Micro Enteric Bacteria 3 Flashcards Preview

ABBEY MSII U6 > Micro Enteric Bacteria 3 > Flashcards

Flashcards in Micro Enteric Bacteria 3 Deck (35):
1

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)

2

what indicates v. cholerae pathogenicity?

o cell wall antigen

3

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

O1 and O139

4

why are O1 and O139 pathogenic?

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

5

how is v cholerae transmitted?

fecal-oral shed by asymptomatic carriers in incubation;
travel to untreated water or undercooked shellfish

6

who is most susceptible to v cholerae? why?

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

7

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

8

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

9

what disease is caused by v cholerae?

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

10

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)

11

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

12

v cholerae treatment

rehydrate and rebalance electrolytes - tetracycline if needed

13

v parahaemolyticus bacteriology

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

14

v parahaemolyticus pathogenesis

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

15

v parahaemolyticus on exam

nausea, vomiting, abdominal cramps, diarrhea, fever;
self limited

16

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

para: gasteroenteritis; vulnificus: cellulitis

17

v parahaemolyticus treatment

previously healthy: oral rehydration: self-limited
iron overload, pre-exsiting liver disease, immunosuppressed, high fever = doxycycline and IV rehydration

18

v vulnificus bacteirology

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

19

v vulnificus pathogenesis

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

20

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

hemolysin, protease exotoxin, siderophores

21

which bug has the highest fatality rate for foodborne disease?

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

22

v vulnificus treatment

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

23

campylobacter bacteriology

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

24

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)

25

what does c. jejuni strongly predispose patients to?

guillain-barre syndrome, reactive arthritis, HUS

26

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

27

what does campylobacter bactermia lead to?

meningitis, vascular infection, abscess

28

campylobacter lab

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

29

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!

30

h pylori bacteriology

curved gram -, similar to campylobacter but strongly UREASE +

31

what organism is also urease positive besides h pylori?

proteus causing UTIs (makes stones)

32

what does h pylori cause?

gastritis, peptic ulcer, MALT lymphoma

33

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)

34

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

35

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