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
how is listeria transmitted to humans?
ingestion of undercooked, refrigerated foods or contact with farm animals
26
how does listeria infect cells?
escapes from phagocytic vacuole with listerolysin | transmits cell to cell with actin based motility
27
what is the result of listeria infection in pregnant women?
it grows in the placenta | can cause neonatal morbility and mortality
28
what is the result of listeria infection in immunocompromised patients?
sepsis and CNS infection
29
how is listeriosis treated in pregnancy or immunocompromise?
ampicillin + gentamicin or trimethoprim + sulfamethoxazole
30
what does listeria cause in previously healthy hosts? how is it treated?
uncomplicated gastroenteritis | rehydrate and report
31
what is the morphology of vibrios?
curved gram negative rods
32
what selective media is used to grow vibrio?
bile salt agar (salt tolerant)
33
what is the best way to prevent vibrio infection? what else is available?
hygiene | modestly effective vaccines
34
what are reservoirs of cholera?
humans and plankton from the indian ocean and the gulf of mexico
35
describe rout and infectious dose of cholera
fecal oral rout with poor stomach acid survival and high infectious dose
36
how does cholera colonize the small intestine? how does it cause disease?
with mucinase | toxin coregulated pilus secretes enterotoxin
37
describe cholera enterotoxin. what does it do?
AB subunit toxin that causes massive watery diarrhea
38
what gene incurs pathogenicity in cholera? what antigens can be used to test for infection?
Choleragen gene carried by lysogenic bacteriophage CTX | O1 and O139 antigens
39
what is the result of infection with non CTX cholera strains?
mild sporadic disease
40
what causes morbidity and mortality in cholera infection?
dehydration and electrolyte imbalance (acidosis and hypokalemia)
41
how is cholera dehydration treated?
with IV lacted ringer solution (not just saline because of acidosis)
42
what may shorten the course of cholerae and parahaemolytcus infection? what is more important?
doxycycline | rehydration
43
what other vibrio are infectious? what diseases are they associated with
parahaemolyticus and vulanis | self limited gastroenteritis and life threatening cellulitis
44
how are non cholera vibrio infections contracted?
handling or eating raw shellfish
45
what are complicating factors of vibrio infections?
liver or kidney disease, immunodeficiency and iron overload
46
describe non cholera vibrio cellulitis. how is it treated?
rapidly progressive, hemorrhagic bullae in a seawater exposed injury. treat with surgical excision then antibiotics
47
describe the morphology and metabolism of campylobacter
curved gram negative rods that are microaerophilic
48
where are campylobacter found?
ubiquitous | reservoir is farm animals
49
what is the result of campylobacter infection?
destructive intracellular infection of intestines with bloody diarrhea
50
what are possible complications of campylobacter infection?
guillaia- barre, reactive arthritis, HUS, meningitis and vascular infection
51
how is campylobacter diagnosed?
microaerophilic culture, gram stain of fecal smear and sigmoidoscopy
52
how is campylobacter infection treated?
with rehydration | antibiotics if high fever or predisposed to complications (immunosuppressed, pediatric)
53
how does H pylori cause disease?
it colonizes the stomach, expresses urease and irritates the stomach lining. destruction is immunogenic (ulcer)
54
what diseases does h pylori predispose to?
gastric cancer and malt lymphoma
55
how is h pylori infection diagnosed?
scope, urea breath, PCR, biopsy
56
how is h pylori infection treated?
combined antibiotics and proton pump inhibitors