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Pathology: Infectious disease section > Bacteria III: Enteric Pathogens > Flashcards

Bacteria III: Enteric Pathogens Flashcards

(70 cards)

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1
Q

what are the most common causes of enteric infections?

A

salmonella and campylobacter

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2
Q

most common contaminants but not serious disease?

A

clostridium perfringins and staph. aureus

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3
Q

less common but fatal diseases?

A

Listeria and E.coli O157:H7

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4
Q

E.coli

A

Enterotoxic, enteroinvasive

0157:H7, other STEC

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5
Q

enteropathic bacteria

A

cholera, E.coli, shigella, Salmonella, Campylobacter, Yersinia

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6
Q

Salmonella

A

S. enteritidis, S. typhinurium, S. typhi

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7
Q

enteropathic bacteria with toxins

A

Staph. aureus, botulism, clostridium perfringens

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8
Q

Enteric Pathogens

A

Bacteria
Viruses: Norwalk, enteroviruses, Polio
Parasites: Giardia, Amoebae, Ascaris, Cryptosporiosis

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9
Q

what is the pathogenesis of enteropathic bacteria?

A
  1. ) ingestion of enterotoxins: absorption of pre-formed toxins, short incubation
  2. ) infection by colonizing toxigenic organisms: hypersecretion reaction from bacterial adherence and toxin secretion, incub. 1-3 days
  3. ) direct invasion of the gut wall: incubation time days-weeks
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10
Q

level of tissue involvement

A

toxin only-> superficial colonization plus toxin-> superficial colonization + inflammation-> mucosal invasion-> mucosal necrosis-> submucosal invasion-> systemic spread

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11
Q

what are important virulence factors from enteropathic bacteria?

A
  1. ) adherence to mucosal cells: Pili, flagella
  2. ) Production of enterotoxins
  3. ) Capacity to invade: intracellular proliferation, cell lysis, and cell-to-cell spread, invasion and cytolysis-> dysentery
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12
Q

Vibrio cholerae enterotoxin

A

prototype secretagogue toxin-

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13
Q

Shigella enterotoxin

A

shiga toxin (cytotoxin)

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14
Q

Stap. enterotoxin

A

T cell super-antigen

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15
Q

what are predisposing factors to enteropathic bacteria?

A 
fecal contamination
IC
antispasmodic drugs
antacids
mucosal disease
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16
Q

what is the clinical presentation to enteropathic bacteria diseases?

A

absorbed toxin-> local (staph) versus systemic (botulism)

secretory diarrhea (cholera)

dysentery (shigella)

systemic illness (typhoid fever)

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17
Q

diarrhea

A

excess fluid: hypersecretion (cholera) or osmotic load (lactose intolerance)

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18
Q

dysentery

A

mucosal invasion: inflammation

loose stool+blood+ leukocytes=dysentery

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19
Q

level o tissus destruction with diarrhea

A

toxin only-> superficial colonization + toxin-> superficial colonization + inflammation

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20
Q

level of tissue destruction with dysentery

A

(diarrhea ones)+ mucosal invasion-> mucosal necrosis-> submucosal invasion-> systemic spread

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21
Q

E. coli characteristics

A

G-, rod, green “sheet” on EMB agar

-coliform (lactose fermenting)

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22
Q

E. coli characteristics of disease

A
  • watery diarrhea, cramping pain, fever, malaise
  • invasive or cytolytic-> dysentery
  • verotoxin (shiga)-> hemolytic uremic syndrome
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23
Q

pathological mechanism of E. coli

A 
invasive disease
toxigenic disease (traveler's diarrhea)
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24
Q

ETEC

A

traveler’s diarrhea
-consumption contamination food
enterotoxin-producing strain

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25
EHEC
severe bloody diarrhea - colitis - consumption of hamburger, dairy, fruit juice with verotoxin producing (shiga toxin) strain (O157:H7)
26
EPEC
enteropathogenic
27
EIEC
enteroinvasive
28
EAEC
enteroaggregative | -pediatric diarrhea in impoverished nations
29
EHEC source
cattle and beef products including hamburger and unpasterized milk
30
O157:H7 mechanism of disease
- small infectious dose - bacteria adhere to cell membrane and colonize large intestine - produce shigatoxin which damage endothelial cells-> inhibits mRNA translation, protein synthesis
31
O157:H7 disease progression
- onset 3-4 days after ingestion of organism - severe abdominal cramping, watery diarrhea progressing to bloody after 3-4 days - occasionally vomiting-> fever low grade or absent - duration average 8 days
32
disease presentation O157:H7
asymptomatic -mild/moderate illness (non-bloody, watery diarrhea, abdominal pain, fever usually absent) -dysentery -hemolytic uremic syndrome children, elderly, acute renal failure (obstruction of glomeruli by microthrombi) -thrombic thrombocytopenic purpura (TTP)
33
other important enteropathic pathogens
O26, O45, O103, O111, O121, O145
34
Shigella characteristics
G-, non-motile, non-coliform
35
shigella pathogenesis
fecal-oral, high-virulent - invasive lesions of colonic mucosa-> spreads to lymph nodes-> DO NOT CAUSE bacteremia to distant organs - exotoxin causes mucosal necrosis-> fibrinosuppurative exudate forms pseudomembrane as in diphtheria
36
Cholera characteristics
G-, comma-shaped, alkali tolerant
37
cholera transmission
direct fecal-oral transmission asymptomatic carriers
38
cholera pathogenesis
- no invasive lesions due to enterotoxin-> inducing secretion of isotonic fluid - deaths-> dehydration and hypovolemic shock
39
V. parahaemolyticus V. vulnificus
halophilic
40
cholera toxin pathogenesis
subunit A binds with ADP-ribosylation factors-> activate GTP-activated adenylate cyclase resulting in cAMP formation-> stimulates secretion of chloride and bicarbonate
41
Salmonella characteristics
G-, non-coliform, H2S production - S. enteritidis, S. typhimurium, S. paratyphi, S. cholerae-suis - S, typhi
42
Salmonella diseases
Typhoid Enteric fever salmonella food poisoning
43
Salmonella food poisoning
vomiting and diarrhea - S. enteritidis and S. typhimurium - eggs, undercooked chicken, meat, contaminated water, turtles, reptiles, cantaloupes, mangoes
44
Salmonella food poisoning characteristics
- superficial lesions of colon | - self-limiting (except in IC)
45
Salmonella food poisoning pathogenesis
- invasive disease-> invade mucosal cells and cause mucosal ulceration - do not produce enterotoxins - multiply within neutrophils and macrophages - G- sepsis
46
what does salmonella cause in children with sickle cell anemia?
osteomyelitis and sepsis
47
Paratyphoid fever
S. typhinurium, S. paratyphi, S. cholera-suis - fever, bacteremia, local lesions - associated with sickle disease, schistosomiasis
48
salmonella typhi
typhoid fever - fecal pathogen - fever with "rose spots" on lower anterior chest and abdomen, hepatosplenomegaly - diarrhea, uncommon, mild-vomiting - incubation period: 10-20 periods
49
systemic involvement in S. typhi
- fever, rash - invasion via involvement of mononuclear phagocytes - splenomegaly; typhoid nodules throughout immune tissue - typhoid nodules in liver - local ulceration of Peyer's patches - colonization of gallbladder in carrier state - neutropenia in peripheral blood
50
C. jejuni
G-, comma-shaped, flagellated | -C. fetus: usually from undercooked beef
51
C. jejuni most common cause of ______
gastritis, diarrhea, and dysentery in US, associated Guillain-Barre neuropathies -major severe disease: including sepsis, in debilitated or IC patients
52
C. jejuni transmission
ingestion of contaminated liquid or solid food - water sources - food-borne - improperly cooked chicken and beef
53
C. jejuni pathogenesis
foul-smelling stools with blood or exudate | -toxin/invasive lesions-> colonic crypt abscesses/adherence
54
Yersinia Entercolitica
``` pediatric -Upper/lower GI ulcerative intestinal lesions like typhoid microabscess and granuloma formation deeply invasive and may be lethal ```
55
How fast does the staph. aureus toxin act?
2-4hours more vomiting than diarrhea resolves 24 hours
56
How fast does the bacillus cereus toxin act?
- Fried Rice syndrome (catering and buffets) - 2-5% food poisoning cases - vomiting (1-5 hours) or diarrhea (8-15)
57
Clostridial characteristics
G+, sporulating anaerobes - highly stable in environment - produce fermentation products and degradative enzymes - elaboration of potent exotoxins, invasive destructive necrotic abscesses
58
Clostridial disease
gut to soil transmission - necrotic tissue or puncture wounds - contaminated food
59
clostridial pathogenesis
local growth-> absorption and distribution of exotoxin | -growth favored in necrotic tissue (b/c of damaging enzymes), anaerobic organisms
60
Clostridial disease: tetanus
contamination of wounds | -neurotoxin: tetanospasmin
61
Clostridial disease: tetanus toxin mechanism
affects presynaptic terminals of inhibitory spinal interneurons resulting in severe convulsive contractions
62
what does the loss of sympathetic inhibition with tetanus toxin cause
``` accelerated HR hypertension cardiovascular instability smooth muscle deficits dysphagia respiratory difficulty ```
63
Gangrene/necrotizing cellulitis Clostridial bacteria?
C. perfringens
64
Gas gangrene from C. perfringins is because of?
gas bubbles caused by fermentation reactions, hemolytic destruction of RBC's
65
what are some of the extracellular necrotizing enzymes Clostridial disease have?
phospholipases, proteinases, poisons, characteristics myonecrosis
66
what do Clostridial diseases usually invade?
invasion of traumatic or surgical wounds such as amputations stumps, foul odor, thin and discolored exudates-> wet gangrene
67
Clostridial disease: gastroenteritis
most common in US -improper preparation of meat and poultry -cooled foods without re-heating (spores survive high heat and sporulate when cooled) -abdominal cramps, watery diarrhea (incub 6-24 hrs) resolves within 24 hours
68
C. difficile
pseudomembranous colitis - enterotoxin A and cytotoxin B - pseudomembrane formation and severe colitis - disruption of bowel NF (antibiotics)
69
Botulism (C. botulinum)
-performed neurotoxin: cleaves synaptobrevin -in honey -blocks release of acetylcholine resulting in descending form of paralysis -cranial nerve defects death-> respiratory muscle paralysis
70
what is the exception for C. botulinum colonization?
usually toxin with bacterial colonization | EXCEPT: neonates (honey) with necrotizing enterocolitis

Pathology: Infectious disease section (11 decks)

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