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victimsofadown
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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
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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
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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
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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.
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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)
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Describe the treatment of Campylobacter
- Fluid and electrolyte replacement
- Antibiotics if symptoms are severe or last more than a week
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Prevention of Campylobacter
- Thorough cooking of food
- Pasteurization of milk and its porducts
- Disinfection of food preparation surfaces
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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
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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
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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
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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
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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
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Describe prevention of Shigella
- Protection of water and food supply, personal hygiene
- highly sensitive to heat (cook/pasteurize)
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Describe treatment of Shigella
- Normally self limiting
- Antibiotics required for complicated cases ONLY
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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
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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
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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
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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
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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
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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
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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)
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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
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Laboratory ID of V. cholerae
- Grows on standard media (MacConkey, blood)
- Oxidase positive
- Further biochemical testing is required
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Describe the treatment of V. cholerae
- Replacement of fluids and electrolytes immediately via I.V. if suspected
- Antibiotics can shorten duration of excretion
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Prevention of V. cholerae
- Reduction of fecal contamination of water/food
- Adequate cooking of food
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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
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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)
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Describe the epidemiology of Y. enterocolitica and Y. pseudotuberculosis
Ingestion of contaminated food (colonized domestic animals, slaughterhouses, raw meat (especially pork))
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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
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Describe Lab ID of Y. enterocolitica and Y. pseudotuberculosis
- Cultured on MacConkey OR cefsulodin-irgasan-novobiosin (selective for Yersinia)
- Serologic tests
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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
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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)
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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
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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
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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
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Describe Y. pestis in the flea
- Releases coagulase that causes blood clot
- Multiplies rapidly
- Regurgitates bacteria when attempting to feed
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Describe Lab ID of Y. pestis
- gram-stained smear, culture from bubo, etc
- MacConkey and blood agars
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Describe treatment of Y. pestis
- Rapid institution of antibiotic therapy is crucial (prevention of septicemia)
- Streptomycin is the drug of choice
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Describe prevention of Y. pestis
- Formalin-killed vaccine is available for high-risk individuals
- Minimize exposure to rodents or fleas
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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.
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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)
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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)
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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)
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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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