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  1. General information about Campylobacter (shape, motility, serotyping, aeration, location/disease)
    • Curved/Spiral (resemble vibrios)
    • darting motility (single, polar flagellum)
    • Numerous (Somatic, flagellar, and capsular antigens)
    • Microaerophilic (no fermentation)
    • Infect intestine, cause ulcerative lesions in jejunum, ileum, or colon
  2. Describe the epidemiology of Campylobacter (reservoirs, transmission)
    • Commensals of many vertebrates (including mammals and fowl) which serve as reservoirs
    • Transmitted primarily via fecal-oral route, direct contact, contaminated meat (especially poultry), or contaminated water
  3. What are the disease states caused by Campylobacter?
    • Intestinal (enteritis, traveler's diarrhea, and pseudoappendicitis) AND extraintestinal (bacteremia, septicemia) disease
    • Fever, headache, myalgia AND abdominal cramping/diarrhea
  4. Why is Campylobacter commensal in fowl?
    • Humans: Circumvents the mucus layer and is internalized by epithelial cells.  This causes inflammatory response
    • Chickens: Reside primarily in the mucosal layer of chickens.  Immune response does not lead to inflammation.
  5. How is Campylobacter identified in the lab?
    • Isolated from feces using Skirrow agar media in microaerophilic conditions
    • Small size utilized to selectively isolate (can pass through membranes with small pores)
  6. Describe the treatment of Campylobacter
    • Fluid and electrolyte replacement
    • Antibiotics if symptoms are severe or last more than a week
  7. Prevention of Campylobacter
    • Thorough cooking of food
    • Pasteurization of milk and its porducts
    • Disinfection of food preparation surfaces
  8. General information about Shigella (gram, shape, disease w/ description, motility, special properties, biochemical rxns)
    • Gram negative
    • Rods
    • Bacillary dysentary (blood and mucus in feces)
    • Motile WITHIN mammalian cells with actin polymerization
    • Intracellular pathogen
    • Cannot ferment lactose
  9. How are Shigella serotypes categorized?  What are they w/ information?
    • 4 subtypes based on LPSO-antigen
    • S. sonnei: (1 serotype) causes most shigellosis in industrialized countries
    • S. flexneri: (14 serotypes) endemic in developing countries, most common worldwide
    • S. dysenteriae: (12 serotypes) cause of epidemic dysentary
    • S. boydii: (18 serotypes) scattered shigellosis
  10. Endemic vs epidemic vs pandemic
    • Endemic: always present in an area
    • Epidemic: dramatic rise of disease in an area
    • Pandemic: dramatic rise of disease in many areas
  11. Describe the transmission of Shigella
    • *LOW INFECTIOUS DOSE (10-200)
    • Fecal-oral route via contaminated food/water and person-to-person contact
    • Transmission can occur by house flies
  12. Describe the symptoms of Shigellosis
    • Bacillary dystentary: self-limiting bloody + mucusy diarrhea, fever, stomach ramps
    • In immunocompromised - mucosal ulceration, rectal bleeding, drastic dehydration leading to death
  13. Describe prevention of Shigella
    • Protection of water and food supply, personal hygiene
    • highly sensitive to heat (cook/pasteurize)
  14. Describe treatment of Shigella
    • Normally self limiting
    • Antibiotics required for complicated cases ONLY
  15. Describe the virulence factors of Shigella and describe them
    • Invasive factors: Type III secretion system alters cytoskeleton to internalize more Shigella
    • Enteric Toxins: Enterotoxins w/ A subunit (toxic) and 5 B subunits (binding) which inhibit protein synthesis by inactivating the ribosome
  16. How is Shigella diagnosed?
    • 1. Stool examination: diagnosed by blood (neutrophils) in fecal smears
    • 2. Cultured test: selective/differential media
    • 3. Antigen-Antibody Test: rapid latex agglutination test
    • 4. PCR-based diagnoses: best method
  17. General information about Vibrio (gram, shape, motility, typing factors, aeration, growth factors)
    • gram negative
    • short, curved, rods
    • "vibrate" via single polar flagellum
    • O and H antigens, but only O antigens are useful for typing
    • Facultative anaerobes
    • Requires NaCl
  18. What are the pathogenic vibrios w/ description?
    • V. cholerae, serogroup O1 strains: epidemic cholera
    • non-O1 V. cholerae: sporadic cases of cholera
    • V. parahaemolyticus and other halophilic: gastroenteritis and extraintestinal infections
  19. Describe the epidemiology of V. cholerae (transmission, reservoirs, vectors, global locations)
    • Contaminated water and food (esp. seafood)
    • No animal reservoirs or vectors
    • Epidemic and endemic around the world (100k deaths), VERY rare in North America
  20. What are the two biotypes for V. cholera serogroup O1 (with description)?
    • V. cholera classic:
    • V. cholera El Tor: more pathogenic
    • Hemolysins, higher carriage rates, ability to survive in water for longer
  21. Describe the pathogensis of V. cholerae (infection, cause of disease, mechanism)
    • Ingestion -> attachment to small intestinal villa, secrete AB-type cholera toxin
    • NONINVASIVE - causes disease through cholera toxin
    • B subunit: binds to GM1 ganglioside receptor of intestinal cells
    • A subunit: two components - A1 and A2 (an inhibitor of A1)
    • Increases cAMP levels, causing ion transport and loss of H2O (similar to E. coli O157:H7)
  22. Describe the symptoms of cholera and risks
    • Massive loss of fluid and electrolytes from hours to days of profuse diarrhea (rice-water stools)
    • Death from severe dehydration may occur in hours if not treated
    • Multiple pandemics in history
  23. Laboratory ID of V. cholerae
    • Grows on standard media (MacConkey, blood)
    • Oxidase positive
    • Further biochemical testing is required
  24. Describe the treatment of V. cholerae
    • Replacement of fluids and electrolytes immediately via I.V. if suspected
    • Antibiotics can shorten duration of excretion
  25. Prevention of V. cholerae
    • Reduction of fecal contamination of water/food
    • Adequate cooking of food
  26. Information about V. parahaemolyticus and other halophilic vibrios (normal location, diseases caused)
    • Require higher-than-usual [NaCl]
    • Common in coastal seawaters
    • V. parahamolyticus associated with GI illness from contaminated seafood
    • Vibriosis is major disease in shellfish, finfish, and shrip aquaculture
  27. What are the medically important genuses of Yersinia and their general disease?
    • Y. enterocolitica and Y. pseudotuberculosis: pathogens of the GI tract
    • Y. pestis: agent of bubonic plague (black death)
  28. Describe the epidemiology of Y. enterocolitica and Y. pseudotuberculosis
    Ingestion of contaminated food (colonized domestic animals, slaughterhouses, raw meat (especially pork))
  29. Describe the disease state caused by Y. enterocolitica and Y. pseudotuberculosis
    • Uncommon cause of enterocolitis (fever, abdominal pain, diarrhea) in US
    • Ulcerative lesions in ileum, nectrotic lesions in Peyers patches, enlargement of lymph nodes
  30. Describe Lab ID of Y. enterocolitica and Y. pseudotuberculosis
    • Cultured on MacConkey OR cefsulodin-irgasan-novobiosin (selective for Yersinia)
    • Serologic tests
  31. Describe treatment and prevention of Y. enterocolitica and Y. pseudotuberculosis
    • Proper handling/preparation of meat
    • Antibiotic therapy is essential for sepsis, but not used in self-limiting enterocolitis
  32. Epidemiology of Y. pestis (reservoirs, vectors, types of infection)
    • Predominantly a zoonosis (animals serve as reservoirs)
    • Urban plague: rats
    • Sylvatic plague: prairie dogs, ground squirrels
    • Fleas are vectors which maintain infection in reservoirs
    • Can also be transmitted by contanimated tissue OR via respiratory route (pneumonic plague)
  33. Describe the cycles of the plague
    • Sylvatic cycle: squirrels, prairie dogs, fleas
    • Urban cycle: rats, fleas
    • Either transferred to human directly by mammal or by flea causing bubonic plague
    • Bubonic plague may progress to pneumonic plague
    • Pneumonic plague RAPIDLY spreads between humans
  34. Describe the pathogenesis of Y. pestis (what happens INSIDE the body to cause disease)
    • Y. pestis carried to regional lymph nodes, ingested by phagocytes
    • Are not destroyed, instead multiply within phagocytes, and are released with increased phagocytic resistance
    • Affected lymph nodes display hemmorhagic necrosis, which can spread to other organs/tissue
  35. What are the various disease states caused by Y. pestis with a description?
    • Bubonic plague: formation of buboes (swelling of infected nodes) typically in groin or axillae
    • Blood pressure drops potentially leading to septic shock
    • Septicemic plague: variation when patient is overwhelmed by bacteremia BEFORE buboes develop
    • Pneumonic plague: bacteria reaches lungs, cause purulent pneumonia.
    • RAPIDLY fatal (48 hours)
    • Highly contagious (respiratory droplets)
    • Plague meningitis: dissemination into meninges
    • May occur with/without buboes
  36. Describe Y. pestis in the flea
    • Releases coagulase that causes blood clot
    • Multiplies rapidly
    • Regurgitates bacteria when attempting to feed
  37. Describe Lab ID of Y. pestis
    • gram-stained smear, culture from bubo, etc
    • MacConkey and blood agars
  38. Describe treatment of Y. pestis
    • Rapid institution of antibiotic therapy is crucial (prevention of septicemia)
    • Streptomycin is the drug of choice
  39. Describe prevention of Y. pestis
    • Formalin-killed vaccine is available for high-risk individuals
    • Minimize exposure to rodents or fleas
  40. General information about H. pylori (shape, motility, aeration, biochemical features, generic disease, site of colonization, amount of infection)
    • curved/spiral organisms
    • corkscrew motility (multiple polar flagella)
    • Microaerophillic
    • Urease production
    • Acute gastritis, diarrhea, and ulcers.  May lead to cancer
    • Colonize the stomach (low pH)
    • Very common (2/3).  Tends to be chronic.
  41. Function of urease in H. pylori
    • Produces ammonia ions and CO2 from urea
    • Ammonia Neutralizes stomach acid in the vicinity of the organism (increases pH)
  42. Mechanism of urease in H. pylori
    • Low pH causes opening of proton-gated urea channel
    • Urea is allowed into the cell and interacts with cytoplasmic urease
    • Urease from lysed bacteria also sticks to membrane surface of intact bacteria (additional activity is provided in this manner)
  43. Describe the laboratory identification of H. pylori
    • Breath tests for urease: patients ingest a solution containing isotope-labeled C urea.  Exhaled CO2 is tested for these isotopes.
    • Serological tests from blood (ELISA)
    • Gastric biopsy (invasive)
  44. Describe the treatment for H. pylori
    • Resistance readily develops, so triple therapy is used
    • triple therapy: 2 antibiotics and a proton pump inhibitor (increases pH which strengthens antibiotics and weakens urease)
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