Micro Enteric Bacteria 3 Flashcards
vibrio cholerae bacteriology
curved, comma-shaped, gram - rod with polar flagellum;
aerobic, facultatively anaerobic;
dual lifecycles (planktonic in indian ocean and pathogenic in drinking water supply)
what indicates v. cholerae pathogenicity?
o cell wall antigen
what o cell wall antigens cause epidemic disease in v cholerae?
O1 and O139
why are O1 and O139 pathogenic?
lysogenic bacteriophage - carries gene for primary choleragen enterotoxin (which is GI exotoxin)
how is v cholerae transmitted?
fecal-oral shed by asymptomatic carriers in incubation;
travel to untreated water or undercooked shellfish
who is most susceptible to v cholerae? why?
people on antacids or with gastrectomy because high infectious dose - usually killed by stomach acid
how does v cholerae cause disease?
if survives past stomach acid - reach small intestine where it secretes MUCINASE to clear path to brush border and attaches using toxin coregulated pilus (TCP) and colonize - then secretes cholera toxin
describe cholera toxin
choleragen: A-B subunit structure - “A” causes persistent activation of adenylate cyclase leading to loss of water adn ions from attached cell
what disease is caused by v cholerae?
massive watery diarrhea - more than any other infectious gastroenteritis - death from dehydration and electrolyte imbalance
what is seen on exam for v cholerae?
“rice water stool” - large volumes of watery diarrhea - no pain, blood or neutrophils in stool but acidosis and hypokalemia from loss of bicarb and K;
dehydration leads to cardiac and renal failure (skin dehydration test)
v cholerae labs
isolated on media - salt-tolerant (because it’s from the ocean!), oxidase positive, ferments sucrose; darkfield microscopy of stool sample reveals motile vibrios
v cholerae treatment
rehydrate and rebalance electrolytes - tetracycline if needed
v parahaemolyticus bacteriology
gram - curved motile rod, oxidase +, saltwater-borne (warm ocean water), halophile
v parahaemolyticus pathogenesis
enters humans through undercooked seafood –> secretes enterotoxin similar to choleragen –> causes diarrhea
v parahaemolyticus on exam
nausea, vomiting, abdominal cramps, diarrhea, fever;
self limited
what disease is commonly caused by v parahaemolyticus? v vulnificus?
para: gasteroenteritis; vulnificus: cellulitis
v parahaemolyticus treatment
previously healthy: oral rehydration: self-limited
iron overload, pre-exsiting liver disease, immunosuppressed, high fever = doxycycline and IV rehydration
v vulnificus bacteirology
gram - curved motile rod, oxidase positive, some encapsulated, salt water born = halophile
v vulnificus pathogenesis
infects shellfish contaminated wounds –> causes cellulitis and rapidly-fatal septicemia when in immunocompromised
what is produced by v vulnificus? (virulence factors)?
hemolysin, protease exotoxin, siderophores
which bug has the highest fatality rate for foodborne disease?
v vulnificus (esp in those with history of chronic liver disease)
v vulnificus treatment
- surgical care: debride early and often
- ceftazidime + doxycycline or antipsudomonal penicillin
- admit/observe for sepsis, DIC, ARDS, renal failure
campylobacter bacteriology
comma or s shaped gram - rod, oxidase and catalase positive, microaerophilic, grows well at 42C, reservoir in guts of domestic animals
campylobacter pathogenesis
transmitted fecal-oral, sexual contact, sick pets with low infectious dose - colonizes both intestines (NOT just M cells!! - just epithelium) causing blood and pus in diarrhea (some have cholera like enterotoxin causing a watery diarrhea)
what does c. jejuni strongly predispose patients to?
guillain-barre syndrome, reactive arthritis, HUS
campylobacter exam
common in children and MSM, incubation in days-week, initially watery foul-smelling diarrhea that progresses to bloody stools with fever and abdominal pain - need to rule out bacteremia
what does campylobacter bactermia lead to?
meningitis, vascular infection, abscess
campylobacter lab
stool sample culture - blood agar with antibiotics to inhibit normal flora - dual temperatures (only grows on 42C), oxidase positive, gram -
campylobacter treatment
rehydrate for simple gastroenteritis - treat if patient is pediactric, high fever, bloody, 8+ stools/day, worsening, more than a week, pregnant, HIV with azithromycin, or erythromycin in peds
DO NOT TREAT THE DIARRHEA!
h pylori bacteriology
curved gram -, similar to campylobacter but strongly UREASE +
what organism is also urease positive besides h pylori?
proteus causing UTIs (makes stones)
what does h pylori cause?
gastritis, peptic ulcer, MALT lymphoma
h pylori pathogenesis
transmission unknown - attach to mucus secreting cells of stomach - secrete urease virulence factor breaking down urea into ammonia which nenutralizes stomach pH allowing bacterial growth and irritating stomach lining - WBC infiltrates also and upregulates caspases (causing apoptosis in nearby cells)
h pylori lab
“urea breath” test - patient ingests radiolabeled urea, if infected will exhale radiolabeled carbon dioxide; biopsy has bacteria visible on gram stain, antigen present in stool, IgG in serum
h pylori treatment
normalize gastric pH with bismuth salts (pepto bismol), proton pump inhibitors to reduce pain and speed healing, kill bacteria with TRIPLE DRUG THERAPY
