Campylobacter

Front 1

T/F
1. camp is #2 cause of diarrhea worldwide.
2. is #1 cause of travelers diarrhea.
3. 50% of raw chicken is infected with camp.

Back 1

1. F - it is #1
2. F- ETEC is
3. T

Front 2

what is the biologic properties of the camp species?

Back 2

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

Front 3

what animal usually contains campylobacter

Back 3

birds - polutry

Front 4

describe campylobacter fetus

Back 4

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

Front 5

describe camp epidemiology

Back 5

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

Front 6

in terms of campylobacter, salmonella, and other causes of gastroenteritis (e coli and such) which is most respondible for illnesses? hospitilizations? deaths?

Back 6

camp. salmonella. others like ecoli (salmonella is close behind it)

Front 7

how is camp spread?

Back 7

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

Front 8

describe the survival of camp in the environment.

Back 8

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

Front 9

describe the disease caused by camp in developed countries.

Back 9

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

Front 10

camp usually infects where in the body?

Back 10

large intestine, but can get up into the small at times

Front 11

what are less common manifestations seen in camp infection?

Back 11

relapsing colitis like crohn's or ulcerative colitis, massive GI hemmorhage, sepsis (esp with C fetus), cholera like watery diarrhea, autoimmune sequelae,

Front 12

since most causes of gastroenteritis exhibit similar symptoms, how do you determine if camp is the problem (what labs)?

Back 12

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

Front 13

describe the pathogenesis of camp.

Back 13

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

Front 14

what are the virulence factors of camp?

Back 14

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)

Front 15

describe the toxins found in camp.

Back 15

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...)

Front 16

what are the causes of guillain barre syndrome?

Back 16

C. jejuni infection (most of cases), cytomegalovirus, epstein barr, m. pneumoniae.

Front 17

describe the types of guillain barre.

Back 17

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

Front 18

how can jejuni cause GBS?

Back 18

some strains have LPS that mimic gangliosides...

Front 19

can ppl infected with jejuni be on some sort of preventative meds for GBS?

Back 19

nope

Front 20

why don't we know more about camp?

Back 20

cannot infect humans for study -> GBS; other animals do not get as sick as we do, so hard to study

Front 21

what is the treatment?

Back 21

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

Front 22

what are the infectious species for humans of camp?

Back 22

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