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46 Cards in this Set

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I. VIBRIO CHOLERAE AND CHOLERA
*
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)
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
C. CLINICAL FEATURES
- painless, profuse WATERY DIARRHEA

- isotonic volume loss (10-15 Liters/ day and dehydration

- low bp
D. TREATMENT
- 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
E. EPIDEMIOLOGY
- 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)
F. PREVENTION (3)
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
*other related pathogens
1) VIBRIO PARAHEMOLYTICS: invasive gastroenteritis from contaminated shellfish

2) VIBRIO VULNIFICUS:
infections in wounds contaminated by seawater or shellfish
II. CAMPYLOBACTER SPECIES
*
A. GENERAL PROPERTIES
- curved, comma-shaped microaerophilic gram -ve rod

- present in lots of animal species

- most common: C. JEJUNI, followed by C.COLI
B. PATHOGENESIS
- 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
C. EPIDEMIOLOGY
- 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
D. HISTORY
- has probably caused disease for centuries but was just recognized as a disease- causing agnet since 1970
E. OCCURANCE
- most commone etiologic agent of diarrhea in the world, surpassing SHIGELLA and SALMONELLA
F. CLINICAL FEATURES
- 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
G. INFECTIOUS DOSE
- usually only need about 500 organisms to cause disease- - just need 1 drop of raw chicken juice
H. DIAGNOSIS
- esablished by culture of stool on selective media

- interestingly grows best at 42 degrees C, which is body temp of chicken
I. TREATMENT
- SUPPORTIVE WITH ANTIMICROBIAL

ERYTHROMYCIN or DIPROFLOXACIN
J. PREVENTION
- pasteurization of milk, avoid undercooked meats
III. YERSINIA PESTIS and PLAGUE
*
A. GENERAL PROPERTIES
- large rod- shaped coccobacillary gram -ve bacteria

- aerobic or facultatively anaerobic, non- lactose fermenter

- family enterobacteriacae, genus includes 2 other zoonotic bacteria
B. PATHOGENESIS
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
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
What are the CHARACTERISTICS of the URBAN PLAGUE? (4)
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
What are the CHARACTERISTICS of the RURAL PLAGUE? (5)
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
D. IMMUNITY
- antibody develops and is protective
- inactivated vaccine protects against bubonic plague
E. CLINICAL FEATURES
1) BUBONIC PLAGUE: fever, malaise, and painful lymphadenopathy

2) PNEUMONIC PLAGUE (1 AND 2): fever, cough, shortness of breath
F. DIAGNOSIS
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
G. TREATMENT/ PROGNOSIS
- TETRACYCLIN, STREPTOMYCIN, CHLORAMPHENICOL

- untreated: mortality rate of about 60- 90%
- treated: 5% mortality rate
H. PREVENTION
- flea control in enzootic areas frequented by humans
- avoid ill rodents
- inactivated vaccine
IV. FRANCISCELLA TULARENSIS and TULAREMIA
*
A. GENERAL PROPERTIES
- cause of TULAREMIA in humans

- small encapsulated pleomorphic gram -ve
B. PATHOGENESIS
- 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
C. EPIDEMIOLOGY
* 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
D. CLINICAL FEATURES
- abrupt onset of : fever chills, malaise

- SPECIFIC SYNDROMES:
1) ULCEROGLANDULAR: most common, skin ulcer and painful adenopathy
E. DIAGNOSIS
- difficult to diagnose and dangerous to culture

- fluorescent antibody staining of node biopsy
F. TREATMENT
STREPTOMYCIN
G. PREVENTION
- check for ticks

- wear protective gloves when dressing animals

- vaccine (live attenuated) for lab workers and trappers
V. BRUCELLA SPECIES and BRUCELLOSIS
*
A. GENERAL PROPERTIES
- PLEOMORPHIC fastidious gram (-)ve
- grows slowly, requires 10% CO2
B. PATHOGENESIS
- 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
C. EPIDEMIOLOGY
*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
D. CLINICAL FEATURES
- 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
E. DIAGNOSIS
- occupational history

- blood culture


- increased serologic titer
F. TREATMENT
- STREPTOMYCIN and TETRACYCLIN

- 25% chance of relapse NAD 1- 13% mortality rate
G. PREVENTION
- pasteurize milk!!

- control of animal resevoir

- vaccinate animals

- test the herd

- workers wear protective gear