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microbiology, exam #2


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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.

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