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

Bacteria III: Enteric Pathogens Flashcards

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
Q

EHEC

A

severe bloody diarrhea

  • colitis
  • consumption of hamburger, dairy, fruit juice with verotoxin producing (shiga toxin) strain (O157:H7)
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26
Q

EPEC

A

enteropathogenic

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27
Q

EIEC

A

enteroinvasive

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28
Q

EAEC

A

enteroaggregative

-pediatric diarrhea in impoverished nations

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29
Q

EHEC source

A

cattle and beef products including hamburger and unpasterized milk

30
Q

O157:H7 mechanism of disease

A
  • small infectious dose
  • bacteria adhere to cell membrane and colonize large intestine
  • produce shigatoxin which damage endothelial cells-> inhibits mRNA translation, protein synthesis
31
Q

O157:H7 disease progression

A
  • 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
Q

disease presentation O157:H7

A

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
Q

other important enteropathic pathogens

A

O26, O45, O103, O111, O121, O145

34
Q

Shigella characteristics

A

G-, non-motile, non-coliform

35
Q

shigella pathogenesis

A

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
Q

Cholera characteristics

A

G-, comma-shaped, alkali tolerant

37
Q

cholera transmission

A

direct fecal-oral transmission asymptomatic carriers

38
Q

cholera pathogenesis

A
  • no invasive lesions due to enterotoxin-> inducing secretion of isotonic fluid
  • deaths-> dehydration and hypovolemic shock
39
Q

V. parahaemolyticus V. vulnificus

A

halophilic

40
Q

cholera toxin pathogenesis

A

subunit A binds with ADP-ribosylation factors-> activate GTP-activated adenylate cyclase resulting in cAMP formation-> stimulates secretion of chloride and bicarbonate

41
Q

Salmonella characteristics

A

G-, non-coliform, H2S production

  • S. enteritidis, S. typhimurium, S. paratyphi, S. cholerae-suis
  • S, typhi
42
Q

Salmonella diseases

A

Typhoid
Enteric fever
salmonella food poisoning

43
Q

Salmonella food poisoning

A

vomiting and diarrhea

  • S. enteritidis and S. typhimurium
  • eggs, undercooked chicken, meat, contaminated water, turtles, reptiles, cantaloupes, mangoes
44
Q

Salmonella food poisoning characteristics

A
  • superficial lesions of colon

- self-limiting (except in IC)

45
Q

Salmonella food poisoning pathogenesis

A
  • invasive disease-> invade mucosal cells and cause mucosal ulceration
  • do not produce enterotoxins
  • multiply within neutrophils and macrophages
  • G- sepsis
46
Q

what does salmonella cause in children with sickle cell anemia?

A

osteomyelitis and sepsis

47
Q

Paratyphoid fever

A

S. typhinurium, S. paratyphi, S. cholera-suis

  • fever, bacteremia, local lesions
  • associated with sickle disease, schistosomiasis
48
Q

salmonella typhi

A

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
Q

systemic involvement in S. typhi

A
  • 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
Q

C. jejuni

A

G-, comma-shaped, flagellated

-C. fetus: usually from undercooked beef

51
Q

C. jejuni most common cause of ______

A

gastritis, diarrhea, and dysentery in US, associated Guillain-Barre neuropathies
-major severe disease: including sepsis, in debilitated or IC patients

52
Q

C. jejuni transmission

A

ingestion of contaminated liquid or solid food

  • water sources
  • food-borne
  • improperly cooked chicken and beef
53
Q

C. jejuni pathogenesis

A

foul-smelling stools with blood or exudate

-toxin/invasive lesions-> colonic crypt abscesses/adherence

54
Q

Yersinia Entercolitica

A 
pediatric
-Upper/lower GI
ulcerative intestinal lesions like typhoid 
microabscess and granuloma formation 
deeply invasive and may be lethal
55
Q

How fast does the staph. aureus toxin act?

A

2-4hours
more vomiting than diarrhea
resolves 24 hours

56
Q

How fast does the bacillus cereus toxin act?

A
  • Fried Rice syndrome (catering and buffets)
  • 2-5% food poisoning cases
  • vomiting (1-5 hours) or diarrhea (8-15)
57
Q

Clostridial characteristics

A

G+, sporulating anaerobes

  • highly stable in environment
  • produce fermentation products and degradative enzymes
  • elaboration of potent exotoxins, invasive destructive necrotic abscesses
58
Q

Clostridial disease

A

gut to soil transmission

  • necrotic tissue or puncture wounds
  • contaminated food
59
Q

clostridial pathogenesis

A

local growth-> absorption and distribution of exotoxin

-growth favored in necrotic tissue (b/c of damaging enzymes), anaerobic organisms

60
Q

Clostridial disease: tetanus

A

contamination of wounds

-neurotoxin: tetanospasmin

61
Q

Clostridial disease: tetanus toxin mechanism

A

affects presynaptic terminals of inhibitory spinal interneurons resulting in severe convulsive contractions

62
Q

what does the loss of sympathetic inhibition with tetanus toxin cause

A 
accelerated HR
hypertension
cardiovascular instability
smooth muscle deficits
dysphagia
respiratory difficulty
63
Q

Gangrene/necrotizing cellulitis Clostridial bacteria?

A

C. perfringens

64
Q

Gas gangrene from C. perfringins is because of?

A

gas bubbles caused by fermentation reactions, hemolytic destruction of RBC’s

65
Q

what are some of the extracellular necrotizing enzymes Clostridial disease have?

A

phospholipases, proteinases, poisons, characteristics myonecrosis

66
Q

what do Clostridial diseases usually invade?

A

invasion of traumatic or surgical wounds such as amputations stumps, foul odor, thin and discolored exudates-> wet gangrene

67
Q

Clostridial disease: gastroenteritis

A

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
Q

C. difficile

A

pseudomembranous colitis

  • enterotoxin A and cytotoxin B
  • pseudomembrane formation and severe colitis
  • disruption of bowel NF (antibiotics)
69
Q

Botulism (C. botulinum)

A

-performed neurotoxin: cleaves synaptobrevin
-in honey
-blocks release of acetylcholine resulting in descending form of paralysis
-cranial nerve defects
death-> respiratory muscle paralysis

70
Q

what is the exception for C. botulinum colonization?

A

usually toxin with bacterial colonization

EXCEPT: neonates (honey) with necrotizing enterocolitis

Pathology: Infectious disease section (11 decks)

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