Enteric Bacterial Infections Flashcards

1
Q

what is the morphology of all foodborne enterobacteriaceae?

A

gram negative rods

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2
Q

how do enterobacteriaceae colonize the lumen of the intestine?

A

they cannot colonize the epithelium in the lumen

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3
Q

how do enterobacteriaceae gain access to the host?

A

they are sampled by M cells of Peyers patches to gain access to the serosa side of the intestine

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4
Q

how do enterobacteriacea avoid the immune system?

A

they use macrophages as trojan horses and infect the lymphatics

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5
Q

what are the diseases caused by Yersinia and salmonella using macrophages as trojan horses?

A

yersina- local false appendicitis

salmonella- systemic enteric fever or post sepsis focal disease

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6
Q

what are the differences in clinical presentation of noninvasive vs invasive/destructive enterobacteriaceae?

A

noninvasive- watery diarrhea

invasive- bloody diarrhea

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7
Q

which enterobacteria are noninvasive?

A

salmonella, enterotoxic e coli and yersinia

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8
Q

which enterobacteria are invasive/destructive?

A

shigella and enterohemorrhagic e coli

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9
Q

what are the common exposures of foodborne enterobacterial infections?

A

proteins

meat for e coli and meat or eggs for salmonella

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10
Q

what causes the most complications of enterobacterial infections?

A

dehydration and electrolyte loss

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11
Q

what life threatening complication may follow gut tissue necrosis?

A

bacteremia

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12
Q

how are virulence factors often carried in enterobacteria?

A

plasmids

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13
Q

what are the common virulence factors for foodborne enterobacteria?

A

fimbriae/pilli for attachment, T3SS for immune evasion and/or host cell invasion and toxins

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14
Q

what determines the disease caused by E coli?

A

the acquired virulence factors make it able to cause certain diseases

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15
Q

which is the only enterobacterial pathogen that is likely to ferment lactose?

A

e coli

pink on MacConckey agar which detects fermentation of lactose

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16
Q

who has the highest risk of developing a foodborne enterobacterial infection? who is at the highest risk for mortality?

A

children

neonates and elderly

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17
Q

which pathogens cause HUS? when does it occur?

A

shigella and enterohemorrhagic E coli

when shiga toxin (protein synthesis inhibitor) reaches the bloodstream

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18
Q

what is one postinfectious sequalae of shigella, salmonella and yersinia infection?

A

reactive arthritis/ reiter’s syndrome

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19
Q

what should be done before treatment of enterobacterial infection?

A

antimicrobial susceptibility testing

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20
Q

how is exposure to enterobacteriacae minimized?

A

sewage treatment, pasteurization, water chlorination, food processing and hand washing

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21
Q

what causes noninfectious bacterial- toxigenic food poisoning?

A

a patient eats a food containing preformed toxins secreted by non GI bacteria

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22
Q

which three pathogens cause toxigenic food poisoning? what happens to the bacteria when they are ingested?

A

staph aureus, B. cereus and C. botulinum

they do not survive ingestion but their toxins cause gastroenteritis

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23
Q

what conditions are suitable for staph aureus and b cereus colonization?
c botulinum?

A

foods left open at room temp

c b- airtight packaged foods (anaerobic)

24
Q

what is the morphology of listeria? what type of hemolysis does it exhibit?

A

gram positive rod

beta hemolytic

25
Q

how is listeria transmitted to humans?

A

ingestion of undercooked, refrigerated foods or contact with farm animals

26
Q

how does listeria infect cells?

A

escapes from phagocytic vacuole with listerolysin

transmits cell to cell with actin based motility

27
Q

what is the result of listeria infection in pregnant women?

A

it grows in the placenta

can cause neonatal morbility and mortality

28
Q

what is the result of listeria infection in immunocompromised patients?

A

sepsis and CNS infection

29
Q

how is listeriosis treated in pregnancy or immunocompromise?

A

ampicillin + gentamicin or trimethoprim + sulfamethoxazole

30
Q

what does listeria cause in previously healthy hosts? how is it treated?

A

uncomplicated gastroenteritis

rehydrate and report

31
Q

what is the morphology of vibrios?

A

curved gram negative rods

32
Q

what selective media is used to grow vibrio?

A

bile salt agar (salt tolerant)

33
Q

what is the best way to prevent vibrio infection? what else is available?

A

hygiene

modestly effective vaccines

34
Q

what are reservoirs of cholera?

A

humans and plankton from the indian ocean and the gulf of mexico

35
Q

describe rout and infectious dose of cholera

A

fecal oral rout with poor stomach acid survival and high infectious dose

36
Q

how does cholera colonize the small intestine? how does it cause disease?

A

with mucinase

toxin coregulated pilus secretes enterotoxin

37
Q

describe cholera enterotoxin. what does it do?

A

AB subunit toxin that causes massive watery diarrhea

38
Q

what gene incurs pathogenicity in cholera? what antigens can be used to test for infection?

A

Choleragen gene carried by lysogenic bacteriophage CTX

O1 and O139 antigens

39
Q

what is the result of infection with non CTX cholera strains?

A

mild sporadic disease

40
Q

what causes morbidity and mortality in cholera infection?

A

dehydration and electrolyte imbalance (acidosis and hypokalemia)

41
Q

how is cholera dehydration treated?

A

with IV lacted ringer solution (not just saline because of acidosis)

42
Q

what may shorten the course of cholerae and parahaemolytcus infection? what is more important?

A

doxycycline

rehydration

43
Q

what other vibrio are infectious? what diseases are they associated with

A

parahaemolyticus and vulanis

self limited gastroenteritis and life threatening cellulitis

44
Q

how are non cholera vibrio infections contracted?

A

handling or eating raw shellfish

45
Q

what are complicating factors of vibrio infections?

A

liver or kidney disease, immunodeficiency and iron overload

46
Q

describe non cholera vibrio cellulitis. how is it treated?

A

rapidly progressive, hemorrhagic bullae in a seawater exposed injury. treat with surgical excision then antibiotics

47
Q

describe the morphology and metabolism of campylobacter

A

curved gram negative rods that are microaerophilic

48
Q

where are campylobacter found?

A

ubiquitous

reservoir is farm animals

49
Q

what is the result of campylobacter infection?

A

destructive intracellular infection of intestines with bloody diarrhea

50
Q

what are possible complications of campylobacter infection?

A

guillaia- barre, reactive arthritis, HUS, meningitis and vascular infection

51
Q

how is campylobacter diagnosed?

A

microaerophilic culture, gram stain of fecal smear and sigmoidoscopy

52
Q

how is campylobacter infection treated?

A

with rehydration

antibiotics if high fever or predisposed to complications (immunosuppressed, pediatric)

53
Q

how does H pylori cause disease?

A

it colonizes the stomach, expresses urease and irritates the stomach lining. destruction is immunogenic (ulcer)

54
Q

what diseases does h pylori predispose to?

A

gastric cancer and malt lymphoma

55
Q

how is h pylori infection diagnosed?

A

scope, urea breath, PCR, biopsy

56
Q

how is h pylori infection treated?

A

combined antibiotics and proton pump inhibitors