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26 Cards in this Set

  • Front
  • Back
EHEC
eating pink hamburgers
does not produce LT or ST but DOES make Shigella-like toxin

Attaches and effaces Large intestine
pediatric diarrhea - copious bloody discharge

HUS - thrombycytopenia, kidney failure
"pedestal formation" on EM

AB treatment is contraversial
Shigella Etiology and Pathogenesis
similar to E coli
Non lactose fermenting gram negative rods
DO NOT produce H2S
DO NOT produce gas

most effective amoung enteric pathogens. S. Sonnei (group D) is most common in US. S. dysenteriae (group A - shiga toxin similar to E coli) most common in 3rd world.

target M cells in Peyer's patches. No bacteremia,
Shiga toxin cleaves 28S rRNA in 80S subunit
Shigella Transmission and Diagnosis
diagnose with Methyl blue and presence of PMNs (does not rule out other invasive pathogens)

transmit human to human
the 4 f's of fecal-oral route
food born more common than water borne

usually children under 10
Shigella Treatment and Prevention
treat with fluid and electrolyte replacement

severe cases treat with Cipro (FQ)

empahsize personal hygiene to prevent
Symptoms of typhoid (salmonella)
necrosis of ileum
fibrinous exudate
abdominal maculopapular lesion
fever
diarrhea, hemorrhage, cholecystitis, kidney damages
Typhoid (salmonella) septicemia
underlying chronic disease - sickle cell anemia or cancer

bacteremia results in osteomyelitis, pneumonia, meningitis
Typhoid (salmonella) Enterocolitis
invasion of subepithelial tissue of small and large intestines

PMN's respond to limit the infection in the gut and surrounding lymph nodes

gastric acid is an important host defense
Salmonella multiplication
salmonella multiplies in lamina propria with uncertain mechanisms

salmonella not killed in macrophages
Treatment of Salmonella
symotomatic relief
select AB's based on resistance

target poultry industry for prevention

vaccine is 50% effective
Yersiniae
gram negative rods
anearobes, zoonotic
do NOT ferment lactose
oxidase negative

plasmids with all virulence genes
Y. Pestis - bubonic and pneumonic plagues - protein capsule
Yersinae enterocolitis
caused by entercolitica and psuedotuberculosis
- identical symptoms as salmonella and shigella -

cause mesenteric adenitis - mimics appendicitis

enterocolitica more common in colder parts of US
Treatment for Yersina
psuedotuberculosis - abscesses - treat with ampicillin and tetracycline

entercolitica - chronic abscesses - treat with ampicillin and chloramphenicol, polymyxin

prevent by water treatment
Clostridium difficile
gram positive - spore forming
strict anaerobe - makes toxins

linked to exposure with C. difficile - psuedomembranous lesions
Antibiotic associated diarrhea
classically associated with the use of clindamycin
now associated with many other broad spectrum AB's

enterotoxin - chemotaxis
cytotoxin B - depolarization of actin
Campylobacter jejuni
gram negative, slender, comma shaped
cannot oxidize or ferment carbs
motile, microaerophilic
catalase and oxidase positive
urease negative
campylobacter enteritis
similar to salmonella and shigella
inflammatory enteritis, throughout whole mucosa
villi atrophy
necrotic debris
thickening of basement membrane
Campylobacter diseases
gastroenteritis - competent immune system
diarrhea and septicemia - in immunocomprimised host

-- associated with Guillan-Barre syndrome --
Treatment of Campylobacter
gastroenteritis is self limiting

erythromycin is AB of choice followed by tetracycline and FQ

systemic infections treated with aminoglycosides
Helicobacter pylori
chronic infection of about 50% of worlds polulation

colonizes gastric mucosa
class 1 carcinogen
very common in patients who die from gastric cancer
H. pylori Diseases
chronic active gastritis
peptic ulcer disease
MALT lymphoma
possible stomach adenocarcinoma
H pylori structrue
gram negative
curved shaped with a bundle of flagella at one end
has Oxidase, Urease, catalase, and phosphatase

2 big virulence factors... Urease and Flagella
Pathogenesis of H pylori
pH must be above 4
stays in mucus layer
and produces urease to buffer acid

produces vacuoloating cytotoxin - VacA
produces CagA - causes more damage when expressed
H pylori chronic gastritis
lymphoplasmacytic infiltrate in the lamina propria of fundus and other regions
H pylori and Adenocarcinoma
most common form of gastric cancer
inflammation and toxin release causes mutations which may lead to adenocarcinoma
H pylori and MALT lymphoma
lymphoid tissue regresses after H pylori is eradicated
treatment of H pylori
pepto bismol inhibits growth

first line: treat with proton pump inhibitor and 2 AB's (clarithromycin and amoxicillin)
-- 1 week, twice a day --

second line: proton pump inhibitor bismuth susalicylate and tetracycline and metrondazone
-- twice a day for 2 weeks --