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24 Cards in this Set
- Front
- Back
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zoonotic
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transfered from animals to humans. campylobacter are normal flora and pathogens for animals
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campylobacter similarities to vibrio
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gram negative bacilli that are motile and oxidase positive
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campylobacter differences to vibrio
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microerophillic, resistant to many antibiotics, very small, do not ferment or oxidze carbohydrates, not halophilic
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Campylobacter jejuni disease
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more common that Salmonella and Shigella, causes gastroenteritis
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Campylobacter jejuni epidemiology
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vast animal reservoirs, assciated with consumption of contaminated water or foods (especially milk, poultry, and meat products)
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Symptoms of Campylobacter jejuni
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acute diarrhea with blood and neutrophils in stool. malaise, fever, and abdominal pain are normal, with destruction of mucosal surfaces common
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infections associated with Campylobacter jejuni
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Guillain-barre syndrome, an immune disorder of the peripheral nervous system
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laboratory diagosis
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grows best under microaerophilic and thermophilic conditions
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treatment of Campylobacter jejuni
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most cases are self limiting
severe cases- antimicrobial treatment drug choice - ciprofloxacin for adults and erythromycin for children |
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Campylobacter fetus causes
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bacteremia infections such as septic thrombophebitis, arthritis, septic abortion and meningitis. (debilitated and immunocompromised individuals are most susceptible)
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Campylobacter fetus resistance
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has capsule like S-protein
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differences in physiologic characteristics between C. jejuni and C. fetus
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C. fetus grows around 37 degrees celcius instead of 42
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general characteristics of Heliobacter
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gram-negative, microaerophilic, spiral bacteria, non-invasive, oxidase and catalase positive, mulitpolar flagella,
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Helicobacter pylori causes
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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
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epidemiology of Helicobacter pylori
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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
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pathogenesis of H. pylori
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potent urease neutralizes teh gastric acids through ammonia production, attaches to epithelial cells with a variety of attachment factors
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clinical manifestations of H. pylori
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chronic gastritis and peptic ulcer disease, persistent inflammation leads to destruction of normal epthelium, loss of mucous layer
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Type I H. pylori
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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
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Type II H. pylori
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does not express VacA or CagA
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virulence factors of H. pylori
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urease, heat shock protein, acid-inhibitory proetien, flagella, adhesins, mucinase, phospholipase, superoxide dismutase and catalase, vacuolating cytoxin
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mucinase and phospholipase
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disrupts gastric mucus
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superoxide dismutase and catalase
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prevents phagocytic killing
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vaculolating cytotoxin
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induces vaculolation in epithelial cells, stimulates neutrophil migration into mucosa
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treatment of H. pylori
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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
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