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423 Cards in this Set

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  • Back
how do anaerobes acquire energy?
via fermentation
where are clostridium found in large numbers as normal flora?
mucous membranes of the mouth, oropharynx, nasopharynx, upper respiratory tract, large intestine and vagina.
can anaerobic bacteria be present as normal flora in areas which are exposed to the atmosphere? how do they survive?
yes, the survive by growing in the skin (not ON the skin). growth occurs in sweat glands, sebaceous glands, hair follicles and beneath dead keratinized cells of the stratum corneum. shielded from O2.
what helps the anaerobes survive in this seemingly exposed environment? how?
facultative bacteria help by consuming the O2 present in the environment.
what bacteria is most present on the skin? how are they classified?
staph. epidermidis is most common on dry skin (g+ cocci, facultative). propionibacterium are most common on oily skin (anaerobe).
where are anaerobes present in smaller numbers?
conjunctiva and small intestine.
where are the greatest number of anaerobes present?
subgingival plaque and the lumen of the colon (where bacteroides outnumber e.coli).
describe 'autoassasination'.
a theory of why anaerobes are sensitive to O2. the normal metabolic activities of the bacteria generate toxic 02 derivatives which may damage the cells.
give an example of an autoassasin. how can it be eliminated?
H202 can be produced via oxidases. it is toxic unless eliminated by catalase or peroxidase.
what produces the superoxide anion? describe it's properties.
it can be produced from the univalent reduction of 02 via flavoprotein oxidase or dehydrogenases. the superoxide anion is highly reactive and toxic.
how are iron-sulfur centers of anaerobic bacteria related to it's 02 reactivity?
these centers may react directly with 02, oxidizing them to a form that is not functional (leading to cell death).
what type of bacteria can survive exposure to 02 for a longer time? some may even be able to grow in very low concentrations of 02.
aerotolerant anaerobes.
what enzymes do aerotolerant anaerobes possess?
enzymes for detoxifying H202, superoxide anion and hydroxyl radical.
what enzyme catalyzes the following rxn?

superoxide anion -> 02 + H202
superoxide dismutase
what enzyme detoxifies H202?
if an obligate anaerobe possesses superoxide dismuatase & catalase, what is likely about it's fxn?
it is more likely pathogenic.
how is aerotolerance helpful in pathogenesis?
it enables the bacteria to invade oxygenated areas indside the body, and to resist 02 dependent bactericidal mechanisms of phagocytes.
how are aerotolerant anaerobes cultured?
they can be streaked on plates on the open bench-top as long as they are then incubated anaerobically.
what are the two ways obligate anaerobes are cultured? solid media in chamber of anaerobic atmosphere.

2.special liquid media with reducing agent to eliminate 02 and lower ox-redox potential.
which method may require mineral oil? what is NOT required of this method that is required of the other?
the reduced liquid media. it does NOT need to be incubated anaerobically, like the rich solid media does.
describe the incubation and growth rate of anaerobes.
incubation lasts several days at 37 degrees C. they are slow growers.
what are the components of compressed anaerobic gas?
10% H2, 5% C, 85% N.
how do gas generating packets work? name any catalysts and indicators. why would they be used?
the packets are added to anaerobe jars and activated by the addition of water. this causes the production of CO2 and H2. The H2 combines with O2 in the jar, making more H2O. a palladium catalyst is necessary, along with a methylene blue indicator strip. these packets are used for small scale experiments.
under which condition is methylene blue colorless?
what are thioglycollate, beta-mercaptoethanol and dithiothreitol examples of? what is their fxn?
they are reducing agents. they maintain anaerobic conditions in cultures.
are these cultures solidified with agar?
NO. small amounts of agar are used, but just enough to prevent convection and mixing of the medium.
what are the components of a thioglycollate broth? where will an obligate anaerobe grow? a facultative?
thioglycollate, broth, methylene blue and agar. anaerobes grow at the bottom. facultatives grow throughout, but most densely at the top (more efficient growth with O2).
what is an anaerobic, gram negative rod found normally in the colon and mouth? what are it's most important pathogens?
bacteroides. B.fragilis, B.thetaiotaomicron and B.melaninogenicus.
what types of antibiotics are bacteroides resistant to? name two specific examples.
aminoglycoside antibiotics. ie, gentamicin and kanamycin.
describe the basic characteristics of B.fragilis.
1.gram negative
2.non-spore forming
4.obligate anaerobe
5.small pleomorphic rod (aka coccobaccilus)
what are clindamycin and metronidazole?
2 antibiotics often effective against anaerobes (including B.fragilis).
is penicillin effective against anaerobes?
name a major virulence factor of B.fragilis. what are it's actions?
it's polysaccharide capsule. it is anti-phagocytic and promotes abscess formation.
can B.fragilis cause septic shock? is this a major concern? why or why not?
septic shock is less likely via B.fragilis b/c it's LPS has very weak endotoxic activity and it's lipid A structure is somewhat different than other gram negative bacteria.
how does B.fragilis respond to O2?
it's an aerotolerant anaerobe. it produces superoxide dismutase and catalase.
what does BF toxin cause? how is it transferred? what is it's origin?
it is a toxin from an enterotoxigenic strain of B.fragilis. it is transferred between people and it is a protease which originates from a small pathogenicity island.
what does B.fragilis produce?
neuraminidase, lipase and protease.
what does B.fragilis cause?
intra-abdominal, lung, brain and pelvic abscesses; also, peritonitis and septicemia. endocarditis (uncommon).
what bacteria produce a black iron-containing pigment? what medium is needed for this pigment production?
porphyromonas and prevotella. a medium with blood is needed.
where can porphyromonas and prevotella be isolated from? what do they cause?
both can be isolated from the oral cavity. prevotella comes from the vagina. they can cause infections of the head, neck and respiratory tract, chronic periodonitis, pelvic or abdominal infections.
what obligate anaerobe has a fully toxic endotoxin? what does this make them capable of causing? where are they commonly found?
fusobacterium, found in the oral cavity. they can cause septic shock and vascular collapse.
what is the most frequent cause of human infections?
fusobacterium nucleatum. F.necrophorum is also seen.
what prefix indicates anaerobic activity?
what are two 'pepto' bacteria found frequently in mixed anaerobic infections?
peptococcus and peptostreptococcus. *gram positive*
what is a gram positive anaerobic rod (normal skin flora)associated with inflammatory process in acne?
propionibacterium acnes
where are eubacterium and bifidobacterium normally found? what are they?
found in fecal flora, they are gram positive anaerobic rods. may cause infxn.
name seven characterisitics of endogenous anaerobic infxns.
1.proximity to colonized mucosal surfaces.
3.foul-smelling discharge
4.gas in tissues
5.necrotic tissue
6.mixed infxn response to aminoglycosides. respond to clindamycin or metronidazole(flagyl)
what are the basic characterisitics of clostridium?
1.large, anaerobic
2.gram positive, spore forming rods.
3.common in soil and GI human/animals
clostridium's main virulence is due to______?
protein exotoxins, including cytolytic and histolytic enzymes which degrade tissue.
name the 4 major clostridium pathogens and their MO.
c.tetani (tetanus)
c.perfringens (gas gangrene)
c.botulinum (botulism)
c.dificile (pseudomembranous colitis)
what do colonies of clostridium tetani look like? how do the individual bacterium appear?
ground-glass appearance, hemolytic and thin.
individually: round terminal spores of thin rods, peritrichous flagella.
how does c.tetani bacteria present? how has it entered the body?
it presents as convulsive contraction of voluntary mm, initially at site of injury.
spores enter the wound and multiply, producing toxin.
what conditions are necessary for the flourishing of c.tetani?
lowered ox-redox potential is needed via tissue damage and mixed bacterial flora.
what is the main virulence factor of c.tetani and how does it work?
1.tetanospasmin is an exotoxin released by autolysis, not secretion.'s located on a plasmid and split into two more toxic fragments via proteolytic cleavage. binds peripheral nerve endings, gets transported to the cell body in the spinal cord.'s then transported to inhibitory interneurons where it binds gangliosides in synaptic membranes and inhibits rls of inhibitory neurotransmitter.
how do you treat c.tetani?
1.passive immunization with antitoxin (immediate).
2.surgical debridement
4.booster of tetanus toxoid (formalin inactivated toxin)
what bacterium has oval, subterminal spores and large grayish colonies? hemolysis is usually present.
what is the cause of death for c.tetani?
respiratory failure
what causes the flaccid paralysis resulting from classical c.botulinum?
a neurotoxin which inhibits acetylcholine.
is food borne botulism an infection or intoxication? what is the difference?
it's an intoxication meaning that the bacteria itself is no longer present, but the toxins made by the bacteria (c.botulinum) ARE.
how is classical botulism contracted? how can the toxic qualities be overcome?
it's contracted via canned food where the bacterium has grown anaerobically and produced toxin. the toxins are heat-labile, so cooking the food will destroy them.
how is wound botulism contracted? is this form a concern in the US?
spores infect the wound and toxin is produced in vivo. very rare in the US.
an infant was recently fed honey and presents with general FTT. what is the problem? the tx?
infant botulism via spores in the honey. respiratory support may be needed, but most recover spontaneously.
where does infant botulism work?
it colonizes the GI tract of newborns and produces toxin in vivo. therefore it causes an INFECTION.
what are the c.botulinum toxins? where are they found and how strong are they?
there are Ag variations A-H, highly NEUROTOXIC. they are located on genome of lysogenic bacteriophage and 1-2 micrograms will kill a human.
which form of botulism does NOT require antibiotics? why?
food-borne botulism (classical) b/c it is an intoxication, not an infection. there are no bacteria present to kill.
what is the general tx for all botulism?
1.trivalent antitoxin (against forms A,B and E)
2.ventilation support
3.antibiotics for wound and infant forms.
what are the general characterisitics of c.perfringens?
1.large rods, encapsulated in tissue and non-motile.
2.rare spores (oval, sub-terminal, non-bulging)
3.rapid growth, double zone of hemolysis on anaerobic blood agar plate
4.ferment carbs in mm with gas production
5.up to 12 varied toxins produced.
what are some clinical results of c.perfringens infection?
1.wound poisoning
2.uterine infection, septic abortion.
3.septicemia poisoning
5.enteritis necroticans.
why is c.perfringens called 'gas gangrene'?
in the case of wound infection, the spores germinate and the bacteria multiplies. the bacteria then ferments carbs to produce a gas which distends the tissue and interferes with blood supply. necrotizing toxins are produced.
how does the tissue necrosis lead to death?
the more tissue necrosis, the more opportunity for the anaerobic bacteria to grow, causing hemolytic anemia and ultimately severe toxemia and death.
what are the top three causes of food poisoning?
how is c.perfringens treated?
mainly via surgical debridement (perhaps amputation).
massive antibiotic therapy and hyperbaric O2 treatment.
a patient being treated with clindamycin for a bacterial infection suddenly presents with diarrhea and necrotic pseudomembranous plaques on the bowel mucosa. what has happened?
the clindamycin has disrupted normal bowel flora, allowing for overgrowth of antibiotic resistant C.difficile.
what is C.difficile MO?
it produces a potent cytotoxin which causes diarrhea, kills colon epithelial cells resulting in necrotic pseudomembranous plaques on the bowel mucosa.
is c.difficile only present during infection?
no, it is present as endogenous flora in low levels of some people. it is kept at low levels via competition with other normal flora.
how is c.difficile diagnosed? how can it be treated?
dx via cytotoxin in the stool.
to tx, stop giving initial antibiotic. replace fluids and rx metronidazole (2nd choice = vancomycin).
what anaerobic gram positive spore forming rod can cause peritonitis, bowel perforation and death?
how is salmonella most commonly spread? give an ex. does it cause disease in humans or animals?
it's spread via contaminated water or food or direct fecal-oral spread. intact eggs improperly stored can cause salmonella. causes disease in humans and animals.
what are salmonella's general characteristics?
gram negative rods
oxidase negative
ferment glucose
what are the six serogroups of salmonella?
A,B,C1, C2, D and E
can salmonella ferment lactose? is it motile?
salmonella cannot ferment lactose but IS motile.
what bacteria produces gas from glucose and produces hydrogen sulfide? what is the exception?
salmonella produces gas from glucose and produces hydrogen sulfide. S.typhi does NOT produce gas.
how common is salmonella exposure? is it highly toxic?
exposure is frequent but a very large innoculum is needed for infection.
what are salmonella's most important virulence factors?
it's an intracellular pathogen involved with invasiveness and serum resistance. it can survive and grow within epithelial cells and macrophages.
does salmonella produce exotoxins or endotoxin?
some of the virulence factors of salmonella are genetically regulated so they are not expressed ____ but are _____ when the bacteria enter the macrophages.
in vitro, induced.
what encodes the virulence of salmonella?
pathogenicity islands SPI1 (invasive) and SPI2 (survival inside macrophages).
how does the type III protein secretion system work, regarding salmonella?
genes carried by SPI1 and 2 which fxn by injecting bacterial effector proteins into target host cells.
the effector proteins interact with intracellular host cell components (ie cytoskeleton) and modify host cell activity in ways that favor pathogenesis.
how does salmonella invade epithelial cells and macrophages?
the trigger mechanism. the effector proteins cause actin filament polymerization, inducing macropinocytosis. (lots of salmonella taken into the cell via macropinocytotic vacuoles)
name the five virulence factors of salmonella.
1. invasion of epithelial
2. survival in macrophages
3. serum resistance (c' res.)
4. LPS (endotoxin and serum res. via long O-Ag coat)
5. capsule,Vi Ag(anti-phag against PMNs, serum res.)
how can salmonella present clinically?
1.enteric fever
4.asymptomatic carriage
typhoid fever is the prototype of what salmonella dz? what strain causes it? what are it's symptoms?
prototype of enteric fever, caused by S.typhi. it is characterized by high fever and abdominal symptoms.
what illness is caused by S.paratyphi A, S.schottmuelleri and S.hirschfeldii?
paratyphoid fever
how is typhoid fever contracted? what type of infection is it?
it's contracted via the fecal-oral route and bacteria are shed in stool at some stages of the dz. it is a SYSTEMIC infxn, organisms present in blood at low titer, and in some organs.
during invasion phase of typhoid fever, what may patient experience?
humans are the only host for which enteric fever strains?
S.tyhpi and S.paratyphi
which strains of salmonella can cause sepsis? what are common secondary infections?
s.choleraesuis and S.dublin. secondary local supparative infections can result: endocarditis, osteomyelitis and septic arthritis.
how is septicemia characterized via salmonella infection?
organisms are present in large numbers in blood without concurrent involvement in GI tract.
what is gastroenteritis know as?
what are the symptoms of salmonella 'food poisoning'? when do they first appear?
symptoms begin 6-48 hrs after consuming contaminated food/water. initially have nausea, vomiting and diarrhea. loose, moderate volume stools (no blood or mucus USUALLY). fever and abdominal cramping are common.
what causes entercolitis?
live bacteria in the gut, not preformed toxins. the ingested bacteria infects the gut mucosa.
what is the usual cause of entercolitis/gastroenteritis in the US?
salmonella enteriditis, the typhimurium serotype.
is salmonella enteriditis invasive? how? is it systemic?
it is mildly invasive, frequently infecting mesenteric lymph nodes. it only reaches the blood 5% of the time.
how should salmonella enteriditis be treated?
if uncomplicated, antibiotics will only prolong the carrier state. fluid balance should be maintained.
how long are salmonella bacteria excreted after a treated infection?
50% still excrete after one month. 1/20 excrete 5 months later.
how is a salmonella carrier defined?
someone who continues to excrete salmonella after one year.
what is the most common reservoir of salmonella bacteria in carriers?
the gall bladder
which species of salmonella are most likely to be involved in carriers?
s.paratyphi A
s.paratyphi B
what gram negative rod is most closely related to e.coli?
how is shigella transmitted?
it's harbored in humans and transferred by contaminated food, water and direct fecal-oral spread.
why is shigella considered a higly virulent organism?
as few as 10-100 organisms can cause infxn.
what are some general characteristics about shigella?
2.typically lactose negative gas from fermentable carbs.
4.specific lipopolysaccharide O antigens
5.they have no H antigens
which serologic shigella group contains only one type? (name the group and type)
group D, Shigella sonnei
which shigella are groups A-C?
A: dysenteriae
B: flexneri
C: boydii
which shigella species cannot ferment mannitol?
which shigella can ferment lactose (albeit v.slowly)?
S. sonnei
which bacteria causes 60-80% of shigellosis?
S. sonnei
which causes 20-40% of shigellosis?
what is the most communicable bacterial diarrhea? where is it usually spread?
bacillary dysentery, within infected family or day care center.
what is the primary virulence factor of shigella? what are it's toxin activities?
invasiveness is primary. it has enterotoxic, cytotoxic and neurotoxic activities.
EHEC strains of e.coli produce a verotoxin which is similar to the toxin produced by_____?
how does the shigella toxin work? what bacteria is this similar to?
it invades the epithelium of the large bowel and spreads cell-to-cell via actin comets. listeria does this too.
how is ulceration of the colonic mucosa caused via shigella?
micro-abscesses form and ultimately coalesce.
what mechanism does shigella use for invasion?
the trigger mechanism via the type III secretion system.
how are the virulence factors of shigella encoded? why isn't this considered a pathogenicity island?
a large virulence plasmid (220 kb) goes thru the M cells on peyer's patches. path. islands are integrated into the chromosome, this plasmid is not.
what are the symptoms of shigella?
scant bloody diarrhea with mucus and pus
why do patients experience voluminous watery diarrhea during the early stages of shigella?
the small intestine is infected.
how does salmonella cause bacteremia? does shigella?
salmonella invades beyond the mucosa to reach the lamina propria and mesenteric lymph nodes, causing bacteremia. shigella does not.
how is treatment administered?
symptoms subside in a week, organisms continue to excrete for a week. antibiotics shortens symptom durations and shedding. fluids must be replaced.
are there antibiotic resistant strains of shigella? is a carrier state common?
there are antibiotic resistant strains. carrier state is rare.
what type of organism are motile via a polar flagella and capable of growing on a simple media?
pseudomonas is often found in what type of environment? what can be done to prevent their accumulation?
they are often found in moist environments. proper chlorination of things like whirlpool baths will eliminate them.
pseudomonas is capable of doing anaerobic respiration if _____?
NITRATE is available to serve as a terminal electron acceptor in the place of oxygen.
what is pseudomonas strongly associated with? what is their main classification?
they are strongly associated with plant material. they are gram negative rods, oxidase positive and obligate aerobes.
some pseudomonas produce a polysaccharide capsule making them _____?
what is the most common strain of the gram negative rod which causes enteric dz but is not a member of enterobacteriacae?
psuedomonas aeruginosa
pyocyanin and fluorescin are examples of what?
pyocyanin: a bluish-green pigment produced by p.aeruginosa.

fluorescin: greenish-yellow pigment made by p.aeruginosa.
what smell do cultures of p.aeruginosa give off?
a 'grape-like' aroma.
who is most likely to be infected with p.aeruginosa? can it be treated with antibiotics?
immunocompromised hosts, ie cystic fibrosis, leukemia,long term IV or urinary catheterization, invasive surgical procedure or severe burns.
it is resistant to numerous antibiotics.
what types of infections are caused by p.aeruginosa?
septicemia, endocarditis, pulmonary infxn, ear infxn, burn wound infxn, UTI, gastroenteritis, eye infxn and musculoskeletal infxn.
has the genome for p.aerginosa been sequenced? what is unusual about it?
yes, it was sequenced in 2000. it has 6.3 million base pairs (5,600 genes). largest bacterium ever sequenced.
what are the virulence factors of p.aeruginosa (generally)?
polysaccharide capsule
exotoxin A
exoenzyme S
extracellular proteases
where does the pili of p.aeruginosa adhere?
respiratory epithelium
which virulence factor of p.aeruginosa allows for attachment to tracheal epithelium in cystic fibrosis patients?
the mucoid polysaccharide capsule.
which p.aeruginosa virulence factor exerts lethal action on a variety of eukaryotic cells by irreversibly blocking protein synthesis?
exotoxin A
which virulence factors use ADP ribosyltransferase? how is one factor using it differently than usual?
exotoxin A and exoenzyme S both use ADP ribosyltransferase. S doesn't transfer ADP to EF2, like A does. it transfers it to a small G protein (RAS) which causes collapse of the cytoskeleton.
how common is exoenzyme S? what type of system does it use?
it's found in 40% of clinical isolates. it has an effector protein which is injected into cells via the type III secretion system encoded on the chromosome of P.aeruginosa.
this pore forming pr- is toxic for most kinds of eukaryotic cells, including PMNs. it was formerly called 'leukocidin'. what is it?
what protein breaks down elastin in blood vessel walls, resulting in hemorrhage and necrosis?
elastase, an extracellular protease.
alkaline protease is responsible for what action?
it's capable of degrading some of the components of complement, IgG and IgM and other human proteins. it is also an extracellular protease.
what are two enzymes (virulence factors) which inhibit neutrophil function? what is their classification and function? which bacteria are they virulence factors for?
elastase and alkaline protease. they are extra-cellular protease which spread the infection in vivo. these are virulence factors for p.aeruginosa
which virulence factor of p.aeruginosa causes cell membrane damage and tissue destruction?
phospholipase c breaks down phospholipids (including lecithin).
what does the endotoxin of p.aeruginosa cause?
fever, shock, etc.
what are the general characteristics of vibrionaceae?
1.facultative gram negative curved rods.
2.motile via single polar flagellum
3.oxidase positive
4.grow well in alkaline media
5.simple nutritional requirements
how many serotypes of v.cholera are known? which is the main source of epidemic cholera?
there are 139 serotypes. O1 is known for epidemic cholera.
what are the biotypes of v.cholera O1? what are the three serological subtypes?
classical and El Tor are the biotypes. subgroups are ogawa, inaba and hikojima.
what is another antigenic descriptor of v.cholera?
the H (flagellar) antigens.
how is v.cholera spread?
contaminated water or food. it can live freely in brackish water, may infect shellfish. a large dose is needed for infxn.
where does v.cholera remain during infection? which particular cells get colonized?
the lumen of the small intestine. the surface of the brush-border cells are colonized.
is this an intoxication or infection (by v.cholera)?
what are the clinical symptoms of v.cholera and what causes it?
rice-water stool caused by an enterotoxin.
how does the v.cholera toxin work?
the B subunit binds the toxin to receptor, gets the A subunit inside where causes the ADP ribosylation of the G protein (which regulates cAMP). an overproduction of cAMP results, causing hypersecretion of chloride and bicarbonate into the intestinal lumen.
why is the diarrhea of v.cholera so deadly?
the fluid loss is severe (15-20 liters a day). it can cause hypovolemic shock and metabolic acidosis.
an overproduction of cAMP results in _____?
derangement of ion transport: a cascade that results in hypersecretion of chloride and bicarbonate into the intestinal lumen, and hence a net osmotic efflux of water.
what type of media do vibrionaceae thrive in?
alkaline (ph 9-9.6). sensitive to acid.
about 10 hours after eating sushi on a cruise ship a patient suffers an explosive diarrhea only to recover uneventfully. what caused this?
what pathogenic strain does v.parahaemolyticus produce?
kanagawa hemolysin
where is v.parahaemolyticus commonly found?
it grows best in high (8%) salt, it inhabits coastal waters and estuaries everywhere.
a rapidly progressing wound infection after exposure to contaminated seawater may be caused by______?
what is the mortality rate of v.vulnificus septicemia if not immediately treated with antibiotics? does anything predispose patients to this condition?
mortality rate is 50%. liver disease can cause predisposition to this septicemia.
what organism is the MAIN cause of gastrointestinal dz (more than salmonella and shigella combined)?
what are some general characterisitics of campylobacter?
1.slender, gram negative curved rod.
2.oxidase positive
3.highly motile
how can campylobacter be cultured?
a special selective culture media is needed, using antibiotics which inhibit the growth of normal enteric flora. the plates are incubated microaerophilically and at high temperatures.
where is campylobacter found? how are large outbreaks caused?
it is common among animals. human outbreaks are often due to consumption of contaminated food, water, etc.
what are the symptoms of a campylobacter infection?
bloody, muco-purulent diarrhea affecting both large and small intestine with fever and abdominal cramps. most infections are self-limiting and subside in 7 days.
what campylobacter strain has been found to cause bacteremic infections in compromised hosts?
camylobacter fetus
classify heliobacter.
1.gram negative
2.highly motile
3.oxidase positive
5.strongly curved
6.difficult to culture
what gram negative, curved rod is strongly associated with gastritis, duodenitis and peptic, duodenal ulcers?
where is H.pylori found? what does it produce to allow for it's survival?
it's found in the mucus layer overlying the gastric epithelium or adherent to it's surface. it produces urease to help it survive in stomach's low pH.
what is vacuolating cytotoxin?
an exotoxin produced by H.pylori. it's named for it's cytopathic effect on culture cells.
some strains of H.pylori inject effector proteins into gastric epithelial cells. how?
a 40 kb pathogenicity island encodes for a type IV secretion system which injects the effector protein.
what is IL-8?
a proinflammatory cytokine induced via h.pylori.
what has proven to be the most effective treatment of h.pylori?
a combination of bismuth subsalicylate with two antibiotics.
what is CagA?
a protein of unknown function produced by H.pylori.
what short gram negative rod or cocci reproduce by binary fission?
the rickettsiae
what does the genome of rickettsia prowazekii resemble?
mitochondrial DNA
what type of organism is rickettsiae? what enzymes does it lack?
it's an obligate intracellular parasite. it lacks enzymes for nucleotide synthesis.
what is unusual about the cell membrane of rickettsiae?
more permeable. when outside the host cell it loses small molecules like coenzyme Q, NAD and ATP.
where do rickettsiae usually reside? how is this related to human contraction?
they usually live as non-pathogenic parasites in arthropods. infection can be caused by arthropod bite or via scratching arthropod fesces into broken skin.
what are common symptoms of rickettsiae?
fever and rash.
how do the organisms of rickettsiae work?
they proliferate in endothelial cells and cause leakiness of blood vessels. they are widely disseminated in the blood.
recovery from a rickettsiae infection usually leads to what?
what is the vector and reservoir of rocky mountain spotted fever?
tick, dog.
when does transovarial transmission occur?
in ticks and mites.
what is the vector and reservoir of epidemic typhus? of brill zinsser?
body louse, humans and flying squirrels.
brill zinsser has no arthropod vector, but has a human reservoir characterized by reappearance of disease after it has been quiescent.
how can one test for rickettsiae? what is indicative of infection?
paired acute and convalescent serum. can look for a 4-fold rise in titer or single high titer of IgM, IgA or IgG. species will not be identified.
what test for rickettsiae is only of historical interest?
weil-felix agglutination
what newer tests are being more commonly used to identify the organism?
direct immunofluourescnece or PCR of skin biopsies.
which rickettsiae does not require an arthropod vector? how is it transmitted?
coxiella burnetti (Q fever) is transmitted via respiration.
what is unusual about coxiella burnetti in comparison to other rickettsiae?
it is much more resistant to drying. it may survive for a long time in the environment, forming something spore or cyst-like.
what does coxiella burnetti cause? what is the prognosis?
it causes acute febrile illness, commonly manifested as an atypical pneumonia. it may cause hepatitis or endocarditis.
it is v.seldom fatal, but may become chronic. can see hepatomegaly and thrombocytopenia.
what is a common host for coxiella burnetti? how is it transmitted to humans?
ticks, insects, birds, sheep, cattle, goat. cattle can pass the organism into milk. there is NO human to human transmission.
how is coxiella burnetti (q fever) diagnosed in the lab?
via serology.
what causes human monocytic ehrlichiosis?
ehrlichia chaffeensis
how is ehrlichia chaffeensis transmitted? how is it diagnosed?
it's transmitted to humans via ticks, but deer are the reservoir. there is usually no rash and it's diagnosed via indirect immunoflouresence using acute and convalescent serum, or by PCR or culture.
what organism replicates in macrophages and monocytes with formation of inclusion bodies called morulae, which are aggregates of bacteria?
ehrlichia chaffeenesis
what bacteria causes human granulocytic ehrlichiosis (HGE)?
ehrlichia granulocytophilia.
what two bacteria resemble rocky mountain spotted fever?
ehrlichia chaffeenesis and ehrlichia granulocytophilia.
where is ehrlichia granulocytophilia found?
upper midwest and northeast.
what is the vector and reservoir of e.granulocytophilia? what other disease may it be transmitted with?
it's vector is ticks within the genus ixodes. deer and rodents are the reservoir. it may be transmitted with lyme disease.
what is unusual about the pathogenesis of ehrlichia granulocytophilia?
it can invade, survive and replicate within neutrophils. it produces proteins which block the apoptosis of neutrophils, prolonging it's survival.
how does e.granulocytophilia replicate?
it replicates in granulocytes (neutrophils) with inclusion bodies (morulae).
how is e.granulocytophilia diagnosed? what sorts of problems can it cause?
it is diagnosed in 4-fold antibody titer to E.equi or by PCR.
it may cause heart problems in humans.
what are two pathogens common in dogs? what ehrlichia do they resemble? what is unique about one?
e.canis and e.ewingii. they resemble e.chaffeensis. e.ewingii grows in granulocytes.
describe the elementary body of chlamydiae. what is unusual about it's cell wall?
a dense spherical body, 0.2-0.4 micrometers in diameter surrounded by rigid cell wall. the cell wall contains no pep-g, even though chlamydiae genome sequences show the capability to make pep-g. the cell wall is rigid b/c of disulfide cross linking in the major outer membrane protein, a porin.
how much DNA is present in chlamydiae as compared to e.coli?
about 1/4th of the DNA.
what is reductive evolution? what chlamydiae species have demonstrated this?
it is elimination of genes which have demonstrated no usefulness in intracellular existance. c.trachomatis and c.pneumoiae do this.
how is chlamydia treated in the laboratory?
with giamesa stain.
what is the pathogenic cycle of chlamydiae?
the elementary body enters the mucosal epithelial cell, transforms into a reticulate body, then BACK to an elementary body. it's vacuole and the cell lyse, releasing hundreds of elementary bodies.
how do elementary bodies enter the host cell? what happens when the elementary body transforms to a reticulate body?
the EB enters the host cell via receptor mediated endocytosis. the rigidity of the EB is reduced via reduction of disulfide linkages. the cell ENLARGES to form a reticulate body.
describe the reticulate body of chlamydiae.
it is 1 micrometer in diameter, and looks like a gram negative bacterial cell. they replicate by binary fission and are NON-INFECTIOUS.
what happens at the conclusion of the chlamydial life cycle?
the reticulate body differentiate back into EBs. the late inclusion body (vacuole) contains > 100 EBs.
how long does the chlamydial life cycle take?
48-72 hours.
what are some general characteristics of chlamydiae?
1.obligate intracellular parasites.
2.synthesize v.little ATP. few biosynthetic capabilities. characterized by latency, inapparent infection, scarring and carrier state.
4.Abs produced with no effect.
what are the two diseases caused by chlamydia trachomatis? how are they defined antigenically?
trachoma types A-C are the most common cause of blindness. types D-K cause sexually transmitted diseases and other diseases caused by secretions from infected genitourinary tracts.
what is the reservoir of trachoma and how is it transmitted? how is it diagnosed?
infected humans are the reservoir. it can be transmitted via fingers, fomites and flies. it is diagnosed via conjunctival scrapings, looking for inclusion bodies.
what sexually transmitted bacterium is found 8x more in asymptomatic females than n.gonorrhea? what is the asymptomatic finding?
chlamydia trachomatis, D-K.
cervicitis is often found in asymptomatic females.
how does chlamydia trachomitas affect men? women? newborns?
it causes non-gonococcal urethritis in men. cervicitis, PID, ectopic pregnancy and infertility among women. it is the most common cause of neonatal conjunctivitis and a common cause of neonatal pneumonia in children under 8 wks of age.
what is a complication following chlamydial infection where you can't see, pee or climb a tree?
reiter's syndrome. it is characterized by arthritis, urethritis and conjunctivitis. usually affects those with who are genetically predisposed.
what is often the cause of swimming pool conjunctivitis in adults?
chlamydia trachomatis.
what affect does chlamydia trachomatis infection have on HIV susceptibility?
it increases transmission of HIV 3-5 fold.
what are common lab dx techniques for c.trachomatis?
innoculation of cell cultures looking for tell-tale inclusion bodies via staining or flourescent antibodies. PCR test.
what venereal disease is characterized by antigenic types L1, L2 and L3?
lymphogranuloma venereum (LGV)
how is LGV transmitted and what is it's pathogenesis?
it's transmitted via sexual contact thru minute abrasions. it infects reticuloendothelial cells and causes lesions in local lymph nodes. rupture of these lymph nodes causes abscesses, fistulas, sinus tracts or fissure formation.
what is the cause of a systemic influenza like disease which may also manifest as a severe pneumonia? how is it transmitted?
chlamydia psittaci. it is transmitted via respiratory route by exposure to infected birds who excrete the organism thru fesces and nasal discharge.
how does chlamydia psittaci affect humans?
the organisms travel through the blood to the reticuloendothelial cells of the liver and spleen, multiply there and invade the lungs by hematogenous seeding.
how can chlamydia psittaci be diagnosed in the lab?
a 4 fold titer of acute and convalescent serum.
what is a problem regarding transmission of chlamydia psittaci?
latency in the reservior. an asymptomatic bird my transmit the dz. stress may cause clinical dz in an animal with latent infection.
what strain of chlamydia has been found to cause upper and lower respiratory tract infections, bronchitis, pneumonia and sinusitis? how is it transmitted?
chlamydia pneumonia. it is transmitted from human to human through the respiratory route.
where has c.pneumonia been isolated from? what types have arteries are involved?
human atheromatous plaques (via immunochemistry and PCR). coronary and carotid arteries have been shown to be involved.
what is unusual about the spirochetes?
they are spiral shaped and very long. they have a corkscrew motility and are very flexible.
how are spirochetes visualized?
with darkfield microscopy or special staining techniques. they do not grow in vitro.
name two spirochetes common in the tropics which cause non-venereal chronic skin lesions.
treponema pertenue (yaws) and treponema carateum (pinta).
what causes syphilis? what type of bacteria is this?
treponema palladium, a spirochete.
what are the stages of syphilis and how are they characterized?
primary: hard chancre, infectious.
secondary: rash, HIGHLY infectious.
tertiary: cardiovascular, CNS lesions - no longer infectious.
when can congenital syphilis occur?
if a pregnant woman has the active stage of syphilis, treponema can cross the placenta into the fetus past the first trimester.
how is syphilis diagnosed in the lab? what is unusual about the Abs produced in response to infection?
serological tests detect Abs. Abs may be produced against cardiolipin (non-treponomal) as well as treponomal Ags.
what causes louse-borne relapsing fever? what causes it?
borrelia recurrentis. the organism changes it's angtigenic structure, enabling it to evade host defense.
what is the cause of lyme disease? what are some of the disease manifestations?
burrelia burgdorferi. there are characteristic skin lesions and arthritis.
what does ANUG stand for? what causes it?
acute necrotizing ulcerative gingivitis, cause by borrelia vincenti.
what spirochete is transmitted via animal urine, causes systemic infection which finally localizes in the kidney?
leptospira interrogans.
what is considered a poor prognosis of leptospira interrogans?
hemorrhage, jaundice and azotemia (too much urea/nitrogen in the blood).
is penicillin effective against spirochetes?
what is the difference between spirilla and spirochetes?
spirilla and spirochetes are both spiral shaped, but spirilla have rigid cell walls. spirochetes have flexible cell walls, typical of gram negative bacteria.
are spirochetes motile? how?
yes via axial fibrils (periplasmic flagella).
what are the three genera of spirochetes? how can they be told apart?
borrelia are thicker and longer with coarse irregular coils and many axial fibrils. treponema are tight and regular.
leptospira are the same size as treponema, but the cells are hooked at ends.
what do borrelia and treponemes have in common?
both are microaerophilic and very difficult to grow in culture.
which spirochete can be grown in culture on special medium and is an obligate aerobe?
what is a non-pathogenic treponeme that can be grown in culture? what pathogenic treponeme is it antigenically related to?
REITER treponeme (T.phagedenis). it is partially related to T.pallidum.
what are general features of yaws and pinta? what are the official names of these dz?
they are tropical dz, causing chronic skin lesions.
non-venereal, associated with poor personal hygeine and insect vectors.
they can give a false positive for syphilis and respond to penecillin.
t.pertenue = yaws (tropics)
t.carateum = pinta (s.america)
which spirochete causes syphilis?
treponema pallidum
where does initial infection of t.pallidum occur?
through host mucocutaneous tissues, usually in erogenous zones.
what type of dz is syphilis? how does this occur?
it's a systemic dz from the onset. after infection through mucocutaneous tissue, the organism travels through the lymphatics to reach systemic circulation.
what is the first sign of infection with t.pallidum? is it very obvious?
first there is a papule, which turns into a painless, ulcerated hard chancre which heals spontaneously in 3-6 wks. most don't notice the chancre. it is highly infectious! after healing it will continue to spread to other tissues.
what signifies the secondary stage? when does it occur?
weeks to months after the end of the primary stage, the patient will become ill with fever, sore throat, headache, generalized lymphadenopathy and prominent mucocutaneous lesions over much of the body.
what is a macular rash over the trunk, limbs, soles of feet and hands indicative of?
secondary stage of syphilis
what are condylomata lata?
lesions of secondary syphilis which occur as coalesced masses on moist areas of the skin.
where do lesions of secondary syphilis occur as white patches?
mucous membranes
what do the primary and secondary phases have in common?
both appear to resolve spontaneously while the organism continues to spread.
what characterizes the latent phase of syphilis?
there are no signs or symptoms, pt is NOT infectious but there is positive serology. patient may remain in this phase forever.
what are symptoms of late (tertiary) stage syphilis?
GUMMAS are the least serious, localized relatively quiescent granulomatous lesions of the dermal elements or supporting structures of the body.

more serious manifestations:
neuro and cardiovascular syphilis, which can result in death.
at what stages of syphilis is the patient infectious?
primary and secondary.
what characterizes lesions of LATE syphilis?
very FEW spirochetes. these are mainly due to hypersensitivity rxn of the immune system.
a pregnant female is infected with syphilis. what are the risks for the fetus?
spontaneous abortion
severe developmental abnormalities
serious dz may progress AFTER birth even if no dev. abnormalities are apparent.
when can a syphilis-infected pregnant woman transmit the dz to the fetus?
at ANY stage of infection (even latent or tertiary).
what techniques are used to directly visualize t.pallidum? at what stages are these appropriate?
during primary and secondary infection ONLY:
darkfield microscopy
fluorescent antibody technique
special stain (silver nitrate)
what is 'reagin' in the context of t.pallidum?
it's an anti-cardiolipin antibody. a negative test indicates succesful tx of syphilis infection.
how do the serological tests for t.pallidum work? name two tests.
they test for the non-treponemal Ag cardiolipin using RPR (rapid plasma reagin) or VDRL (venereal disease research lab).

treponemal Ags are studied using FTA (fluorescent treponemal Ab) and FTA-ABS(FTA-absorbed).
how does the FTA test work? the FTA-ABS test? what are you testing for?
FTA: indirect FA test using anti-human Ig labeled with flourescein

FTA-ABS: like FTA but the patient's serum is first absorbed with non-pathogenic treponeme to remove nonspecific treponemal Abs.

testing for treponemal Ag
what causes a false positive for RPR/VDRL?
drug addiction
connective tissue dz
immune disorder
what is commonly the cause of a false positive syphilis diagnosis via the FTA-ABS test?
non-venereal treponoma infection or colonization, immune disorders.
what is the tx for t.pallidum? how must it be administered and why?
penicillin is effective for t.pallidum but it must be administered either frequently over a long period of time or in large doses. this is b/c t.pallidum is a slow-growing organism.
what is characteristic of the borrelia species?
relapsing fever, lyme dz. transmission via arthropods. long thick spirochetes with loose irregular coils.
what causes louse borne relapsing fever? how is it transmitted?
borrelia recurrentis. transmitted directly from person to person by the louse.
what causes tick borne relapsing fever? how is it transmitted?
borrelia hermsii.
it's a zoonosis in which soft-bodied ticks transmit the spirochetes to humans from an animal reservoir (infected rodents)
which borrelia is associated with crowding, poverty and a cold climate?
borrelia recurrentis, louse borne relapsing fever.
which borrelia is associated with vacationing, outdoor activity and warmer weather?
borellia hermsii, tick borne relapsing fever.
what is the 'relapse' aspect of borrelia recurrentis and hermsii due to?
the emergence of a new antigenic type due to a special genetic mechanism.
borrelia recurrentis and hermsii present the same clinical picture. describe it.
sudden onset of chills, fever, headache, muscle pain, vomiting and diarrhea.
how often do louse and tick born relapsing fever relapse?
typically 2-3 times, but up to 13x has been documented.
how are the borrelia diseases tested for?
the spirochetes are readily seen in wright, giemsa or gram stains of blood from people in the active stage of relapse.
are there serological tests for borrelia?
NO serological test for relapsing fever.
what is erythema chronicum migrans? what does it indicate?
it's a lesion with a red flat border and central clearing. it is the characteristic skin lesion of lyme disease, borrelia burgdorferi. it appears after incubation period of 3-30 days.
how is lyme disease transmitted?
to humans by hard bodied ticks (ixodes) from infected rodents, deer and domestic pets.
besides erythema chronicum migrans, what are the initial symptoms of borrelia burgdorferi?
flu-like symptoms, lasting a month.
what happens to patients with untreated borrelia burgdorferi?
in a high percentage of patients, untreated lyme dz results in neurologic and cardiac symptoms. this can develop into arthralgias (neuralgic pain in a joint or joints) and arthritis.
where are spirochetes present in lyme dz?
during early dz they are in the blood and CSF, but not easily detected by microscopic examination. during LATE dz, few spirochetes are present. pathogenesis is believed to be due to immunological cross reaction.
how can lyme dz diagnosis be confirmed?
serological testing.
what causes an oral infection characterized by painful inflammation and necrosis of the gingiva?
borrelia vincenti (ANUG- acute necrotizing ulcerative gingivitis)
what is the fusospirochetal complex?
an abundant mixture of borrelia spirochetes and fusiform gram-negative anaerobic bacteria found in tissue infected with ANUG. it's believed to cause ANUG. it's detected via gram-staining.
what causes borrelia vincenti? what can treat it?
stress, anxiety and neglect of oral hygeine can cause ANUG. it can be treated with penicillin and improved oral hygeine.
what spirochete is known as infectious jaundice? weil's dz? canicola fever?
what are some characteristics of leptospires?
slender, tightly coiled with hooks at ends. two axial filaments.
obligate aerobes.
can be cultured on ordinary lab media containing animal serum at 25 degrees C.
how is leptospirosis transmitted? what is the usual portal of entry?
it's primarily an animal dz transmitted accidentally to humans via indirect contact with urine. wide range of infected animals (dogs, cats, rodents, horses, pigs). contact may be thru contaminated water.
portal of entry: abraded skin or exposed mucus membranes.
what is the pathogenic species of leptospira? which serotypes are pathogenic to humans?
leptospira interrogans.
3 pathogenic to human:
pomona (pig)
canicola (dog)
icterohaemorrhagiae (rat)
what occupations are at a larger risk for this dz?
sewer workers
swine herders
slaughterhouse workers
which organs are involved with leptospirosis? what are the signs?
brain, lungs, liver and kidney (where the spirochetes finally colonize).
signs are fever, chill, headache, photophobia, GI distrubance, mm pain. occurence of hemorhhage, jaundice (icterus) and azotemia indicate poor prognosis.
how is leptospirosis diagnosed in the lab?
darkfield microscopy of blood and CSF (1st week) or urine (after 1st week).
culture: flecher's medium, aerobic incubation at 25 degrees celsius. blood CSF week 1. urine post week 1.
microscopic agglutination test can be used to detect presence of Ab in serum.
if jaundice is present in a leptospirosis infection, what is the mortality rate?
how is leptospirosis treated?
antibiotics are effective early. dz can be controlled via prevention of water contamination.
why are mycobacterium difficult to classify?
they are genetically related to gram positive bacteria but they do not stain well with gram stain.
how are mycobacteria stained?
with an acid fast stain
what is characteristic about the mycobacteria?
it's genome has a high GC content. it has a thick waxy cell wall composed of, among others, mycolic acid.
what is the generation time of m.tuberculosis? are mycobacterium known as fast or slow growers?
m.tuberculosis has a 24 hour generation time. mycobacterium are known for SLOW growth.
what strains of mycobacterium cause tuberculosis?
m.tuberculosis (humans)
m.bovis (humans, BCG vaccine strain)
m.microti (infect voles)
m.africanum (human localized in africa)
how is m.tuberculosis transmitted?
it is transmitted from someone in an ACTIVE stage of infection. it is transmitted via respiratory/aerosols.
where must the bacilli of m.tuberculosis get deposited in order for infection to occur?
how does m.tuberculosis develop once contracted?
macrophages engulf the bacilli and a granuloma will form within the macrophage. the granuloma degenerates, bacilli multiply extracellularly for the first time in vivo. tissue is eroded into the adjacent airway and a cavity is formed. now it can spread.
how is m.tuberculosis spread?
via cavity formation and expulsion of bacteria from liquefied center of the granuloma into the environment.
are latent individuals infectious? why?
no, they are not infectious b/c their granulomatous are static and walled off.
what kind of parasite is m.tuberculosis?
a facultative intracellular parasite of macrophages.
how is control of the TB infection predominantly done?
through cell mediated immunity.
what are risk factors for active m.tuberculosis?
2. senescence
3. poor nutrition
4. chronic medical conditions
what is the current vaccine for tuberculosis? what is the strategy for TB in the US?
the BCG vaccine via the m.bovis strain. it's efficacy varies widely but is generally not considered effective against adult TB. US will test for dz and then treat.
what is purified protein derivative used for?
PPD. it's the skin test for TB. a positive test is indicated by the size of the raised area that results from the injection or puncture. this indicates exposure, not active/latent.
why are mycobacteria acid fast?
the lipid and waxy constituents of the cell.
how is mycobacterium treated in the laboratory?
it's a BSL 3 bacteria, requiring tremendous caution.
what are the two most common testing techniques for tuberculosis?
PPD and sputum testing. sputum can be smear tested or cultured.
how long does the latent stage of TB last?
can last forever.
what is significant about the genome of m.leprae?
it's 1/2 the size of m.tuberculosis, making it impossible to culture on artificial media.
what kind of energy production does m.tuberculosis undergo?
it's an obligate AEROBE.
where is m.leprae found? what type of organism is it?
humans and armadillos (tx and la). it's an acid fast bacilli.
which strain of m.leprae is similar to TB? what are the symptoms?
tuberculoid leprosy. it forms organized granulomas (like TB) but they cause nerve damage to nearby dermal and autonomic nerve fibers.
which strain of m.leprae has a longer incubation period?
lepromatous leprosy (8-12 yrs) compared with tuberculoid leprosy (2-5 yrs).
what is a major difference between tuberculoid leprosy and lepromatous leprosy?
tuberculoid has a strong cell mediated immunity TH1 response. lepramatous does not - and only poorly formed granulomas are present.
why do neurological symptoms result from lepromatous leprosy? what area of the body does it prefer to grow?
the bacteria replicate in schwann cells, causing neuro symptoms. it prefers to grow on cool areas (nose, fingers).
which genus of mycobacterium produces a toxin? what does the toxin do?
m.ulcerans produces a polyketide toxin, mycolactone. it's responsible for ulceration of the skin and blunting of the immune response.
how can m.ulcerans be treated?
with surgical excision of ulcer is at nodular stage. antibiotics cannot penetrate.
what does MOTTS stand for? where are they found? what is their characteristic drug response?
mycobacteria other than tuberculosis (MOTTS).
found in water and soil. they are more likely to resist 1st line anti-TB drugs than m.tb
what is a slow growing, non pigmented bacteria which causes pulmonary dz, regional adenitis and disseminated dz?
what are the clinical manifestations of m.avium in normal patients? those who are immunocompromised?
lung dz.
disseminated dz.
what is lady windermere syndrome?
m. avium disease found in little old ladies of fastidious nature. they do not cough or spit and this causes a poorly draining lung region to develop. this encourages the formation of MAC.
where is m.kansasii found? what are it's symptoms?
environmental water.
pulmonary dz, cervical lymphadenitis in children.
what bacteria causes swimming pool granuloma, fish handler's nodule or surfer's nodule?
what is the leading cause of scrofula or cervical lymphadenitis in children (1-5)?
how can infectious units of a virus be determined?
1.plaque formation (lysis)
2.pock formation
3.focus formation (proliferation)
4.serial dilution (cytopathic changes)
5.serial dilution (characteristic symptoms)
what are the consequences of viral infections?
1.cell death & lysis
2.proliferation of host cell
3.fusion of membranes on adjacent cells
4.inclusion bodies
what is often found in the formation of a multinucleate giant cell?
F proteins
which consequence of viral infection can lead to cancer? how does it work?
transformation. normal cells progress to malignant cells with loss of contact inhibition and uncontrolled proliferation.
what are examples of genes which lead to cell transformation (via viruses)?
ras and myc
what is hemagglutinin used for? how does it work?
some viruses (influenzae) are capable of binding to rbcs. the agglutination forms a lattice that coats the 'well'.
+ test for virus = rbc stay suspended
- test = rbc form button at bottom
what is another characteristic of transformation?
viral genomes are integrated into the genome of the cell.
name 6 ways in which viral products can be observed.
1.immunological means
2.complement fixation fluorescent antibody
4.western blot
7.DNA probes
how are southern blots performed?
DNA is extracted from speciman thought to contain virus.
which viral observation technique requires hybridization with a radiolabeled probe?
in situ hybridization
which viral product observation technique is most useful when there is a very small sample of blood available?
PCR- polymerase chain reaction
name seven methods used for testing Ab activity in order to detect presence or absence of virus.
1.neutralization of infectivity mechanisms
2.complement fixation
3.hemagglutination inhibition
4.latex agglutination
6.indirect fluorescent antibody
7.western immunoblot
what are some neutralization mechanisms?
1.absorption of virus to cells is hindered
2.virus capsid is stabilized, preventing the uncoating of a viral molecule.
3.membrane fusion (and therefore entry into cells) is inhibited.
how is a viral presence diagnosed?
with an acute and convalescent serum indicating a 4x rise in titer.
what immunoglobulin can be tested for to indicate viral presence? (positive test indicated by high levels of this Ig)
what are the various tests to detect viral presence ultimately used for?
2.retrospective determination
3.determine need for immunization
4.establish if infection was caused
name five ways that immunity to viral infections comes about.
1.neutralization by antibodies
2.cell-mediated immunity
4.natural killer cells
what form of cell mediated immunity is important for recovery from primary infection and preventing re-infection?
cytotoxic t-cells!
A cell that is actively infected with virus can then process the endogenously produced viral antigens and present them to cytotoxic T-Cells. These T-cells are activated and are then produce cytotoxic substances
what are two innate forms of immunity which aid in response to viral infections?
natural killer cells
complement fixation
how are MHC I molecules involved in the immune response against viruses?
1.the down regulation of MHC I by some viruses stimulates NK cells

2.MHC I bind viral peptides and display them to cytotoxic T cells which destroy virally infected cells.
what are the most important cytokines in the antiviral immune response? what sorts of viruses induce them? what is their specificity? what is it's action?
type one interferons (alpha & beta)
induced by active and inactive viruses.
they are host specific.
they inhibit protein synthesis, degrade viral mRNA and promote apoptosis of virally infected cells.
what type of cytokine can make adjacent cells more resistant to infection via inhibtion of protein translation?
type one interferons.
what interferon is involved in cell mediated immunity?
type II gamma interferon
what is it called when little or no cell mediated immunity is induced? what is an example of dz which can cause this in fetal life?
immunological tolerance. rubella.
what causes most of the symptoms of chronic hepatitis B?
the host immune system. cytotoxic T cells kill virus infected cells and cause liver damage.
what is unusual about the immune response brought about by flaviviruses?
the presence of some antibody to the virus enhances multiplication of the virus. Abs are NON-NEUTRALIZING.
what are some patterns of viral pathogenesis?
1.local infections
2.disseminated infections
3.inapparent infection
4.persistant infections
5.chronic infections
what are some characteristics of a disseminated infections?
1.local multiplication at the site of entry
2.spread through the lymphatics to bloodstream. (primary viremia)
3.multiplication at secondary sites.
4.secondary viremia
5.infection of the target organ
which steps of a disseminated infection are asymptomatic?
multiplication at site of entry thru secondary viremia.
what is a characteristic of a persistant infection? a chronic infection?
persistant = herpes
chronic = hepatitis B
how can viral diseases be controlled?
1.public health surveillence
3.isolation of cases of dz
4.passive immunization immunization
how are most virus vaccines prepared?
in tissue culture
what are some characteristics of attenuated vaccines?
many years of immunity
IgG and IgA
good CMI
rare reversion to virulence
what are some characteristics of inactivated vaccines?
less yrs of immunity than activated
IgG only
poor CMI
no reversion to virulence
what is required to eliminate a virus from a population? animal reservoir
2.good vaccine
3.few or no subclinical cases (no latency!) antigenic type or only a few
what factors contribute to creation of a new viral disease?
genetic changes
genetic reassortment
how do the dynamics of parasitism contribute to virus creation?
a parasite needs to be transmissable and evolution favors transmissability.
what can usually be said about a new viruses virulence?
newer = more virulent
when does reassortment of a virus occur?
in viruses with segmented genomes (h.influenzae)
how are viruses treated?
immune serum (more effective early)
how can viral diseases be controlled?
1.public health surveillence
3.isolation of cases of dz
4.passive immunization immunization
how are most virus vaccines prepared?
in tissue culture
what are some characteristics of attenuated vaccines?
many years of immunity
IgG and IgA
good CMI
rare reversion to virulence
what are some characteristics of inactivated vaccines?
less yrs of immunity than activated
IgG only
poor CMI
no reversion to virulence
what is required to eliminate a virus from a population? animal reservoir
2.good vaccine
3.few or no subclinical cases (no latency!) antigenic type or only a few
what factors contribute to creation of a new viral disease?
genetic changes
genetic reassortment
how do the dynamics of parasitism contribute to virus creation?
a parasite needs to be transmissable and evolution favors transmissability.
what can usually be said about a new viruses virulence?
newer = more virulent
when does reassortment of a virus occur?
in viruses with segmented genomes (h.influenzae)
how are viruses treated?
immune serum (more effective early)
what are some unique features of baltimore virus groups III, IV and V?
1.replicate in cytoplasm
2.genetic material replicates by synthesis of complementary RNA.
3.genomes code for RNA dependent RNA poly
4. viruses show a HIGHER MUTATION rate (lack of proofreading enzymes)
what are class III viruses?
what are three examples of class III viruses?
rotavirus (gastroenteritis in infants)

orbivirus (colorado tick fever, viremia infects RBC precursors)

orthoreovirus (usually inapparent, mild cold)
what is unique about class IV viruses?
they are ssRNA +viruses. the RNA alone is infectious.
give five examples of class IV viruses.
what sorts of infections do picornoviridae cause? how is it defined?
cytolytic infections
naked icosahedral nucleocapsid
what are some examples of the enteroviruses caused by class III picornoviridae?
ECHO viruses
enterovirus 70
enterovirus 71
of those infected with poliovirus, how many suffer dz?
4-8% have mild dz
1-2% have nonparylytic aseptic meningitis
<1% have flaccid paralysis
how are the coxsackie viruses A and B classified? what are some symptoms?
they are class III +ssRNA viruses, picornoviridae. they cause aseptic meningitis, common cold, myocarditis, herpangina and pleurodynia.
what +ssRNA virus group is responsible for the norwalk virus and hepatitis E? what is it's shape?
it's a naked icosahedral nucleocapsid.
which two +ssRNA virus groups are enveloped?
what viral group causes arboviruses (man = dead end host) and rubiviruses? what class are these in?
class III (+ssRNA)
which genera of class III viruses causes west nile virus? what other dz does it cause that leads to cirrhosis?
flaviviridae. also causes hepatitis C.
what is the physical appearance of the coronaviridae? what recent virus outbreak was a coronaviridae?
it's an enveloped helical nucleocapsid surrounded by petal shaped projections. SARS.
what do the capsid cores of -ssRNA viruses contain? what is it for?
RNA dependent RNA polymerase called RNA transcriptase to make +strand mRNA
name six -ssRNA virus groups.
1.orthomyxoviridae (influenza viridae)
which -ssRNA virus has a segmented genome? what is it's physical appearance?
it contains eight segments of RNA.
it's a helical nucleocapsid with a lipid containing envelope added at the cell membrane. outer surface of envelope has glycoprotein spikes (H and N).
how is the subtype of influenza defined?
the H and N glycoprotein spikes on the outer surface of the cell envelope.
which class V virus causes parainfluenza? what other illnesses does it cause? what is it's major effect on the cell?
mumps, measles & respiratory synctial virus.
major effect on cell = syncytia formation.
what is the structure of paramyxoviridae?
it's an enveloped helical nucleocapsid, genomes are not segmented.
what is the shape of the rhabdoviridae? what does it cause?
they are bullet shaped enveloped helical nucleocapsids. it is responsible for the rabies virus.
what causes the ebola virus? what is it's shape?
it's a long pleomorphic enveloped helical nucleocapsid
what is another segmented class V virus besides orthomyxoviridae?
what illnesses is arenaviridae responsible for? does it have an envelope?
lassa virus
lymphocytic choriomeningitis (LCM)
yes, it has an envelope
what is an unclassified RNA virus? what is it associated with and why?
Hepatitis D
it's dependent on Hepatitis B to provide the genetic information for it's envelope protein. infection with HDV causes a more severe hepatitis than infxn with hep B (more cytopathic on liver cells).
what are class VI viruses? what do they contain? what do they make?
they are RNA viruses which replicate with a DNA intermediate. the enveloped virus particle has a capsid with two identical copies of +ssRNA per virus particle. and tRNA needed for tsc and reverse transcriptase.
they make a DNA intermediate for replication using reverse transcriptase.
what is a subfamily of class VI? what are the human viruses within that subclass?
1.HTLV-I and II
which class VI virus are responsible for most lymphoid leukemias?