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46 Cards in this Set
- Front
- Back
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I. VIBRIO CHOLERAE AND CHOLERA
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A. GENERAL PROPERTIES OF VIBRIO CHOLERA (6)
What does it look like? How does it grow on its special media? How do you abolish motility? What exotoxins does it produce? |
- motile gram -ve fermenter, comma shape, polar flagellum
- yellow opaque colonies on special TCBS medium (the usual media for enteric pathogens, such as EMB, may inhibit growth - motility abolished by antiserum - produces: - O and H antigens - endotoxin - and potent enterotoxin (CHOLERA TOXIN which is an exotoxin) - major colonization factor is the TOXIN COREGULATED PILUS (TCP) |
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B. PATHOGENESIS
Can it survive in the stomach? Where does Cholera toxin bind? What does neuraminidase do? How do you get massive intestinal fluid loss? |
- gastric acid inactivates ingested organisms, but some survive
- organisms enter the small bowel and bind to the epithelium by an unknown mechanism - TCP is expressed and bacteria form microcolonies in intestinal crypts - CHOLERA TOXIN is expressed and secreted, binds to GM1 gangliosides of cell membrane - NEURAMINIDASE of V. CHOLERA converts other gangliosides to GM1 and thereby increases amount of toxin binding sites - CHOLERA TOXIN enters the intestinal cells by endocytosis and stimulates adenylate cyclase and camp production- - which result in massive intestinal fluid loss via 2 mechanisms: 1) villus cells: decreased NACL absorption from gut 2) secretory cells: increased CL and increased HCO3 secretion into gut, along with H20 |
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C. CLINICAL FEATURES
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- painless, profuse WATERY DIARRHEA
- isotonic volume loss (10-15 Liters/ day and dehydration - low bp |
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D. TREATMENT
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- replace fluid using same concentrations of electroplyte
- IV fluid or oral rehydaration solutions both acceptable - Cholera cot facilitates measurement of stool volume - antibiotics (TETRACYCLINE) reduce duration of diarrhea from 5-10 days to 1-3 days. - ERYTHROMYCIN and CHLORAMPHENICOL are the derivatives |
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E. EPIDEMIOLOGY
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- disease is limited to humans and associated with poverty and asociated with poverty and inadequate sanitation- - it is endemic in some regions such as south-central and souteast asia - - but it is mainly in africa
- have accounts of cholera since BC - 7th pandemic began in 1961 and in 1992 and spread to latin america- - which represented the first cholera outbreak in the Western world in more than a century. - it spread rapidly with hundreds of thousands of cases and mortality rate of about 1%, and cholera is more of a world wide concern now than it was in 1992 - found a new serogroup (o139) in madras and it has a spread throughout the world - outbreaks are related to contaminated water, shellfish, and other seafood - infectious dose influences mode of transmission- - need a lot of bacteria to get infected in water and food (10^9) |
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F. PREVENTION (3)
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1) WATER: bottled and carbonated or boiled
2) FOOD: dry, steaming, careful of shellfish 3) VACCINE: A) current inacticvated vaccine: crude bacterial suspension- - not recommended B) live attenuated vaccine- - do not manufacture |
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*other related pathogens
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1) VIBRIO PARAHEMOLYTICS: invasive gastroenteritis from contaminated shellfish
2) VIBRIO VULNIFICUS: infections in wounds contaminated by seawater or shellfish |
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II. CAMPYLOBACTER SPECIES
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A. GENERAL PROPERTIES
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- curved, comma-shaped microaerophilic gram -ve rod
- present in lots of animal species - most common: C. JEJUNI, followed by C.COLI |
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B. PATHOGENESIS
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- ingest organisms in contaminated food/ water
- when they arrive in the small and large bowel, they cause invasive inflammatory process - the organisms rarely enter the bloodstream - usually recover and get specific ab- mediated immunity |
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C. EPIDEMIOLOGY
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- it's a zoonotic disease: so it's tranferred from animals to humans- - especially poultry
- more than half chicken in grocery stores have campylobacter - the cases are usually sporadic than epidemic and tend to peak in the summer and fall - usualy has a point- contaminated source- - unpasteurized milk - doesn't make animals ill and human to human transmission is rare |
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D. HISTORY
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- has probably caused disease for centuries but was just recognized as a disease- causing agnet since 1970
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E. OCCURANCE
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- most commone etiologic agent of diarrhea in the world, surpassing SHIGELLA and SALMONELLA
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F. CLINICAL FEATURES
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- incubation 3-5 days
- symptoms include: fever, malaise, headache, fever, abdominal pain, diarrhea for a few days to a week - 1/ 1000 develop autoimmunity to nervous system with paralysis |
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G. INFECTIOUS DOSE
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- usually only need about 500 organisms to cause disease- - just need 1 drop of raw chicken juice
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H. DIAGNOSIS
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- esablished by culture of stool on selective media
- interestingly grows best at 42 degrees C, which is body temp of chicken |
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I. TREATMENT
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- SUPPORTIVE WITH ANTIMICROBIAL
ERYTHROMYCIN or DIPROFLOXACIN |
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J. PREVENTION
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- pasteurization of milk, avoid undercooked meats
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III. YERSINIA PESTIS and PLAGUE
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A. GENERAL PROPERTIES
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- large rod- shaped coccobacillary gram -ve bacteria
- aerobic or facultatively anaerobic, non- lactose fermenter - family enterobacteriacae, genus includes 2 other zoonotic bacteria |
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B. PATHOGENESIS
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1) EXTRACELLULAR PATHOGEN:
- anti- phagocytic capsule required for virulence (F1 antigen) - other anti- phagocytic properties present before visible capsule (V, W, antigens) - anti- phagocytic properties present at 37 degrees C BUT not at 28 degrees B. INTRACELLULAR: - persistence within mammalian monocytes C. TOXINS: - classical LPS toxin - an exotoxin |
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C. EPIDEMIOLOGY
What is the general transmission? What are the steps involved? |
* This is the cycle of transmission involving mammals (usually rodents) and their associated ectoparasites (usually fleas) with incidental involvement of humans
1) TRANSMISSION FROM FLEA TO MAMMAL (BUBONIC) - flea acquires y. pestis after a blood meal - Y. pestis multiplies and obstructs the foregut - then when it bites its host to feed, it regurgitates the organisms onto the bite - organisms enter the lymphatic system 2) TRANSMISSION FROM MAMMAL TO MAMMAL (1 PNEUMONIC) - bubonic plague leads to 2dary pneumonia in index xase - spread via respiratory droplets in a contact |
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What are the CHARACTERISTICS of the URBAN PLAGUE? (4)
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1) 3 major epidemics
2) EPIZOOTICS among urban black rats and their fleas 3) humans get involved as rats dies and fleas try and find a new host 4) initial cases bubonic, then pneumonic |
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What are the CHARACTERISTICS of the RURAL PLAGUE? (5)
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1) sporadic human cases related to travel or residence in rural/ semi- rural areas
2) enzootic and epizootic pattern among wild rodents and their fleas 3) distribution: india, south america, south africa, and southern ussr 4) us cases: 10 cases/ year in southwestern US 5) mode of aqcuisition in US is via FLEA BITE |
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D. IMMUNITY
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- antibody develops and is protective
- inactivated vaccine protects against bubonic plague |
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E. CLINICAL FEATURES
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1) BUBONIC PLAGUE: fever, malaise, and painful lymphadenopathy
2) PNEUMONIC PLAGUE (1 AND 2): fever, cough, shortness of breath |
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F. DIAGNOSIS
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1) BUBO ASPIRIATE: gram stain, and +ve culture
2) BLOOD CULTURE: usually positive with numbers > 10^6 3) SEROLOGY: 4 x rise in antibody to F1 capsule is diagnostic |
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G. TREATMENT/ PROGNOSIS
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- TETRACYCLIN, STREPTOMYCIN, CHLORAMPHENICOL
- untreated: mortality rate of about 60- 90% - treated: 5% mortality rate |
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H. PREVENTION
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- flea control in enzootic areas frequented by humans
- avoid ill rodents - inactivated vaccine |
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IV. FRANCISCELLA TULARENSIS and TULAREMIA
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A. GENERAL PROPERTIES
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- cause of TULAREMIA in humans
- small encapsulated pleomorphic gram -ve |
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B. PATHOGENESIS
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- TICK BITE: organisms injected directly while feeding or bite wound contaminated by feces
- organisms cause skin lesions, enter lymphatics, produce local lymphadenopathy then bacteremia with granuloma formation in reticuloendothelial system (spleen and liver) - intracellular survival in monocytes - ENDOTOXIN plays role in initial systemic symptoms |
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C. EPIDEMIOLOGY
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* it's a zoonotic disease transmitted from infected animals or arthropods
* it has a widespread distribution in northern hemisphere in 100 wild animals, 9 domestic birds, insects, and water ROUTES OF HUMAN INFECTION: 1) RABBIT: hand contact or ingestion partly cooked meat; winter disease in eastern US 2) ARTHROPOD-BORNE: ticks, deer flies, and others- - it's a summer disease in western US |
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D. CLINICAL FEATURES
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- abrupt onset of : fever chills, malaise
- SPECIFIC SYNDROMES: 1) ULCEROGLANDULAR: most common, skin ulcer and painful adenopathy |
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E. DIAGNOSIS
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- difficult to diagnose and dangerous to culture
- fluorescent antibody staining of node biopsy |
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F. TREATMENT
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STREPTOMYCIN
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G. PREVENTION
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- check for ticks
- wear protective gloves when dressing animals - vaccine (live attenuated) for lab workers and trappers |
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V. BRUCELLA SPECIES and BRUCELLOSIS
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A. GENERAL PROPERTIES
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- PLEOMORPHIC fastidious gram (-)ve
- grows slowly, requires 10% CO2 |
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B. PATHOGENESIS
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- causes infectious ABORTION of cows, sheep, pigs, and goats
- disease of reticuloepithelial system in humans - organisms are ingested by PMN, multiply in monocytes, and then form granulomas in liver, kidney, spleen, and marrow |
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C. EPIDEMIOLOGY
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*this is a zoonotic disease common in developing countries due to transmission from unpastuerized cheese and milk- - it is uncommon in the US, and most cases are in the midwest
1) B. ABORTUS: cows; tissue contact or millk 2) B. SUIS: pigs; tissue contact, airborne, abattoir workers at high risk 3) B. MELITENSIS: goats, sheep; unpastuerized milk, goat cheese |
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D. CLINICAL FEATURES
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- systemic and non- focal, including FUO (FEVER OF UNDERTERMINED ORIGIN)
- symptoms: fever, chills, malaise, headache and arthralgias (joint pain) - intracellular persistance causes prolonged initial symptoms and high risk of relapse |
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E. DIAGNOSIS
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- occupational history
- blood culture - increased serologic titer |
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F. TREATMENT
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- STREPTOMYCIN and TETRACYCLIN
- 25% chance of relapse NAD 1- 13% mortality rate |
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G. PREVENTION
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- pasteurize milk!!
- control of animal resevoir - vaccinate animals - test the herd - workers wear protective gear |
