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35 Cards in this Set

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General properties of Vibrio cholerae

G?
Motile?
Metabolism?
shape?

Colonies?
Medium?
Produces what?
Major colonization factor?
How do you abolish motility?
G -
Motile - via polar flagellum
Fermenter
comma shape

yellow, opaque
TCBS medium, vibrio selective (this is the usual media for enteric pathogens like EMB, may inhibit growth)

O, H Antigens, endotoxin, potent enterotoxin (=cholera toxin, an exotoxin)

toxin coregulated pilus (TCP)

via antiserum
Vibrio cholerae pathogenesis:
bacteria from contaminated water or food -> gastric acid inactivates most ingested organisms, but some survive -> enter small bowel, bind to epithelium via unknown mechanism -> bacteria express TCP and form colonies in intestinal crypts -> cholera toxin is expressed and secreted -> binds to GM1 gangliosides of intestinal wall cell membrane -> neuraminidase of V. cholerae converts other gangliosides of the plasma membrane to GM1 (increases toxin binding sites) -> cholera toxin enters cells via endocytosis -> stimulates adenylate cyclase and cAMP production -> massive intestinal fluid loss due to villus cells (decreased NaCl absorption from gut), and secretory cells (increased Cl and HCO3 secretion into gut, along with water)
Clinical features of cholera:
painless, profuse watery diarrhea

isotonic volume loss (10-15L/day) and dehydration, low BP ("shock"), potential death
Cholera treatment:
replace fluid with same electrolyte concentration

rehydrate via IV or orally

measure stool volume with cholera cot

Antibiotics to reduce duration of diarrhea from 5-10 days to 1-3 days (tetracyclin)
Cholera epidemiology

infects who?
associated with what?
endemic to where?
Historical accounts?
History of Pandemics?
Current worldwide cholera status?
infects only humans

assoc with poverty and poor sanitation

Endemic in south-central, southeast asia, and South America (since 1992), recently assoc with refugee camps in Africa (mainly)

Accounts since BC

seven pandemics since 1800 - focus in a common delta of the Ganges and Brahmaputra rivers
7th pandemic began in 1961 and spread to latin america in 1992 = first western cholera outbreak in more than a century, spread rapidly with hundreds of thousands of cases, mortality rate 1%

A new serogroup O139 arose in Madras in 1992, has spread rapidly throughout the world, Cholera is more of a worldwide problem now than it was in 1992
History of cholera spread:

What are outbreaks often related to?

Infectious dose?
discovered by father of epidemiology John Snow that the 1855 outbreak in London was centered around the broadstreet pump

outbreaks related to contaminated water, shellfish and other seafood

infectious dose influences the possible modes of transmission of enteric pathogens
Largest infectious doses may be from water or food, smaller infectious doses may be from contact
Preventing cholera:
water precaution: bottled and carbonated, chlorinated, boiled
Food precautions: dry, steaming hot, special attention to shellfish
Cholera vaccine
1) Current inactivation vaccine: crude bacterial suspension, 50% effective, not recommended even for travel
2) live attenuated vaccine: effective in N. American clinical trials, unproven in field studies, common mild side effects, licensed but not manufactured
Campylobacter

General:
Gram
shape
metabolism
location
causative agents (bacteria)
gram - rod
curved or comma shape
microaerophilic
present in numerous animal species
C jejuni is most common, followed by C. coli
Campylobacter pathogenesis:
ingested with food or water -> some survive gastric acid -> to sm and lg bowel to cause invasive inflamm process -> rarely, enter the blood stream -> usually recovery and specific Ab-mediated immunity are characteristic
Campylobacter epidemiology:

type of transmission?
Commonly found in?
Cases/outbreaks?
zoonotic (transmitted to humans from animals), doesn't make animals ill, rare human to human transmission

>50% raw chicken in US grocery stores has Campylobacter

cases typically sporadic, not epidemic, tend to peak in summer/early fall
multiple cases simultaneously point to common contaminated source (e.g. unpasteurized milk)
Campylobacter history:
probably caused disease for centuries, but wasn't isolated until 1968, and not recognized as cause of diarrheal illness until 1970s
Campylobacter occurrence:

common?
how many in US?
most commonly affected?
*Most common* cause of diarrhea in the world (far more than salmonella and shigella)

>1 million reported US cases/year

infants-young adults most commonly affected in developing countries, infants in developing countries
Campylobacter clinical features:

incubation
symptoms
sequelae
3-5 day incubation

Prodromal symptoms = fever, malaise, headache -> fever, abd pain, diarrhea for a few days-week

1 in 1000 develop autoimmunity to nerves -> can cause paralysis that lasts for several weeks (requires intensive care)
campylobacter

infectious dose:

Diagnosis:
<500 organisms (1 drop of raw chicken juice)

stool culture on selective media, incubate in 5-10% oxygen at 37 or 42 degrees C (42 is optimal and is also body T of poultry)
Campylobacter

treatment:

Prevention:
for all: supportive therapy
for some: antimicrobial therapy (erythromycin or ciprofloxacin)

pasteurize milk, avoid undercooked meat esp poultry
Yersinia pestis

causes what:

general properties:
Gram
shape/size
metabolism
Family, genus, species
plague (includes bubonic and penumonic)

G-, large, rod-shaped or coccobacillary
aerobic or facultatively anaerobic, non-lactose fermenter

Family: Enterobacteriacae
Genus: Yersinia
Species: pestis and two other zoonotic bacteria, pseudotuberculosis and enterocolitica
Y. pestis

pathogenesis:
Extracellular
Intracellular
Toxins
extracellular pathogen:
capsule is antiphagocytic
-F1 Ag for virulence
- anti-phagocytic properties present before the capsule - V and W Ags
- antiphagocytic properties are present at 37 degrees C (mammal) but not 28C (flea)

Intracellular pathogen:
- persists within mammalian monocytes

Toxins:
- classical LPS endotoxin
Y. pestis epidemiology

General Transmission cycle:
*cycle of transmission involving mammals, usually rodents, and their associated ectoparasites, usually fleas, with incidental human involvement
Y. pestis epidemiology

2 types of general transmission
1) From flea to mammal (Bubonic)
- flea acquires Y.pestis after a blood meal -> Y. pestis multiplies -> obstructs foregut -> obstructed flea attempts to feed, regurgitates 24,000 organisms on bite site -> organisms enter lymphatics, cause regional adenitis ("bubo") in the mammal

2) From mammal to mammal (Primary pneumonic)
- bubonic plague -> secondary pneumonia in first case -> spread via resp droplets to cause primary pneumo in a contact
Y. pestis epidemiology

1) Urban plague:

2) Rural plague:
- sporadic human cases related to?
- patterns among wild rodents and their fleas
- Distribution
- US # cases per year
- mode of acquisition in US
Domestic/murine
-3 major human epidemics (A.D. 546, 1346, 1894)
- Epizootics (animal epidemics) among urban black rats and their fleas (Xenopsylla cheopis)
- Humans become involved as rats die and their fleas seek new hosts
- initial cases = bubonic, then pneumonic

Sylvatic
- sporadic human cases related to travel or residence in rural or semi-rural areas
- enzootic and epizootic patterns among wild rodents and their fleas
- Distributed in India, S. America, S. Africa, S USSR
- US 10 cases per year in SW US
- mode of acquisition in US = flea bite
Y. pestis

Immunity:

Clinical features:
1) Bubonic plague
2) Pneumonic plague
Ab develops and is protective
Inactivated vaccine, was used to vietnam troops

1) (Flea bite) fever, malaise, painful lymphadenopathy
2) fever, cough, SOB
Y. pestis

Diagnosis:
Bubo aspirate: usually Gram stain and culture positive, confirm by fluorescent antibody (FA)

Blood culture: usually positive, may have very high # organisms, >10^6 visible on peripheral smear

Serology: 4x's increase in Ab to F1 capsule is diagnostic (passive hemagglutination)
Y. pestis

Treatment/prognosis:
treatment
mortality
US mortality

Prevention:
10 days tetracyclin, streptomycin or chloramphenicol
Mortality 60-90% if untreated, 5% with early antibiotics
US mortality 15% overall

flea control programs in enzootic areas frequented by humans
avoid ill rodents
inactivated vaccine
Franciscella tularensis

causes what, in who?
characteristics (gram, shape)
causes tularemia in humans
G -, small, pleomorphic, unencapsulated
Franciscella tularensis

Pathogenesis:
tick bite
- organisms injected directly during feeding
or
- bite wound contaminated by tick feces

organisms cause skin lesion -> enter lymphatics -> local lymphadenopathy -> bacteremia -> granuloma formation in reticuloendothelial system (spleen, liver) -> intracellular survival in monocytes -> endotoxin plays role in initial systemic symptoms
Franciscella tularensis

Epidemiology:
transmitted from where?
location?
2 routes of human infection?
transmitted from infected animals or arthropods
widespread distribution in N. Hemisphere (found in 100 wild mammals, 9 domestic animals, birds, insects, water)
1) Rabbit: hand contact or ingestion of partially cooked rabbit meat (winter disease in E. US)
2) Arthropod-borne: ticks, deer flies etc (summer disease in W. US)
Franciscella tularensis

Clinical features:
prodromal symptoms
specific symptoms
mortality
abrupt onset of fever, chills, malaise

Specific symptoms include ulceroglandular (most common, skin ulcer, painful adenopathy - inguinal, axillary)

1% mortality with treatment
Franciscella tularensis

Diagnosis: (3)
difficult and dangerous to culture (lab accidents)

fluorescent Ab stain of node biopsy

serologic
Franciscella tularensis

Treatment:

Prevention:

What causes relapses?
streptomycin bactericidal

Rx for 7-10 days (alternative tetracyclin to 14 days)


Ticks: check for tick frequently in endemic areas, remove by mouth parts

Rabbits/muskrats: wear protective gloves when dressing animals

Vaccine: live attenuated, for lab workers, at risk trappers
Relapses occur from intracellular parasite
Brucella species

Cause what?

General:
Gram
shape
growth/metabolism
Oxygen requirements
Brucellosis

G -, pleomorphic, grows slowly, requires 10% CO2 for optimal growth
Brucella

Pathogenesis:
causes infectious abortion in cows, sheep, pigs, goats (localizes in placenta due to erythritol - a sugar found in animals)

In humans - disease of reticuloendothelial (RE) system (aka mononuclear phagocyte system)

organisms ingested by PMN -> multiply in monocytes -> form granulomas in the liver, kidney, spleen, marrow
Brucella

Epidemiology:
type of disease?
common where? why?
uncommmon where?
3 species:
Epidemiological studies done where?
zoonotic disease

common in developing countries because of transmission from unpasteurized milk and cheese

uncommon in US (200 cases/yr), most from midwest (Illinois, Iowa)

1) B. abortus (cattle): contaminated milk or direct tissue contact
2) B. suis (swine): tissue contact, airborn, abattoir workers at high risk (slaughterhouse)
3) B. melitensis (goats, sheep): unpasteurized milk, goat cheese

epidemiological studies done in abattoirs
Brucella

Clinical features:
symptoms
intracellular persistence ->
systemic, non-focal, FUO (fever of unknown origin), chills, myalgias (muscle pain), headache, arthralgias (joint pain)

intracellular persistence -> prolonged initial symptoms and high risk of relapse
Brucella

Diagnosis:
based on
Occupational history
Blood Culture: 21 day incubation, common prolonged bacteremia
Serologic: 4x titer increase
Brucella

Treatment:
how long?
percent relapse and mortality?

Prevention:
Streptomycin and tetracycline for 3 weeks, then only tetracycline for 3 weeks
25% relapse, 1-13% mortality

Pasteurization of milk and cheese

Control of animal reservoir via
1) vaccinate young female calves with B. abortus vaccine
2) Herd testing: Ab test on pooled milk samples from herd -> individual animal testing -> destruction of positive animals

Occupational protection: mesh gloves and eye protection