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IM INFECTIOUS > ACUTE INFECTIOUS DISEASE > Flashcards

ACUTE INFECTIOUS DISEASE Flashcards

1
Q
  • passage of abnormally liquid or unformed stools at an increased frequency
  • Stool weight >200 g/day
A

DIARRHEA

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2
Q

TWO COMMON CONDITIONS, USUALLY ASSOCIATED

WITH THE PASSAGE OF STOOL TOTALING <200 G/D

A

|. Pseudodiarrhea

2. Fecal Incontinence

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3
Q
  • frequent passage of small volumes of |
  • often associated with rectal urgency, tenesmus, or a feeling of incomplete evacuation
  • accompanies IBS or proctitis
A

PSEUDODIARRHEA

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4
Q
  • involuntary discharge of rectal contents

- most often caused by neuromuscular disorders or structural anorectal problems

A

FECAL INCONTINENCE

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5
Q

DURATION OF DIARRHEA

A
  • acute if <2 weeks
  • persistent if 2-4 weeks
  • chronic if >4 weeks in duration.
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6
Q
  • > 90% of cases of acute diarrhea are caused by infectious agents vomiting, fever, and abdominal pain.
  • 10% are caused by medications, toxic ingestions, ischemia, food indiscretions, and other conditions.
A

sACUTE DIARRHEA

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7
Q

PATHOGENIC MECHANISMS OF ACUTE DIARRHEA

A
  • INOCULUM SIZE
  • ADHERENCE
  • TOXIN PRODUCTION
  • INVASION
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8
Q

INOCULUM SIZE: 10-100 bacteria or cysts

A

Shigella, enterohemorrhagic Escherichia coli, Giardia lamblia, or Entamoeba

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9
Q

INOCULUM SIZE

105-108

A

Vibrio organism

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10
Q

INOCULUM SIZE:

The infective dose varies widely, depending on the species, host and food vehicle

A

Salmonella

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11
Q

ADHERENCE

specific surface adhesins, including the toxin-coregulated pilus

A

V. cholerae

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12
Q

ADHERENCE

produces an adherence protein called colonization factor antigen

A

Enterotoxigenic E. coli

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13
Q

ADHERENCE

produce virulence determinants

A

Enteropathogenic/Enterohemorrhagic E. coli

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14
Q

TOXIN PRODUCTION

cause watery diarrhea by acting directly on secretory mechanisms in the intestinal mucosa.

A

Enterotoxin

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15
Q

TOXIN PRODUCTION

cause destruction of mucosal cells and associated inflammatory diarrhea

A

Cytotoxins

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16
Q

TOXIN PRODUCTION

which act directly on the central or peripheral nervous system

A

Neurotoxins

17
Q
  • prototypical enterotoxin

- heterodimeric protein composed of one A and five B subunits

A

Cholera toxin

18
Q

Cholera toxin contains the enzymatic activity of the toxin

A

A subunit

19
Q

Cholera toxin binds holotoxin to the enterocyte surface receptor, the ganglioside GMI, increase in cAMP

A

B subunit pentamer

20
Q

similar to cholera toxin and causes secretory diarrhea by the same mechanism.

A

heat-labile enterotoxin (LT)

21
Q

one form of which causes diarrhea by activation of guanylate cyclase and elevation of intracellular cGMP

A

heat-stable enterotoxin (ST)

22
Q
  • destroy intestinal mucosal cells and produce the syndrome of dysentery
  • Shigella dysenteriae type |, Vibrio parahaemolyticus,
    and Clostridium difficile.
A

BACTERIAL CYTOTOXINS

23
Q

produce potent cytotoxins and have been associated with outbreaks of hemorrhagic colitis and hemolytic-uremic syndrome

A

S. dysenteriae type I and Shiga toxin-producing strains of E. coli

24
Q
  • usually produced by bacteria outside the host and therefore cause symptoms soon after ingestion
  • which act on the central nervous system to produce vomiting.
  • staphylococcal and Bacillus cereus toxins
A

Neurotoxins

25
Q

Bacteria cause Neurotoxins

A
  • staphylococcal

- Bacillus cereus toxins

26
Q

INVASION

invasion of mucosal epithelial cells, intraepithelial multiplication, and subsequent spread to adjacent cells

A

Shigella and enteroinvasive E. coli

27
Q

INVASION
causes inflammatory diarrhea by invasion of the bowel mucosa, but generally is not associated with the destruction of enterocytes or the full clinical syndrome of dysentery.

A

Salmonella

28
Q

INVASION
can penetrate intact intestinal mucosa, multiply intracellularly in Peyer’s patches and intestinal lymph nodes, and then disseminate through the bloodstream to cause ENTERIC FEVER

A
  • Salmonella Typhi

- Yersinia enterocolitica

29
Q

asyndrome characterized by fever, headache, abdominal
pain, splenomegaly, and leukopenia, relative bradycardia
(faget’s sign).

A

ENTERIC FEVER

30
Q

HOST DEFENSES

A
  • Intestinal Microbiota
  • Gastric Acid
  • Intestinal Motility
  • Intestinal Mucin
  • Immunity
  • Genetic Determinants
31
Q
  • act as an important host defense mechanism, preventing colonization by potential enteric pathogens.
  • Persons with fewer intestinal bacteria: infants or patients receiving antibiotics
A

INTESTINAL MICROBIOTA

32
Q
  • Alterations in gastric pH due to Gastric surgery have increased frequency to Salmonella, G. lamblia, and a variety of helminths
  • Antacids, proton pump inhibitors, or H2 blockers
  • Rotavirus- a microorganisms that can survive the extreme acidity of the gastric environment and is highly stable to acidity.
A

GASTRIC ACID

33
Q
  • Impaired intestinal motility the frequency of bacterial overgrowth and infection of the small bowel with enteric pathogens is increased.
  • Opiates
  • Antimotility drugs
  • Anatomic Abnormalities
  • Hypomotility states
A

INTESTINAL MOTILITY

34
Q
  • A complex layer of mucus, produced by specialized secretory cells
  • Comprises glycoproteins and a range of antimicrobial molecules and secreted immunoglobulins directed against specific microbial antigens
  • pathogens can penetrate the mucus layer by secreting enzymes to degrade the mucus or through flagella-mediated motility.
  • Shigella, secrete toxins that can diffuse through the mucus layer and disrupt the underlying epithelium.
A

INTESTINAL MUCIN

35
Q

systemic IgG and IgM as well as secretory IgA.

A

Humoral immunity

36
Q

may be the first line of defense against many gastrointestinal pathogens.

A

Mucosal immune system

37
Q

show increased susceptibility to disease due to V. cholerae, Shigella, E. coliO\57, and norovirus.

A

blood group O

IM INFECTIOUS (13 decks)

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