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2: Enteric Dudes Flashcards

1
Q

top 5 pathogens contributing to domestically acquired foodborne illnesses in US

A
  1. norovirus
  2. salmonella, non typhoidal
  3. c. perfringens
  4. campylobacter spp.
  5. s. aureus
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2
Q

top 4 pathogens contributing to domestically acquired foodborne illnesses resulting in deaths in US

A
  1. Salmonella, nontyphoidal
  2. Toxoplasma gondii
  3. Listeria
  4. Norovirus
  5. Campylobacter
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3
Q

most common causes of foodborne illnesses that cause the most hospitalizations

A

Salmonella non typhi

Campylobacter

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4
Q

which two dudes are common contaminants but do not cause serious disease (toxin-mediated)

A

C. perfringens

S. aureus

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5
Q

which two dudes are less common, but can cause fatal disease?

A

Listeria

E. coli O157:H7

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6
Q

list the enteropathic bacteria

A 
EHEC 
EIEC 
cholera 
shigella 
salmonella - typhi and non typhi 
campylobacter 
yersinia 
S. aureus (toxin) 
botulism (toxin) 
c. perfringens (toxin) 
B. cereus (toxin)
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7
Q

enteropathic viruses

A

norwalk virus
enterovirus
polio virus

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8
Q

enteropathic parasites

A

giardia
amoebae
ascaris
cryptosporiosis

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9
Q

general pathogenesis of enteropathic bacteria

A
  1. ingestion of enterotoxins
    - absorption of preformed toxin, short incubation time - hours
  2. infection by colonizing toxigenic organisms
    - hypersecretion reaction from bacterial adherence and toxin secretion
    - incubation 1-3d
  3. direct invasion of gut wall
    - incubation time extended: days-weeks
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10
Q

important virulence factors for adherence to mucosal cells

A

pili

flagella

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11
Q

important virulence factors for production of enterotoxins

A
  • prototype secretagogue toxin (vibrio cholerae)
  • cytotoxins - Shiga toxin (shigella, E. coli O157:H7)
  • T cell super Ag’s (staph enterotoxins)
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12
Q

important virulence factors for capacity to invade

A
  • intracellular proliferation, cell lysis, and cell-to-cell spread
  • invasion and cytolysis result in bloody/pus diarrhea (dysentery)
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13
Q

predisposing factors for enteropathic bacteria

A
  • fecal contamination
  • immunosuppression
  • antispasmodic drugs (less movement through gut means more chance of overgrowth)
  • antacids
  • mucosal disease
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14
Q

clinical presentation of enteropathic bacterias

A
  • disease from absorbed toxin: local (staph) vs. systemic (botulism)
  • secretory diarrhea (cholera)
  • dysentery (shigella)
  • systemic illness (typhoid fever)
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15
Q

diarrhea vs. dysentery

A

diarrhea: excess fluid
- hypersecretion
- osmotic load (lactose intolerance)

dysentery: mucosal invasion
- inflamamtion + necrosis of wall
- loose stool + blood + leukocytes

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16
Q

levels of tissue involvement/destruction in diarrhea

A
  • toxin only (no bacteria)
  • superficial colonization + toxin
  • superficial colonization + inflammation
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17
Q

levels of tissue involvement/destruction in dysentery

A
  • mucosal invasion
  • mucosal necrosis
  • submucosal invasion
  • systemic spread
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18
Q

general characteristics of E. coli

A

G(-)
rods
green sheen on EMB agar
coliform - ferment lactose

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19
Q

characteristics of E. coli disease

A

depends on strain:

  • watery diarrhea, cramping pain, fever, malaise
  • invasive or cytolytic disease (dysentery)
  • verotoxin (shigatoxin) - hemolytic uremic syndrome
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20
Q

hemolytic uremic syndrome

A

shiga toxin binds to glomerular endothelium -> clotting/inflammation

anemia
hemoglobinuria
renal failure

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21
Q

pathogenic mechanisms of E. coli

A
  • invasive disease (migrants, Indian reservations)

- toxigenic disease (traveler’s diarrhea)

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22
Q

why do you not use imodium with Montezuma’s revenge?

A

it is an anti-motility drug: less motility of gut means more chance of overgrowth, easier overgrowth

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23
Q

describe ETEC

A

watery “traveler’s diarrhea” from consumption of food contaminated with enterotoxin-producing strain

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24
Q

describe EHEC

A

severe bloody colitis from consumption of hamburger, dairy products, or fruit juice, contaminated with invasive, verotoxin-producing (shiga toxin) strain (mainly O157:H7)

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25
Q

describe EAEC

A

primarily pediatric diarrhea in impoverished nations

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26
Q

describe where EHEC cannot grow

A

doesn’t ferment sorbitol or grow at 45 degrees

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27
Q

sources of O157:H7

A
  • cattle and beef products (hamburgers, unpasteurized milk)
  • other ag products contaminated by products
  • outbreaks: hamburgers, spinach, sprouts

-rarely transmitted person to person

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28
Q

O157:H7 mechanism of disease

A
  • small infectious dose (less than 100 dudes)
  • bacteria adhere to cell membrane, colonize large intestine
  • produce shigatoxins -damage endothelial cells (inhibits mRNA translation, protein synthesis)
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29
Q

O157:H7 disease course

A
  • onset 3-4d after ingestion
  • severe abdominal cramping, watery diarrhea progressing to bloody after 3-4d
  • occasionally vomiting
  • fever low grade or absent
  • duration average 8d
30
Q

O157:H7 disease presentations

A
  • asymptomatic
  • mild/moderate illness (just watery diarrhea, abdominal pain, rare vomit, no fever)
  • dysentery (grossly bloody diarrhea, severe abdom pain)
  • hemolytic uremic syndrome (3-5% fatality rate, kids and elderly, acute renal failure - obstruction of glomeruli by microthrombi)
  • TTP = thrombotic thrombocytopenic purpura (type of DIC)
31
Q

how often do STEC non O157:H7 cause disease?

A

5-10% cause serious illness

32
Q

what are STEC non O157:H7 associated with?

A

Stx2 and eae (intimin) genes (not as frequent or severe as O157:H7

33
Q

general characteristics of shigella

A

G(-)
non-motile
non-coliform

34
Q

how do you get shigella

A

fecal/oral transmission

daycare centers
MSM

35
Q

pathogenesis of shigella

A
  • invasive lesions of colonic mucosa which spreads to lymph nodes
  • do NOT cause bacteremia
  • exotoxin causes mucosal necrosis - fibrinosupporative exudate forms pseudomembrane as in diphtheria
  • highly virulent: 12 dudes can cause disease
36
Q

general characteristics of cholera

A

G(-)
comma
alkali tolerant

37
Q

transmission of cholera

A
  • direct fecal-oral transmission

- asymptomatic carriers

38
Q

pathogenesis of cholera

A
  • no invasive lesions
  • pathogenicity entirely due to enterotoxin
  • induces secretion of isotonic fluid
  • deaths due to dehydration and hypovolemic shock
39
Q

where is cholera endemic?

A

endemic in India; recent pandemics in S. America

40
Q

toxin of cholera - mechanism

A
  • subunit A binds with ADP-ribosylates EF-2
  • activates GTP-activated adenylate cyclase resulting in cAMP formation
  • stimulates secretion of chloride and bicarb
41
Q

hallmark symptom of cholera

A

rice water diarrhea

42
Q

general characteristics of salmonella

A

G(-)
non coliform
H2S production

43
Q

three forms of disease from salmonella

A
  • typhoid (typhoid mary)
  • enteric fever
  • salmonella food poisoning
44
Q

salmonella food poisoning: organisms

A

S. enteritidis

S. typhimurium

45
Q

salmonella food poisoning: transmission

A
  • eggs
  • undercooked chicken or meat
  • contaminated waters
  • turtles/reptiles
  • cantaloupes
  • mangos
46
Q

salmonella food poisoning: symptoms

A

vomiting and diarrhea (gastroenteritis)

superficial lesions of colon
usually mild, self-limiting except in immunosuppressed
local epidemics traced to a single food source

47
Q

salmonella food poisoning: pathogenic mechanisms

A
  • invades mucosal cells - mucosal ulceration (superficial)
  • NO enterotoxins
  • multiply w/i neutrophils and macrophages
  • can cause G(-) sepsis
48
Q

normally osteomyelitis is caused by S. aureus. but in kids with sickle cell anemia, what is the main cause?

A

Salmonella!!

49
Q

salmonella paratyphoid fever: organisms

A
  • S. typhinurium
  • S. paratyphi
  • S. cholerae-suis
50
Q

salmonella paratyphoid fever: symptoms

A
  • fever
  • bacteremia
  • local lesions

associated with sickle cell disease, shistosomiasis

51
Q

salmonella typhi - systemic disease. describe

A

typhoid fever

  • fever
  • rose spots on lower anterior chest and abdomen
  • hepatosplenomegaly
  • carrier state - 3-5% in gall bladder (not dissolved by bile)
  • mild vomiting
  • diarrhea uncommon
52
Q

salmonella typhi pathogenesis

A
  • systemic involvement: fever, rash
  • invasion via involvement of mononuclear phagocytes
  • results in splenomegaly; typhoid nodules throughout lymphoid tissues
  • local ulceration of Peyer’s patches
  • colonization of gallbladder in carrier state
  • neutropenia in peripheral blood
53
Q

general characteristics of campylobacter enteritis (jejuni)

A

G(-)
comma
flagella

54
Q

campylobacter jejuni presentation

A

one of the most common causes of gastritis, diarrhea, and dysentery in US - mostly self limited

55
Q

campylobacter jejuni long term sequelae

A

associated with Guillain-Barre neuropathies

56
Q

transmission of campylobacter jejuni

A
  • ingestion of contaminated liquid or solid food, usually from animals (zoonotic)
  • also think about when camping
57
Q

campylobacter jejuni pathogenesis

A
  • foul-smelling stools with blood or exudate***
  • toxin/invasive lesions (colonic crypt abscesses)/adherence

-septicemia rare

58
Q

yersinia entercolitica: who do you normally see it in + transmission

A

-mostly pediatric

  • raw or undercooked pork
  • unpasteurized milk
59
Q

yersinia entercolitica pathogenesis

A
  • upper and lower GI
  • ulcerative intestinal lesions like typhoid fever, but NO systemic disease
  • microabscess and granuloma formation
  • deeply invasive and may be lethal (if extensive necrosis of GI tract)
60
Q

rapid acting toxins: staph aureus

A
  • common form of food poisoning from pre-formed toxin (enterotoxin)
  • 2-4h
  • more vomit than diarrhea
  • resolves within 24h
61
Q

rapid acting toxins: b. cereus

A
  • fried rice syndrome
  • associated with catering and buffets
  • only 2-5% of food poisoning cases
  • vomiting (1-5h) or diarrhea (8-15h), depends on strain
  • production of enterotoxins (cereulide)
62
Q

general characteristics of clostridiums

A 
G(+) 
spore forming 
anaerobes 
environmentally stable 
produce fermentation products and degradative enzymes
63
Q

what are clostridial diseases associated with?

A

elaboration of potent exotoxins and/or with invasive, destructive necrotic abscesses

64
Q

transmission of clostridial diseases

A

“gut and soil” cycle - spores

  • contamination of wounds (puncture wounds, necrosis)
  • contamination of food (not killed during cooking)
65
Q

pathologic mechanisms of clostridial diseases

A
  • action of specific exotoxins cause specific disease even in absence of direct infection
  • local growth leads to absorption and distribution of toxin
  • spores difficult to kill
  • growth favored in necrotic tissue/anaerobic environments
  • growth accompanied by necrosis induced by several tissue damaging enzymes from bacteria
66
Q

tell me EVERYTHING about C. tetani

A
  • contamination of puncture wounds/necrotic tissue
  • local growth + dissemination of toxin
  • neurotoxin tetanospasmin
  • affects presynaptic terminals of inhibitory spinal interneurons, resulting in severe convulsive contractions
  • loss of sympathetic inhibition: high HR, HTN, CV instability, smooth muscle deficits (dysphagia, resp difficulty)
67
Q

tell me all about C. perfringens

A
  • gangrene/necrotizing cellulitis
  • extracellular necrotizing enzymes (characteristic myonecrosis)
  • invasion of traumatic/surgical wounds such as amputation stumps
  • foul odor, thin and discolored exudate, wet gangrene
  • gas gangrene: gas bubbles caused fermentative rxns; hemolytic destruction of RBCs
68
Q

tell me about clostridial gastroenteritis

A
  • one of the most common US forms of food poisoning
  • improper preparation of meat, poultry w/ spores
  • abdominal cramps + watery diarrhea
  • incubation 6-24h
  • usually resolves w/i 24h b/c no necrotic tissue for organism to grow in
69
Q

tell me about C. diff

A
  • pseudomembranous colitis
  • diarrhea, clinical toxemia
  • enterotoxin (toxin A) and cytotoxin (toxin B)
  • nosocomial: associated w/ antibiotics, chemotherapy
  • almost always hospital acquired, but if community acquired, shows suppression of gastric acid
70
Q

tell me about botulism

A
  • preformed neurotoxin cleaves synaptobrevin
  • present in honey, improperly home canned foods
  • usually does not involve direct infection of victim
  • blocks release of ACh resulting in descending paralysis
  • also get CN defects (diplopia, dysphagia)
  • descending flaccid paralysis
  • usually toxin w/o bacterial colonization
  • *exception: neonates (honey) with necrotizing enterocolitis

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