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22 Cards in this Set

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  • Back
1. camp is #2 cause of diarrhea worldwide.
2. is #1 cause of travelers diarrhea.
3. 50% of raw chicken is infected with camp.
1. F - it is #1
2. F- ETEC is
3. T
what is the biologic properties of the camp species?
gram neg curved rod or spiral, microaerophilic and fastidious, motile with a flagellum at one or both ends, oxidase positive, urease neg, needs 37 C + to grow, Has LPS with serotypes resulting from H and O antigens
what animal usually contains campylobacter
birds - polutry
describe campylobacter fetus
systemic infections (bacteremia, septic arthritis, endocarditis...) in immunocompromised, occasional diarrrhea, S protein forms capsule like structure that helps org resist complement mediated lysis (note protein capsule, not polysac). usually seen in cattle and sheep causing septic abortion
describe camp epidemiology
commensal in birds and other animals, sporadic cases - no outbreaks, usually in summer due to bar b q-ing on own, more often in children and young adults
in terms of campylobacter, salmonella, and other causes of gastroenteritis (e coli and such) which is most respondible for illnesses? hospitilizations? deaths?
camp. salmonella. others like ecoli (salmonella is close behind it)
how is camp spread?
raw or undercooked pultry (1 drop of juice may be enough), unpasteurized milk, NOT raw eggs, stuff contaminated with bird/animal feces, contaminated water, infected dog or cat, infected small child, may have some asymptomatic carraige
describe the survival of camp in the environment.
not very hardy, dies on dry surfaces, freezes, acid less than 5, salt... biofilms of other orgs may enhance its survival esp in the setting of a farm
describe the disease caused by camp in developed countries.
onset is 2-10 days, ab pain, fever, diarrhea (often bloody and pus filled), headache, nausea, occasional vomiting, diarrhea may become watery, ab pain may last longer than diarrhea, usually resolves in 1 week, fatalities rare and limited to immunocompromised and very young
camp usually infects where in the body?
large intestine, but can get up into the small at times
what are less common manifestations seen in camp infection?
relapsing colitis like crohn's or ulcerative colitis, massive GI hemmorhage, sepsis (esp with C fetus), cholera like watery diarrhea, autoimmune sequelae,
since most causes of gastroenteritis exhibit similar symptoms, how do you determine if camp is the problem (what labs)?
darting motility in fresh stool specimens, vibrio like org seen in gram stain (these two give presumptive diagnosis). culture needs microaerobic environment, filtration will reduce other bacs bc camp is very small, selection against other bacs using antibiotics, do not use cephalothin if C. upsaliensis is suspected. also have non culture methods of PCR and DNA probes
describe the pathogenesis of camp.
infectious dose: 500-10000, susceptible to stomach acid so those on antacids are more susceptible, infects jejunum, ileum, and LI (mainly in LI), avoidance of immune system, epi damage, and inflammation, may have some invasion
what are the virulence factors of camp?
motility and chemotaxis, adherence via outer membrane proteins, flagella, LPS, and CadF that binds fibronectin, can invade through epi via transcellular or paracellular (bw cells) to tissue via microtubules and/or actin as well as cia (camp invasion antigens from flagella); iron aquisition without siderophores, capsular polysaccharide (possible role in adherence), LPS (variable, molecular mimicry, and inflammation)
describe the toxins found in camp.
cytolethal descending toxin (3 genes and thus three subunits: A, B, C; B is active), found in C. jejuni, fetus, and coli; DNAse activity from epi cell necrosis and immune cell apoptosis; likely to be involved in pathogenesis and immune cell evasion. Cholera like toxin (?) (probly not). Hemolysin: seen in chickens for cecal colonization, role in human disease unknown (maybe iron aquisition...)
what are the causes of guillain barre syndrome?
C. jejuni infection (most of cases), cytomegalovirus, epstein barr, m. pneumoniae.
describe the types of guillain barre.
acute or chronic inflammatory demyelinating polyneuropathy: typical with myelin sheath and schwann cells targeted. Acute motor axonal neuropathy is like AIDP but attacks gangliosides and thus more severe symptoms. Miller Fisher syndrome: gangliosides of facial and cranial nerves hit (ataxia and paralysis of eye muscles). NOTE the last two are associated with C. jejuni
how can jejuni cause GBS?
some strains have LPS that mimic gangliosides...
can ppl infected with jejuni be on some sort of preventative meds for GBS?
why don't we know more about camp?
cannot infect humans for study -> GBS; other animals do not get as sick as we do, so hard to study
what is the treatment?
wait it out and give oral rehydration therapy. If immunocompromised or sever infection give erythromycin. If not erythro give tetracycline or fluoroquinolones... NOTE widespread antibiotic reistance to most beta lactams and fluoroquinolone resistance is on the rise due to use in agriculture world
what are the infectious species for humans of camp?
jejuni is most common in US, coli is second most common, upsaliensis needs special culture, fetus causes bacteremia like typhoid, lari is in seagulls, and concisus is a periodontal disease that is possibly opportunistic