80% of lunch.
B. Long term goal (met, partially met, not met)
Unable to assess at this time.
Chart data acquired via client chart, Kingman Regional Medical Center, March 10, 2009.
Client data acquired in interview with client, Kingman Regional Medical Center, March 10, 2009.
Barbara E. Gould, Med. (2006). Pathophysiology for the Health Professions; Third Edition. Toronto, Ontario, Canada: Elseveir Inc.
RBC Count. (2009) Retrieved March 17, 2009, from MedlinePlus Web site; http://www.nlm.nih.gov/medlineplus/ency/article/003644.htm
Hemoglobin. (2009) Retrieved March 17, 2009, from MedlinePlus Web site; http://www.nlm.nih.gov/medlineplus/ency/article/003645.htm
Hematocrit (HCT). (2009) Received March 17, 2009, from MedlinePlus Web site; http://www.nlm.nih.gov/medlineplus/ency/article/003646.htm
Platelet Count. (2009) Received March 17, 2009, from MedlinePlus Web site; http://www.nlm.nih.gov/medlineplus/ency/article/003647.htm
Differential. (2006) Received March 17, 2009, from RnCeus Web site; http://www.rnceus.com/cbc/cbcdiff.html
Blood Differential. (2009) Received March 17, 2009, from MedlinePlus Website; http://www.nlm.nih.gov/medlineplus/ency/article/003657.htm
Eosinophil Count – Absolute. (2009) Received March 17, 2009, from MedlinePlus Web site; http://www.nlm.nih.gov/medlineplus/ency/article/003440.htm
Serum Chloride. (2009) Received March 17, 2009, from MedlinePlus Web site; http://www.nlm.nih.gov/medlineplus/ency/article/003485.htm
BUN. (2009) Received March 17, 2009, from MedlinePlus Web site; http://www.nlm.nih.gov/medlineplus/ency/article/003474.htm
Albumin – Serum. (2009) Retrieved March 17, 2009, from MedlinePlus Web site; http://www.nlm.nih.gov/medlineplus/ency/article/003480.htm
Total Protein and A/G Ratio. (2009) Retrieved March 17, 2009, from Lab Tests Online Web site; http://www.labtestsonline.org/understanding/analytes/tp/test.html
ALT. (2009) Retrieved March 17, 2009, from MedlinePlus Web site; http://www.nlm.nih.gov/medlineplus/ency/article/003473.htm
Cholesterol – Test. (2009) Retrieved March 17, 2009, from MedlinePlus Web site; http://www.nlm.nih.gov/medlineplus/ency/article/003492.htm
Judith Hopfer Deglin and April Hazard Vallerand. (2005) Davis’s Drug Guide for Nurses: Tenth Edition. Philadelphia, PA: F.A. Davis Company.
Marilynn E. Doenges, Mary Frances Moorhouse, and Alice C. Murr. (2006) Nursing Care Plans. Philadelphia, PA: F.A. Davis Company.
|Posted by: treacherous Mar 31 2009, 03:38 AM|
|Ack! Cut that out. It hurts me head.|
|Posted by: granobulax Mar 31 2009, 03:42 AM|
Your head hurts? I can't imagine why. You should try WRITING one. There's TRUE writing
|Posted by: treacherous Mar 31 2009, 03:43 AM|
Hall of Fame worthy.
|Posted by: granobulax Mar 31 2009, 03:50 AM|
Should I post it on the FPL?
|Posted by: treacherous Mar 31 2009, 02:25 PM|
Everyone would vote for it, because they'd feel guilty that they don't get it.
|Posted by: Pseudonym Mar 31 2009, 08:34 PM|
Your name is really granobulax
|Posted by: granobulax Mar 31 2009, 10:31 PM|
|No, that's not my real name. My first name is Josh and there's only one other person on this site who knows my last name.|
|Posted by: Jailer411 Apr 1 2009, 12:01 AM|
|Posted by: granobulax Apr 1 2009, 04:59 AM|
He know's it too?
|Posted by: treacherous Apr 1 2009, 11:51 AM|
|Posted by: granobulax Apr 2 2009, 09:20 PM|
| Well, today I got the worst test grade I've recieved since being in the nursing program. I failed the test by 1% at a 74%
Now, my test grade average for the semester is an 80%, only 5% above failing.
|Posted by: L Bison Apr 2 2009, 09:28 PM|
| Omg that is so long just scrolling past it makes my head spin.
Ew your name is suckness you're granobulax really and don't lie about it lol.
That's bad about the test (I think, in all honesty I don't really know but it seems like it sucks a lot.)
|Posted by: granobulax Apr 2 2009, 09:39 PM|
One is entitled to their own opinion.
And yes, the test grade wreaks of "suckness".
|Posted by: L Bison Apr 2 2009, 09:43 PM|
| Lol sorry bad day, I don't always think about my wording when I'm in this kind of mood.
Any way you can improve the grade?
|Posted by: granobulax Apr 2 2009, 10:24 PM|
Yeah, study harder for the next test
I'm doing alright in that I have one more test and a final exam. I'd have to get a 60% on my next test to be concidered failing which ain't happenin.
I'll do fine, I'm just disappointed that I failed this test is all.
|Posted by: L Bison Apr 2 2009, 10:27 PM|
| Ah ok well at least you should pass then.
It is annoying to fail stuff though, I get irritated if I just get a slightly low grade in something (even if it isn't important lol.)
|Posted by: Solomon Apr 2 2009, 10:28 PM|
Aw don't worry bud.
The sun'll come out
Bet your bottom dollar
There'll be sun!
Just thinkin' about
Clears away the cobwebs,
And the sorrow
'Til there's none!
When I'm stuck a day
I just stick out my chin
The sun'll come out
So ya gotta hang on
Come what may
I love ya
|Posted by: Solomon Apr 2 2009, 10:30 PM|
I know! I KNOW!
|Posted by: granobulax Apr 2 2009, 10:47 PM|
You do too?
I'd better stop telling people my full name!
|Posted by: Solomon Apr 2 2009, 10:51 PM|
Of course I know Mr. [Your name has been ommited to protect your identity]
|Posted by: Jailer411 Apr 3 2009, 12:36 AM|
Your name is in your e-mail address.
|Posted by: granobulax Apr 3 2009, 01:26 AM|
Of course it is, but I haven't emailed bloody in almost a year. Does he still have it?
|Posted by: Bloody_Freak Apr 3 2009, 02:44 AM|
It's your contact name for me.
|Posted by: granobulax Apr 3 2009, 03:01 AM|
Wow, I need to stop giving out my email. Half of the Haven knows my full name then!
|Posted by: granobulax Apr 3 2009, 03:10 AM|
|Has anyone seen Ethan lately?|
|Posted by: treacherous Apr 3 2009, 03:52 AM|
Yeah, I was thinking that. I'm worried.
|Posted by: granobulax Apr 3 2009, 03:54 AM|
I hope he's just on vacation.
|Posted by: granobulax Apr 3 2009, 04:20 AM|
| I updated my avatar.
|Posted by: M Bison Apr 3 2009, 07:22 AM|
He's not. Trust me.
|Posted by: treacherous Apr 3 2009, 11:44 AM|
|The evil dictator got him.|
|Posted by: granobulax Apr 3 2009, 02:13 PM|
|Posted by: Pseudonym Apr 3 2009, 09:44 PM|
|Posted by: Darkender Apr 3 2009, 10:48 PM|
|I hate you guy's avatars because I cant tell who's writing what.|
|Posted by: Solomon Apr 4 2009, 02:22 PM|
|Posted by: M Bison Apr 4 2009, 07:28 PM|
What can I say? I do my job.
|Posted by: granobulax Apr 5 2009, 12:59 AM|
|So, he was banned?|
|Posted by: Solomon Apr 5 2009, 01:00 AM|
|Posted by: Jailer411 Apr 5 2009, 01:02 AM|
Just like Hamboy.
|Posted by: Solomon Apr 5 2009, 01:06 AM|
You've been reading old topics haven't you?
|Posted by: Jailer411 Apr 5 2009, 01:14 AM|
|Posted by: Granobulax Apr 8 2009, 07:27 PM|
| Here's my latest note-card for my microbiology class. It's 7,500 words long and will be compressed onto a 3x5 card with font 3.
Mitochondria bacteria cell symbiotic relationship established w/ cells ring shaped chromosome don’t have more than 100-150 genes can be rod shaped or nearly spherical produce some of their own proteins divide at their won schedule some antibiotics can attack the mitochondria and kill them in the end kill us some Eukaryotic cells don’t have mito instead have hydrogenosomes related structure provide atp for anaerobic creatures much less efficient lacks the citric acid cycle enzymes and usually also cristae chloroplast bacteria structures have circular dna molecule like bacteria pigments are different from bacterial photosynthetic pigments capture light energy and using it to create glugose molecules then it is modified to do what the cell needs are the site of photosynthetic energy production and co2 fixation in eukaryotic phototrophs multi types of chloroplasts relationships of mitochondria and chloroplasts to bacteria all contain dna circular the eukaryotic nucleus contains genes derived from bacteria ones that have to do w/ mechanical parts mitochondria and chloroplasts contain their own ribosomes cell structures that function in protein synthesis these are basically the same as bacteria antibiotic specificity several affect the ribosomes function also the mitochondria and chloroplasts endoplasmic reticulum and Golgi complex The endoplasmic reticulum (ER) is a network of membranes continuous with the nuclear membrane. Two types of endoplasmic reticulum are recognized; rough, which contains attached ribosomes, and smooth, which does not. Smooth ER participates in the synthesis of lipids and in some aspects of carbohydrate metabolism. Rough ER, though the activiety of its ribosomes is a major producer of glycoproteins and also produces new membrane material that is transported throughout the cell to enlarge the various membrane systems before cell division. The Golgi complex consists of a stack of membranes distinct from the ER but that functions in concert with the ER. In the Golgi complex, products of the IR are chemically modified and sorted into those destined for secretion—for example, hormones or digestive enzymes—and those that function in other membranous structures in the cell. Golgi arise from the division of preexisting Golgi and contain various enzymes that modify secretory and membrane proteins differently, depending on their final destination in the cell. Many of the modifications are glycosylations (addition of sugar residues) that convert the proteins into specific glycoproteins. Lysosomes a packet that buds off the Golgi that contains digestive enzymes also helps repair cell destroys things in the cell that become nonfunctional microtubules microfilaments and intermediate filaments these are protein structures that allow the cell to form for example cilia flagella they also have internal functions of the cell give the cell a shape flagella and cilia are present on many eukaryotic MOs organelles of motility allowing cells to move by swimming cilia are short flagella that beat in synchrony to propel the cell usually quite rapidly flagella are long appendages present singly or in groups that propel the cell along most cells other than animal cells have a cell wall they have a extracellular matrix (ECM) in which cells are embedded is present outside the cytoplasmic membrane. Protists Giardia doesn’t have mitochondria causes’ giartiasis waterborne diarrheal disease common in US last about 2-6 wks w/ cramps not going to die only attacks mammals Trichomonas causes vaginal problems STD Trypanosoma agent that causes things like sleeping sickness transmitted by vector lives in circulatory system leaves you open to other things that can now kill you nonphotosynthetic have flagella Euglena free living most are photosynthetic creature but some when in dark become predatory some purely predatory ciliates covered w/ cilia paramecium uses cilia to obtain food and movement can detect chemicals in water also when moving if it runs into something the cilia move in the opposite direction how this coordination occurs isn’t understood also they’re the most complex of the single cell creatures they have structures that do what our kidneys do whey rid them of excess water have thin almost cell wall that gives structure has mouth like structure has anus like structure fairly benign creatures dinoflagellates about 60% marine and 40% fresh water cell wall present of related cellous material have 2 flagella of diff lengths w/ differ points of insertion into the cell transverse and longitudinal in general good causes red tides because of agricultural runoff that produce a neurotoxin which kill fish important probably wont hurt you some say that it causes lung damage and ulcerations in humans ecologically photosynthetic apicomplexans/sporozones plasmodiums the malarial parasite nonmotile creatures all are parasitic all require vectors 4 strains that cause malaria in humans malaria causes more grief in human population than any other creature malaria tropical disease 6-8 hundred million people are affected 2-6 million people die from malaria per yr not actually dying from malaria but it weakens you and you die from something else more economic damage is done that any other disease because of the pattern it shows doesn’t go away on own get it fell ok invade red blood cells and multiplies after 2-3 months a pattern develops anywhere from 28-32 days your red blood cells rupture fell like crap ache tired 1st wk after feel little better 2nd wk feel little better 3rd wk feel little better 4th wk feel fine the red blood cells rupture again cycle starts cant work so damages the economy now can be killed by meds they can form resistance to meds so new ones have to be made oomycetes doesn’t attack humans directly this is and agricultural pest has changed history because of the agricultural aspects their ex potato famine in Ireland diatoms and golden algae photosynthetic doesn’t cause disease important ecologically because of food sources for creatures and o2 production sarcodina these are amoeba and most are friends to us entamobas are a gastrointestinal parasites sm and lg intestinal parasite upsets the balance it’s an ulceration of the intestinal tract that results in a bloody diarrhea most will resolve itself some can go dormant then reoccur over and over Fungi Some fungi are aquatic, living primarily in freshwater, and a few marine fungi are also known. Most fungi, however, are terrestrial. They inhabit soil or dead plant matter and play crucial roles in the mineralization of organic carbon. A large number of fungi are plant parasites. Also establish symbiotic associations with many plants, facilitating the plant’s acquisition of minerals from soil and many fungi contribute beneficially to human life through fermentation and the synthesis of antibiotics. Nutrition and physiology—are chemoorganotrophs, typically with simple nutritional requirements, and most are aerobes. They feed by secreting extracellular enzymes that digest complex organic materials, such as polysaccharides or proteins, into their monomeric constituents, sugars, peptides, amino acids, and so on. As sources of energy, carbon, and other nutrients. Recycle, nonliving organic material, As parasites use the same mode of nutrition but take up their nutrients from the living cells of the plants and animals they infect and invade. Major ecological activity of fungi, especially basidiomycetes, is the decomposition of wood, paper, cloth, and other products derived from these natural sources can use the cellulose or lignin present as carbon and energy sources. Many fungi can grow at environmental extremes of low pH or high temperature (up to 62°C; common contaminants of food products and surfaces of all sorts. Morphology and spores-Most are multicellular, forming a network of filaments called hyphae are often separate, with cross-walls dividing each hyphae into separate cells. Each hyphal filament grows mainly at the tip Hyphae typically grow together across a surface and form compact tufts, collectively called a mycelium, or mold from the mycelia mat, hyphal branches may reach up into the air above the surface, and on these aerial branches spores called conidia are formed Conidia are asexual spores and they’re often pigmented and resistant to drying The fruiting bodies can release millions of spores that are spread by wind, water, or animals to new habitats where the spores can then germinate. Cell walls resemble plant cell walls in basic structure, but not in their chemistry most contain chitin, a polymer of the glucose derivative arranged in the walls in microfibrillar bundles are typically 80-90% polysaccharide, with proteins, lipids, polyphosphates, and inorganic ions making up the wall-cementing matrix symbioses- Most plants are dependent on fungi to facilitate their uptake of minerals from soil. The fungi form symbiotic associations with the plant roots called mycorrhizae help the plant obtain phosphate and other minerals and also water from the soil fungi obtain nutrients such as sugars from the plant root pathogenic fungi form specialized hyphae, called haustoria, that penetrate the plant cell wall and make the cell’s cytoplasm available for fungal nutrition. In humans, fungal disease, called mycoses, range from relatively minor and easily cured conditions, such as athlete’s foot, to serious, life-threatening systemic mycoses, such as histoplasmosis. Reproduction- Most fungi reproduce primarily by asexual means. Fungi reproduce asexually in three ways; by the growth and spread of hyphal filaments, by asexual production of spores or by simple cell division as in budding yeasts sexual spores- some produce spores as a result of sexual reproduction sexual spores can originate from the fusion of two haploid cells to yield a diploid cell; this then undergoes meiosis and mitosis to yield individual haploid spores. Algae there are unicellular red algae green algae start of plant life they bear chloroplasts lack phycobilins have photosynthetic pigments similar to plants most inhabit freshwater some are marine and some found in moist soils or snow morphology ranges from filamentous to colonial and multicellular most have complex life cycle w/ both asexual and sexual reproductive stages there are very small algae known At the colonial level of organization in green algae is Volvox This algae forms colonies composed of several hundred flagellated cells involved in motility and photosynthesis and several other cells that specialize in reproduction. Sterilization killing everything in the vegetative stage (when it’s doing what its doing) and the endospore stage decontamination to make an object not dangerous to you in vitro control is outside the body in vivo control is inside the body harder than in vitro control lots of antibiotics that are found are harmful to us as well so we can’t use physical control heat sterilization you add energy to the protein molecules and dna in this process you are denaturizing the protein and make unstable so it can no longer function also change shape of dna the time it takes depends on the heat requirements of the creature ex kill vegatitative form easier w/ lower heat endospore higher temps needed how long varies as well depending on the creature and stages they are in type of heat also important have dry and moist moist has better penetrating power than dry and given the temp produces faster reduction in the number of living organisms endospores being killed q/ heat remember that they have small acid soluble spore proteins which take more energy to disrupt them and they stabilize everything they are also dry which adds stability mechanisms used in heat control autoclave is a sealed heating devise that allows the entrance of steam under pressure (a big pressure cooker) heat kills not pressure usually runs 15 min w/ 15lbs pressure reaching temps of about 125-126°C almost enough to kill everything may not kill the extreme thermophiles great if not worried about chemical structure of things being autoclaved pasteurization uses heat to reduce the numbers of Mos doesn’t kill everybody just things ready to germinate quickly gives longer shelf life heat to as high of temps as can w/o changing the nature of it for short periods of time then cooled like a radiator radiation sterilization soft (uv light) good for some functions and not for others uv has very little penetrating power uv can cause cataracts kills superficially does not penetrate even a piece of paper what the uv does is add energy to the protein and dna causing extra connection between the adjacent nucleotides which means the dna can’t control the cell functions normally can’t repo normally and the cell will die also cause mutations in the cells growth process Ionizing (hard) penetrates these are high energy particles that penetrate readily may interact directly with molecule and destabilize it so it breaks generates electrons hydroxyl radicals (free radials ) that attach to other molecules in that cell and oxidate them and cause damage and hydride radicals capable of altering dna and protein which leads to death of cell mos are much more resistant to hard radiation than multicellular organisms common source is x rays starting to use as a way to preserve food 2 problems one bogus you get damage from eating this and the other good nutrient value is damaged especially the vitamins filter sterilization good for gases and some fluids 3 basic types better the job done more cost depth have layers of fibers which can be all differ kinds of fibers depending on what you are treating or being handled like the ones brought for vacuums the fibers just criss cross crating spaces for entrapment great for dust some pollen doesn’t do well for trapping mos membrane has higher complexity composed of high tensile strength polymers manufactured to contain a lg number of tiny holes or pores which can be controlled during manufacturing does pretty good job on bacterial agents nucleation track (nuclepore) subcategory of membranes create a membrane that is a solid structure that responds to radio activity it is zapped with this and crates the holes which can be tiny enough to catch bacteria as sm as 0.1 um in diameter and 20 um in length some virus’ can be killed in these physical ways chemical control antimicrobial agent is one that destroys or makes not grow or repo ones that kill are known as –cidal agents ones that inhibit growth are known as –static agents there are differences in the mode of action static agents prevent growth of culture the number of viable cells are the same as total cell count haven’t killed any cidal agents kills the bacteria but doesn’t destroy the cells total cell count remains the same but the viable cell count declines to 0 a lytic agent kills the bacterial cells by lysing them it just physically destroys them all cells die agents for external use sterilants destroy all forms of microbial life including endospores used on thing that can’t withstand heat disinfectants goal is to kill as many vegetative forms of mos as you can on inanimate objects like tables, floors sanitizer goal is not to kill but reduce the numbers of mos to a safe number used on inanimate objects used on food contact equipment like meat slicer and nonfood contact like tables walls antiseptics and germicides these are agents for living tissue such as ethanol can be used as both the efficacy of chemical antimicrobial agents organic material if you have sm amount the cleaning agent will work better than lg amount the agent will interact w/ the organic material more and reduce the efficacy biofilms may slow or completely prevent penetration of agents endospores also affect the efficacy of the agent temp and pH also effect the use of agents agents used in vivo some things to be considered here are the antimicrobial spectrum of activity mode of action one reason that antibiotics have been failing is the over usage of broad spectrum which breed resistance synthetic antimicrobial drugs things that are not antibiotics they act in differ sorts of ways mode of action are doing same kind of things growth factor analogs is a chemical that can fit in and take the place of another chemical usually taking about chemical subunit when it fits in it render the lger molecule inactive sulfa drugs they attack folic acid they fit in but when they are there its not folic acid produced it’s a useless molecule growth factor analogs so the same kind of things but in vitamins sulfa drugs work well in humans because we can’t produce our own folic acid we don’t have the metabolic process to screw up in terms of sulfa drugs bacteria do some plant could be affect by sulfa but mammals don’t w/ growth factor analogs have to be carful not to give if it will mess up something we produce isonaizid interfere with the growth of cell walls of the tb bacteria wont mess with our metabolic processes we don’t have cell walls you can be allergic to any of them nucleic acid base analogs have to b a little careful with these they interfere with the production of thymine and uracil of the bacterium by exposing the creature to the nucleic acid base blocks nucleic acid synthesis quinolones here even w/ circular dna molecule there is a lot of twisting you have groups of enzymes called gyrases the quinolones interfere with the folding up processes of the bacterial dna doesn’t hurt us because we have diff enzymes these are bacteria specific processes that are going on naturally occurring antimicrobial drugs; antibiotics are produced by bacteria and fungi they are used as war agents against each other we use some of these for our own purposes protein production antibiotics such as aminoglycosides, macrolides, and tetracyclines our ribosomes are different enough so that these antibiotics screw up their protein production but not ours these 3 interfere w/ the ribosome dna gyrase(nalidixic acid, ciprofloxacin, novobiocin) and rna elongation(actinomycin) interfere w/ the transcription and production of the messages the materials that carry the information from the dna molecule to the ribosome penicillins and cephalosporins synthetic penicillins is have org and chg little prevent production of cell wall if the cell goes to divide no cell wall stuff leaks out cell dies cephalosporins do the same in little differ way dapotomycin operates on the cell membrane interferes w/ functioning of the plasma membrane induces a rapid chg of the cell by depolarization of the membrane the cell loses control of itself and what goes in and out then it dies platensimycins screws up fatty acid production makes so can’t produce cell walls and other lipids steriol antibiotics that mess w/ cell wall synthesis are cycloserine vancomycin bacitracin penicillins cephalosporins monobactams carrbapenema folic acid metabolism trimethoprim sulfonamides cytoplasmic membrane structure and function polymyxins daptomycins lipis biolynthesis plantesimyvin protein synthesis trna mupirocin puromycin protein synthesis 30sfactor tetracyclines spectinomycin streptomyclin gentamicin kanamycin amikacin mitrofurans protein synthesis 50s factor erythromycin(macrolides) chloramphenicol clindamycin lincomycin dna directed rns polymerase rifampin streptovaricins rna elongation actinomycin dna gyrase nalidixic acid ciprofloxacin novobiocin antiviral drugs very few that do much of anything chemotherapeutic agents limited in what they do you have nucleoside analogs nearly all work by inhibiting elongation of the viral nucleic acid chain by a nucleic acid polymerase the reverse transcriptase inhibitors work in the same way protease inhibitors are enzymes which build protein structures stop production of the capsid influenza antiviral agents The adamantanes amantadine and rimantadine are synthetic amines that interfere with an influenza A ion transport protein, inhibiting virus uncoating and subsequent eplication. The neutaminidase inhibitors oseltamivir (tamiflu®) and zanamivir (Relanza®) block the active site of neuraminidase in influenza A and B viruses, inhibiting virus release from infected cells. Zanamivir is used only for treatment of influenza, whereas oseltamivir is used for both treatment and prophylaxis. The adamantanes are less useful than the neuraminidase inhibitors because resistance to adamantanes develops rapidly in strains of influenza virus interferons are chemical messages sent from one cell to another a cell is infected message is sent to another cell(healthy) and says I’m infected when the cell gets the message it starts doing the antiviral things that it can so it prevents new cells from being infected complex to work with created in tiny amounts tissue specific toxic at high levels if it is a virulent and the virus takes over interferon can’t be produced in time antifungal drugs ergosterol inhibitors Ergosterol in fungal cytoplasmic membranes replaces the cholesterol found in animal cytoplasmic membranes. Can get as cream or pill echinocandins screw up the fungi cell wall resistance mechanisms at least six different reasons, some microorganisms are naturally resistant to certain antibiotics. (1) The organism may lack the structure an antibiotic inhibits. (2) The organism may be impermeable to the antibiotic. (3) The organism may be able to alter the antibiotic to an inactive form(4) The organism may modify the target of the antibiotic(5) The organism may develop a resistant biochemical pathway.(6) The organism may be able to pump out an antibiotic entering the cell, a process called efflux resistance can be genetically encoded by the microorganism on either the bacterial chromosome or on a plasmid called an R not all bacteria will use one or the other to resistance often the resistant is a combo of things preventing resistance immunize to prevent common diseases avoid unnecessary introduction of parenteral devices such as catheters target the pathogen access the experts practice anti microbial control use local data treat infection not contamination treat infection not colonization treat with least exotic antimicrobial agent that will eliminate the pathogen monitor antimicrobial use isolate the pathogen break the chain of contagion formation of new it’s a pain According to pharmaceutical industry estimates, about 7 million candidate compounds must be screened to yield a single useful clinical drug. Drugs effective in the laboratory must then be tested for efficacy and toxicity in animals and finally in clinical tries in humans. Animal testing requires multiple trials over several years to ensure that the candidate drug is both effective and safe. Clinical trials in humans to check efficacy and safety take additional years for each drug. The total time for discovery and development for each drug typically takes 10-25 years before it is approved for clinical use The cost of discovery and development, from the laboratory through clinical trials, is estimated at over $500 million for each new drug approved for human use. Bacteriophages are viruses that infect bacteria Phages interact with individual bacterial cell surface components and show specificity for particular bacterial species. The attached phage enters the cell, replicates, and kills the bacterial host in the process. Efficacy and efficiency largely untested somewhat controversial can acquire resistance to a phage bacterio phage therapy will likely be susceptible to resistance, just as for most chemical antimicrobial agents. Interactions with humans colonization by microorganisms in utero develop in a sterile environment and have no exposure to microorganisms once birth happen you are contaminated to mos as you grow you build up the mos that will live with you depending on what you eat depends on what you will have where you live will also affect based on what you are exposed to pathogens host what the organism lives on they carry it parasite another organism that lives on or in the host and cause damage not kill pathogens an organism usually a microorganism that causes disease so don’t hurt us a pathogen will cause medical problems pathgenicity the ability of a parasite to inflict damage on the host virulence the degree of pathogenicity displayed by a pathogen opportunistic pathogen an organism that causes disease in the absence of normal host resistance in normal place doesn’t cause problems infection and disease infection refers to any situation in which a microorganism is established and growing in a host, whether or not the host is harmed acute problems. Disease is damage or injury to the host that impairs host function. Cause major problems host parasite interactions the conditions have to be proper for growth such as pH, osmotic pressure ect if conditions not right they won’t infect infection process 2 places you get infections skin if there is a break most effected is the mucous membranes lining or the respiratory system lining of the urogenital and gastrointestinal system these barriers are broken easily it depends on who the infector is for where they will infect normal microbial inhabitance of skin not a favorable place for abundant growth most associated directly or indirectly with sweat glands thrive in warm humid places order results from the mos hair follicles provide attractive habitat for mos just below the skin sweat has lysimes that lyce the mos this is a built in defense Although the resident microflora remains more or less constant, various environmental and host factors may influence its composition. (1) The weather may cause an increase in skin temperature and moisture, which increases the density of the skin microflora. (2) The age of the host has an effect; young children have a more varied microflora 3) Personal hygiene influences the resident microflora; individuals with poor hygiene usually have higher microbial population densities on their skin. Organisms that cannot survive on the shin generally succumb from either the skin’s low moisture content or low pH 4) life style someone who works outside will have more diverse microbiota than someone inside normal inhabitance of the oral cavity the avrg person has 5-600 species of bacteria living in mouth most arnt doing anything just digesting food saliva has lysozyme that causes the cell to lyse most have adapted new ones will be affected if you don’t brush your teeth there are mos that attach and create biofilms mostly in the gingival cavity you may get a thick enough plaque layer that as a waste product produce acid that cause tooth decay have anaerobic process most of these bacteria are going to be facultative anaerobes or aerotolerant carry on fermentation produce acid cavities depend on what you eat more futosose more damage lack of brushing teeth more damage normal inhabitance of the gastrointestinal track depending on what part you look at it has a pretty well developed microbial community varies on where you talking about esophagus not much living there the gut nasty place to live low pH digestive enzymes found in almost everyone is the helicobacter can lead to ulcers a lot of the stomach probably have 7-80 species living there hard to culture and sm intestine has differ pHs more live in the lower part more complex ecosystem bacteria are hard to culture lg intestine about 700 living there all normally good for you some pathogens but in sm numbers so can’t compete with good so don’t harm you until you take antibiotic that kills off good ones and release the sm pops a lot are neither helping nor harming you they contribute by vitamin synthesis, b12 gas production odor production organic acids production glycosidase reactions steroid metabolism 1/3 of the weight of fecal matter is mad up by bacteria you are many ecosystems walking around other body regions respiratory tract fairly clean find most in nasal cavity pharynx little bit live in trachea shouldn’t have any in lungs urogenital tract not much lives here more in female than male female have higher infection rate than males harmful microbacteria humans entry of pathogen into the host specific adherence most pathogens are host and tissue specific only going to attack what its adapted to attack evolutionary chg is now some can attack birds and us ect invasion can be difficult has to find a breach in skin or mucous some can secrete digestive enzymes that make a hole in that membrane not anybody that does this with the skin so it would be mucous colonization and growth you can be invaded by something and that’s ok as long as you don’t have a great deal of colonization and growth this makes the difference between an infection and disease colonization depends on host factors nutrients, pH, temp have to be right for the organism or no growth of the colony localization in the body also plays a part most are fairly localized in the body if extensive bacterial growth in tissues occurs, some of the organisms are usually shed into the bloodstream in large numbers, a condition called bacteremia. Widespread infections of this type almost always start as a local infection in a specific organ such as the kidney, intestine, or lung. Some bacteria don’t need to become very infective or widespread to kill you virulence attenuation decrease or loss of virulence the longer the culture sits the less strength it has and numbers it has stops growing toxicity and invasiveness toxicity is the ability of an organism to cause disease by means of a toxin that inhibits host cell function or kills the host cell invasiveness is the ability of a pathogen to grow in host tissue in such lg numbers that it inhibits host function both causes tissue damage toxin by producing exotoxins that destroys tissue and the other by physically destroying tissues virulence factors the more virulent the disease the greater the affect hyaluronic acid lots of organisms produce Hyaluronidase digests the intercellular matrix, enabling these organisms to spread from an initial infection site. Bacteria can also produce particular enzymes that break down differ parts of a cell can produce other things that also add to the virulence such as enzymes that break down blood clots in a wound that surround a bacteria some may produce coagulase which cause clots to occur prevent antibodies from getting to them Exotoxins toxins produced by the bacteria and released into its environment as its growing cytolitic produce proteins that damage the host cytoplasmic membrane causing cell lysis and death caring on chemical warfare punches a hole in the plasma membrane allowing outside stuff to come in and cell contents to go out disrupting cell function protein synthesis inhibitors atacks the cell and may shut down various functions inhibit protein synthesis tetanus and botulinum C.botulinum sometimes grows directly in the body causing infant or wound botulism and also grows and produce toxin in improperly preserved food death is usually from respiratory failure due to flaccid muscle paralysis toxin is produced as the waste product of these guys The action of botulinum toxin from Clostridium botulinum. (a) Upon stimulation of peripheral and cranial nerves, acetylcholine (A) is normally released from vesicles at the neural side of the motor end plate. Acetylcholine then binds to specific receptors on the muscle, inducing contraction. ( Botulinum toxin acts as the motor end plate to prevent release of acetylcholine (A) from vesicles, resulting in a lack of stimulus to the muscle fibers, irreversible relaxation of the muscles, and flaccid paralysis C tetany grows in the body in deep wounds punctures that become anoxic does not invade the body from initial site of infection it can spread via neural cells cause spastic paralysis leading to death The action of tetanus toxin from Clostridium tetany. (a) Muscle relaxation is normally induced by glycine ( release from inhibitory interneurons. Glycine acts on the motor neurons to block excitation and release of acetylcholine (A) at the motor end plate. ( Tetanus toxin binds to the interneuron to prevent release of glycine from vesicles, resulting in a lack of inhibitory signals to the motor neurons, constant release of acetylcholine to the muscle fibers, irreversible contraction of the muscles, and spastic paralysis. Enterotoxins are exotoxins produced that deal with the gut lining cause leaking of gut endotoxins are made up of parts of the cell wall of bacteria they’re cell bound and released in lg amounts only went lyses as long as the cell is alive it fine if antibiotics given and person gets worse they’re in crisis stage then get better can cause fever diarrhea, rapid decrease in lymphocyte, leukocyte, and platelet numbers, release of cytokines chemicals released from one cell and cause something to happen in another allows fluid into cell by wreaking the capillaries which then cause blood volume to drop means b/p is going to drop and the generalized inflammation lg doses can cause death host factors in infection age- young people who haven’t developed a good immune system older people alter about 55 the immune system becomes more changeable stress- hormones released in stress can inhibit normal immune responses diet- inadequate diets low in protein and calories alter the normal flora, allowing opportunistic pathogens a better chance to multiply and increasing susceptibility of the host to known pathogens. Compromised one in whom one or more resistance mechanisms are inactive and in whom the probability of infection is therefore increased people who get sick in the hospital are said to have nosocomial infections also people already sick, smoke drink too much have poor diet fill own gas take breathing in the fumes may be compromised genetic component some respond quicker innate resistance to infection the factors are things with you at all times things that prevent infectious agents from entering you your resistance as a species allows you not to get some diseases some do cross EX Anthrax infects a variety of animals, causing diease symptoms varying from mild pustules in cutaneous anthrax in humans to fetal blood poisoning in cattle. However, pulmonary, or airborne anthrax, such as that induced by weaponized strains use for bioterrorism is almost universally fetal in humans tissue specificity if pathogens adhere to an exposure site if it is not compatible with their nutritional and metabolic need they can’t colonize you won’t get tb of the foot physical and chemical barriers nature of the skin and secretions of the skin immunity innate/nonspecific immunity the bodies built in ability to recognize and destroy pathogens or their products responds to every invader the same way adaptive/specific immunity the acquired ability to recognize and destroy a pathogen or its products and is activated by exposure of the immune system to the pathogen. Adaptive responses are directed at discrete molecules called antigens (what your body is recognizing as being a nonself entity) on pathogens designed to attack only that one pathogen each has differ response some can cross over to protect both such as cow pox and small pox if you get cow pox you don’t get small pox you have to be exposed to agents to get immunity to them cells and organs of the immune system blood and lymph components if o2 stressed higher number of rbc if disease stressed higher number of leukocytes white blood cells always about the same number of trmylocytes produced all carried in plasma a liquid containing proteins other solutes and suspended cells the remaining fluid is called serum which contains no cells or clotting proteins does contain soluble antibody proteins innate immune responses type of response depend on how bad the problem is generally the first responder is the phagocytes they engulf the cells 3 parts to this process the first is monocytes don’t do anything the differentiate into dendritic cells and macrophages these are lg cells with the capability of engulfing things macrophages especially the macrophage engulfs whatever it might be into a special vacuole digestive enzymes dumped in the macrophage and dendritic cells spend most of their time digesting things neutrophils quicker than macrophages more often 1st on scene cause smaller cells they engulf limited in the numbers they can engulf they eat so many then die most buss in a wound is these APCS antigen presenting cells basis for the specific immune response macrophages with specialized functions the macrophage can detect the difference between your cells and invading cells inhibiting phagocytes some bacteria can get around the macrophages some let themselves get engulfed then reproduce inside it others will secrete chemicals that neutralize the macrophages chemicals some produce leukocidins proteins that kill the macrophage capsules bigger infection the body might show inflammation is a nonspecific reaction to toxins and pathogens. Inflammation causes redness (erythema), swelling (edema), pain, and heat, usually localized at the site of infection. The molecular mediators of inflammation include a group of proteins called cytokines and chemokines. These proteins are produced by various immune cells, but especially by phagocytes and lymphocytes. Process is increase the blood vessel permeability and chemotacic attraction of phagocytes also fever is good bacteria can’t get iron out of blood as easy and become less efficient if you have a systemic infection better not to have temp low but not too high systemic inflammation and septic shock if you have the capillaries all over body dilating the b/p drops a lot if this is low enough you have a short period of time before you die the fluid lost from the cardiovascular system can be a problem also high fever Complement system real important component in generalized sock what’s involved with it is a number of proteins is a system that responds in a cascade action to infection minor infection one response little more infection more response major infection big response the difference between this and the specific immune response is that it doesn’t matter what you’re infected with it’s the degree of infection by anything C3 is stimulated by antibody binding to antigen this initial protein is split into 2 components amongst them do 3 differ things C3a interacts with mast cells these are modified white blood cell that have particles of histone ( proteins that play a role in inflammation of spots ) in them histones are stimulated to be released by mast cells then you enhance the inflammation there C3b they attach to cell body surface area to allow the macrophage to latch onto the thing easier if the proteins are on the surface proteins on the surface provide appoint of attachment for antibodies this is a direct interaction between the complement protein and the bacteria if this doesn’t work protein C5 is stimulated splits up into 2 parts C5a is going to stimulate more mast cells and attract macrophages and neutrophiles C5b is going to interact with C6 which stimulated C7 C8 C9 and maybe some others what these proteins do is organize themselves and again this is not exactly what happening but from a functional point of view what they do is punch a hole in the cell wall of the bacterium they organize themselves to keep the cell open so materials will leak out and the bacteria are lysised these proteins are circulating in the blood stream now the adaptive response 2 basic kids of cells t cell receptors and the cells that are doing things are the t cells called this because they mature in the thymus what it does is get close to the bad cell and releases proteins that punch holes in it can do this one at a time move around in body cell mediated immunity the killing of bad cells B cells are fixed cells what it does is detects antigens in your system then produces antibodies to attack the antigen 3 general characteristics of this apply to both T and B cells specificity- immune cells recognize and react with individual molecules called antigens via direct molecular interactions memory- the immune response to a specific antigen is faster and stronger upon subsequent exposure because the initial antigen exposure induced growth and division of antigen reactive cells resulting in multiple copies of antigen reactive cells tolerance- immune cells aren’t able to react with self antigen. Self-reactive cells are destroyed during development of the immune response. Antigens and antigen presentation- Antigens are substances that react with antibodies or TCRs. Most, but not all, antigens are immunogens, substances that induce and immune response. Intrinsic Properties of Immunogens- Molecular size is an important component of immunogenicity. Low-molecular weight compounds called haptens cannot induce an immune response but can bind to antibodies. Haptens can include sugars, amino acids, and other low-molecular weight organic compounds. Most immunogens have a molecular weight of 10,000 or greater. Thus, sufficient molecular size is an indication of potential immunogenicity. Complex, nonrepeating polymers such as proteins are usually effective immunogens. Molecular complexity of a substance is another predictor of immunogenicity. Starch is a polymer. Large, complex macromolecules in insoluble or aggregated form. Usually excellent immunogens. Extrinsic Properties of Immunogens- Extrinsic factors also influence immunogenicity. Include the dose, rout, and foreign nature of the immunogen Larger dose = greater response. Doses of 10 u.g. to 1g are effective in most mammals. Immunizations given by parenteral routes, usually by injection, are normally more effective than those given topically or orally. Most important extrinsic feature is that an effective immunogen must be foreign with respect to the host. Self-antigens are not recognized, and thus individuals are tolerant of their own self-molecules. Antigen binding by antibodies and T cell receptors- the antibody or RCR does not interact with the antigenic macromolecule as a whole, but only with a distinct portion of the molecule called an antigenic determinant or epitope. Antigenic determinants may include sugars, amino acids, and other organic molecules. Antibodies interact with accessible surface antigenic determinants. A sequence of four to six amino acids is the optimal size of an antigenic determinant on a protein. The surface of a bacterial cell or virus consists of a mosaic of proteins, polysaccharides, and other macromolecules, all with individual determinants. TCRs recognize determinants only after the immunogens have been partially degraded. Degraded immunogens are then presented to T cells on the surface of specialized APCs or target cells. Specificity is not absolute, and an individual antibody or TCR may react to some extent with several different but structurally similar determinants. The antigen that induced the antibody or TCR is called the homologous antigen, and the noninclucing antigens that react with the antibody are called heterologous antigens. Antigen presentation to T lymphocytes- The T cell receptor (TCR) is a membrane-spanning protein that extends from the T cell surface into the extracellular environment. Each T cell has thousands of copies of the same TCR on its surface. Consists of two polypeptides, and a chain and a B chain. Major histocompatibility complex (MHC) proteins- MHC proteins are encoded by a linked set of genes found in all vertebrates called the MHC. In humans, collectively called human leukocyte antigens or HLAs. MHC protein function primarily as antigen-presenting molecules, binding pathogen-derived antigens and displaying these antigens for interaction with TCRs. Antigen presentation- the MHC proteins expressed on the cell surface reflect the composition of the proteins inside the cell. T helper cells: activating the immune response- Tí1 cells and Macrophage activation- Macrophages play a central role as APCs in both antibody-mediated and cell-mediated immunity. Macrophages engulf antigens that are then processed and present antigen to Tí cells. Macrophages take up and kill foreign cells, and ability stimulated by Tí1 cells and the cytokines they produce. Tí1-activated macrophages kill intracellular bacteria that normally multiply in nonactivated macrophages or other cell types. Some bacteria survive and multiply within macrophages. Tí2 cells and B cell activation- Tí2 cells play a pivotal role in B cell activation and antibody production. B cells make antibodies. Mature B cells are coated with antibodies that act as antigen receptors. Antigen binds to the B cell antigen receptors, but the B cell does not immediately produce soluble antibodies. The bound antigen is first endocytosed and degraded in the B cell. Peptides from the degraded antigen are then presented on the B cell’s MHC II proteins. Antibodies- antibodies, or immunoglobulins (Ig), are protein molecules that interact specifically with antigenic determinants. They are found in the serum and other body fluids such as gastric secretions and milk. Serum containing antigen-specific antibody is called antiserum. Immunoglobulin G structure- IgG, the most common circulating antibody, has a molecular weight of about 150,000and is composed of four polypeptide chains. Heavy chains and light chains- Each IgG heavy chain is composed of several distinct parts called domains, the variable, and constant. The antigen-binding site- The antigen binding site of IgG and all other antibodies forms by cooperative interaction between the variable domains of both heavy and light chains. T cell-B cell interactions- a reactive B cell exposed to antigen for the first time binds the antigen through its antigen-specific surface receptor; membrane-bound antibody. Antigen-antibody complex is then internalized, and the antigen is processed to peptides for loading onto MHC II proteins. Generation of antigen receptor diversity- Each individual is capable of producing billions of different antibodies and TCRs, with each receptor aimed to specifically interact with one of the countless antigens in our environment. Immune receptor diversity is generated by a unique mechanism exclusive to only T and B cells. Antibody production and immune memory- Starting with B cell, antibody production begins with antigen exposure and culminates with the production and secretion of an antigen specific antibody according to the following sequence: 1) Antigens are spread via the lymphatic and blood circulatory systems to nearby secondary lymphoid organs such as lymph nodes, spleen, or mucosal-associated lymphoid tissue. 2) Following the initial antigen exposure, each antigen stimulated B cell multiplies and differentiates to form antibody-secreting plasma cells and memory cells. Plasma cells are relatively short-lived but produce and secrete large amounts of mostly IgM antibody in the primary antibody response. 3) The memory B cells generated by the initial exposure to antigen may live for years. If there is a later reexposure to the immunizing antigen, memory B cells need no T cell activation. A rise in antibody titer is called the secondary antibody response.
|Posted by: Darkender Apr 9 2009, 02:18 AM|
Trying to make yourself a vet.
|Posted by: Jailer411 Apr 9 2009, 10:27 PM|
Not really,I just got bored.
Also, I like seeing how members used to act back then. Funny stuff.
|Posted by: treacherous Apr 9 2009, 10:29 PM|
and what was so funny about how I acted?
|Posted by: Jailer411 Apr 9 2009, 10:30 PM|
I read all of the RP party threads.
|Posted by: Darkender Apr 9 2009, 10:53 PM|
The only person that I remember changing is Leo Sanders.
|Posted by: Bandit Apr 9 2009, 10:54 PM|
Yep, that guy was annoying.
|Posted by: Darkender Apr 9 2009, 10:58 PM|
|Posted by: Jailer411 Apr 9 2009, 10:59 PM|
|Posted by: Darkender Apr 9 2009, 11:04 PM|
I wonder why people think its named after me...
|Posted by: Jailer411 Apr 9 2009, 11:07 PM|
Let's find out.
|Posted by: Darkender Apr 9 2009, 11:12 PM|
|Posted by: Jailer411 Apr 9 2009, 11:13 PM|
:Jailer411:, yup, still not working
|Posted by: Bandit Apr 9 2009, 11:15 PM|
|Grano is very popular. I wonder if he was in High school.......|
|Posted by: The Ripper Apr 10 2009, 03:13 AM|
|Hey Grano, http://www.bloodcalibur.com/forums/|
|Posted by: Granobulax Apr 21 2009, 04:09 AM|
|Posted by: Granobulax Apr 21 2009, 04:11 AM|
| Here's my next study card. It's almost 13,000 words long and is over 80,000 characters which is why it won't fit in one post. Well, here it is, my 3x5 card...
Chapter 30 Immunity and prevention of infectious diseases: Immunity generated by natural exposure to pathogens is an effective way to resist infections. We can safely induce adaptive immune responses to various pathogens and their products. Artificial immunization remains our best weapon against many infectious diseases. Natural Immunity: Both the innate and adaptive immune responses protect the host from infections by pathogens, and both innate and adaptive immunity are essential for survival. Adaptive immunity and prevention of infectious disease: animals normally develop natural active immunity by acquiring a natural infection that initiates an adaptive immune response. Natural active immunity is the outcome of exposure to antigens through infection and usually results in protective immunity conferred by antibodies and T cells. The importance of active immunity in disease resistance is shown in individuals who are immunocompromised due to certain genetic disorders or infection. There is also natural passive immunity. For example, for several months after birth, newborns have maternal IgG antibodies, transferred across the placenta before birth, in their blood. IgA antibodies are also transferred in breast milk from colostrum. Active and passive immunity are contrasted in and actively through immune responses to infections, or naturally and passively through antibody transfer across the placenta or in breast milk. Artificial immunity and immunization: The purposeful artificial induction of immunity to individual infectious diseases is a major weapon for the treatment and prevention of diseases. There are two ways by which artificial immunity can be induced. An individual may be purposefully exposed to a controlled dose of harmless antigen to induce formation of antibodies, a type of immunity called artificial active immunity because the individual promotes vaccination. Alternatively, an individual may receive injections of an antiserum (serum containing antibodies from the blood of an immune individual) or purified antibodies (immunoglobulin or gamma globulin) derived from an immune individual. This is called artificial passive immunity because the individual receiving the antibodies played no active part in antibody production. In active immunity, introduction of antigen induces changes in the host: The immune system produces large quantities of antibodies and T cells in the primary response. A second (“booster”) dose of the same antigen results in a faster response resulting in much higher levels of antibodies and T cells. This is known as a secondary immune response, or a memory response. Active immunity often remains throughout life as a result of immune memory. These antibodies gradually disappear from the body of a passively immunized individual. Artificial passive immunity is usually therapeutic. Immunization: The antigen or antigen mixture used to induce artificial active immunity is known as a vaccine or an immunogen, and the process of generating an artificial active immune response is immunization. Immunization with a vaccine designed to produce active immunity may introduce risks for infection and other adverse reactions. To reduce risks, pathogens or their products are often inactivated. For example, many immunogens consist of pathogenic bacteria killed by chemical agents. Many exotoxins can be modified chemically so they retain their antigenicity but are no longer toxic. Such a modified exotoxin is called a toxoid. Immunization with live cells or virus is usually more effective than immunization with dead or inactivated material. It is often possible to isolate a mutant strain of a pathogen that has lost its virulence but still retains the immunizing antigens; strains of this type are called attenuated strains. Most effective viral vaccines are attenuated. Attenuated vaccines tend to provide long-lasting T cell-mediated immunity , as well as a vigorous antibody response and a stron secondary response upon reimmunization. However, the attenuated strains are difficult to select, standardize, and maintain. Bacterial vaccines are nearly always provided in an inactivated form. Immune response diseases: Immune reactions can cause host cell damage and disease. Hypersensitivity responses are inappropriate immune responses that result in host damage. Hypersensitivity diseases are categorized according to the antigens and effector mechanism that produce disease. Superantigens are proteins produced by certain bacteria and viruses that cause widespread stimulation of immune cells, resulting in host damage by activating massive inflammatory responses. Allergy, hypersensitivity, and autoimmunity: Antibody-mediated immediate hypersensitivity is commonly called allergy. Cell-mediated reactions also cause disease in the form of delayed hypersensitivity. Autoimmune diseases are mediated by immune reactions directed against self antigens. These diseases are categorized as type I, II, III, or IV hypersensitivities based on symptoms and immune effectors. Immediate hypersensitivity: Immediate hypersensitivity, or type I hypersensitivity, is caused by release of vasoactive products from IgE antibody-coated mast cells. Immediate hypersensitivity reactions occur within minutes after exposure to antigen. Immediate hypersensitivity reactions can be very mild or can cause a life-threatening reaction called anaphylaxis. Antigens that cause type I hypersensitivities are called allergens. About 20$ of the population suffers from immediate hypersensitivity allergies to pollens, molds, animal dander; certain foods, insect venoms, and other agents. Almost all allergens enter the body at the surface of mucous membranes. Mast cells are nonmotile granulocytes associated with the connective tissue adjacent to capillaries throughout the body. Cross-linking of two or more IgEs by an antigen triggers the release of soluble allergic mediators from the mast cells, a process called degranulation. These mediators cause allergic symptoms within minutes of antigen exposure. In general, these symptoms are relatively short-lived. The primary chemical mediators released from mast cells are histamine and serotonin that cause rapid dilation of blood vessels and contraction of smooth muscle, initiating the symptoms of systemic anaphylaxis. These symptoms include severe respiratory distress caused by bronchial edema, vasodilation, flushed skin, mucus production, sneezing, and itchy, watery eyes. A person can die from anaphylactic shock. Fortunately, most allergic reactions are limited to mild local anaphylaxis with symptoms such as itchy, watery eyes. Less serious allergic symptoms are treated with drugs called antihistamines that neutralize the histamine mediators. Delayed-type hypersensitivity: Delayed-type hypersensitivity (DTH) or type IV hypersensitivity is cell-mediated hypersensitivity characterized by tissue damage due to inflammatory responses produced by TH1 inflammatory cells. Delayed-type hypersensitivity symptoms appear several hours after secondary exposure to the eliciting antigen, with a maximal response usually occurring in 24-48 hours. Typical antigens include certain microorganisms, a few elf-antigens, and several chemicals that covalently bind to the skin, creating new antigens. Hypersensitivity to these newly treated antigens is known as contact dermatitis. An example of delayed-type hypersensitivity is the development of immunity to the casual agent to tuberculosis, mycobacterium tuberculosis. Autoimmune diseases: T and B cells destined to react with self-antigens are normally eliminated during the process of lymphocyte maturation. In some individuals, T and B cells can be activated to produce immune reactions against self-proteins, leading to autoimmune diseases. TH1-mediated delayed hypersensitivity can cause autoimmune responses directed against self-antigens, as is the case for allergic encephalitis. In type I (juvenile) diabetes mellitus; TH1 cells cause inflammatory reactions that destroy the beta cells of the pancreas. Some autoimmune diseases are caused by autoantibodies, antibodies that interact with self-antigens. In many cases, antibodies are directed to certain organ-specific antigens. For example, in Hashimoto’s disease, autoantibodies are made against thyroglobulin, a product of the thyroid gland. The disease affects thyroid function and is classifies as type II hypersensitivity: Antibodies interact with antigens found on the surface of host cells and initiate destruction of the tissue. Systemic lupus erythematosus (SLE) is an example of a disease caused by type III hypersensitivity: This disease and others like it are caused by autoantibodies directed against soluble, circulating self-antigens. In SLE, the antigens include nucleoproteins and DNA. Antibodies bid to soluble proteins, producing insoluble immune complexes. Disease results when circulating antigen-antibody complexes deposit in different body tissues such as the kidneys, lungs, and spleen. Superantigens: Certain exotoxins, the superantigens, act indirectly on host cells. These exotoxins do not act directly on host cell targets, but rather subvert the immune system to cause extensive host cell damage. Superantigen activation of T cells: Superantigens are proteins capable of eliciting a very strong response because they activate more T cells than a normal immune response. Superantigens are produced by many viruses and bacteria and interact with TCRs. Streptococci and staphylococci produce several different and very potent superantigens. Superantigen interaction with the TCR differs from conventional antigen-TCR binding. Autoimmune diseases of humans: Juvenile diabetes; pancreas; cell-mediated immunity and autoantibodies against surface and cytoplasmic antigens of islets of Langerhans (II and IV), Myasthenia gravis; skeletal muscle; autoantibodies against acetylcholine receptors on skeletal muscle (II), Doodpasture’s syndrome; kidney; autoantibodies against basement membrane of kidney glomeruli (II), Rheumatoid arthritis; cartilage; autoantibodies against self IgG antibodies, which form complexes deposited in join tissue, causing inflammation and cartilage destruction (III), Hashimoto’s disease (Hypothyroidism); thyroid; autoantibodies to thyroid surface antigens (II), Male infertility (some cases); sperm cells; autoantibodies agglutinate host sperm cells (II), Pernicious anemia; intrinsic factor; autoantibodies prevent absorption of vitamin B12 (III), Systemic lupus erythematosus; DNA, cardiolipin, nucleoprotein, blood clotting proteins; autoantibody response to various cellular constituents results in immune complex formation (III), Addison’s disease; adrenal glands; autoantibodies to adrenal cell antigens (II), Allergic encephalitis; brain; cell-mediated response against brain tissue (IV), Multiple sclerosis; brain; cell-mediated and autoantibody response against central nervous system (II and IV) Chapter 32 Immunology and clinical diagnostic methods: Immunoassays are used in clinical, reference, and research laboratories to detect specific pathogens or pathogen products. Immunoassays for infectious disease: Many immunoassays utilize antibodies specific for pathogens or their products for in vitro tests designed to detect individual infectious agents. In some cases, patient immune responses are monitored to obtain evidence for infection by a pathogen. Antibody titers, skin tests, and the diagnosis of infectious disease: Isolation of a pathogen is not always possible or practical to confirm diagnosis of an infectious disease. An alternative approach that provides strong circumstantial evidence for infection by a particular pathogen is to measure antibody titer (quantity) against an antigen or antigens produced by the suspected pathogen. If an individual is infected with a suspected pathogen, the immune response—in this case, the antibody titer—to that pathogen should be elevated. Tests such as agglutination, enzyme-linked immunosorbent assay, and radioimmunoassay are commonly used. The titer is defined as the highest dilution (lowest concentration) of serum at which the antigen-antibody reaction is observed. These methods are called serological tests because they make use of patient serum antibodies. A single measure of antibody titer indicates previous infection or exposure to a pathogen. In most cases the mere presence of antibody does not indicate active infection. Antibody titers typically remain detectable for long periods after a previous infection has been resolved. To link an acute illness to a particular pathogen, it is essential to show a rise in antibody titer in serum samples taken from a patient during the acute disease and later during the covalescent phase of the disease. Frequently, the antibody titer is low during the acute stage of the infection and rises during convalescence. A rise in antibody titer is the best indication that the illness is due to the suspected pathogen. In some cases, the presence of antibody in the serum may be due to a recent immunization. Skin testing is another method for determining exposure to a pathogen. The most commonly used skin test is the tuberculin test, which consists of an intradermal injection of a soluble extract from cells of Mycobacterium tuberculosis. A positive inflammatory reaction at the site of injection within 48 hours indicates current infection or previous exposure to M. tuberculosis. Skin tests are routinely used for diagnosing tuberculosis, Hansen’s disease (leprosy), some fungal diseases, and other infectious disease in which the antibody response is weak or nonexistent. If a pathogen is extremely localized, there may be little induction of an immunological response and no rise in antibody titer or skin test reactivity, even if the pathogen is proliferating profusely at the site of infection. A good example is gonorrhea, caused by infection of mucosal surfaces with Neisseria gonorrhoeae. Gonorrhea does not elicit a systemic or protective immune response, there is no antibody titer or skin test reactivity, and reinfection or individuals are common. In vitro antigen-antibody reactions: Serology—The study of antigen-antibody reactions in virto is called serology. Serological reactions are used for many diagnostic immunology tests. Antigen-antibody reactions rely on the specific interaction of antigenic determinants with the variable region of the antibody molecule. Various serological tests are used to identify antigens, depending on the properties of the antigen and on the conditions chosen for reaction. Specificity and sensitivity: The usefulness of a serological test for diagnostic purposes depends on the test’s specificity and sensitivity. Specificity is the ability of an antibody preparation to recognize a single antigen. Optimal specificity implies that the antibody is specific for a single antigen, will not cross-react with any other antigen, and therefore will not provide false positive results. Specificity must be defined in terms of reactions with positive- and negative- control antigens. Specificity for each test must be determined experimentally and verified every time the test is used. Sensitivity defines the lowest amount of an antigen that can be detected. The highest level of sensitivity requires that the antibody in a test be capable of identifying a single antigen molecule. High sensitivity prevents false-negative reactions. The amount of antigen detected by each test system is proportional to the amount of antibody used. ELISA tests require 100,000 times less antibody and can detect 1 million times less antigen (0.1-1.0 ng quantities) than precipitation tests. Thus, ELISA tests are amon the most sensitive serological tests. Neutralization: Neutralization is the interaction of antibody with antigen to block or distort the antigen sufficiently to reduce or eliminate its biological activity. Neutralization reactions can occur in vitro or in vivo. Neutralization of a microbial toxin by specific antibody occurs when the toxin and specific antibody combine in such a way that the active portion of the toxin is blocked. Neutralization reactions can block the effects of many bacterial exotoxins. An antiserum containing an antibody that neutralizes a toxin is called an antitoxin. Antitoxin therapy is used to treat botulism, tetanus, and diphtheria, all diseases that result from bacterial exotoxins. Neutralization reactions may also occur when viruses are bound by specific antibodies. Neutralization reactions can be used for in vitro testing using patient serum, but are not used in routine diagnostic laboratories because neutralization tests require biologically active test systems. Precipitation: Precipitation results from the interaction of a soluble antibody with a soluble antigen to form an insoluble complex. Antibody molecules generally have two antigen binding sites (that is, they are bivalent). Therefore, each antibody can bind two separate antigen molecules. Precipitation occurs maximally, however, only when there are optimal proportions of the two reacting substances. The presence of either antigen or antibody in excess quantities results in the formation of soluble immune complexes. Precipitating reactions carried out in agar gels, called immunodiffusion tests, are used to study the specificity of antigen-antibody reactions. Both antigen and antibody diffuse outward from separate wells cut in an agar gel, and precipitation bands form in the region where antibody interacts with antigen in optimal proportions. If two antigens in adjacent wells are identical, they will form a single, fused, precipitin band. This is called a line of identity. If adjacent wells contain one antigen, a line of partial identity will form. Agglutination: Agglutination is the visible clumping of a particulate antigen when mixed with antibodies specific for the particulate antigens. Agglutination tests are about 100 times more sensitive than precipitation tests and are widely used in clinical and diagnostic laboratories; they are simple to perform, highly specific, inexpensive, rapid, and reasonably sensitive. Standardized agglutination tests are used for the identification of blood group (red blood cell) antigens as well as many pathogens and pathogen products. Direct agglutination: Direct agglutination results when soluble antibody causes clumping due to interaction with an antigen that is an integral part of the surface of a cell or other insoluble particle. Direct agglutination procedures are used for the classification of antigens found on the surface of red blood cells (erythrocytes). Agglutination of red blood cells is called hemagglutination and is the basis for human blood typing. Passive agglutination: Passive agglutination is the agglutination of soluble antigens or antibodies that have been adsorbed or chemically coupled to cells or insoluble particles such as latex beads or charcoal particles. The insolubilized antigen or antibody can then be detected by agglutination reactions. The cell or particle serves as an inert carrier. Passive agglutination reactions can be up to five times more sensitive than direct agglutination tests, significantly increasing sensitivity. The agglutination of antigen-coated or antibody-coated latex beads by complementary antibody or antigen form a patient is a typical method of rapid diagnosis. Small latex beads coated with a specific antigen are mixed with patient serum on a microscope slide and incubated for a short period. If patient antibody binds the antigen on the bead surface, the mildy white latex suspension will become visibly clumped, indicating a positive agglutination reaction. Latex agglutination is also used to detect bacterial surface antigens by mixing a small amount of a bacterial colony with antibody coated latex beads. Latex agglutination tests are also used to detect serum antibodies directed against the body’s own Ig, DNA, and other macromolecules. Fluorescent antibodies: Antibodies can be chemically modified with fluorescent dyes. These modified antibodies can then be used to detect antigens on intact cells. Fluorescent antibodies are widely used for diagnostic and research applications. Fluorescent methods: Distinct direct and indirect fluorescent antibody-staining methods are used. In the direct method, the antibody targeted against the surface antigen is itself covalently linked to the fluorescent dye. In the indirect method, the presence of a nonfluorescent antibody on the surface of a cell is detected by the use of a fluorescent antibody directed against the nonfluorescent antibody. Applications: In a typical test using fluorescent antibodies, a specimen containing a suspected pathogen is allowed to react with a specific fluorescent antibody and observed with a fluorescent microscope. If the pathogen contains surface antigens reactive with the antibody, the pathogen cells fluoresce. Fluorescent antibody assays are also used to aid in the diagnosis of noninfectious diseases. Fluorescent antibodies can also be used to separate mixtures of cells into relatively pure populations or to define the numbers of individual cell types in complex mixtures such as blood. Cells labeled with fluorescent antibodies can be visualized, counted, and separated ith an instrument called a fluorescence cytometer, or fluorescence activated cell sorter (FACS). Enzyme-linked immunosorbent assay and radioimmunoassay: Enzyme-linked immunosorbent assay (ELISA) and radio-immunoassay (RIA) methods are very sensitive immunological assays and are therefore widely used in clinical and research applications. ELISA and RIA employ covalently bonded enzymes and radioisotopes, respectively, to label antibody molecules, allowing detection of very small quantities of antigen-antibody complexes. ELISA: in ELISA, an enzyme is covalently attached to an antibody molecule, creating an immunological tool with high specificity and high sensitivity. The enzyme’s catalytic properties and the antibody’s specificity are unaltered. Typical bound enzymes include peroxidase, alkaline phosphatase, and B-galactosidase, all of which catalyze reactions that develop colored products that can be detected in very low amounts. Two different ELISA methodologies are used, one for detecting antigen (direct ELISA) and the other for detecting antibodies (indirect ELISA). For detecting antigens such as virus particles from a blood or fecal sample, the direct ELISA method is used. The specimen is added to the wells of a microtiter plate previously coated with antibodies specific for the antigen to be detected. If present in the sample, the virus particle will be bound by the antibodies. After washing away unbound material, a second antibody containing a conjugated enzyme is added. The second antibody is also specific for the antigen, and it binds to other exposed antigenic determinants. Following a wash, the enzyme activity of the bound material in each microtiter well is determined by adding the substrate for the enzyme. The enzyme catalyzes the conversion of the substrate to a colored product, which is detected with a spectrophotometer. The color produced is proportional to the amount of antigen present. To detect antibodies in human serum, an indirect ELISA is employed. An indirect ELISA is widely used to detect antibodies to human immunodeficiency virus (HIV) in human body fluids. Modified rapid ELISA procedures use reagents adsorbed to a fixed support material such as paper strips, nitrocellulose or plastic membranes, or plastic “dipsticks.” These tests cause a color change on the strip or stick in a very short time. These rapid “point of care” tests are diagnostic aids for infectious diseases such as HIV-AIDS or “strep throat.” Radioimmunoassay: Radioimmunoassay (RIA) employs radioisotopes as antibody or antigen conjugates instead of the enzymes used in ELISA. The isotope iodine-125 (125I) is commonly used as the conjugate because antibodies or antigens can be readily iodinated without disrupting their immune specificity. RIA is used clinically to measure rare serum proteins such as human growth hormone, glucagon, vasopressin, testosterone, and insulin present in humans in extremely small amounts. RIAs are also used in some tests for illegal drugs. In most cases, a direct RIA is employed. The direct assay is a two-step procedure. First, a series of microtiter wells are prepared containing known concentrations of pure antigen. Radiolabeled antigen-specific antibodies are added to the wells, and the radioactivity bound in each of these standard wells is measured. Next, a sample from a patient is boud to another well, and radioactive antibodies are added and measured, as before. The amount of radioactive bound by the patient sample is then compared to a standard plot generated from binding data obtained using the pure antigen, and the concentration of antigen in the patient sample is interpolated from the standard plot. RIA has the same sensitivity range as ELISA and can also be performed very rapidly. RIA is often used only when ELISA is not sufficiently specific or sensitive. Chapter 33 Principles of epidemiology: Individuals may acquire pathogens through infected vectors and vehicles and spread the pathogens to other members of a population. Epidemiology is the study of the occurrence, distribution, and determinants of health and disease in a population. It deals with public health. Many infectious diseases are adequately controlled in developed countries. Worldwide infectious diseases remain serious public health problems, accounting for nearly 30% of the 56 million annual deaths. The science of epidemiolody: to cause diseas, a pathogen must grow and reproduce in the host. For this reason, epidemiologists track the natural history of pathogens. In many cases, an individual pathogen cannot grow outside the host; if the host dies, the pathogen also dies. Pathogens that kill the host before they move to a new host will become extinct. Most host-dependent pathogens must therefore adapt to coexist with the host. A well-adapted pathogen lives in balance with its host, taking what it needs for existence and causing only a minimum of harm. Such pathogens may cause chronic infections in the host. When equilibrium between host and pathogen exist, both host and pathogen survive. New natural pathogens sometimes emerge for which the individual host, and sometimes the entire species, has not developed resistance. Such emerging pathogens often cause acute infections, characterized by rapid and dramatic onset. Organisms in the genus Clostridium, ubiquitous inhabitants of the soil, are occasional accidental human pathogens, causing life-threatening diseases such as tetanus, botulism, gangrene, and certain gastrointestinal diseases. The epidemiologist traces the spread of a disease to identify its origin and mode of transmission. The vocabulary of epidemiology: A disease is an epidemic when it occurs in an unusually high number of individuals in a population at the same time; a pandemic is a widespread, usually worldwide, epidemic. An endemic disease is one that is constantly present, usually at low incidence, in a population. An endemic disease implies that the pathogen may not be highly virulent, or the majority of individuals in the selected population may be immune, resulting in low disease incidence. As long as an endemic situation exists, the infected individuals are reservoirs of infection, providing a source of viable infectious agents from which other individuals may be infected. The incidence of a particular disease is the number of new and existing disease cases reported in a population in a given time period. The prevalence of a given disease is the total number of new and existing disease cases reported in a population in a given time period. A disease outbreak occurs when a number of cases are observed, usually in a relatively short period of time, in an area previously experiencing only sporadic cases of the disease. Diseased individuals who show no symptoms or only mild symptoms have what are called subclinical infections. Subclinically infected individuals are frequently carriers of a particular disease. Mortality and morbidity: The incidence and prevalence of disease, as determined from statistical analyses of illness and death records, is and indicator of the public health of a selected group such as the total global population or the population of a localized region, such as a city, state, or country. Mortality is the incidence of death in the population. In developing countries, infectious diseases are still major causes of mortality. Morbidity refers to the incidence of disease in populations and includes both fatal and nonfatal diseases. Morbidity statistics define the public health of a population more precisely than mortality statistics because many diseases have relatively low mortality. Disease progression: 1. Infection: The organism invades, colonizes, and grows in the host. 2. Incubation period: A period of time elapses between infection and the appearance of disease symptoms. 3. Acute period: The disease is at its height, with overt symptoms such as fever and chills. 4. Decline period: Disease symptoms are subsiding, any fever subsides, usually following a period of intense sweating, and a feeling of well being develops. 5. Convalescent period: The patient regains strength and returns to normal. Disease reservoirs and epidemics: Reservoirs are sites in which infectious agents remain viable and from which infection of individuals may occur. Reservoirs may be either animate or inanimate. Some pathogens are primarily saprophytic, only incidentally infect humans, and cause disease. For example, Clostridium tetany normally inhabits the soil. For many other pathogens, living organisms are the only reservoirs. In these cases, the reservoir host is essential for the life cycle of the infectious agent. The staphylococci and streptococci are examples of human-restricted pathogens, as are the agents that cause diphtheria, gonorrhea, and mumps. Zoonosis: A disease that primarily infects animals but is occasionally transmitted to humans is called a zoonosis. Occasionally, transmission is from animal to human; person-to-person transfer of these pathogens is rare, but does happen. Factors leading to the emergence of zoonotic disease include the existence of the infectious agent, the proper environment for propagation and transfer of the agent, and the presence of the new susceptible host. Easiest way to stop zoonosis is to kill the carrier. Carriers: A carrier is a pathogen-infected individual showing no signs of clinical disease. Carriers are potential sources of infection for others. Carriers may be individuals in the incubation period of the disease, in which case the carrier state precedes the development of actual symptoms. For such acute carriers, the carrier state lasts for only a short time. Chronic carriers may spread disease for extended periods of time. Carriers can be identified in populations using diagnostic techniques such as culture or immunoassay surveys. A classic example of a chronic carrier was the woman known as Typhoid Mary. Infectious disease transmission: Epidemiologists follow the transmission of a disease by correlating geographic, climatic, social, and demographic data with disease incidence. These correlations are used to identify possible modes of transmission. A disease limited to a restricted geographic location may suggest a particular vector; malaria, a disease of tropical regions, is transmitted only by mosquito species restricted to tropical regions. Pathogen survival depends on efficient hot-to-host transmission. Pathogens often have modes of transmission that are related to the preferred habitat of the pathogen in the body Respiratory pathogens are typically airborne whereas intestinal pathogens are spread through contaminated food or water. Pathogens can be classified by their mechanism of transmission, but all mechanisms have these stages in common. 1. escape from the host, 2. travel, and 3. entry into a new host. Pathogen transmission can be by direct or indirect mechanisms. Direct host-to-host transmission: Host-to-host transmission often occurs when an infected host transmits a disease directly to a susceptible host without the assistance of an intermediate host or inanimate object. Some pathogens are extremely sensitive to environmental factors such as drying and heat and are unable to survive for significant periods of time away from the host. These pathogens, transmitted only by intimate person-to-person contact such as exchange of body fluids in sexual intercourse, include those responsible for sexually transmitted diseases such as syphilis and gonorrhea. Direct contact also transmits skin pathogens such as staphylococci and fungi. Indirect host-to-host transmission: Indirect transmission of an infectious agent can be facilitated by either living or inanimate agents. Living agents transmitting pathogens are called vectors. Commonly, arthropods insects or vertebrates act as vectors. Arthropod vectors may not be hosts for the pathogen, but may carry the agent from one host to another. Many arthropods obtain their nourishment by biting and sucking blood, and if the pathogen is present in the blood, the arthropod vector may ingest the pathogen and transmit it when biting another individual. Inanimate agents such as bedding, toys, books, and surgical instruments can also transmit disease. These inanimate objects are collectively called fomites. Food an water are potential disease vehicles. Fomites can also be disease vehicles, but major epidemics originating from a single-vehicle source are typically traced to food or water because these are consumed in large amounts by many individuals in a population. Epidemics: Major epidemics are usually classified as common-source or host-to-host epidemics. A common-source epidemic arises as the result of infection of a large number of people from a contaminated common source such as food or water. Such epidemics are often caused by a breakdown in the sanitation of a central food or water distribution system. Waterborne and foodborne diseases are generally controlled by public health measures. The disease incidence for a common source outbreak is characterized by a repid rise in a peak because a large number of individuals become ill within a relatively brief period of time. The incidence of a common-source illness also declines rapidly. In a host-to-host epidemic, the disease incidence shows a relatively slow, progressive rise and a gradual decline. A host-to-host epidemic can be initiated by the introduction of a single infected individual into a susceptible population. The pathogen then replicates in susceptible individuals, reaches a communicable stage, and is transferred to other susceptible individuals, where it again replicates and becomes communicable. The host community: Coevolution of a host and a parasite: A classic example of host and pathogen coevolution occurred when a virus was intentionally introduced for purposes of controlling feral rabbits in Australia. Rabbits introduced into Australia form Europe in 1895 spread until they were over-running large parts of the continent and causing massive crop and vegetation damage. Although coevolution of host and pathogen may be common in diseases that rely on host-to-host transmission, for pathogens that do not rely on host-to-host transmission, as mentioned for Clostridium, there is no selection for decreased virulence to support mutual coexistence. Herd immunity: Herd immunity is the resistance of a group to infection due to immunity of a high proportion of the members of the group. If a high proportion of individuals in a group are immune to an infectious agent, then the whole population will b protected. A higher proportion of individuals must be immune to prevent an epidemic by a highly virulent agent or one with a long period of infectivity and a lower proportion for a less virulent agent or one with a brief period of infectivity. For poliovirus immunization in the United States, studies of polio incidence in large populations indicate that if a population is 70% immunized, polio will be essentially absent from the population. A value of about 70% of the population immunized has also been estimated to confer herd immunity for diphtheria. Healthcare-associated infections: A healthcare associated infection (HAI) is a local or systemic condition resulting from an infectious agent or its products that occurs during admission to a healthcare facility and that was not present on admission. HAIs cause significant morbidity and mortality. About 5% of patients admitted to healthcare facilities acquire HAIs, also called nosocomial infections. Some nosocomial infections are acquired from patients with communicable diseases, but others are caused by pathogens that are selected and maintained within the hospital environment. The hospital environment: Infectious diseases are spread easily and rapidly in hospitals for several reasons. 1. Many patients have low resistance to infectious disease because of their illness. 2. Healthcare facilities treat infectious disease patients, and these patients may be pathogen reservoirs. 3. Multiple patients in rooms and wards increase the chance of cross-infection. 4. Healthcare personnel move from patient to patient, increasing the probability f transfer of pathogens. 5. Healthcare procedures such as hypodermic injection, spinal puncture, and removal of tissue samples or fluids, breach the skin barrier and may introduce pathogens into the patient. 6. In maternity wards of hospitals, newborn infants are unusually susceptible to certain infections because they lack well-developed defense mechanisms. 7. Surgical procedures expose internal organs to sources of contamination, and the stress of surgery often diminishes the resistance of the patient to infection. 8. Certain therapeutic drugs, such as steroids used for controlling inflammation, increase the susceptibility to infection. 9. Use of antibiotics to control infections selects for antibiotic-resistant organisms. Infection sites: Of the 99,000 estimated deaths caused by HAIs in 2002, 36,000 were from pneumonia, 31,000 from bloodstream infections, 13,000 from urinary tract infections, 8,000 from surgical site infections, and 11,000 for all other sites. Healthcare-associated pathogens: Healthcare-associated pathogens preferentially infect several sites in the body, notably in urinary tract, blood, and the respiratory tract. One of the most important and widespread hospital pathogen is Staphylococcus aureus. It is the most common cause of blood infections. Escherichia coli is the most common cause of urinary tract infections in hospitals. Public health measures for the control of disease: Public health refers to the health of the general population and to the activites of public health authorities in the control of disease. Controls directed against the reservoir: When the disease reservoir is primarily in domestic animals, the infection of humans can be prevented if the disease is eliminated from the infected animal population. Immunization or destruction of infected animals may eliminate the disease in animals and in humans. When the disease reservoir is a wild animal, eradication is much more difficult. Rabies is a disease that occurs in both wild and domestic animals but is transmitted to domestic animals primarily by wild animals. Thus, control of rabies in domestic animals and in humans can be achieved by immunization of domestic animals. When humans are the disease reservoir, control and eradication can be difficult, especially if there are asymptomatic carriers. Certain diseases that are limited to humans have no asymptomatic phase. If these can be prevented through immunization or treatment with antimicrobial drugs, the disease can be eradicated if those who have contracted the disease and all possible contacts are strictly quarantined, immunized, and treated. Controls Directed against transmission of the pathogen: The transmission of pathogens in food or water can be eliminated by preventing contamination of these sources. Water purification methods and food protection laws have greatly decreased the probability of transmission of pathogens to humans. Transmission of respiratory pathogens is difficult to prevent. Attempts at chemical disinfection of air have been unsuccessful. Air filtration is a viable mthod but is limited to small, enclosed areas. Immunization: Smallpox, diphtheria, tetanus, pertussis, measles, mumps, rubella, and poliomyelitis have been controlled primarily by means of immunization. 100% immunization is not necessary for disease control in a population, although the percentage needed to ensure disease control varies with infectivity and virulence of the pathogen and twith the living conditions of the population. Quarantine: Quarantine restricts the movement of a person with active infection to prevent spread of the pathogen to other people. The length of quarantine for a given disease is the longest period of communicability for that disease. To be effective, quarantine measures must prevent the infected individual from contacting unexposed individuals. Quarantine is not as severe as measure as strict isolation, which is used in hospitals for unusually infectious and dangerous diseases. By international agreement, six diseases require quarantine: smallpox, cholera, plague, yellow fever, typhoid fever, and relapsing fever. Surveillance: Surveillance is the observation, recognition and reporting of diseases as they occur. The Centers for Disease Control and Prevention (CDC) in the United States, through the National Center for Infectious Diseases (NCID), operates a number of surveillance programs. Emerging and reemerging diseases: Alterations in the pathogen, the environment, or the host population contribute to the spread of new diseases with potential for high morbidity and mortality. Diseases that suddenly become prevalent are emerging diseases. Emerging infections are not limited to “new” diseases but also include reemerging diseases that were previously under control; reemerging diseases are especially a problem when antibiotics become less effective and public health system fail. Emerging epidemic diseases are not a new phenomenon. Some of the diseases that rapidly and sometimes catastrophically emerged in the past were syphilis and plague. Emergence factors: some factors responsible for emergence of new pathogens are 1. Human demographics and behavior; 2. Technology and industry; 3. Economic development and land use; 4. International travel and commerce; 5. Microbial adaption and change; 6. Breakdown of public health measures; and 7. Abnormal natural occurrences that upset the usual host pathogen balance. The demographics of human populations have changed dramatically in the last two centuries. In 1800, less than 2% of the world’s population lived in urban areas. Today nearly one-half of the world’s population lives in cities. The numbers, sizes, and population density in modern urban centers make disease transmission much easier. Human behavior also contributes to disease spread. For example, sexually promiscuous practices in population centers have been a major contributing factor to the spread of hepatitis and AIDS. Technological advances and industrial development have a generally positive impact on living standards worldwide. Transportation, bulk processing, and central distribution methods have become increasingly important for quality assurance and economy in the food industry. However, these same factors can increase the potential for common-source epidemics when sanitation measures fail. For example, a single meat processing plant spread Escherichia coli to at least 500 individuals in four states in the United States. Economic development and changes in land use can also promote disease spread. For example, Rift Valley fever, a mosquito-borne viral infection, has been on the increase since the completion of the Aswan High Dam in Egypt in 1970. Lyme disease, the most common vectorborne disease in the United States, is on the rise largely due to changes in land use patterns. Reforestation and the resulting increase in populations of deer and mice have resulted in greater numbers of infected ticks, the arthropod vector. International travel and commerce also affect the spread of pathogens. For example, filoviruses, a group of RNA viruses, cause fevers culminating in hemorrhagic disease in infected hosts. Travel of potential hosts to or from endemic areas is usually implicated in disease transmission. Sporadic Ebola outbreaks in central Africa, often characterized by mortality rates greater than 50%, highlight a group of viral hemorrhagic fever pathogens for which there is no immunity or therapy. Biological warfare and biological weapons: Biological warfare is the use of biological agents to incapacitate or kill a military or civilian population in an act of war or terrorism.
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Chapter 34 Airborne transmission of diseases: Aerosols, such as those generated by a human sneeze are important vehicles for person-to-person transmission. Airborne pathogens: MOS found in air are derived from soil, water, plants, animals, people, and other sources. In outdoor air, soil organisms predominate. Indoors, the concentration of MOS is considerably higher than outdoors, especially for organisms that originate in the human respiratory tract. Most MOS survive poorly in air. Pathogens are effectively transmitted among humans only over short distances. Certain pathogens survive under dry conditions and can remain alive in dust for long periods of time. Gram-positive bacteria (Staphylococcus, Streptococcus) are in general more resistant to drying than gram-negative bacteria because of their thick, rigid cell wall. The waxy layer of Mycobacterium cell walls resists drying and promotes survival. The endospores of endospore-forming bacteria are extremely resistant to drying. Large numbers of moisture droplets are expelled during sneezing. Each infectious droplet is about 10 u.m. in diameter and may contain one or two microbial cells or virions. Respiratory infections: Different organisms characteristically colonize the respiratory tract at different levels. The upper and lower respiratory tracts offer different environments, favoring different MOS. Bacterial and viral pathogens: Most human respiratory pathogens are transmitted from person to person because humans are the only reservoir for these pathogens. Streptococcal diseases: The bacteria Streptococcus pyogenes and Streptococcus pneumonia are important human respiratory pathogens; both organisms are transmitted by the respiratory route. S. pneumonia is found in the respiratory flora of up to 40% of healthy individuals and can cause severe respiratory disease in compromised individuals. Streptococci are nonsporulating, homofermentative, aerotolerant, anaerobic gram-positive cocci that typically grow inelongated chains. Pathogenic strains of S. pneumonia typically grow in pairs or short chains, and virulent strains produce an extensive polysaccharide capsule. Streptococcus pyogenes: epidemiology and pathogenesis: also called group A Streptococcus (GAS), is frequently isolated from the upper respiratory tract of healthy adults. S. pyogenes is the cause of streptococcal pharyngitis, better known as “strep throat”. Streptococcal pharyngitis produce a toxin that lyses red blood cells in culture media, a condition called B-hemolysis. Streptococcal pharyngitis is characterized by a severe sore throat, enlarged tonsils with exudates, tender cervical lymph nodes, a mild fever, and general malaise. Can also cause related infections of the inner ear, the mammary glands, infections of the superficial layers of the skin and erysipelas. Untreated streptococcal infections can lead to serious diseases such as scarlet fever, rheumatic fever, acute glomerulonephritis, and streptococcal toxic shock syndrome. Certain GAS strains carry a lysogenic bacteriophage that encodes streptococcal pyrogenic exotoxin A, SpeB, SpeC, and SpeF. These exotoxins are responsible for most of the symptoms of streptococcal toxic shock syndrome and scarlet fever. Spe’s are superantigens that recruit massive numbers of T cells to the infected tissues. Toxic shock results when the activated T cells secrete cytokines, which activate large numbers of cells, causing systemic inflammation and tissue destruction. Occasionally GAS causes fulminant invasive systemic infection such as cellulitis, and necrotizing fasciitis. These diseases cause inflammation and extensive tissue destruction resulting in death in about 15% of the estimated 11,000 cases per year. Timely and adequate treatment of the infection stops production of the superantigen and its effects. Other streptococcal syndromes: Untreated or insufficiently treated S. pyogenes infections may lead to other diseases, even in the absence of active infection. These severe nonsuppurative poststreptococcal diseases usually occur about 1 to 4 weeks after the onset of a strep infection The immune response produces antibodies that cross-react with host tissue antigens on the heart, joints, and kidneys, resulting in damage to these tissues. The most serious of these diseases is rheumatic fever caused by rheumatogenic strains of S. pyogenes. These strains contain cell surface antigens that are similar to heart valve and joint antigens. Rheumatic fever is an autoimmune disease, with antibodies directed against streptococcal antigens also reacting with heart valve and joint antigens. Another nonsuppurative disease is acute poststreptococcal glomerulonephritis. Streptococcus pneumonia: causes invasive lung infections that often develop as secondary infections to other respiratory disorders. Strains that are encapsulated are particularly pathogenic because they are potentially very invasive. Cells invade alveolar tissues of the lung, where the capsule enables the cells to resist phagocytosis and elicit a strong host inflammatory response. Pneumonia can result from accumulation of recruited phagocytic cells and fluid. The S. pheumoniae cells can then spread from the focus of infection as a bacteremia, sometimes resulting in bone infections, inner ear infections, and endocarditis. Untreated invasive disease has a mortality rate of about 30%. Even with antimicrobial treatment, it has up to 10% mortality. Diagnosis is based on the culture of gram-positive diplococci from either patient sputum or blood. An effective vaccine is available for prevention of infection by at least two-thirds of the 90 known strains. Penicillins are the agents of choice for treatment. Most strains respond quickly to penicillin therapy. Erythromycin is the drug of choice for penicillin-resistant organisms. Corynebacterium and diphtheria: Corynebacterium diphtheriae causes diphtheria, a severe respiratory disease. C. diphtheria is a gram-positive, nonmotile, aerobic bacterium that forms irregular rods that may appear as club-shaped cells during growth. It enters the body via the respiratory route, with cells lodging in the throat and tonsils. It’s spread from healthy carriers or infected individuals to susceptible individuals by airborne droplets. Previous infection or immunization provides resistance to the effects of the potent diphtheria exotoxin. The organism produces a neuraminidase capable of splitting N-acetylneuraminic acid and this may enhance the invasion process. The inflammatory response of throat tissues to infection results in formation of a characteristic lesion called a pseudomembrane, which consists of damaged host cells and cells of C. diphtheriae. Pathogenic strains lysogenized by bacteriophage B produce a powerful exotoxin. Diphtheria toxin inhibits eukaryotic protein synthesis and thus kills cells. The pseudomembrane may block the passage of air, and death from diphtheria is usually due to a combination of the effects of partial suffocation and tissue destruction by exotoxin. In untreated infections, the toxin can cause systemic damage to the heart, kidneys, liver, and adrenal glands. It is isolated from the throat and is diagnostic for diphtheria. Prevention of diphtheria is accomplished with a highly effective vaccine. Penicillin, erythromycin, and gentamicin are generally effective for stopping growth and further toxin production, but do not alter the effects of preformed toxin. Diphtheria antitoxin contains neutralizing antibodies. Early administration of both antibiotics and antitoxin is necessary for effective treatment of the acute disease. Bordetella and pertussis: Pertussis is a serious respiratory disease caused by infection with Bordetella pertussis, a small, gram-negative, aerobic coccobacillus that is a member of the Betaproteobacteria. Pertussis, also known as whooping cough, is an acute, highly infectious respiratory disease now observed frequently in school-age children under 19 years of age. Infants less than 6 months of age have the highest incidence of disease. B. pertussis attaches to cells of the upper respiratory tract by producing a specific adherence factor called filamentous hemagglutinin antigen, which recognizes a complementary molecule on the surface of host cells. Once attached, it grows and produces pertussis exotoxin. This toxin induces synthesis of cyclic adenosine monophosphate, which is at least partially responsible for host tissue damage. It also produces an endotoxin, which may induce some of the symptoms of whooping cough. Whooping cough is characterized by a recurrent, violent cough that can last up to 6 weeks. Spasmodic coughing gives the disease its name. Worldwide, there are up to 50 million cases and 300,000 pertussis deaths each year. In the U.S., there was 25,616 cases in 2005 and caused about 14 deaths. Up to 32% of coughs lasting 1-2 weeks or longer may be caused by B. pertussis. Diagnosis can be made by fluorescent antibody staining of a nasopharyngeal swab specimen or by culture. A vaccine consisting of proteins derived from B. pertussis is part of the routinely administered DTaP vaccine. They are killed by ampicillin, tetracycline, and erythromycin, although antibiotics alone do not seem to be sufficient to kill the pathogen in vivo. Whooping cough remains infectious for up to 2 weeks following commencement of antibiotic therapy, immune response may be more important than antibiotics for eliminating from the body. Mycobacterium, tuberculosis, and Hansen’s disease: Tuberculosis (TB) is caused by the gram-positive, acid-fast bacillus Mycobacterium tuberculosis. A related species, Mycobacterium leprae, causes Hansen’s disease (leprosy). All mycobacteria share acid-fast properties due to the waxy mycotic acid constituent of their cell wall. M. Tuberculosis is easily transmitted by the respiratory route; even normal conversation can spread the organism from person to person. Over 14,000 new cases of TB and over 700 deaths occur each year in the U.S., Worldwide, it accounts for almost 1.6 million deaths per year. The interaction of the human host is determined both by the virulence of the strain and the resistance of the host. Cell-mediated immunity plays a critical role in the prevention of active disease after infection. It can be classified as a primary infection or postprimary infection. Primary infection typically results from inhalation of droplets containing viable M. tuberculosis bacteria from an individual with an active pulmonary infection. The inhaled bacteria settle in the lungs and grow. The host responds with an immune response resulting in a delayed-type hypersensitivity reaction and the formation of activated macrophages. In individuals with low resistance, the bacteria are not controlled and the pulmonary infection becomes acute, leading to the extensive destruction of lung tissue, the spread of the bacteria to other parts of the body, and death. In most cases of TB, acute infection does not occur. The infection remains localized, and appears to end. This initial infection hypersensitizes the individual and consequently alters the response of the individual to subsequent exposures. Tuberculin test can be used to measure this hypersensitivity. Tuberculin elicits a local immune inflammatory reaction within 1-3 days at the site of and intradermal injection. The reaction is characterized by induration and edema. A positive tuberculin test does not indicate active disease. Individuals who have a positive TB test are generally treated with antimicrobial agents for long periods of time. Secondary infections often progress to chronic infections that result in destruction of lung tissue, followed by partial healing and calcification at the infection site. TB may spread by coughing or speaking. TB is highly contagious patients must be hospitalized in negative-pressure rooms. Antimicrobial therapy of TB has been a major factor in control or the disease. Streptomycin was the first effective antibiotic, but the real revolution came with isonicotinic acid hydrazide, called isonaizid. It affects the synthesis of mycolic acid. Mycolic acid is a lipid that complexes with peptidoglycan in the mycobacterial cell wall. Treatment is typically achieved with daily doses of isoniazid and rifampin for 2 months, followed by biweekly doses for a total of 9 months. Failure to complete the entire prescribed treatment may allow the infection to be reactivated and may be more resistant. Neisseria meningitides, meningitis, and meningococcemia: Meningitis is an inflammation of the meninges, the membranes that line the central nervous system, especially the spinal cord and brain. Meningitis can be caused by viral, abacterial, fungal, or protest infections. Neisseria meningitides, often called meningococcus, is a gram-negative, nonsporulating, obligately aerobic, oxidase-positive, encapsulated diplococcus. At least 13 pathogenic strains are recognized, bsed on antigenic differences in their capsular polysaccharides. Meningococcal meningitis often occurs in epidemics, usually in closed populations such as military installations and college campuses. Up to 30% of individuals carry it in the nasopharynx with no apparent harmful effects. In an acute infection, the bacterium is transmitted to the host, usually via the airborne route, and attaches to the cells of the nasopharynx. Once there the organism gains access to the bloodstream, causing bacteremia and upper respiratory tract symptoms. The bacteremia sometimes leads to fulminant meningococcemia, characterized by septicemia, intravascular coagulation, shock, and death in over 10% of cases. Meningitis is characterized by sudden onset of headache, vomiting, and stiff neck, and can progress to coma and death in a matter of hours. Up to 3% of acute victims die. Colonies showing gram-negative diplococcus morphology and a positive oxidase test are presumptively identified as Neisseria. Penicillin G is the drug of choice. Chloramphenicol is the accepted alternative agent of infections in penicillin-sensitive individuals. Broad-spectrum cephalosporins are also effective. Vaccines consisting of purified polysaccharides or polysaccharides conjugated to proteins from the most prevalent pathogenic strains are available and are used to immunize susceptible individuals. Acute meningitis is usually caused by one of the pyogenic bacteria such as Staphylococcus, streptococcus, or Haemophilus influenza. Several viruses cause meningitis, herpes simplex virus, lymphocytic chriomeningitis virus, mumps virus, and a variety of enteroviruses. Viral meningitis is less severe than bacterial meningitis. Viruses and respiratory infections: The most prevalent human infectious diseases are caused by viruses. Most viral diseases are acute, self-limiting infections. Measles: Rubeola or 7-day measles usually affects susceptible children as an acute, highly infectious, often epidemic disease. It is a paramyxobirus, a negative-strand RNA virus that enters the nose and throat by airborne transmission, quickly leading to systemic viremia. Symptoms start with nasal discharge, redness of the eyes, cough, and fever. As the disease progresses, fever and cough appear and rapidly intensify, and a rash appears; symptoms generally persist for 7-10 days. Circulating antibodies to measles virus are measurable about 5 days after initiation of infection, and both serum antibodies and cytotoxic T lymphocytes combine to eliminate the virus from the system. Postinfection complications include inner ear infection, pneumonia, and measles encephalomyelitis. Worldwide there are over 600,000 annual deaths because the disease is highly infectious. Active immunization is done with an attenuated virus. Mumps: is caused by a paramyxovirus and is also highly infectious. Mumbs is spread by airborne droplets, and is characterized by inflammation of the salivary glands, leading to swelling of the jaws and neck. The virus spreads through the bloodstream and may infect other organs, including the brain, testes, and pancreas. Severe complications include encephalitis. The host immune response produces antibodies ot surface proteins, and leads to a quick recovery. An attenuated vaccine is effective for preventing. Rubella; German measles or 3-day measles is caused by a single-stranded, positive-sense RNA virus of the togavirus group. Disease symptoms resemble measles but are generally milder. Rubella is less contagious than true measles. It can cause stillbirth, deafness, heart and eye defects, and brain damage in live births. An attenuated virus is administered for immunization. Chickenpox and shingles: Chickenpox is a common disease caused by the varicella-zoster virus (VZV), a DNA herpesvirus. It is highly contagious and is transmitted by infectious droplets. The virus enters the respiratory tract, multiplies, and is quickly disseminated via the bloodstream, resulting in a systemic popular rash that quickly heals, rarely leaving disfiguring marks. An attenuated virus vaccine is now used in the U.S. Reported annual incidence is now about 32,000 cases per year. VZV establishes a lifelong latent infection in nerve cells. The virus occasionally migrates from this reservoir to the skin surface, causing a painful skin eruption referred to as shingles (Zoster). Colds: are the most common of infectious diseases. Colds are viral infections that are transmitted via droplets spread from person to person in coughs, sneezes, and respiratory secretions. Colds are usually of sort duration, and the symptoms are milder than other respiratory diseases such as influenza. Each person averages over three colds per year throughout his or her lifetime. Symptoms include rhinitis, nasal obstruction, watery nasal discharges, and a general feeling of malaise, usually without fever. Rhinoviruses, a positive-sense, single-stranded RNA viruses of the picornavirus group are the most common causes of colds. 115 different rhinoviruses have been identified. 25% of colds are due to other viruses Coronaviruses cause 15% of all colds. Adenoviruses, coxsackie viruses, respiratory syncytial viruses (RSV), and orthomyxoviruses are collectively responsible for about 10% of colds. Colds generally induce a specific, local, neutralizing IgA antibody response. The number of potential infectious agents makes immunity due to previous exposure very unlikely. Aerosol transmission spreads colds. Direct contact and fomite contact are also methods of transmission. Most antiviral drugs are ineffective. Pyrazidine derivative has shown promise for preventing colds after virus exposure. Influenza: is caused by an RNA virus of the orthomyxovirus group. Influenza virus is a single-stranded, negative-sense, helical RNA genome surrounded by an envelope made up of protein, a lipid bilayer, and external glycoproteins. There are three different types; influenza A, B, and C. Influenza A is the most important human pathogen. Unique reassortments result in antigenic shift, a major change in a protein coat antigen resulting from the total replacement of an RNA segment. Antigenic shift can immediately and substantially alter on of the two glycoproteins important in the attachment and eventual release of virus from host cells, hemagglutinin and heuraminidase. The H and N glycoprotein antigens can also acquire minor antigenic changes due to point mutations in the coding sequences that alter one or more amino acids. These limited mutations create slightly altered antigens, a phenomenon called antigenic drift. It is transmitted from person to person through the air, primarily in droplets expelled during coughing and sneezing. It infects the mucous membranes of the upper respiratory tract and occasionally invades the lungs. Symptoms include a low-grade fever lasting for 3-7 days, chills, fatigue, headache, and general aching. Recovery is usually spontaneous and rapid. Most of the serious consequences of influenza infection occur from bacterial secondary infections in persons whose resistance has been lowered by the influenza infection. Death, if it occurs, is usually due to the bacterial infection. Annually causes 3-5 million cases of severe illness and 250.000-500,000 deaths worldwide. A new avian influenza strain, the influenza A H5N1 strain, also called avian influenza, can be spread human to human only after prolonged close contact. Influenza epidemics can be controlled by immunization. The choice of appropriate vaccines is complicated by the large number of existing strains and the ability of existing strains to undergo antigenic drift and antigenic shift. Immunization is recommended for those individuals most likely to acquire the disease and develop serious secondary illnesses. Direct contact transmission of diseases: Some pathogens are spread primarily by direct contact with an infected person or by contact with blood or excreta from an infected person. Staphylococcus: contains pathogens of humans and other animals. Commonly infect skin and wounds. Result from the transfer of staphylococci in normal flora from an infected asymptomatic individual to a susceptible individual. Are nonsporulating gram-positive cocci that divide in several planes to form irregular clumps. Are resistant to drying and are readily dispersed in dust particles through the air and on surfaces. Two species are important; Staphylococcus epidermidis, a nonpigmented species usually found on the skin or mucous membranes, and Staphylococcus aureus, a yellow-pigmented species. S. aureus is more commonly associated with human disease. Both species are frequently present in the normal microbial flora of the upper respiratory tract and the skin. It causes diseases including acne, boils, pimples, impetigo, pneumonia, osteomyelitis, carditis, meningitis, and arthritis. They are said to be pyogenic. Healthy individuals are often carriers and resident staph in the upper respiratory tract or skin seldom causes disease. Serious infections often occur because of hormonal changes, debilitating illness, wounds, or treatment with steroids or other drugs that compromise immunity. At least four different hemolysins have been recognized. Hemolysins cause the red blood cell lysis. S. aureus is also capable of producing an enterotoxin associated with foodborne illness. All staph also produce catalase, which distinguishes staph from strep. Another substance produced by S aureus is coagulase. Clotting induced by coagulase makes it difficult for host defense agents to come into contact with the bacteria and preventing phagocytosis. Most strains also produce leukocidin, a protein that destroys leukocytes. S. enterotoxin A, another superantigen, causes a form of food poisoning. After ingestion, the toxin stimulates T cells localized along the intestine, resulting in a massive T cell response and release of inflammatory mediators. Outcome is the severe but short-lived diarrhea and vomiting associated with food poisoning. Antimicrobial drug therapy is a major problem in healthcare environments. Over 100,000 cases of infection with methicillin-resistant S. aureus (MRSA) are reported each year in healthcare facilities. Some community-acquired staph infections are still treatable with penicillin. Carriers of known pathogenic strains must be either excluded or treated with topical or systemic antimicrobial drugs to eliminate the pathogens. Helicobacter pylori and gastric ulcers: Is a gram-negative, highly motile, spiral shaped bacterium that is related to Campylobacter. Has one to six polar flagella at one end. H pylori is a pathogen associated wit gastritis; ulcers, and gastric cancers. Colonizes the non-acid-secreting mucosa of the stomach and the upper intestinal tract. Up to 80% of gastric ulcer patients have concomitant H. pylori infections. Person-to-person contact and ingestion of contaminated food or water are the probable transmission methods with no known nonhuman reservoir. Occurs in high incidence in certain families and prevalence in the population increases with age. Sometimes occurs in epidemic clusters. A major preventable and treatable cause of may gastric ulcers. It is slightly invasive and colonizes the surfaces of the gastric mucosa. Pathogen products and host responses cause inflammation, tissue destruction, and ulceration. Urease, vacA, and lipopolysaccharide may contribute to localized tissue destruction and ulceration. Antibodies are usually present in infected individuals but are not protective and do not prevent colonization. Chronic gastritis due to untreated infection may lead to gastric cancers. Signs of infection include belching and stomach pain. Diagnosis requires culture or observation from a biopsy. Antibodies are not reliable indicators of acute, active disease. Most patients relapse within 1 year after long-term treatment of ulcers with antacid preparations. Treating ulcers as an infectious disease, permanent cures are often obtained. It’s usually treated with a combination of drugs including metranidazole, tetracycline or amoxicillin, and a bismuth-containing antacid preparation. Administered for 14 days, abolishes the infection and provides a long-term cure. Hepatitis viruses: Hepatitis is a liver inflammation commonly caused by an infectious agent. It sometimes results in acute illness followed by destruction of functional liver anatomy and cells, a condition known as cirrhosis. An infection can cause chronic or acute disease; some forms lead to liver cancer. A restricted group of viruses is often associated with liver disease. Hepatitis A virus is transmitted from person to person or by ingestion of focally contaminated food or water. Often called infectious hepatitis, usually causes mild, even subclinical infections, but rare cases of severe liver disease occur. Most significant food vehicles are shellfish from water polluted by human fecal material. Numbers of infections has moved downward partly due to an effective vaccine. Over 30% of individuals in the U.S. have antibodies. Infection due to hepatitis B virus is often called serum hep. It is a hepadnavirus, a partially double-stranded DNA virus. Particle containing the viral genome is called a Dane particle. Causes acute, often severe disease that can lead to liver failure and death. Chronic infection can lead to cirrhosis and liver cancer. Is usually transmitted by a parentaral route. May also be transmitted though exchanges of body fluids. New infections are decreasing due to an effective vaccine. Over 150,000 people worldwide and nearly 5,000 people in the U.S. die each year. Hepatitis C virus is also transmitted parenterally. Generally produces a mild or even asymptomatic disease at first but up to 85% of individuals develop chronic hep, up to 20% leading to chronic liver disease and cirrhosis. Chronic infection leads to hepatocarcinoma in 3-5% individuals. Latency period can be several decades. HCV related deaths due to chronic HCV infections that develop into liver cancer is the most common liver disease in the U.S. Hepatitis E virus transmits via an enteric route. An acute, self-limiting hep that varies in severity. Symptoms include fever, jaundice, icterus, hepatomegaly, and cirrhosis. Mild hep is minor elevation of liver enzymes. Infection with HAV or HBV can be prevented with effective vaccines. Universal precautions are standards developed for personnel handling infectious waste and body fluids. Pooled human immune gamma globulin can be used to prevent HAV infection if given soon after exposure. Pro post-exposure prevention of HBV infection, specific hep B immune globulin, coupled with administration of the HBV vaccine has been effective. In some cases, antiviral drugs are effective. Interferon a is effective against HCV when combined with the drug ribavirin. HBV can be treated with foscarnet, ribvirin, lamivudine, and ganciclovir. Sexually transmitted infections: or STI’s, also called sexually transmitted diseases (STDs) or venereal diseases, are caused by bacteria, viruses, protists, and even fungi. Pathogens are generally found only in body fluids from the genitourinary tract that are exchanged during sexual activity. Typically very sensitive to drying and other environmental stresses. Their habitat, the human genitourinary tract, is a protected, moist environment. These pathogens preferentially and sometimes exclusively colonize the genitourinary tract. Diagnosis and treatment is very challenging. Up to one-third of all STIs are in teenagers with multiple sex partners. Many STIs have minor symptoms. Most STIs are controllable with appropriate medical intervention. Delay or lack of treatment can lead to long-term problems such as infertility, cancer, heart disease, degenerative nerve disease, berth defects, stillbirth, or destruction of the immune system. Their spread can be controlled by sexual abstinence or by the use of barriers such as condoms. Gonorrhea and syphilis: are preventable, treatable bacterial STIs. The overall pattern of disease differs between the two. Gonorrhea is very prevalent, and often asymptomatic. Is often unrecognized and remains untreated. Syphilis has a low prevalence and exhibits very obvious symptoms in its primary stage and infected individuals usually seek immediate treatment. Neisseria gonorrhoeae, often called the gonococcus, causes gonorrhea. Is a gram-negative, nonsporulating, obligately aerobic, oxidase-positive diplococcus related biochemically and phylogenetically to Neisseria meningitides. Is very sensitive to drying and normally does not survive away from the mucus membranes of the genitourinary tract. Gonococci are killed rapidly by drying, sunlight, and ultraviolet light. Can be transmitted only by intimate person-to-person contact. Enters the body by way of the mucus membranes of the genitourinary tract. Symptoms are quite different in the male and female. In females, gonorrhea is characterized by a mild vaginitis that is difficult to distinguish from vaginal infections caused by other organisms. In females can lead to pelvic inflammatory disease (PID). PID is a chronic inflammatory disease that can lead to sterility. In the male it causes a painful infection of the urethral canal. Untreated both in males and females include damage to heart valves and joint tissues due to immune complex deposition. Also causes eye infections in newborns. Prophylactic treatment of the eyes of all newborns with an ointment containing erythromycin. Treatment with penicillin has been successful. Strains of N. gonorrhoeae resistant to penicillin are now widespread. Quinolones ciprofloxacin, oflaxacin, or levofloxacin were also used but has developed resistance. Strains resistant to penicillin and quinolones respond to alternative antibiotic therapy with a single dose of the B-lactam antibiotics ceficime or ceftriaxone. 50% of gonorrhea patients are also infected with Chlamydia trachomatis. Incidence remains relatively high for the following reasons: (1) Acquired immunity does not exist; repeated reinfection is possible. (2) The use of oral contraceptives alters the local mucosal environment in favor of the pathogen. (3) Symptoms in the female are so mild that the disease may be unrecognized, and an infected female with multiple partners can infect many males. Syphilis is caused by a spirochete, Treponema palladium. Extremely sensitive to environmental stress, it’s normally transmitted from person to person by intimate sexual contact. Is often transmitted at the same time as gonorrhea. Syphilis is potentially more serious than gonorrhea. Worldwide, it kills over 150,000 people per year, whereas gonorrhea kills only 1,000 per year. Syphilis does not pass though unbroken skin and initial infection takes place through tiny breaks in the epidermal layer. In the male, initial infection is usually on the penis; in the female it is most often in the vagina, cervix, or perineal region. In about 10% of cases, infection is extragenital, usually in the oral region. The disease acquired by infants is called congenital syphilis. Syphilis is an extremely complex disease and may progress into any of three stages, but always begins with a localize infection called primary syphilis. In primary syphilis, T. pallitum multiplies at the initial site of entry, and a characteristic primary lesion called a chancre forms within 2 weeks to 2 months. In most cases the chancre heals spontaneously and T. pallidum disappears from the site. Some cells spread from the initial site to various parts of the body such as the mucous membranes, the eyes, joints, bones, or central nervous system, where extensive multiplication occurs. A hypersensitivity reaction to the treponomes often takes place, revealed by the development of a generalized skin rash; this rash is the key symptom of secondary syphilis. The secondary rash papules may contain T. pallidum, making them highly infectious. Eventually the spirochetes are cleared from the secondary lesions and infectivity is reduced. About one-fourth of infected individuals undergo a spontaneous cure. Another one-fourth exhibit no further symptoms. About half of untreated individuals undergo a spontaneous cur. Another one-fourth exhibit no further symptoms. About osf of untreated patients develop tertiary syphilis, with symptoms ranging from relatively mild infections of the cardiovascular system or central nervous system. Involvement of the nervous system can cause generalized paralysis or other severe neurological damage. Low numbers of T. Pallidum ar present in individuals with tertiary syphilis, and most of the symptoms probably result from inflammation due to delayed hypersensitivity reactions to the spirochetes. Chancre, is diagnostic for the disease. Infected individuals generally seek treatment. Penicillin is highly effective. Primary and secondary stages can usually be controlled by a single injection of benzathine penicillin G. Tertiary syphilis, penicillin treatment must be extended for longer periods of time. The incidence of primary and secondary syphilis in the U.S. has decreased over the last two decades. Chlamydia, herpes, trichomoniasis, and human papillomavirus: These diseases are very prevalent in the population and are much more difficult to diagnose and treat than are syphilis and gonorrhea. Chlamydia: A number of sexually transmitted diseases can be ascribed to infection by the obligate intracellular bacterium Chlamydia trachomatis. Over 900,000 cases are reported, and there may be over 4 million new cases each year. This organism is the cause of the most prevalent STI and communicable disease in the U.S. It also causes a serious eye infection called trachoma. Strains responsible for STIs are distinct from those causing trachoma. May also be transmitted congenitally to the newborn causing conjunctivitis and pneumonia. Nongonococcal urethritis (NGU) due to C. trachomatis is one of the most frequently observed STDs in males and females. Infections are often inapparent. In a small percentage of cases, chlamydial NGU leads to serious acute complications, including testicular swelling and prostate inflammation in men, and cervicitis, pelvic inflammatory disease, and fallopian tube damage in women; cells of C. trachomatis attach to microvilli of fallopian tube cells, enter, multiply and eventually lyse the cells. Untreated NGU can cause infertility. Chlamydia NGU is relatively difficult to diagnose by traditional isolation an identification method, but can be cultured. Tests have been developed include nucleic acid probe tests, nucleic acid amplification tests, fluorescent antibody tests, and enzyme-linked immunosorbent assay tests. Treatment is initiated with azithromycin or doxycycline. Is frequently observed as a secondary infection following gonorrhea. If both are transmitted to a new host, treatment of gonorrhea with cefixime or ceftriaxone is usually successful but dos not eliminate the Chlamydia. Patients treated for gonorrhea are also given azithromycin or doxycycline to treat the potential coinfection. Lymphogranuloma venereum is a sexually transmitted disease caused by distinct strains of C. trachomatis. Occurs most frequently in males and is characterized by infection and swelling of the lymph nodes in and about the groin. Chlamydial cells may travel to the rectum and cause a painful inflammation of rectal tissues called proctitis. Lymphogranuloma venereum has the potential to cause regional lymph node damage and proctitis. Herpes: Herpesviruses are a large group of complex double-stranded DNA viruses. Herpes simplex viruses are responsible for cold sores and genital infections. Herpes simplex virus type 1 (HSV-1) infects the epithelial cells around the mouth and lips, causing cold sores. HSV-1 may occasionally infect other body sites including the anogenital regions. It’s spread via direct contact or through saliva. The incubation period is 3-5 days and the lesions heal without treatment in 2-3 weeks. Is most likely spread by contact with infectious lesions. Latent herpes infections are common, with the virus persisting in nerve tissue. Recurrent infections are due to a periodic triggering of virus activity by unknown or indeterminant causes. Oral herpes HSV-1 is quite common and has no harmful effects on the host beyond the discomfort of the oral blisters. Herpes simplex virus 2 HSV-2 infections are associated with the anogenital region. Painful blisters occur on the penis of males or on the cervix, vulva, or vagina of females. Infections are transmitted by direct sexual contact and the disease is easily transmitted when active blisters are present but may also be transmitted during asymptomatic periods. HSV-2 occasionally infects other sites such as the mucous membranes of the mouth. It can be transmitted to a newborn at birth. Diseased newborns vary from latent infection to systemic disease resulting in brain damage or death. To avoid infections in newborns, caesarean section is advised. Long-term effects are not yet fully understood. Significant correlation between genital herpes and cervical cancer in females. They are presently incurable, a limited number of drugs have been successful in controlling the blister stages. Guanine analog acyclovir is effective in limiting the shed of active virus from blisters and promoting the healing of blistering lesions. Acyclovir, valcyclovir, and vidarabine are nucleoside analogs inhibiting viral DNA replication. Trichomoniasis: Nongonococcal urethritis may also be caused by infections with the protest Trichomonas vaginalis. It does not produce the resting cells or cysts important to the life cycle of many protists. Transmission is usually from person to person by sexual intercourse. Can survive for 1-2 hours on moist surfaces, 30-40 minutes in water, and up to 24 hours in urine or semen. Is sometimes transmitted by toilet seats, sauna benches, and paper towels. It infects the vagina in women, the prostate and seminal vesicles of men, and the urethra of both male and female. Many cases are totally asymptomatic in males. In women, is characterized by a vaginal discharge, vaginitis, and painful urination. More common in females and 25-50% of sexually active women are infected. 5% of men are infected. Metronidazole is effective in treating the trichomoniasis. Human papillomaviruses (HPV): comprise a family of double stranded DNA viruses. Of more than 100 different strains, about 30 are transmitted sexually; several of these cause genital warts and cervical cancer. 20 million people in the U.S. are infected, 80% of women over age 50 have had at least one HPV infection. Most infections are asymptomatic, some progress to genital warts. Others cause cervical neoplasia, a few progresses to cervical cancers. Most infections resolve spontaneously but there is no adequate treatment or cure. HPV vaccine has been developed. Designed to provide immunity to the most oncogenic viral strains. HIV: is divided into two types, HIV-1 and HIV-2. HIV-1 is genetically similar but distinct from HIV-2. HIV-2 is less virulent than HIV-1 and causes a milder AIDS-like disease. More than 99% of AIDS cases are due to HIV-1. HIV-1 is a retrovirus. The genome contains 9,749 nucleotides in each of its two identical single-stranded RNA molecules. Using the viral RNA as a template, reverse transcriptase in the intact virion catalyzes formation of a complementary single-stranded DNA molecule. The enzyme then converts the complementary DNA (cDNA) into double-stranded DNA, which intergrates into the host cell genome. HIV-infected individuals will continue to rise. In the U.S., the numbers of newly diagnosed HIV infections are increasing, and declines in HIV morbidity and mortality attributable to combination antiretroviral therapy have ended.
|Posted by: Pseudonym Apr 21 2009, 10:32 PM|
|I'm confused, are you using that to study, or bringing it into the test? Are you bringing it into an essay? Has anyone else adopted your methods?|
|Posted by: Granobulax Apr 22 2009, 12:55 AM|
I'm condensing it all on a 3x5 note card and taking it to class. I have to bring a magnifying glass to read it
|Posted by: videogameman Apr 22 2009, 02:19 AM|
|HOLY! WAY too long for me to read.|
|Posted by: Granobulax Apr 22 2009, 03:26 AM|
Aw, come on. It'll only take an hour or two to read...
|Posted by: Pseudonym Apr 22 2009, 08:34 PM|
I'm confused, why? What do you gain from putting it on a note card?
|Posted by: Granobulax Apr 22 2009, 08:50 PM|
The answers to the questions. The test questions are essay questions so it helps tremendously.
|Posted by: Pseudonym Apr 22 2009, 09:05 PM|
|You can bring the answers into class for a test?|
|Posted by: Granobulax Apr 22 2009, 09:24 PM|
Yes, as long as you take the time to make the card. Do you have any idea how long it took to make that card?
|Posted by: Pseudonym Apr 22 2009, 09:40 PM|
It isn't just copying of a textbook?
What are the criteria for what you can bring in, only one note-card?
Do other people do it too?
|Posted by: Granobulax Apr 23 2009, 05:02 AM|
Well, technically it is copying from a text book except you do have to read the material because you have to downsize the material greatly. If I coppied all of the material from the text book I have, I would need several note cards at size one font.
Yes, we can have only one note card for the test.
Yes, everyone that wants a good grade on the test makes a note card. My professor likes a LOT of information on a given essay question to be discussed in our answers.
|Posted by: Granobulax Apr 29 2009, 01:31 AM|
| I started 7 IV's today! Yay!
It's so much fun sticking people with needles
|Posted by: Ethan Apr 29 2009, 02:24 AM|
|OMG Grano, that's gotta hurt your eyes reading all that stuff.|
|Posted by: Granobulax Apr 29 2009, 02:25 AM|
Yeah, I had to put it all in font 2.5
Whatdyathink about my starting 7 IVs today?
|Posted by: Ethan Apr 29 2009, 02:33 AM|
Sticking other people with sharp objects sounds fun, is it dangerous if you miss besides hurting? Hey also weird question but did you do any cathers (might be mispelled) yet?
|Posted by: Granobulax Apr 29 2009, 04:10 AM|
If you miss, no, not really. If you do an IV without using sterile technique, you can instil a septic blood infection that if bad enough can kill a person though.
And yes, I have inserted indwelling urinary catheters in both men and women.
|Posted by: The Ripper Apr 29 2009, 04:22 AM|
|Grano, what about those with Typranophobia? (Typranophobia=fear of needles)|
|Posted by: Granobulax Apr 29 2009, 06:06 PM|
Then we give them Lidocaine. It numbs the area before the needle stick.
|Posted by: Granobulax Apr 29 2009, 07:02 PM|
|Do you know what I just noticed? Solomon, Darkender, and I each have more total posts than the entire Electric Ferret forum|
|Posted by: Pseudonym Apr 29 2009, 08:53 PM|
It was recently restarted.
|Posted by: Judge Death Apr 29 2009, 08:57 PM|
Uck! That's... just... uck!
My aunt works the night shift in a hospital too
|Posted by: Granobulax Apr 29 2009, 08:59 PM|
What part is "Uck"? They're all necessary tasks...
|Posted by: Judge Death Apr 29 2009, 09:00 PM|
The urinary catheters.
Has anyone ever had an "accident" when you were putting one in?
|Posted by: Jailer411 Apr 29 2009, 09:03 PM|
If they could have an "accident" then the need for a catheter is gone.
|Posted by: Granobulax Apr 29 2009, 09:06 PM|
| @ Judge Death: No, that's never happened to me but it has happened to other people.
@ Jailer: You're absolutely right... for the most part. Sometimes we have to 'straight cath' them to get a urine sample. Otherwise, you're completely right.
|Posted by: Jailer411 Apr 29 2009, 09:08 PM|
|Posted by: Pseudonym Apr 29 2009, 09:57 PM|
|Nurse Grano, what is the most devastating possible consequence of a sneeze?|
|Posted by: Judge Death Apr 29 2009, 10:18 PM|
I know this on. Careful brain surgery... *long blip*
|Posted by: Granobulax Apr 30 2009, 03:36 AM|
I looked around and found no reasonable cases of death from sneezing. Here's what I did gather though.
"Allergy affects 1 in 5 Australians, yet is often considered more a nuisance than a major disease. Unfortunately, those with severe allergies have a miserable time, and end up physically and emotionally exhausted. Severe allergies have a major impact on quality of life, sleep quality, mood, work performance in adults and learning in children. Severe hay fever is also associated with a number of medical complications, such as more frequent sinus and middle ear infections, and harder to control asthma."
So, allergies with severe complications such as asthma are the worst, but it's not caused by sneezing. Sneesing is a symptom of those problems. I see no real threat by sneezing at all. Sneezing is the bodies way of excreting material, that's all.
|Posted by: Pseudonym May 9 2009, 01:15 AM|
| Grano, I need help for Bio homework, we're doing diseases.
I need the
Cause (Bacteria, Virus, Toxin)
Treatable or not
How is it contracted
for eight diseases:
The Black Plague
Before you accuse me of cheating, this is a research project.
|Posted by: Shadow Fenrir May 9 2009, 01:21 AM|
| Thank god for Living Enviroment and Biology.
The Black Plague: Bacteria
E. Coli: Bacteria
Lyme's Disease: Bacteria
|Posted by: Granobulax May 9 2009, 03:56 AM|
I would look those up for you, but I'm too busy studying for my finals next week. I think the majority of those are in my previous note cards if you want to read through those or you could probably google them and get all of the information.
Sorry, wish I could be more help, but I'm barely passing my nursing class and I need a passing grade on the final to pass.
I'm only on here a few minutes at a time any more lately
|Posted by: treacherous May 9 2009, 04:33 AM|
|Grano, I called you and you have not returned my call. You better be hella busy. And you better pass this nursing thing.|
|Posted by: Shadow Fenrir May 9 2009, 05:03 AM|
|Thanks alot, that stupid dyke...gotta screw Grano over...WTH.|
|Posted by: Marvel Man May 9 2009, 06:40 AM|
| Good Luck with your nursing test.
|Posted by: Granobulax May 11 2009, 05:02 AM|
| While things between my wife and I have become civilized, I find myself falling into an ever increasing depression. The sheer loneliness that I feel right now is excruciating. The only think keeping me going is the need to be the best father to my daughter that I can and that means finishing school.
However, I find myself attempting to study and I can't help but have my mind wander, falling ever deeper into the depths of my tourment.
I will overcome this, I know I will. My spirit is too great to be dampened by this ordeal for too long, I just wish I knew how long the pain is going to last. I wish she could just be dead to me in my heart, but I can't. I still love her and it's tearing me apart.
I'm sure everyone is getting sick of my self loathing but this is one place where I can express my feelings. I want to express my deepest gratitude to all that have lent an ear in my time of need. Know this, I will get through this one way or another and I have each and every one of you to thank for helping me along the way.
I especially want to thank treacherous. You have been more than an internet friend to me. I want you to know that I think of you more as a brother than just a friend. You have gone over and above anything a mere internet friendship can go to help me out. As long as you stick around on these boards, I'll never leave. Thank you so much.
Sorry if I'm a bit "wishy washy," it's just been an emotional day for me. Even as I sit here, typing this post, I'm crying. One day, I'll be happy again. Life is like a rollercoaster. It has its ups and downs. I happen to be on the bottom of the ride, but I have that uphill swing to look forward to.
|Posted by: treacherous May 11 2009, 11:41 AM|
| Grano's so emotional.
Move to Tennessee. We'll hang out.
|Posted by: Granobulax May 11 2009, 06:50 PM|
Yeah, last night was a bad night. I'm better today.
As far as moving to Tennessee, as tempting as that may be at the moment, I wouldn't want to move so far away from my daughter. Ha! That's the second time in the last day I've been offered to move across country One of my best friends tried to get me to move to South Carolina.
I do, however, make frequent trips to Texas. Perhaps some day I'll swing on up to Tennessee just to hang out for a day though
|Posted by: treacherous May 11 2009, 08:23 PM|
|We'll show you the finest in southern cookin'.|
|Posted by: Marvel Man May 11 2009, 09:06 PM|
I used to live in the South, so I'm still a Titans/Vols Fan. Plus, I like Chattanogah/Nashville (Spelling).
|Posted by: Bassetman May 11 2009, 09:14 PM|
|Posted by: treacherous May 11 2009, 09:26 PM|
GO TITANS!! I'm from Nashville.
@I don't know much about Paramore or whatever, but I know that Franklin is where all the Richie Riches live.
|Posted by: Marvel Man May 11 2009, 10:38 PM|
|Posted by: Granobulax May 12 2009, 05:08 PM|
| The Titans were such a let down in the playoffs last year
I'm not a Titans fan per se, but I usually root for them when they're up against a team that I don't like.
Tell me all you Titans fans, does that one yard still get under your skin? *If you're a true Titans fan, you'll know what I'm talking about*
|Posted by: Solomon May 12 2009, 09:34 PM|
| It does for me. I had 25 bucks riding on that game.
|Posted by: Granobulax May 13 2009, 03:34 AM|
Wow, that game was in 2000. So, let's assume that you were the youngest age capable of legally gambling which is 21, then you are at the very least 30 years old...
|Posted by: Granobulax May 13 2009, 04:49 AM|
| Here's my final note card for microbiology. It's my longest one yet, so I'll have to post it in two parts.
Chapter 12: Genetic engineering: Genetic engineering refers to the use of in vitro techniques to alter genetic material in the laboratory. Cloning the gene via mRNA- The standard way to obtain an intron-free eukaryotic gene is to clone it via its mRNA. Since introns are removed during the processing of mRNA, the mature mRNA carries an uninterrupted coding sequence. The isolated mRNA is used to make complementary DNA (cDNA) using the retroviral enzyme reverse transcriptase. Tissues expressing the gene of interest often contain large amounts of the desired mRNA. In a typical mammalian cell, about 80-85% of the RNA is ribosomal RNA, 10-15% is transfer RNA, and only 1-5% is mRNA. Once mRNA has been isolated, it is necessary to convert the genetic information into DNA. This is done by the enzyme reverse transcriptase. This enzyme is essential for retrovirus replication and copies information from RNA into DNA, a process called reverse transcription. Reverse transcriptase makes DNA that is complementary to the mRNA. Double-stranded cDNA contains the coding sequences of interest but lacks introns. It can then be inserted into a plasmid or other vector for cloning. Finding the gene via the protein: Knowing the sequence of a gene allows for the construction of a synthetic and complementary DNA molecule to use as a prove. This can then be used to find the gene in a gene library. Knowledge of the amino acid sequence of a protein can also be used to construct a probe or even to synthesize a whole gene. For certain small proteins there may be good reason to synthesize the entire gene. Many mammalian proteins are made by protease cleavage of larger precursors. Thus, to produce a short peptide hormone, such as insulin, it may be more efficient to construct an artificial gene that encodes just the final hormone rather than the larger precursor protein from which it is derived naturally. Many human and viral proteins have been expressed at high yield under the control of bacterial regulatory systems. Restriction and modification enzymes: All cells contain enzymes that can chemically modify DNA in one way or another. One major class of such enzymes is the restriction endonucleases, or restriction enzymes. Restriction enzymes recognize specific base sequences within DNA and cut the DNA. In vivo, restriction enzymes protect prokaryotes from hostile foreign DNA such as virus genomes. Restriction enzymes are also essential for in vitro DNA manipulation, and their discovery gave birth to the field of genetic engineering. Gel electrophoresis: separation of DNA molecules- Because the base sequences recognized by many restriction enzymes are four to six nucleotides long, they cut DNA molecules into segments that range in length from a few hundred to a few thousand base pairs. The fragments generated can be separated from each other by gel electrophoresis and analyzed. Electrophoresis is a procedure that separates charged molecules migrating in an electrical field. The molecules are separated in a porous gel, rather than in free solution. When an electrical current is applied, nucleic acids move through the gel toward the positive electrode due to their negatively charged phosphate groups. Small or compact molecules migrate more rapidly than large molecules. The gel can be stained with a compound that binds to DNA and the DNA will then fluoresce orange under ultraviolet light. Steps in gene cloning: 1. Isolation and fragmentation of the source DNA. 2. Inserting the DNA fragment into a cloning vector. 3. Introduction of the cloned DNA in a host organism. Some cells contain the desired cloned gene, whereas other cells may contain other cloned genes from the same source DNA. Such a mixture is known as a DNA (gene) library. Making a gene library by cloning random fragments of a genome is called shotgun cloning and is widely used in genomic analyses. Cloning genes into plasmid vectors: Many vectors include features similar to those of pUC19. Sometimes insertional inactivation can be detected by selection, rather than by screening. Cloning using plasmid vectors is versatile and widely used in genetic engineering, particularly when the fragment to be cloned is fairly small. Plasmids are often used as cloning vectors if expression of the cloned gene is desired, since regulatory genes can be engineered into the plasmid to obtain expression of the cloned genes under specific conditions. Reporter genes: The benefit of locating a cloning site within a gene whose activity is easy to assay. In this application, the lacZ gene used as a reporter gene. The key property of a reporter gene is that it encodes a protein that is easy to detect and assay. They may be used to signal the presence or absence of a particular genetic element or DNA inserted within a vector. They can also be fused to other genes or to the promoter of other genes so that expression can be studied. Hosts for cloning vectors: To obtain large amounts of cloned DNA, an ideal host should grow rapidly in an inexpensive culture medium. The host should also be nonpathogenic, be capable of incorporating DNA, be genetically stable in culture, and have the appropriate enzymes to allow replication of the vector. The most useful hosts for cloning are microorganisms that are easily grown and for which we have much information. Transfection of eukaryotic cells: Eukaryotic microorganisms and animal and plant cells can take up DNA in a process that resembles bacterial transformation. Because the word “transformation” is used to describe the conversion of mammalian cells to a cancerous state, the introduction of DNA into mammalian cells is usually called transfection. Transfection of cultured animal cells was originally accomplished by precipitating DNA in such a way that the cells would take it up by phagocytosis, which is possible because animal cells do not have cell walls. DNA can also be injected directly into the nucleus, a technique called microinjection. Chapter 23: Principles of Microbial Ecology- Ecological Concepts: An ecosystem is the sum total of all of the organisms and abiotic factors in a particular environment. An ecosystem contains many different habitats, portions of the ecosystem best suited to one or a small number of microbial populations. Microorganisms are found anywhere higher organisms are and many more places. The type of microorganism in an ecosystem depends on the species composition, population sizes, and physiological state of the microorganisms in each habitat. The rates of activities are controlled by the nutrients and growth conditions. Symbiosis is defined as a relationship between two or more organisms that share a particular ecosystem. Parasitism is a form of symbiosis in which one member in the relationship is harmed in the process. A parasite is an organism that obtains its nutrients from another organism, the host. Mutualism is a symbiotic relationship in which both species benefit. Commensalism is a symbiotic relationship in which one species benefits while the other is neither armed nor helped. Bacteria that inhabit the animal gut are mostly commensal while other bacteria excrete essential nutrients and are mutualistic. Species richness is the total number of different species present in a habitat. Species abundance is the proportion of each species in the ecosystem. Richness and abundance depends on the amount of nutrients available. In rich soil, high species richness is abundant with most species in moderate abundance. In extreme environments, richness is often very low, but abundance of one or two species is very high. The Microbial Habitat: Microorganisms are found in every habitat that sustains life. They live in soil, water, extreme environments, on or within higher organisms, and even intracellularly within higher organisms. Differences in the type and quantity of resources and the physiochemical conditions of a habitat define the niche for niche particular microorganism. For every organism, there exists at least one niche, their prime niche, in which that organism is most successful. The organism dominates the prime niche but may inhabit other niches. Microenvironment is the niche where a microorganism actually lives and metabolizes. A microbial niche will be very small. Outer zones of the soil particle may be fully oxic while only a short distance away remains completely anoxic. Anaerobic organisms could thrive near the center, microaerophiles further out and obligately aerobic organisms in the outermost fully oxic region. Nutrient levels and growth rates: Resources typically enter the ecosystem intermittently. A large pulse of nutrients may be followed by a period of nutrient deprivation in “Feast or famine.” The organisms will store materials when they get them. Bacteria that grow in the soil can grow as little as 1% of the maximal growth rate. Microbial competition and cooperation: Competition may be intense with the outcome dependent on rate of nutrient uptake, inherent metabolic rate and, growth rate. Ome microorganisms work together to carry out transformation that cannot be accomplished alone which is called syntrophy. Biofilms: assemblages of bacterial cells attached to a surface and enclosed in an adhesive matrix excreted by the cells. Usually a mixture of polysaccharides. Usually contain several porous layers. Can contain one or several species. Biofilm formation: Attachment of a cell to a surface is a signal for biofilm-specific genes. Once committed, the cells lose its flagella. The mechanism is yet to be discovered, but the cells know a suitable surface to attach to. Intracellular communication is important in developing and maintaining biofilm. Biofilms: Advantages and control- Four reasons for formation. One, self-defense. Biofilms resist phagocytosis. Second, allows cells to maintain a favorable niche. Third, allows bacteria to live in close association with each other which allows for increased chance for survival. Fourth is the typical way bacterial cells grow in nature. Biofilm Control: Biofilms are protected from the immune system, antibiotics, and other antimicrobial agents that fail to pierce the biofilm. They are implicated in medical and dental conditions which include periodontal disease, kidney stones, tuberculosis, Legionnaire’s disease, and staph infections. Industrial biofilms can slow the flow of water, oil, or other liquids through pipelines and can accelerate corrosion. Although water pipe biofilms mostly contain harmless microorganisms, if pathogens successfully colonize the biofilm, standard chlorination practices may be insufficient to kill them. New antimicrobial agents that can penetrate biofilm, as well as drugs that prevent biofilm formation by interfering with intercellular communication, are being developed. Freshwater, soil and plant microbial ecosystems: Freshwater environments- Oxygenic phototrophs suspended freely in the water are called phytoplankton and include algae and cyanobacteria. The term “plankton” means “floating” and these organisms can exist throughout the water column of lakes, sometimes accumulating in large numbers at a particular depth. Phototrophs attached to the bottom or sides of a lake or stream are benthic species. Because oxygenic phototrophs obtain their energy from light and use water as an electron donor to reduce CO2 to organic matter, they are called primary producers. The activity of guilds of heterotrophic microorganisms depends on the rate of primary production. Oxygenic phototrophs produce new organic material as well as oxygen. Oxygen relationships in lakes: significant photosynthetic production of oxygen occurs only in the surface layers of a lake or ocean, where light is available. Once oxygen is consumed in freshwater lakes, the deep layers become anoxic. The bottom layers contain anaerobic prokaryotes and a few anaerobic eukaryotes. A transition occurs in anoxic waters from respiratory metabolisms to fermentative and methanogenic metabolisms. Many lakes in temperate climates become stratified, with the warmer and less dense surface layers, called the epilimnion, separated from the colder and denser bottom layers, called the hypolimnion. The thermocline is the transition zone from epilimnion to hypolimnion. After stratification sets in during the early summer, the bottom layers become anoxic. In temperate lakes in the late fall and early winter, the surface waters become colder and thus more dense than the bottom layers. This causes the cold water to sink and the lake to “turn over,” leading to reaeration of the bottom waters. Rivers and streams: Oxygen depletion in freshwater ecosystems is undesirable because many aquatic animals die under even very temporary anoxia. Anoxia results in the production by anaerobic bacteria of odoriferous compounds. As in lakes, nutrient inputs to rivers and streams from sewage or other pollutants can also trigger mass blooms of cyanobacteria, algae and aquatic plants. Biochemical oxygen demand: the microbial oxygen-consuming capacity of a body of water called its biochemical oxygen demand (BOD). The BOD of water is determined by taking a sample, aerating it well to saturate the water with dissolved O2, placing it in a sealed bottle, incubating for a standard period of time in the dark, and determining the residual oxygen in the water at the end of incubation. A BOD determination gives a measure of the amount of organic material in the water that can be oxidized by the microorganisms present there. We see that in freshwater habitats the oxygen and carbon cycles are linked. Terrestrial environments: The word soil refers to the loose outer material of Earth’s surface. Soil develops over long periods of time. Soil composition: Composed of at least four components. (1) Inorganic mineral matter; (2) organic matter; (3) air and water; and (4) living organisms. Soil formation: Soils form as a result of combined physical, chemical, and biological processes. Populations of chemoorganotrophs increase as the degree of plant cover increases. Carbon dioxide produced during respiration becomes dissolved in water to form carbonic acid, which slowly dissolves the rock. Freezing, thawing, and other abiotic processes assist soil formation. As weathering proceeds, the soil increases in depth. Eventually, the movement of materials downward results in the formation of soil layers, called a soil profile. Soil as a microbial habitat: The most extensive microbial growth takes place on the surfaces of soil particles. Even a small soil aggregate can contain many different microenvironments. One of the major factors affecting microbial activity in soil is the availability of water. Water is held in the soil in two ways—by absorption onto surfaces or as free water in thin sheets or films between soil particles. The other major factor affecting microbial activity in soils is the extent of the resources present. The greatest microbial activity is in the organic-rich surface layers. The numbers and activity of soil microorganisms depend to a great extent on the kinds and amounts of nutrients present. Deep subsurface microbiology: Although microbial numbers are much lower than in the A horizon soil, a variety of microorganisms inhabit deep subsurface soils. Microorganisms in the deep subsurface have access to nutrients because groundwater flows through their habitats. Plants as microbial habitats: The rhizosphere is the region immediately outside the root. It is a zone where microbial activity is usually high. The rhizoplane is the actual root surface. Microbial numbers are almost always higher in the rhizosphere and rhizoplane that in regions of the soil devoid of roots. Roots excrete significant amounts of sugars, amino acids, hormones, and vitamins. The phylosphere is the surface of the plant leaf. Under conditions of high humidity, the microflora of leaves may be quite high and include fungi. Plant pathogens are called phytopathogens. Phytopathogens can cause disease in plants in different ways. Some cause the breakdown of key plant components, while others cause direct physical damage to the plant. Other phytopathogens cause growth-related problems manifested in reduced biomass, seeds, fruits, or other plant components. The deep sea and Barophilism: Visible light penetrates no further than about 300 m in pelagic waters; this region is called the photic zone. Beneath the photic zone, down to a depth of about 1,000 m, there is still considerable biological activity. Water at depths greater than 1,000 m is much less biologically active and is known as the deep sea. Organisms that inhabit the deep sea face three major environmental extremes: (1) low temperature, (2) high pressure, and (3) low nutrient levels. Deep-sea waters are completely dark, such that photosynthesis is impossible. Microorganisms that inhabit the deep sea are chemotrophic and are able to grow under high pressure and oligotrophic conditions in the cold. Bacteria isolated from marine waters below 100 m are psychrophilic or psychrotolerant. Deep-sea microorganisms must also be able to withstand the enormous hydrostatic pressures. An organism growing at a depth of 5,000 m must be able to withstand pressures of 500 atm. Some organisms simply tolerate high pressure bud don’t grow best under pressure; these are called barotolerant. Others actually grow best under pressure; these are called barophilic. Organisms isolated from surface waters down to around 3,000 m are typically barotolerant. Cultures derived from samples taken at greater depths, 4,000-6,000 m, are typically barophilic. In even deeper waters (10,000 m), extreme barophiles are present. Molecular effects of high pressure: Pressure decreases the affinity of enzymes for their substrates. The enzymes of extreme barophiles must fold in such a way as to minimize pressure-related effects. Other pressure-sensitive targets include protein synthesis and transport. Chapter 24: Nutrient cycles, bioremediation, and symbioses: The carbon and oxygen cycles- Global carbon cycling requires the activities of both microorganisms and macroorganisms. The carbon cycle: on a global basis, carbon is cycled through all of Earth’s major carbon reservoirs; the atmosphere, the land, the oceans and other aquatic environments, sediments and rocks, and biomass. Carbon reservoirs: the largest carbon reservoir is in the sediments and rocks of Earth’s crust. From the viewpoint of living organisms, a large amount of organic carbon is found in land plants. More carbon is present in dead organic material, called humus. Humus is a complex mixture of organic materials that is derived from dead soil microorganisms that have resisted decomposition along with resistant plant organic materials. The most rapid means of global transfer of carbon is via the CO2 of the atmosphere. Carbon dioxide is removed from the atmosphere primarily by photosynthesis of land plants and marine microorganisms and is returned to the atmosphere by respiration of animals and chemoorganotrophic microorganisms. The single most important contribution of CO2 to the atmosphere is microbial decomposition of dead organic material, including humus. Importance of photosynthesis in the carbon cycle: Most organic carbon comes from photosynthesis. Phototrophic organisms are therefore the foundation fo the carbon cycle. Phototrophic organisms are abundant in nature only in habitats where light is available. Oxygenic phototrophic organisms can be divided into two groups; plants and microorganisms. Decomposition: Photosynthetically fixed carbon is eventually degraded by microorganisms, and tow major forms of carbon remain; methane and carbon dioxide. In anoxic habitats CH4 is produced from the reduction of CO2 with H2 and from certain organic compounds such as acetate. Virtually any compound can eventually be converted to CH4. H2generated from the fermentative degradation of organic compounds by syntrophs gets consumed by methanogens and converted to CH4. Methane produced in anoxic habitats is insoluble and flows to oxic environments where it is oxidated to CO2 by methanotrophs. All organic carbon eventually returns to CO2 and the carbon cycle is complete. The nitrogen cycle: the element nitrogen, N, a key constituent of cells, exists in a number of oxidation states. Four major microbial nitrogen transformations; nitrification, denitrification, anammox, and nitrogen fixation. Nitrogen fixation: nitrogen gas (N2) is the most stable form of nitrogen and is a major reservoir for nitrogen on earth. The nitrogen recycled on Earth is mostly in fixed forms of nitrogen, such as ammonia and nitrate. Denitrification: Under most conditions, the end product of nitrate reduction is N2, NO, or N2O. The reduction of nitrate to gaseous nitrogen compounds, called denitrification, is the main means by which gaseous N2 is formed biologically. On the on hand, denitrification is a detrimental process. On the other hand, denitrification can aid in wastewater treatment. Ammonia fluxes, nitrification, and anammox: Ammonia is released during the decomposition of organic nitrogen compounds such as amino acids and nucleotides, a process called ammonification. Much of the ammonium released by aerobic decomposition in soils is rapidly recycled and converted to amino acids in plants and microorganisms. Because ammonia is volatile, some of it can be lost from alkaline soils by vaporization. Ammonia constitutes only about 15% of the nitrogen released to the atmosphere. Nitrification, the oxidation of NH3 to NO3, occurs in well-drained soils at neutral pH though the activities of the nitrifying bacteria. Nitrification produces nitrate. One common inhibitor is a substituted pyridine called nitrapyrin. Nitrapyrin specifically inhibits the first step in the nitrification, the oxidation of NH3 to NO2. Ammonia can be catabolized anaerobically by Brocadia and related organisms in the process called anammox. The sulfur cycle: the bulk of the sulfur on Earth is in sediments and rocks in the form of sulfate minerals, although the oceans constitute the most significant reservoir. Sulfate-reducing bacteria are a large and highly dierse group. In many anoxic habitats, sulfate reduction is limited by the low levels of sulfate. It only occurs where significant amounts of organic material are present. Sulfide is commonly detoxified in the environment by combitation with iron. Sulfide and elemental sulfur oxidation/reduction: Under oxic conditions, sulfide rapidly oxidizes spontaneously at neutral pH. Sulfur-oxidizing chemolithotrophic bacteria can catalyze the oxidation of sulfide. Significant amounts of sulfide are oxidized by bacteria only in areas in which H2S emerging from anoxic areas meets O2 from oxic areas. Elemental sulfur is chemically stable but is readily oxidized by sulfur-oxidizing chemolithotrophic bacteria. Elemental sulfur is insoluble, and thus the bacteria that oxidize it must attach to the sulfur crystals to obtain their substrate. Elemental sulfur can be reduced as well as oxidized. The bulk of sulfur-reduction in nature is carried out by the phylogenetically distinct sulfur reducers. The iron cycle: On the surface of Earth, iron exists naturally in two oxidation states, ferrous (Fe2+) and ferric (Fe3+). Iron cycles primarily between the ferrous and ferric forms. Fe3+ is reduced both chemically and as a form of anaerobic respiration, and Fe2+ is oxidized both chemically and as a form of chemolithotrophic metabolism. Bacterial iron reduction: Ferric iron reduction is common in waterlogged soils, bogs, and anoxic lake sediments when this iron-laden water reaches bacteria. Ferric iron can also form complexes with various organic constituents. Acid mine drainage: Bacterial oxidation of sulfide minerals is the major factor in acid mine drainage. Microbial bioremediation: the term bioremediation refers to the cleanup of oil, toxic chemicals, or other pollutants from the environment by microorganisms. Microbial leaching of ores: the acid production and mineral dissolution by acidophilic bacteria can be put to use in the mining of metal ores. If the concentration of metal in the ore is low, microbial leaching is practiced. Leaching is especially useful for copper ores because copper sulfate, formed during the oxidation of copper sulfide ores, is very water-soluble. The leaching process: In microbial leaching, low-grade ore is dumped in a large pile and a dilute sulfuric acid solution is percolated down through the pile. The liquid emerging from the bottom of the pile is rich in dissolved metals and is transported to a precipitation plant where the desired metal is precipitated and purified. Mercury and heavy metal transformations: Same process as bioremediation. Petroleum biodegradation: petroleum is a rich source of organic matter, and because of this, microorganisms readily attack hydrocarbons when petroleum is brought into contact with air and moisture. In oil spills, bioremediation is desirable and can be promoted by the addition of inorganic nutrients. The importance of prokaryotes to petroleum bioremediation has been demonstrated in several major crude oil spills in recent years. Both anoxic an oxic biodegradation is possible. Hydrocarbon decomposition: Diverse bacteria, fungi, and a few cyanobacteria and green algae can oxidize petroleum products aerobically. Oil-oxidizing activity is most extensive if temperature and inorganic nutrient concentrations are optimal. Hydrocarbon-degrading bacteria attach to the oil droplets and eventually decompose the oil and disperse the slick. In large oil spills, volatile hydrocarbon fractions evaporate quickly, leaving medium- to longer- chain aliphatic and aromatic components for cleanup crews and microorganisms to tackle. Microorganisms consume oil by oxidizing it to CO2. When bioremediation activities have been promoted by inorganic nutrient application, oil-oxidizing bacteria can grow quickly after an oil spill. Certain oil fractions, such as those containing branched-chain and polycyclic hydrocarbons, remain in the environment. Interfaces where oil and water meet often form on a large scale. Gasoline and crude oil storage tanks are potential habitats for hydrocarbon-oxidizing microorganisms. Petroleum production: In addition to microbial degradation of petroleum, some microorganisms can also produce petroleum, particularly certain green algae. It excretes long-chain hydrocarbons that have the consistency of crude oil. Biodegradation of Xenobiotics: A xenobiotic compound is a synthetic chemical that is not naturally occurring. Xenobiotics include pesticides, polychlorinated biphenyls, munitions, dyes, and chlorinated solvents. Many xenobiotics differ chemically in such a major way from anything organisms have naturally experienced that they degrade extremely slowly, if at all. Pesticide catabolism: some of the most widely distributed xenobiotics are pesticides, which are common components of toxic wastes. Pesticides include herbicides, insecticides, and fungicides. If a xenobiotic substance can be biodegrade, it will eventually disappear from a habitat. Such degradation in the soil is desirable because toxic accumulations of the compound are avoided. The relative persistence rates of xenobiotics are only approximate because environmental factors—temperature, pH, aeration, and organic matter content of the soil. Pesticides can also be removed by volatilization, leaching, or spontaneous chemical breakdown. Some compounds may be degraded either partially or totally provided that some other organic material is present as primary energy source. This is a phenomenon called cometabolism. Reductive dechlorination: In this process, chlorinated organic compounds are used as terminal electron acceptors under anoxic conditions. Aerobic dechlorination: The aerobic biodegradation of chlorinated aromatic compounds occurs by way of oxygenase enzymes. In the aerobic catabolism of 2,4,5-T, following dechlorination, a dioxygenase enzyme breaks down the aromatic ring. Biodegradable plastics: Plastics are xenobiotic polymers of various types. Many of these synthetic polymers remain essentially unaltered for decades in landfills and refuse dups. This problem has fueled the search for biodegradable alternatives—called biopolymers. Photobiodegradable plastics are polymers whose structure is altered by exposure to ultraviolet radiation. Starch-based plastics incorporate starch as a link to shorten fragments of a second biodegradable polymer. Animal-microbial symbioses: Ruminants are herbivorous mammals that possess a special digestive organ, the rumen. Cellulose and other plant polysaccharides are digested with the help of microorganisms. Cows, sheep, and goats are ruminants. Food remains in the rumen about 9-12 hours. During this period cellulolytic microorganisms hydrolyze cellulose to free glucose. The glucose then undergoes bacterial fermentation with the production of volatile fatty acids. These fatty acids pass through the rumen wall into the bloodstream and are oxidized by the animal as its main source of energy. In addition to their digestive functions, rumen microorganisms synthesize amino acids and vitamins that are the main source of these essential nutrients for the animal. Because the rumen is anoxic, anaerobic bacteria naturally dominate. Changes in the microbial composition of the rumen can cause illness or even death of the animal. The rumen has a characteristic fauna composed almost exclusively of ciliated protists. Many of these protists are obligate anaerobes that contribute to the overall process. Hydrothermal vent microbial ecosystems: Underwater hot springs are called hydrothermal vents. Two major types; warm vents emit hydrothermal fluid and hot vents, called black smokers because the mineral-rich hot water forms a dark cloud of precipitated material upon mixing with cold seawater. Hydrothermal ven animals can exist in permanent darkness because they are nourished through a symbiotic association with autotrophic bacteria. Large numbers of sulfur-oxidizing chemolithotrophs live near sulfide-emitting hydrothermal vents. Some vents support nitrifying, hydrogen-oxidizing, iron- and manganese-oxidizing bacteria, or methylotrophic bacteria. Some chemolithotrophs have evolved associations with hydrothermal vent animals. Plant-microbial symbioses: Lichens and mycorrhizae- Lichens are leafy or encrusting microbial symbioses often found growing on bare rocks, tree trunks, house roofs, and the surfaces of bare soils. Lichens consist of a mutualistic relationship between two microorganisms, a fungus, and an alga. The alga is the phototrophic partner and produces organic matter, which is then used for nutrition of the fungus. The fungus, unable to carry out photosynthesis, provides a firm anchor within which the phototrophic component can grow protected from erosion by rain or wind. Mycorrhizae are mutualistic associations of plant roots and fungi. There are two classes of mycorrhizae. In ectomycorrhizae, fungal cells form an extensive sheath around the outside of the root with only a little penetration into the root tissue itself. In endomycorrhizae, the fungal mycelium becomes deeply embedded within the root tissue. Mist mycorrhizal fungi do not catabolize cellulose and other leaf litter polymers. They catabolized simple carbohydrates and typically have one or more vitamin requirements. They obtain their carbon from root secretions and get inorganic minerals from the soil. The mycorrhizal plant can absorb nutrients from its environment for efficiently and thus has a competitive advantage. Chapter 26: Biotechnology- Genetically engineered somatotropin: Growth hormone, or somatotropin, consists of a single polypeptide encoded by a single gene. Lack of somatotropin results in hereditary dwarfism. The somatotropin gene was cloned as cDNA from the mRNA. The cDNA was then expressed in a bacterial expression vector. The main problem with producing relatively short polypeptide hormones such as somatotropin is their susceptibility to protease digestion. This problem can be countered by using bacterial host strains defective for several proteases.. When somatotropin is used to remedy human growth defects, it is desirable to avoid side effects from the hormone’s prolactin activity. Site-directed mutagenesis of the somatotropin gene was used to genetically engineer somatotropin that no longer binds with the prolactin receptor. It is possible not merely to make genuine human hormones, but also to alter their specificity and activity to make them better pharmaceuticals. Genetically engineered vaccines: Vaccines are substances that elicit immunity to a particular disease when injected into an animal. Typically, vaccines are suspensions of killed or modified pathogenic microorganisms or viruses. Genetic engineering can be applied in many different ways to the production of vaccines. Recombinant vaccines: Recombinant DNA techniques can be used to modify the pathogen itself. One can delete pathogen genes that encode virulence factors but leave those whose products elicit an immune response. This yields a recombinant, live, attenuated vaccine. One can add genes from a pathogenic virus to another ,relatively harmless virus, referred to as a carrier virus. Such vaccines are called vector vaccines. This approach induces immunity to the pathogenic viral disease. One can even combine the two approaches. A polyvalent vaccine is a single vaccine that immunizes against two different diseases. Vaccinia virus is widely used to prepare live recombinant vaccines for human use. Genes to be put into vaccinia virus are first inserted into an Escherichia coli plasmid that contains a fragment of the vaccinia thymidine kinase (tdk) gene. This recombinant plasmid is then transformed into animal cells whose own thymidine kinase gene is inactivated. Homologous recombination occurs between the two versions of the tdk gene—one on the plasmid and the other on the virus. Some viruses therefore gain a disrupted tdk gene plus its foreign insert. Vaccinia virus does not actually need thymidine kinase to survive. Consequently recombinant vaccinia viruses can still infect human cells and express any foreign genes they carry. Subunit vaccines: recombinant vaccines do not have to include the entire suite of proteins from the pathogenic organism. Subunit vaccines may contain only a specific protein or proteins from a pathogenic organism. For viruses this protein is often the coat protein(s). The coat proteins are purified and used in high dosage to elicit a rapid and high level of immunity. Fragmentation of viral DNA by restriction enzymes; cloning viral coat protein genes into a suitable vector; providing for proper promoters, reading frame, and ribosome-binding sites; and reinsertion and expression of the viral genes in a microorganism. Cultured insect or mammalian cells are often employed as hosts to prepare such recombinant vaccines. Transgenic organisms: A transgene is a gene from one organism that has been inserted into a different organism. A transgenic organism is one that contains a transgene. A related term is genetically modified organism (GMO). Much of the DNA manipulation is carried out using bacteria and their plasmids long before the engineered transgene is finally inserted into the plant or animal. Transgenic animals in pharming: transgenic animals can be used to produce proteins of pharmaceutical value—a process called pharming. Some proteins have been genetically engineered such that they are secreted in high yield in animal milk. This is convenient for several reasons. First, this allows larger volumes of material to be made more simply and cheaply than by bacterial culture. Second, a milk-processing industry already exists, so little new technology is needed to purify the protein. Third, milk is a natural product that most humans can tolerate, so purification away from possibly toxic bacterial proteins is unnecessary. Goats have proven useful for making several human proteins including tissue plasminogen activator, which is used to dissolve blood clots. Improving livestock and other food animals by transgenics: Livestock may be engineered to improve their productivity, increase their nutritional value, and increase disease resistance. Transgenic livestock are produced that do not necessarily have commercial value but demonstrate the feasibility of certain genetic techniques. One scheme to improve the nutrition of livestock is to insert entire metabolic pathways from bacteria into the animals. A notable technical success has been the insertion into pigs of a gene fro Escherichia coli that helps degrade organic phosphate. Pigs have also been genetically engineered to increase their levels of omega-3 fatty acids. These fatty acids reduce heart disease but are found in significant amounts only in cold-water fish, such as salmon, and a few other rare foods. The enzyme encoded by fat1 converts the less healthy but more common omega-6 fatty acids into omega-3 fatty acids. Another interesting practical example of a transgenic animal is the “fast-growing salmon” These transgenic salmon are not actually larger than normal salmon but simply reach market size much faster. Gene therapy: The use of genetic engineering to treat human genetic diseases as well as attack cancer cells is known as gene therapy. In replacement gene therapy, a nonfunctional or dysfunctional gene in an individual is “replaced” by a functional gene. It is not the defective gene that is replaced but instead, its function. Major obstacles to this approach exist in successfully inserting the required gene therapy and in successfully inserting the required gene into cell lines that will perpetuate the genetic alteration. The first genetic disease for which the use of gene therapy was approved was a form of severe combined immune deficiency (SCID). This disease is caused by the absence of adenosine deaminase (ADA) in bone marrow cells and leads to a crippled immune system. The gene therapy approach used a retrovirus as a vector to carry a wild-type copy of the ADA gene. T cells were removed from the patient and infected with the retrovirus carrying the ADA gene. The corrected T cells were then placed back in the body. Technical problems with gene therapy: Some of the current difficulties are related to the vectors being used. Although using retroviral vectors gives stable integration of the transgene, the site of insertion is unpredictable and expression of the cloned gene is often transient. The vectors also have limited infectivity and are rapidly inactivated in the host. Transgenic plants in agriculture: Genetic engineering can modify plant DNA and then use it to transform plant cells by either electroporation or particle gun methods. One can use plasmids from the bacterium Agrobacterium tumefaciens, which naturally transfer DNA directly into the cells of certain types of plants. Plants can often be regenerated from just a single cell. It is possible to culture plant cells in vivo. After genetically altered clones hav been selected, the cells are induced to grow back into whole plants by treatment with plant hormones. The public knows these plants as genetically modified (GM) plants. Herbicide and insect resistance: Major areas targeted for genetic improvement in plants include herbicide, insect, and microbial disease resistance, as well as improved product quality. The main GM crops today are soybeans, corn, cotton, and canola. Almost all the GM soybeans and canola planted were herbicide resistant , whereas the corn and cotton where herbicide resistant or insect resistant, or both. Herbicide resistance is genetically engineered into a crop plant to protect it from herbicides applied to kill weeds. Many herbicides inhibit a key plant enzyme or protein necessary for growth. Insect resistance; Bt toxin- One widely used approach is based on introducing the genes encoding the toxic protein of bacillus thuringeinsis into plants. B. thuringeinsis produces a crystalline protein called Bt-toxin that is toxic to moth and butterfly larvae. Several different approaches were used to enhance the efficacy of Bt-toxin for pest control in plants. One approach was to develop a single set of Bt-toxins that was effective against many different insects. An effective approach to achieve Bt transgene expression and stability was to transfer the gene derectly into the plant genome. With this methodology, transgenic plants that expressed this protein at levels that were extremely toxic to larvae from a number of insect species were obtained. Although transgenic Bt-toxin looked at first to be a great agricultural success, some problems have arisen, in particular, the selection for insects resistant to Bt-toxin. Bt-toxin often kills nontarget insects, some of which may be helpful. Bt-toxin is hamless to mammals, including humans. Chapter 35: Vectorborne and Soilborne Microbial Diseases- Rabies: occurs primarily as an epizootic disease in animals but is spread as a zoonotic disease to humans under certain conditions. The reservoirs of rabies in the U.S. are wild animals, primarily raccoons, skunks, coyotes, foxes, and bats. Over 50,000 people die every year primarily in developing countries. In the U.S., over 20,000 individuals receive postexposure prophylaxis annually. Is caused by a rhabdovirus, a negative-strand RNA virus that infects cells in the central nervous system of most warm-blooded animals, leading to death if not treated. Present in the saliva of rabid animals, enters the body through a wound from a bite or through contamination of mucous membranes by infected saliva. Rabies virus multiplies at the site of inoculation and then travels to the central nervous system. The incubation period in humans is 9 months. The virus proliferates in the brain, leading to fever, excitation, dilation of the pupils, excessive salication, and anxiety. A fear of swallowing develops from uncontrollable spasms of the throat muscles. Death eventually results from respiratory paralysis. In humans, an untreated rabies infection that becomes symptomatic is almost always fetal. The patient is immunized with a rabies virus vaccine. Because of the very slow progression of rabies in humans, this combination of passive and active immune therapy is nearly 100% effective. Fewer than three cases of human rabies are reported in the U.S each year. If all or even most of the disease reservoir are immune, the disease can be stopped and possibly eradicated. Subunit vaccines are available. Because these are oral vaccines, they have been used to immunize local populations of susceptible wild animals. Hantavirus Syndromes: Cause several severe diseases including Hantavirus pulmonary syndrome (HPS), an acute respiratory and cardiac disease, and hemorrhagic fever with renal syndrome (HFRS), an acute disease characterized by shock and kidney failure. Both diseases are caused by Hantavirus transmission from infected rodents. There have been 453 cases of HPS with 160 deaths (35%) from 1993 to 2006 in the U.S. The genus Hantavirus is a member of the Bunyaviridae, a family of enveloped segmented, negative-strand RNA virus. Includes viruses that cause either HPS or HFSR. Related to hemorrhagic fever viruses such as Lassa fever virus and Ebola virus and occasionally transmitted to humans from animal reservoirs. Are handled with biosafety level-4 precautions. Infect mice and rats of several species, lemmings, and voles. HFRS strains are more commonly implicated in outbreaks in the Eastern Hemisphere and Europe. The HPS strains are more prevalent in the Western Hemisphere. Most commonly transmitted by inhalation of virus-contaminated rodent excreta. The virus is most commonly spread via aerosols from dust generated from mouse droppings or dried urine. HPS is characterized by a sudden onset of fever, myalgia, thrombocytopenia, leukocytosis, and pulmonary capillary leakage. Death occurs within several days in about 35% of cases. The HFRS strains cause as little as 1% mortality. There is no virus-specific treatment or vaccine for hantaviruses. Infection can be prevented by avoiding contact with rodents and rodent habitat. Arthropod-Transmitted Diseases: Rickettsial Diseases: Are small bacteria that have a strictly intracellular existence in vertebrates, usually mammals, and are also associated at some point in their life cycle with blood-sucking arthropods such as fleas, lice, or ticks. Cause diseases in humans and animals, the most important are typhus fever, Rocky Mountain spotted fever, and ehrlichiosis. Closely related to human mitochondria. The Typhus Group: Rickettsia prowazekii- Transmitted from human to human by the common body or head louse. Humans are the only known mammalian host for typhus. Cells are introduced through the skin when a puncture caused by a louse bite becomes contaminated with louse feces. During an incubation period of 1-3 weeks, the organism multiplies inside cells lining the small blood vessels. Symptoms of fever, headache, and general body weakness then appear. Five to nine days later, a characteristic rash is observed in the armpits and generally spreads over the body except for the face, palms, and soles. Untreated typhus includes damage to the CNS, lungs, kidneys, and heart. Mortality rate of 6-30%. Tetracycline and chloramphenicol are most commonly used to control. The Spotted Fever Group: Rickettsia rickettsii- Is transmitted to humans by various ticks. 1000 people acquire the disease every year in the U.S. Acquired from tick fecal matter, which enters the body during a bite, or by rubbing infectious material into the skin by scratching. Grows within the nucleus of the host cell as well as in host cell cytoplasm. Following an incubation period of 3-12 days, characteristic symptoms, including fever and a severe headache, occur. Within 3-5 days, a rash breaks out on the whole body. Gastrointestinal problems are usually observed as well. Clinical symptoms may persist for over 2 weeks if the disease is untreated. Tetracycline or chloramphenicol generally promotes a prompt recovery if administered early and have less tan 1% mortality. 30% in untreated cases. Lyme Disease: An emerging tickborne disease that affects humans and other animals. Most prevalent tickborne disease in the U.S. Caused by Borrelia burgdorferi. Is spread primarily by the deer tick. Deer and the white-footed field mouse are prime reservoirs in the northeastern U.S. Other parts of the country, different species of rodents and ticks transmit. 24,000 cases are reported each year. Transmitted to humans while the tick is obtaining a blood meal. A systemic infection develops. Symptoms include headache, backache, chills, and fatigue. In 75% of cases, a large rash known as eryghema migrans is observed. During this acute stage, Lyme disease is treatable wit tetracycline or penicillin. Untreated, may progress to a chronic stage weeks to months after the tick bite. Chronic Lyme disease is characterized by arthritis in 40-60% of patients.
|Posted by: Granobulax May 13 2009, 04:49 AM|
|Neurological involvement such as palsy, weakness in the limbs, and facial ticks in 15-20% and heart damage in about 8% of patients. May lie dormant causing additional chronic symptoms, including visual disturbances, facial paralysis, and seizures. No toxins or other virulence factors have yet been identified. Resembles symptoms of chronic syphilis. For protection, it is advisable to wear protective clothing. Insect repellant containing DEET is very effective. Treatment of early acute Lyme disease can be with doxycycline, amoxicillin, or cefuroxime axetil for fourteen days. Malaria: Arthropod mosquito vector that has played an important role in the development and spread of human culture and has even affected human evolution. Estimates set the incidence to 350 million people worldwide, and each year over 1 million of these will die. Four species infect humans and cause malaria. Humans are the only reservoirs for the four species. Mosquitoes spread the protest from person to person. Malaria is not a disease of temperate or colder regions. The disease is associated with wet low-lying areas where mosquitoes breed. Malaria means “Bad air.” Prophylaxis usually accomplished with chloroquine. Does not kill sporoziotes, merozoites, and gametes outside the cells. Closely related drug primaquine does. Treatment with both produces a cure. May recur years after the primary infection. The most effective control measure is to interrupt the life cycle by eliminating the Anopheles mosquito. Two approaches to mosquito control; (1) elimination of habitat by drainage of breeding areas, or (2) elimination of the mosquito by insecticides. There are bout 1,500 cases and 5 deaths in the U.S. each year. West Nile Virus: causes West Nile fever. Transmitted through the bite or a mosquito. Can invade the nervous system of its warm-blooded host. A member of the flavivirus group. From 1999 to 2001, there were 149 cases and 18 deaths. By 2002, 884in Illinois and nationwide were 4,156. In 2006, there were 9,186 cases. Transmitted to hosts by the bite of an infected mosquito. 130 species of birds are known host reservoirs. Mosquito vectors transmit to new hosts in new areas, moving in a wavelike fashion across the continent. Humans and other animals are terminal hosts because they do not develop the viremia necessary to infect mosquitoes. Mortality rate is at about 4%. Most human infections are asymptomatic or very mild. After an incubation period of 3-14 days, about 20% of infected individuals develop West Nile fever, a mild illness lasting 3-6 days. May be accompanied by headache, nausea, myalgia, rash, lymphadenopathy, and malaise. Transmission is seasonal and is dependent on exposure to the mosquito population. The primary means of control is by limiting exposure to the disease vector. Should avoid mosquito habitat by wearing appropriate mosquito-resistant clothing and applying insect repellents containing DEET. Spread can be controlled by destruction of mosquito habitat and application of insecticides. There is no effective human vaccine. Treatment is rest, fluids, and symptomatic relief of fever and pain. Plague: has caused more deaths than any other infectious disease except for malaria and TB. Rats are the primary disease reservoir. Humans are accidental hosts. Fleas are intermediate hosts and vectors. Most cases in the U.S. are in the SW states. Is endemic among wild rodents. Is transmitted by the rat flea. Cells multiply in the flea’s intestine and are transmitted to a healthy animal in the next bite. Once in humans, typically travel to the lymph nods, where thy cause swelling. Swollen nodes are called buboes and for this reason are often called bubonic plague. Encapsulated Y. pestis prevents phagoctosis and destruction by cells of the immune system. Eventually enter the bloodstream, causing septicemia. Dark splotches on the skin give the plague its name, the “Black Death.” If not treated prior to the septicemic stage, the symptoms of plague usually progress and cause death within 3-5 days. Pathogenesis is not clearly understood. Exotoxin, murine toxin, is produced by virulent strains. Murine toxin is a respiratory inhibitor. Pneumonic plague occurs when cells of Y pestis are either inhaled directly or via the blood or lymphatic circulation. Septicemic plague is the rapid spread throughout the body via the bloodstream and usually causes death. Can be successfully treated with streptomycin or gentamycin. If treatment is started promptly, mortality can be reduced to 1-5%. Control is accomplished through surveillance and control of animal reservoirs, vectors, and human contact. Fungal Diseases: Commonly found as free-living saprophytes. The fungi include yeasts, which grow as single cells and molds. Most fungi are harmless to humans. Fifty species cause human disease. Cause disease through three major mechanisms. First trigger immune responses that result in allergic reactions. Reexposure may cause allergic symptoms. A second fungal disease producing mechanism involves mycotoxins. Aflatoxins are highly toxic and carcinogenic. The third mechanism is called mycoses. The growth of a fungus on or in the body is called a mycosis that range in severity from relatively innocuous, superficial lesions to serious, life-threatening diseases. Mycoses fall into three categories. The first are superficial mycoses where fungi colonize the skin, hair, or nails and infect only the surface layers. They are benign and self limiting. Spread is by personal contact with an infected person, contact with contaminated surfaces, or by contact with contaminated shared articles. Treatment is with topical miconazole nitrate or griseofulvin. The subcutaneous mycoses are a second category that involves deeper layers of skin. Treatment is with oral potassium iodide or oral ketoconazole. The systemic mycoses are the third and most serious. Involve internal organs and are subclassified as primary or secondary infections. Most antibiotics that inhibit fungi also affect their hosts. Tetanus: is a serious, often life-threatening disease. Causes over 200,000 deaths per year worldwide. Caused by an exotoxin produced by Clostridium tetani. Gains access through a soil-contaminated wound. In the wound, anoxic conditions allow germination of endospores, growth of the organism, and production of a potent Exotoxin, tetanus toxin. The incubation time may take from 4 days to several weeks. The toxin directly affects the release of inhibitory signaling molecules in the nervous system. These inhibitory signals control the “relaxation” phase of muscle contraction. The result is rigid paralysis of the voluntary muscles. Death is usually due to respiratory failure, and mortality is relatively high at 15%. Control measures focus on prevention. The toxoid vaccine is completely effective for disease prevention. Treatment of serious cuts, lacerations, and punctures includes administration of a “booster” tetanus toxoid immunization. Acute tetanus is treated with antibiotics, usually penicillin. Treatment cannot provide a reversal of symptoms, because toxin that is already bound to tissues cannot be neutralized. Chapter 36: Water borne diseases- Waterborne diseases are the most important diseases in the world. Mostly in developing countries. More mortality and morbidity are caused by this than anything else. Few agents that cause diseases and are pretty easy to take care of. Public health and water quality: Can’t tell anything by color just by looking at it. In looking at community water, two kinds of concerns to have. (1) The microorganism load of that water. (2) Waters chemical load. Most water disease causing agents in water have a shorter lifespan than E. Coli in testing water. If you don’t find E coli then from a pacterial perspective it’s probably ok. If you do find E. coli it may mean that the water may or may not be ok to drink. The E. coli itself is ok, but if fount it’s an indicator that there is fecal matter in the water. Worried about I coli because it’s a proxy for disease causing agents. Another reason to test for E. coli first is it’s easy to test for as other agents are not. Filtration and chlorination of water significantly decreases microbial numbers. Sometimes there is contamination after the water has been treated like in the pipes. Wastewater and sewage treatment: Wastewater is contaminated water. Domestic sewage is water contaminated with fecal matter. Liquid industrial waste is not always organic matter but is also chemical waste. Water treatment: Raw wastewater coming in and screen it to get the fish etc out, then you have sedimentation where the insoluble sludge and soluble liquid goes into secondary treatments. Both are treated differently with the idea of lowering the organic matter. Insoluble content is treated by anoxic digestion which leads to digested sludge drying, incineration, use as fertilizer or burial. Soluble is treated using oxidation by means of activated sludge tricking filter and aeration, then is disinfected. Then to treated effluent to stream. You can also use tertiary treatment. You remove most of the nutrients from the water by means of physiochemical or biological process, employing bioreactors, precipitation, filtration, or chlorination procedures. Drinking water purification: Start with raw water that contains sedimentation. You remove the sedimentation, then coagulation where you form and remove floc, containing insoluble material and microorganisms. Met, filtration where you remove all remaining particulates, organic and inorganic compounds. Next is chlorination. Kill remaining microorganisms. Next is storage, where need to prevent growth of new inocula. Last is distribution. The goal is to lower the risk of getting disease through water. There can be problems with this and you could get a disease. Sources of waterborne infection: Potable water recreational water. Cholera is a severe diarrheal disease that is now largely restricted to the developing parts of the world. Is caused by Vibrio cholera. Typically transmitted through ingestion of contaminated water. Is also associated with food consumption. Two distinct strains of cholera are recognized. Known as the classic and the El Tor biotypes. Highest prevalence of cholera is in developing countries, especially in Africa. Epidemic cholera occurs frequently in areas where sewage treatment is either inadequate or absent. For the few possibly endemic cases, raw shellfish seem to be the most common vehicle, presumably because cholera appears to be free-living in coastal waters in endemic areas, adhering to marine microflora. After a person ingests a substantial number of cholera cells, the cells take up residence in the small intestine. The ingestion or 108 and 109 cholera vibrios is generally required to cause disease. Even lower cell numbers can initiate infection if cholera is ingested with food, presumably because the food protects the vibrios from stomach acidity. Cholerae attaches to epithelial cells in the small intestine where it grows and releases enterotoxin. Cholera enterotoxin causes severe diarrhea that can result in dehydration and death unless the patient is given fluid and electrolyte therapy. The enterotoxin causes fluid losses of up to 20L per day. The mortality rate from untreated cholera is typically 25-50%. Natural infection and the current vaccines provide variable, short-term immunity. Public health measures such as adequate sewage treatment and a reliable source of safe drinking water are the most important measures for preventing cholera. V. cholera is emiminated from wastewater during proper sewage treatment and drinking water purification procedures. For individuals traveling in cholera-endemic areas, careful attention to personal hygiene and avoidance of untreated water or ice, raw foods, fish, and shellfish offer protection against contracting cholera. Cholera treatment is simple, effective, and inexpensive. Intravenous or oral liquid and electrolyte replacement therapy is the most effective means of cholera treatment. Oral treatment is preferred because no special equipment or sterile precautions are necessary. Streptomycin or tetracycline may shorten the course of infection and the shedding of viable cells, but antibiotics are of little benefit without simultaneous fluid and electrolyte replacement. Giardiasis is caused by Giardia intestinalis that is usually transmitted to humans in focally contaminated water, although foodborne and sexual transmission of giardiasis has also been documented. Giardiasis is an acute gastroenteritis caused by this organism. The protest cells, called trophoziotes produce a resting stage called a cyst. The cyst has a thick protective wall that allows the pathogen to resist drying and chemical disinfection. After a person ingests the cysts in contaminated water, the cysts germinate, attach to the intestinal wall, and cause the symptoms of giardiasis, an explosive, foul-smelling, watery diarrhea. Intestinal cramps, flatulence, nausea, weight loss, and malaise as well. Symptoms may be acute or chronic. Many infected individuals exhibit no symptoms but act as carries, indicating that G. intestinalis can also establish itself in a stable symptom-free relationship with it’s host. Cysts are resistant to chlorine and UV radiation and most past outbreaks have been associated with water systems that used only chlorination as a means of water purification. Water subjected to proper clarification and filtration followed by chlorination or other disinfection is generally free of Giardia cysts. Giardiasis can be contracted from ingestion of water from infected swimming pools or lakes. Beavers and muskrats are frequent carriers of Giardia and may transmit cells or cysts to water supplies, making the water a possible source of human infection. The drugs quinacrine, furazolidone, and metronidazole are useful in treating acute giardiasis. Cryptosporidiosis is caused by the protest Cryptosporidium parvum. Lives as a parasite in warm-blooded animals. Cells that invade and grow intracellularly in mucosal epithelial cells of the stomach and intestine. The protest produces thick-walled, chlorine-resistant, infective cells called oocyts, which are shed into water in high numbers in the feces of infected warm-blooded animals. The infection is passed on when other animals consume the focally contaminated water. Cryptosporidium cysts are highly resistant to chlorine and UV radiation disinfection. Therefore, sedimentation and filtration methods must be used to remove Cryptosporidium from water supplies. It is also a parasite in diary cattle. Is usually a self-limiting mild diarrhea that subsides in 2 weeks or less in normal individuals. Treatment is unnecessary for those with uncompromised immunity. For individuals undergoing immunosuppressive therapy, discontinuation of immunosuppressive drugs is recommended. Immunocomomised individuals should be given supportive therapy such as intravenous fluids and electrolytes. Legionellosis is caused by legionella pneumophila. The organism can be isolated from terrestrial and aquatic apitats as well as from legionellosis patients. L. pneumopila is present in small numbers in lakes, streams, and soil. It’s relatively resistant to heating and chlorination, so it can spread through water distribution systems. It’s commonly found in large numbers in cooling towers and evaporative condensers of large air conditioning systems. The pathogen grows in the water and is disseminated in humidified aerosols. Human infection is by way of airborne droplets, but the infection is not spread from person to person. L. pneumophila has also been found in hot water tanks and whirlpool spas where it can grow to high numbers in warm, stagnant water. Epidemiological studies indicate that L. pneumophila infections occur at all times of the year, primarily as a result of aerosols generated by heating/cooling systems and common practices such as showering or bathing. Prevention of legionellosis can be accomplished by improving the maintenance and design of water-dependent cooling and heating systems and water delivery systems. The pathogen can be eliminated from water supplies by hyperchlorination or by heating to warmer than 63°C. In the body, L. pneumophila invades and grows in alveolar macrophages and monocytes as an intracellular parasite. Infections are often asymptomatic or produce a mild cough, sore throat, mild headache, and fever. These mild, self-limiting cases, called Pontiac fever, are generally not treated and resolved in 2-5 days. Elderly individuals, whose resistance has been previously compromised often acquire more serious infections resulting in pneumonia. Certain serotypes of L. pneumophila are strongly associated with the pneumonic form of the infection. Prior to the onset of pneumonia, intestinal disorders are common, followed by high fever, chills, and muscle aches. These symptoms precede the dry cough and chest and abdominal pains typical of legionellosis. Death occurs in up to 10% of cases and is usually do to respiratory failure. Can be treated with the antibiotics rifampin and erythromycin. Intravenous administration of erythromycin is the treatment of choice. Typhoid fever is caused by salmonella typhi. Although S. typhi may also be transmitted by contaminated food and by direct contact from individuals, the most common and serious means of transmission worldwide is through water. Fortunately, typhoid fever has been virtually eliminated in developed countries, primarily due to effective water treatment procedures. Viruses can also be transmitted in water and cause human disease. Quite commonly, enteroviruses such as poliovirus, norovirus and hepatitis A virus are shed into the water in fecal material. The most serious of these is poliovirus, but wild poliovirus has been eliminated from the Western Hemisphere and is endemic only in Nigeria, Afghanistan, Pakistan, and India. Although viruses can survive in water for a relatively long period, they are inactivated by disinfection with agents such as chlorine. Amobiasis: certain amoebas inhabit the tissues of humans and other vertebrates, usually in the oral cavity or intestinal tract, and some of these are pathogenic. Worldwide, Entamoeba histolytica is a common pathogenic protest transmitted to humans, primarily by contaminated water and occasionally through contaminated food. E. histolytica produce cysts. Cysts ingested by humans germinate in the intestine, where amoebic cells grow both on and in intestinal mucosal cells. Many infections are asymptomatic, but continued growth may lead to invasion and ulceration of the intestinal mucosa, causing diarrhea and severe intestinal cramps. With further growth, the amoebae can invade the intestinal wall, a condition called dysentery, characterized by intestinal inflammation, fever, and th passage of intestinal exudates, including blood and mucus. If not treated ,invasive trophoziotes of E histolytica can invade the liver and occasionally the lung and brain. Growth in these tissues can cause severe abscesses and death. I. histolytica amoebiasis can be treated with the drugs dehydroemetine for invasive disease and diloxanide furoate for certain asymptomatic cases, as in immunocompromised individuals, but amoebicidal drugs are not universally effective. Spontaneous cures do occur, suggesting that the host immune system plays a role in ending the infection. However, protective immunity is not an outcome of primary infection and reinfection is common. The disease is kept at very low incidence in regions that practice adequate sewage treatment. Naegleria fowleri can also cause amoebiasis, but in a very different form. N. fowleri is a free-living amoeba found in soil and in water runoff. N. fowleri infections usually result from swimming or bathing in warm, soil-contaminated water sources such as hot springs or lakes and streams in the summer. This free-living amoeba enters the body through the nose and burrows directly into the brain. Here, the organism propagates, causing extensive hemorrhage and brain damage. This condition is called meningoencephalites. Death usually results within a week. Prevention can be accomplished by avoiding swimming in shallow, warm, fresh water in summer, such as farm ponds, and shallow lakes and rivers. Swimmers are advised to avoid stirring up bottom sediments, the natural habitat of the pathogen. If a definitive diagnosis can be done quickly, the drug amphotericin B is used to treat infections. Chapter 37: Foodbourne diseases- food spoilage in the degree of possible spoilage depends on the water content of the food. Foods are classified into 3 categories. 1 perishable food-fresh food items. 2 semiperishable food- potatoes and nuts. 3 stable or nonperishable food- flour and sugar. Food preservation: cold is not a preservative, it only slows the spoilage process down. Pickling and acidity at low ph won’t spoil or the low ph slows sown the process. Drying and dehydration are good ways of preserving things. Dehydration pulls more water out than drying itself. Heating pasteurization uses flash heating. It does not prevent spoilage. Aseptic food processing: food stored under sterile conditions and can be kept for a longer shelf life. Chemical preservations are also carcinogens, like bacon has nitrites. Irradiation- goal is to kill all. It will change the chemical nature of the food. Fermentation is another way. Food intoxication is disease that results from ingestion of foods containing preformed microbial toxins. Staphylococcal food poisoning is often caused by toxins produced by the bacterium Staphylococcus aureus. Staph are normal members of the local flora of the skin and upper respiratory tract of nearly all humans and are often opportunistic pathogens. Staph is frequently associated with food poisoning because it can grow in many common foods, and some strains produce several heat-stable enterotoxins. If the enterotoxin is consumed in food, gastroenteritis characterized by nausea, vomiting, and diarrhea, occurs within 1-6 hours. The foods most commonly involved are custard and cream filled baked goods, poultry, meat, and meat products, gravies, egg and meat salads, puddings, and creamy salad dressings. If such foods are refrigerated immediately after preparation, they usually remain safe because staph grows poorly at low temperatures. However, foods of this type are often kept at room temperature in kitchens or outdoors at picnics. The food, if inoculated with staph from an infected food handler, supports rapid bacterial growth and enterotoxin production. Even if the toxin-containing foods are reheated before eating, the heat-stable toxin may remain active. Live staph need not be present in foods causing illness. The illness is soley due to the preformed toxin. Staph produce at least seven different but related enterotoxins. Most strains of staph produce only one or two of these toxins, and some strains are nonproducers. However, any one of these toxins can cause staphylococcal food poisoning. In the intestine, superantigens activate a general inflammatory response that causes gastroenteritis and significant fluid loss. The symptoms of S. aureus food poisoning can be quite severe but are typically self-limiting, usually resolving within 48 hours as the toxin is shed from the body. Severe cases may require treatment for dehydration. Treatment with antibiotics is not useful because staph food poisoning is caused by a preformed toxin, not an active bacterial infection. Staph food poisoning can be prevented by proper sanitation and hygiene in food production, food preparation, and food storage. As a rule, foods susceptible to colonization by staph and kept for several hours at temperatures above 4°C should be discarded rather than eaten. Clostridium perfringens food poisoning: is caused by C. perfringens commonly found in soil, it also lives in small numbers in the intestinal tract of many animals and humans and is therefore found in sewage. Perfringens food poisoning requires the ingestion of a large dose of C. perfringens in contaminated cooked or uncooked foods, especially high-protein foods such as meat, poultry, and fish. Large numbers of C. perfringens can grow in meat dishes cooked in bulk. In such food preparations, heat penetration is often insufficient, and surviving C perfringens begin to sporulate in the intestine, which coincides with production of the perfringens enterotoxin. When ingested, perfringens enterotoxin alters the permeability o the intestinal epithelium, leading to nausea, diarrhea, and intestinal cramps, usually with no fever. The onset of perfringens food poisoning begins about 7-15 hours after consumption of the contaminated food but usually resolves within 24 hours, and fatalities are rare. Because C. perfringens food poisoning is self-limiting, antibiotic treatment is not indicated. Supportive therapy can be used in serious cases. Prevention of perfringens food poisoning requires measures to prevent contamination of raw and cooked foods and control of cooking and canning procedures to ensure proper heat treatment of all foods. Cooked foods should be refrigerated as soon as possible to rapidly lower temperatures and inhibit C perfringens growth. Botulism is a severe, often fetal, food poisoning that occurs following the consumption of food containing the exotoxin produced by C. botulinum. This bacterium normally inhabits soil or water, but its endospores may contaminate raw foods before harvest or slaughter. If the foods are properly processed so that the C. botulinum endospores are removed or killed, no problem arises; but if viable endospores are present, they may germinate and produce toxin. Even a small amount of the resultant neurotoxin can be dangerous. Bodulinum toxin is a neurotoxin that causes flaccid paralysis, usually affecting the autonomic nerves that control body functions such as respiration and heartbeat. At least seven distinct bodulinum toxins are known. However, because the toxins are destroyed by heat, thoroughly cooked food, even if contaminated with toxin, can be totally harmless. Most cases of foodborne botulism are caused by eating foods that are not cooked after processing. Over 60% of all botulism cases in the U.S. are infants. All forms of botulism are quite rare. Death occurs from respiratory paralysis or cardiac arrest due to the paralyzing action of the botulinum neurotoxin. Treatment involves administration of botulinum antitoxin. If the diagnosis is early, and mechanical ventilation for flaccid respiratory paralysis. In infant botulism, C. botulinum and toxin are often found in bowel contents. Infant botulism is usually self-limiting, and most infants recover with only supportive therapy, such as assisted ventilation. Antitoxin administration is not recommended. Respiratory failure causes occasional deaths. Prevention of botulism requires maintaining careful controls over canning and preservation methods. Susceptible foods should be heated to destroy endospores; boiling for 20 minutes destroys the toxin. Home-prepared foods are the most common source of foodborne botulism outbreaks. In addition, feeding honey to children under 2 years of age is not recommended because honey is an occasional source of C. botulinum endospores. Salmonellosis is a gastrointestinal disease typically caused by foodborne salmonella infection. Symptoms begin after the pathogen colonizes the intestinal epithelium. Related to Escherichia coli and other enteric bacteria, salmonella normally inhabits the animal intestine and is thus found in sewage. There are seven evolutionary groups or subspecies of Salmonella enteric. Most human pathogens fall into group I, designated as a single subspecies, S. enteric; subspecies enterica. Salmonella Typhi causes the serious human disease typhoid fever but is very rare in the U.S. The ultimate sources of te foodborne salmonellas are the intestinal tracts of humans and warm-blooded animals, and several mechanisms may introduce these organisms into the food supply. The organism may reach food by fecal contamination from food handlers. Food production animals such as chickens, pigs, and cattle may also harbor Salmonella serotypes that are pathogenic to humans and may pass the bacteria to finished fresh foods such as eggs, meat, and dairy products. Salmonella food infections are often traced to products such as custards, cream cakes, meringues, pies, and eggnog made with uncooked eggs. Other foods commonly implicated in salmonellosis outbreaks are meats and meat products such as meat pies, cured but uncooked sausages and meats, poultry, milk, and milk products. Ingestion of food containing viable Salmonella results in colonization of the small and large intestine. Onset of the disease occurs 8-48 hours after ingestion. Symptoms include the sudden onset of headache, chills, vomiting, and diarrhea, followed by a fever that lasts a few days. The disease normally resolves without intervention in 2-5 days. After recovery, patients may shed Salmonella in feces for several weeks. Some patients recover and remain asymptomatic, but shed organisms for months or even years. They are chronic carriers. A few serotypes of Salmonella may also cause septicemia and enteric or typhoid fever. The pathogenesis of Salmonella infections starts with uptake of the organisms from the gut. Salmonella ingested in food or water invades phagocytes and grows as an intracellular pathogen, spreading to adjacent cells as host cells die after invasion. Pathogenic Salmonella uses a combination of endotoxin, enterotoxin, and cytotoxin to damage and kill host cells, leading to the classic symptoms of salmonellosis. For interocolitis, treatment is usually unnecessary, and antibiotic treatment does not shorten the course of the disease or eliminate the carrier state. Antibiotic treatment significantly reduces the length and severity of septicemia and typhoid fever. Mortality due to typhoid fever can be reduced to less than 1% with appropriate antibiotic therapy. Multi-drug-resistant Salmonella are significan clinical problem. Properly cooked foods are generally safe if consumed immediately. Any foods that become contaminated by an infected food handler can support the growth of Salmonella if the food s are held for long periods of time, especially without heating or refrigeration. Salmonella infections are more common in summer than in winter, probably because warm environmental conditions generally favor the growth of microorganisms in foods. Although local laws and enforcement vary, because of the lengthy carrier state, infected individuals are often banned from work as food handlers until their feces are negative for Salmonella in three successive cultures. E. coli produce verotoxin, an enterotoxin similar to one produced by Shingella dysenteriae, the Shiga toxin. After a person ingests food or water, the organism grows in the small intestine and produces verotixin. Verotoxin causes both hemorrhagic diarrhea and kidney failure. This pathogen is the leading cause of hemolytic uremic syndrome and kidney failure. The most common cause of this infection is the consumption of contaminated uncooked or undercooked meat, particularly mass-processed ground meat. Because it grows in the intestines and is found in fecal material, it is also a potential source of waterborne gastrointestinal disease. I. coli also can be the cause of “traveler’s diarrhea,” an extremely common enteric infection causing watery diarrhea in travelers to developing countries. The primary causal agents are the enterotoxigenic E. coli (ETEC). The ETEC strains usually produce one of two heat-labile diarrhea-producing enterotoxins. The prime vehicles are foods such as fresh vegetables and water. The very high infection rate in travelers is due to contamination of local public water supplies. The local population is usually resistant to the infecting strains, presumably because they have acquired resistance to the entimic ETEC strains. Enteropathogenic E. coli (EPEC) strains cause diarrheal diseases in infants and small children but do not cause invasive disease or produce toxins. Enteroinvasive E. coli (EIEC) strains cause invasive disease in the colon, producing watery, sometimes bloody diarrhea. The EIEC strains are taken up by phagocytes, but escape lysis in the phagolysosomes. They grow in the cytoplasm, and move into other cells. This invasive disease causes diarrhea and is common in developing countries. Treatment of E. coli 0157:H7 and other EHEC includes supportive care and monitoring of renal function, blood hemoglobin, and platelets. Antibiotics may be harmful because they may cause the release of large amounts of verotoxin from dying E. coli cells. For other pathogenic E. coli infections, treatment usually involves supportive therapy and, for severe cases and invasive disease, antimicrobial drugs to shorten and eliminate infection. The most effective way to prevent infection with foodborne EHEC 0157:H7 is to make sure that meat is cooked thoroughly in general, proper food handling, water purification, and appropriate hygiene prevents the spread of pathogenic E. coli. Traveler’s diarrhea can be prevented by avoiding consumption of local water and uncooked foods. Campylobacter is transmitted to humans via contaminated food, most frequently in poultry, pork, raw shellfish, or in surface waters. C jejuni is a normal resident in the intestinal tract of poultry; virtually all chickens and turkeys normally have this organism. Campylobacter species also infect domestic animals such as dogs, causing a milder form of diarrhea than that observed in humans. Campylobacter infections in infants are frequently traced to infected domestic animals. After a person ingests cells of Campylobacter, the organism multiplies in the small intestine, invades the epithelium, and causes inflammation. Because C. jejuni is sensitive to gastric acid, cell numbers as high as 104 may be required to initiate infection. Ingestion of the pathogen directly in food, or ingestion by individuals taking medication to reduce stomach acid production, bay reduce this number to less than 500 bacteria. Campylobacter infection causes a high fever, headache, malaise, nausea, abdominal cramps, and profuse diarrhea with watery, frequently bloody stools. The disease subsides in about 7-10 days. Spontaneous recovery from Campylobacter infections is often complete, but relapses occur in up to 25% of cases. Erythromycin treatment and quinolone treatment may be useful early in severe diarrheal disease. Adequate personal hygiene, proper washing of uncooked poultry, and thorough cooking of meat eliminate Campylobacter contamination. Listeriosis is caused by Listeria monocytogenes, a gastrointestinal food infection that may lead to bacteremia and meningitis. Is found in soil and water. Virtually no food source is safe from possible L. monocytogenes contamination. Food can become contaminated at any stage during food growth or processing. Food preservation by refrigeration, which ordinarily slows microbial growth. Is ineffective in limiting growth of this psychrotolerant organism. Ready-to-eat meats, fresh soft cheeses, unpasteurized dairy products, and inadequately pasteurized mild are the major food vehicles for this pathogen, even when foods are properly stored at refrigerator temperature. Is an intracellular pathogen. It enters the body through the gastrointestinal tract with ingestion of contaminated food. Uptake of the pathogen by phagocytes results in growth and proliferation of the bacterium, lysis of the phagocyte, and spread to surrounding cells such as fibroblasts. Immunity to L. monocytogenes is mainly TH1 cell-mediated. Particularly susceptible populations include the elderly, pregnant women, neonates, and immunosuppressed individuals. Acute listeriosis is rare and is characterized by septicemia, often leading to meningitis. Intravenous antibiotic treatment with penicillin, ampicillin, or trimethoprim plus sulfamethoxazole is recommended for invasive disease. Prevention measures include recalling contaminated food and taking steps to limit L. monocytogenes contamination at the food-processing site. Because L. monocytogenes is susceptible to heat and radiation. Raw food and food handling equipment can be readily decontaminated. Without pasteurizing the finished food product, the risk of contamination cannot be eliminated because of the widespread distribution of the pathogen. Individuals who are immunocompromised should avoid unpasteurized dairy products and ready-to-eat processed meats. Spontaneous abortion is a frequent outcome of listeriosis. Therefore, to protect the fetus, pregnant women should also avoid foods that may transmit L. monocytogenes.|
|Posted by: Granobulax May 13 2009, 04:51 AM|
|Oh, and if anyone is wondering, NONE of this has been copy and pasted. I've hand typed everything out of a book. I don't have to tell you how time consuming that is.|
|Posted by: Shadow Fenrir May 13 2009, 07:10 PM|
|*Head explodes* That's waaayyy too much to read...|
|Posted by: Solomon May 13 2009, 07:24 PM|
...Who says I did legally.
Who says I didn't?
|Posted by: Solomon May 13 2009, 07:25 PM|
I'm gonna buy you a nice scanner/copier/printer for christmas.
|Posted by: Bassetman May 13 2009, 07:48 PM|
Just for our viewing pleasure?
You shouldn't have.
|Posted by: Granobulax May 13 2009, 07:55 PM|
Yes, I did it all for you Basset.
At least if anyone does a microbiology class on her will already have notes
|Posted by: treacherous May 14 2009, 02:34 AM|
I plan on having microbiology class....never.
|Posted by: Marvel Man May 14 2009, 02:43 AM|
You need a hobby.
|Posted by: Shadow Fenrir May 14 2009, 02:48 AM|
|He used to...|
|Posted by: Granobulax May 14 2009, 03:52 AM|
Ha! I've turned you away from all of this work? Work... the worst of four letter words...
|Posted by: Granobulax May 14 2009, 03:53 AM|
I have a hobby. It's called life. It's a difficult hobby to have, but it pays off in the end.
|Posted by: Marvel Man May 14 2009, 04:14 AM|
I love that game.
|Posted by: Granobulax May 14 2009, 04:35 AM|
My character is going to college.
|Posted by: Marvel Man May 14 2009, 12:46 PM|
Mine dropped out, and became a master thief....
|Posted by: Granobulax May 16 2009, 12:52 AM|
| Well, I did it. I passed my second semester nursing class with a B. I feel pretty good knowing that with working full time, taking Nursing II which is a full time class by itself, taking microbiology and passing that class, and going through a divorce and I still made it despite all odds.
I begin my summer courses on monday. When I get through with them in a month and a half I'll sit for my LPN NCLEX exam. If and when I pass that national test, I'll be a Licenced Practical Nurse.
Then it's on to third semester nursing in the fall.
Wish me luck!
|Posted by: Solomon May 16 2009, 12:58 AM|
All systems go.
|Posted by: Granobulax May 16 2009, 01:03 AM|
|Posted by: Solomon May 16 2009, 01:10 AM|
No problem. Nursey pants.
|Posted by: Jailer411 May 16 2009, 01:18 AM|
| How can a pelvic tumor spread directly to the brain without first involving lung or liver?
|Posted by: Granobulax May 16 2009, 02:30 PM|
|It's called a metastasized tumor. It's spread through the blood vessels or the lymphatic system. These metastic tumors can spread virtually anywhere in the body.|
|Posted by: Granobulax May 18 2009, 04:11 AM|
| Well, I got my "official" grades for my classes today and to my suprise, I got an "A" in microbiology.
So, that's an "A" and a "B" for the semester. Yay!
|Posted by: Granobulax May 19 2009, 03:35 AM|
|I finally talked to treacherous today. He's one cool guy. I also finally got to bash some of you unadulterated without worry of a paper trail.|
|Posted by: Solomon May 19 2009, 03:39 AM|
How could you? I thought we were friends.
|Posted by: GruntKilla06 May 19 2009, 03:41 AM|
Cool. Not me though right?
|Posted by: Granobulax May 19 2009, 03:48 AM|
|Posted by: Granobulax May 19 2009, 03:49 AM|
|Posted by: The Ripper May 19 2009, 03:50 AM|
|I congratulate Grano for passing the semester. It is also astounding for him to talk to treacherous from afar!|
|Posted by: GruntKilla06 May 19 2009, 03:50 AM|
|Posted by: Granobulax May 19 2009, 03:55 AM|
Pssst. If I didn't like ya, I wouldn't be a smart-ass to ya
|Posted by: Solomon May 19 2009, 03:59 AM|
|Posted by: Solomon May 19 2009, 04:00 AM|
Whoa! Is it the 1880's already?!
|Posted by: Granobulax May 19 2009, 04:03 AM|
I knew you were old, but damn!
|Posted by: Solomon May 19 2009, 04:05 AM|
|Im not limited by he human concept of time.|
|Posted by: GruntKilla06 May 19 2009, 04:06 AM|
Why thank you.
|Posted by: The Ripper May 19 2009, 04:14 AM|
Go ask Nietzsche. He has the answer.
|Posted by: Solomon May 19 2009, 04:17 AM|
|Yeah I've gazed into the abyss before. It got scared.|
|Posted by: Granobulax May 19 2009, 04:18 AM|
I don't blame you.
|Posted by: Solomon May 19 2009, 04:22 AM|
|Note to self: Take extra extra long when activating Grano's account, maybe "accidentally" delete it a few times.|
|Posted by: Granobulax May 19 2009, 04:46 AM|
|Good, I'll have a legit excuse not to post matches on CBUB for a while longer|
|Posted by: Solomon May 19 2009, 04:50 AM|
|Note to self: Stop taking notes for yourself on the internet.|
|Posted by: Granobulax May 19 2009, 05:35 AM|
|Posted by: treacherous May 20 2009, 10:27 PM|
|Who's talking to me from afar?|
|Posted by: Granobulax May 21 2009, 01:32 AM|
Yeah, I live in Arizona, not "afar"
|Posted by: treacherous May 21 2009, 03:29 AM|
I live behind Zod in your avatar. Move Zod, you're blocking the sun.
|Posted by: Solomon May 21 2009, 03:30 AM|
|I live in...|
|Posted by: Granobulax May 21 2009, 07:52 AM|
| Watch this video of Kendra!
|Posted by: Granobulax May 21 2009, 02:58 PM|
|Watch my video!|
|Posted by: Bassetman May 21 2009, 07:16 PM|
| Is it fascination that attracts a father to a daughter?
Besides love, anyway.
|Posted by: treacherous May 21 2009, 07:20 PM|
You have to have one. You'll never know until you have one. There is nothing like it.
|Posted by: Granobulax May 21 2009, 11:22 PM|
|Posted by: GruntKilla06 May 22 2009, 02:26 AM|
But I did.
|Posted by: Granobulax May 22 2009, 03:14 AM|
I saw that. Thanks for the comment on it too
|Posted by: treacherous May 22 2009, 03:18 AM|
|Daughters, Got to love em.|
|Posted by: Granobulax May 22 2009, 03:19 AM|
|Yes, especially since ours are so damn cute!|
|Posted by: treacherous May 22 2009, 03:21 AM|
|Posted by: GruntKilla06 May 23 2009, 03:20 AM|
|Posted by: Bassetman May 23 2009, 04:26 PM|
|Posted by: treacherous May 24 2009, 05:04 AM|
|Grano's been gone too long. Looks like somebody needs a call.|
|Posted by: Darkender May 24 2009, 11:05 PM|
Yea, get him back before I become King Poster again.
|Posted by: Granobulax May 24 2009, 11:58 PM|
Been busy. I'm moving to a new place tomorrow but won't have internet. I'll send you my new cell number, my old one was shut off. You'll be my only connection to the Haven for a while.
|Posted by: treacherous May 25 2009, 01:50 AM|
|Ha ha. I'll make up stuff about everybody. Seriously Grano, find a library and get back on the Haven.|
|Posted by: Solomon May 25 2009, 03:53 AM|
|Grano Grano where for art thou Grano|
|Posted by: Granobulax May 25 2009, 05:38 AM|
Deny thy Solomon and refuse thy name;
Or if thou wilt not, be but sworn my love
And I'll no longer be a treacherous.
|Posted by: Pseudonym May 25 2009, 01:34 PM|
|Or you could've used Pseudonym for the pun.|
|Posted by: Solomon May 25 2009, 02:09 PM|
|Posted by: Bandit May 25 2009, 02:54 PM|
|Hey Grano, do you like Hotdogs?|
|Posted by: Granobulax May 25 2009, 04:02 PM|
You're right, I should have used pschewedgum...
|Posted by: Granobulax May 25 2009, 04:03 PM|
You're MC Hammer???
|Posted by: Granobulax May 25 2009, 04:04 PM|
This is a risky question to answer, knowing you...
|Posted by: Solomon May 25 2009, 04:08 PM|
Was it not obvious?
|Posted by: Granobulax May 25 2009, 04:09 PM|
I know, but you're so washed up...
|Posted by: Solomon May 25 2009, 04:11 PM|
|You can't touch this!|
|Posted by: Granobulax May 25 2009, 04:12 PM|
But all I want is a hug...
|Posted by: Solomon May 25 2009, 04:15 PM|
|YOUcan't hug this.|
|Posted by: Bassetman May 25 2009, 04:21 PM|
|Posted by: Granobulax May 25 2009, 09:41 PM|
| Well, this is it for a while. I don't think I'll have time to go to the library for a while and where I'm moving into has no internet. I'll be back, but I don't know how long it'll be. I'll have all of you in my prayers.
Treacherous, you'd better call me from time to time. I gave you my new phone number. I'll look foward to talking to you and getting updates from you.
Until I'm back, this is Grano, signing off til next time.
|Posted by: Bandit May 25 2009, 09:59 PM|
I can not send you anything random now.
YOU SONS OF B****es YOU KILLED HIM!
PULLS OUT TWO AK'S AND GOES TO RAISE HELL IN HAVEN.
|Posted by: Marvel Man May 25 2009, 10:25 PM|
May the Power Cosmic be with you....
|Posted by: treacherous May 26 2009, 12:16 AM|
I'm going to sell your phone number a dollar a pop.
|Posted by: Bassetman May 26 2009, 12:17 AM|
|Posted by: Solomon May 26 2009, 12:32 AM|
See you soon dude.
|Posted by: Darkender May 26 2009, 03:26 AM|
|Posted by: treacherous Jun 2 2009, 12:13 PM|
| I talked to Grano last night. He's moved in with some old lady. He checks on the Haven every now and then at his college, but that's about it. He says he misses everyone and a bunch of other mushy stuff. I threw up a little in my mouth. He also wanted everybody to know (rub it in your faces) that he is undefeated in the FPL against all Haven members (Including me... ).
Too bad he had to face me again...
|Posted by: treacherous Jun 3 2009, 11:47 AM|
|Anybody need to ask Grano anything in his absence?|
|Posted by: Granobulax Jun 3 2009, 03:29 PM|
Threw up in your mouth huh...
Yes, I am undefeated and I'm on the leader board for the first time! Also, I'm only behind your Golem 12-13 so watch out. I may yet remain undefeated on the Haven FPL people...
Well, only can be on for a second. I'll try to get internet on the 10th, but no guarentee. Hope everyone's doing good and I'll see everyone soon.
|Posted by: treacherous Jun 3 2009, 03:33 PM|
|I'm just kidding, nothing you've ever said has made me throw up in my m....BLEGH...gotta go.|
|Posted by: Granobulax Jun 3 2009, 10:27 PM|
Maybe this will make you throw up. We're tied.
|Posted by: treacherous Jun 3 2009, 10:33 PM|
|I will not allow you to have two bragging rights over me. It's your Havenite minions voting against me.|
|Posted by: Marvel Man Jun 3 2009, 10:46 PM|
I voted Grano. He's too nice
|Posted by: Jailer411 Jun 3 2009, 10:55 PM|
I'm coming in for the tie breaker.
|Posted by: Granobulax Jun 3 2009, 11:37 PM|
I swear if I lose by one vote, I'll...
|Posted by: Jailer411 Jun 4 2009, 12:02 AM|
Actually, after reading the two characters, I'm in favor of yours.
Edit: Oh my, I've tied the match again. As it turns out, you were losing 14-13 until I voted.
|Posted by: treacherous Jun 4 2009, 01:29 AM|
|That's right, tell me who your voting for.|
|Posted by: Darkender Jun 4 2009, 01:35 AM|
I voted and I broke the tie.
|Posted by: treacherous Jun 4 2009, 01:40 AM|
|Yeah, looks like I'm bringing the Ban Button back out.|
|Posted by: Solomon Jun 4 2009, 01:48 AM|
|Posted by: treacherous Jun 4 2009, 12:14 PM|
| Excellent battle Grano. That's why you're the Ken to my Ryu. That one had me sweating. It's 1-1 now.
The Great Golem of Warsaw
-over Khazan All-Stars (16 to 15)
Actually now, I think you're becoming more Ryu and I'm Ken.
|Posted by: Granobulax Jun 9 2009, 08:16 PM|
|I just figured out how you won treach, I never had the opportunity to vote. Damn, we would have tied. I'm going to concider our match a tie based on that Oh well, congradulations on a well deserved win and your second HoF character.|
|Posted by: treacherous Jun 9 2009, 10:14 PM|
That really sucks. The match would've disappeared from existence. Okay, you still have one win over me and one tie. I'll go with that.
|Posted by: Granobulax Jun 10 2009, 11:18 PM|
Sweet! I'M STILL UNDEFEATED!!! Muahahahaha!!!
|Posted by: treacherous Jun 11 2009, 02:42 AM|
|Hey, I need to call you. Haven't talked in a while.|