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24 Cards in this Set

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zoonotic
transfered from animals to humans. campylobacter are normal flora and pathogens for animals
campylobacter similarities to vibrio
gram negative bacilli that are motile and oxidase positive
campylobacter differences to vibrio
microerophillic, resistant to many antibiotics, very small, do not ferment or oxidze carbohydrates, not halophilic
Campylobacter jejuni disease
more common that Salmonella and Shigella, causes gastroenteritis
Campylobacter jejuni epidemiology
vast animal reservoirs, assciated with consumption of contaminated water or foods (especially milk, poultry, and meat products)
Symptoms of Campylobacter jejuni
acute diarrhea with blood and neutrophils in stool. malaise, fever, and abdominal pain are normal, with destruction of mucosal surfaces common
infections associated with Campylobacter jejuni
Guillain-barre syndrome, an immune disorder of the peripheral nervous system
laboratory diagosis
grows best under microaerophilic and thermophilic conditions
treatment of Campylobacter jejuni
most cases are self limiting
severe cases- antimicrobial treatment
drug choice - ciprofloxacin for adults and erythromycin for children
Campylobacter fetus causes
bacteremia infections such as septic thrombophebitis, arthritis, septic abortion and meningitis. (debilitated and immunocompromised individuals are most susceptible)
Campylobacter fetus resistance
has capsule like S-protein
differences in physiologic characteristics between C. jejuni and C. fetus
C. fetus grows around 37 degrees celcius instead of 42
general characteristics of Heliobacter
gram-negative, microaerophilic, spiral bacteria, non-invasive, oxidase and catalase positive, mulitpolar flagella,
Helicobacter pylori causes
virtually all cases of type B gastritits, most duodenal ulcers, gastric ulcers, and associated with gastric adenocarcinoma and gastric mucosa-associated lyphone type (MALT) B-cell lymphomas
epidemiology of Helicobacter pylori
half of the world is infected but most do not show signs, worst where sanitation is bad, rate of infection increases as age increases, humans are major resovior of disease
pathogenesis of H. pylori
potent urease neutralizes teh gastric acids through ammonia production, attaches to epithelial cells with a variety of attachment factors
clinical manifestations of H. pylori
chronic gastritis and peptic ulcer disease, persistent inflammation leads to destruction of normal epthelium, loss of mucous layer
Type I H. pylori
expresses cytotoxin (VacA), which induces formation of epithelial cells taht resemple the histological lesions in patient biopsy material, and can also present (CagA) that interacts with several signal tranducton pathways
Type II H. pylori
does not express VacA or CagA
virulence factors of H. pylori
urease, heat shock protein, acid-inhibitory proetien, flagella, adhesins, mucinase, phospholipase, superoxide dismutase and catalase, vacuolating cytoxin
mucinase and phospholipase
disrupts gastric mucus
superoxide dismutase and catalase
prevents phagocytic killing
vaculolating cytotoxin
induces vaculolation in epithelial cells, stimulates neutrophil migration into mucosa
treatment of H. pylori
two week regimen durgh therapy with metronidazole and either tetracycline or amoxicillin, proton pump inhibitor (omeprazole), and bismuth salts. vaccination provides best long term resistance