Micro Enteric Bacteria 3 Flashcards

1
Q

vibrio cholerae bacteriology

A

curved, comma-shaped, gram - rod with polar flagellum;
aerobic, facultatively anaerobic;
dual lifecycles (planktonic in indian ocean and pathogenic in drinking water supply)

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2
Q

what indicates v. cholerae pathogenicity?

A

o cell wall antigen

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3
Q

what o cell wall antigens cause epidemic disease in v cholerae?

A

O1 and O139

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4
Q

why are O1 and O139 pathogenic?

A

lysogenic bacteriophage - carries gene for primary choleragen enterotoxin (which is GI exotoxin)

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5
Q

how is v cholerae transmitted?

A

fecal-oral shed by asymptomatic carriers in incubation;

travel to untreated water or undercooked shellfish

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6
Q

who is most susceptible to v cholerae? why?

A

people on antacids or with gastrectomy because high infectious dose - usually killed by stomach acid

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7
Q

how does v cholerae cause disease?

A

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

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8
Q

describe cholera toxin

A

choleragen: A-B subunit structure - “A” causes persistent activation of adenylate cyclase leading to loss of water adn ions from attached cell

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9
Q

what disease is caused by v cholerae?

A

massive watery diarrhea - more than any other infectious gastroenteritis - death from dehydration and electrolyte imbalance

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10
Q

what is seen on exam for v cholerae?

A

“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)

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11
Q

v cholerae labs

A

isolated on media - salt-tolerant (because it’s from the ocean!), oxidase positive, ferments sucrose; darkfield microscopy of stool sample reveals motile vibrios

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12
Q

v cholerae treatment

A

rehydrate and rebalance electrolytes - tetracycline if needed

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13
Q

v parahaemolyticus bacteriology

A

gram - curved motile rod, oxidase +, saltwater-borne (warm ocean water), halophile

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14
Q

v parahaemolyticus pathogenesis

A

enters humans through undercooked seafood –> secretes enterotoxin similar to choleragen –> causes diarrhea

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15
Q

v parahaemolyticus on exam

A

nausea, vomiting, abdominal cramps, diarrhea, fever;

self limited

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16
Q

what disease is commonly caused by v parahaemolyticus? v vulnificus?

A

para: gasteroenteritis; vulnificus: cellulitis

17
Q

v parahaemolyticus treatment

A

previously healthy: oral rehydration: self-limited

iron overload, pre-exsiting liver disease, immunosuppressed, high fever = doxycycline and IV rehydration

18
Q

v vulnificus bacteirology

A

gram - curved motile rod, oxidase positive, some encapsulated, salt water born = halophile

19
Q

v vulnificus pathogenesis

A

infects shellfish contaminated wounds –> causes cellulitis and rapidly-fatal septicemia when in immunocompromised

20
Q

what is produced by v vulnificus? (virulence factors)?

A

hemolysin, protease exotoxin, siderophores

21
Q

which bug has the highest fatality rate for foodborne disease?

A

v vulnificus (esp in those with history of chronic liver disease)

22
Q

v vulnificus treatment

A
  1. surgical care: debride early and often
  2. ceftazidime + doxycycline or antipsudomonal penicillin
  3. admit/observe for sepsis, DIC, ARDS, renal failure
23
Q

campylobacter bacteriology

A

comma or s shaped gram - rod, oxidase and catalase positive, microaerophilic, grows well at 42C, reservoir in guts of domestic animals

24
Q

campylobacter pathogenesis

A

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)

25
Q

what does c. jejuni strongly predispose patients to?

A

guillain-barre syndrome, reactive arthritis, HUS

26
Q

campylobacter exam

A

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

27
Q

what does campylobacter bactermia lead to?

A

meningitis, vascular infection, abscess

28
Q

campylobacter lab

A

stool sample culture - blood agar with antibiotics to inhibit normal flora - dual temperatures (only grows on 42C), oxidase positive, gram -

29
Q

campylobacter treatment

A

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!

30
Q

h pylori bacteriology

A

curved gram -, similar to campylobacter but strongly UREASE +

31
Q

what organism is also urease positive besides h pylori?

A

proteus causing UTIs (makes stones)

32
Q

what does h pylori cause?

A

gastritis, peptic ulcer, MALT lymphoma

33
Q

h pylori pathogenesis

A

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)

34
Q

h pylori lab

A

“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

35
Q

h pylori treatment

A

normalize gastric pH with bismuth salts (pepto bismol), proton pump inhibitors to reduce pain and speed healing, kill bacteria with TRIPLE DRUG THERAPY