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DERS (GIT) > L9- GI Infections III (non-inflam. diarrhea, bacteria) > Flashcards

L9- GI Infections III (non-inflam. diarrhea, bacteria) Flashcards

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1
Q

define acute diarrhea and the types

A
  • <2 wk duration
  • inflammatory OR non-inflammatory types

Defined as one or more of following:

  • 3 or more loose stools per 24 hrs
  • more frequent stools than what is normal for person
  • adults on Western diet with stool weight >200 g/day
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2
Q

most cases of acute diarrhea are caused by…..

A

infections, 90%

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3
Q

what are the five high-risk American groups for developing acute diarrhea

A

1) travelers (40% of tourist to endemic regions)
2) contaminated food consumers
3) immunodeficient individuals (HIV)
4) daycare attendees and family members
5) institutionalized persons

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4
Q

Non-Inflammatory diarrhea (acute):

  • (1) stool description
  • (2) GIT wall changes
  • (3) other Sxs
  • (4) causes
  • (5) typical affected segment
  • (6) fecal leukocytes present?
A

1- watery, non-bloody (larger volume)
2- mucosal hypersecretion + dec absorption w/o mucosal destruction
3- n/v, abdominal cramping + no fever or systemic symptoms (abrupt onset of diarrhea)
4- viruses, non-invasive bacteria
5- SI
6- no

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5
Q

Inflammatory diarrhea (acute):

  • (1) stool description
  • (2) GIT wall changes
  • (3) causes
  • (4) other Sxs
  • (5) typical affected segments
  • (6) fecal leukocytes present
A

1- bloody diarrhea with pus (smaller stool)
2- mucosal invasion w/ inflammation
3- invasive bacteria, toxin-producing bacteria
4- fever, abdominal pain, tenesmus
5- colon
6- yes

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6
Q

Determine is the following are associated with inflammatory of non-inflammatory acute diarrhea:

  • (1) mostly SI
  • (2) mostly colon
  • (3) watery diarrhea (non-bloody)
  • (4) blood/pus diarrhea
  • (5) fever
  • (6) invasive bacteria cause
  • (7) disrupted mucosal integrity –> tissue destruction
  • (8) fecal leukocytes present
  • (9) large stool volume
A 
1- NI
2- Inflam
3- NI
4- Inflam
5- Inflam (no fever in NI)
6- Inflam (non-invasive bacteria for NI)
7- Inflam (no disruption in NI)
8- Inflam (not in NI)
9- NI (small stools in Inflam)
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7
Q

Eschericha Coli:

  • (1) location / found in
  • (2) bacterial family
  • (3) classic microbial features
  • (4) traditional agar
A

1- normal gut flora
2- enterbacteriaceae

3- Gram(-) rod, facultative anaerobes, catalase(+), oxidase(-), rapid lactose fermenter, motile (multiple flagella)
4- MacConkey agar (pink colonies)

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8
Q

list the important (diarrheal causing) Enterobacteriaceae spp.

A
  • *Escherichia
  • *Shigella
  • *Salmonella
  • *Yersinia

Klebsiella
Proteus

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9
Q

list the important antigenic structures of E. coli

A
  • O Ag, lipopolysaccharide O side chains
  • H Ag, flagella
  • K Ag, capsule
  • cell envelope (cytoplasmic membrane, peptidoglycan, outer membrane)
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10
Q

Associated the correct E. coli Ag with the following descriptions:

(1) subunits of flagella
(2) most external part of cell wall
(3) most external Ag

A

1- H Ag

2- O Ag, lipopolysaccharide consisting of repeating units

3- K Ag (capsule), only in encapsulate species: polysaccharides in some species, proteins in others

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11
Q

E. coli key virulence factors:

  • (1) for adhesion
  • (2) toxins
A

1- pili to attach to mucosa (colonization factor)

2- Exotoxin: heat-labile (LT) and or heat-stable (ST) toxins

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12
Q

ETEC = (1):

  • (2) transmission, include dose
  • primary cause of (3)
A

1- enterotoxigenic E. coli

2- contaminated food, water: 100 million to 10 billions cells required

3- traveler’s diarrhea (up to 40% of travelers in certain regions)

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13
Q

describe ETEC pathogenesis

A

(enterotoxigenic E. coli)

1) ingestion of food w/ bacteria
2) reaches SI
3) attachment via pili and fimbriae (CFA- colonization factor Ags) => colonization
4) produces enterotoxins: LT, ST (heat- labile, stable toxins)

(Note- enterotoxin production inc electrolyte secretion)

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14
Q

Enterotoxins (found in ETEC) are found on bacterial (DNA/prophage/plasmid) and has (2) general structure.

Describe the size and action of both types: (3) LT, (4) ST.

A

1- plasmid encodes (enterotoxins)

2- 1 A subunit, 5 B subunits

3- Heat-labile, LT: MW 80,000, similar to cholera –> activates adenylate cyclase (inc cAMP)

4- Heat-stable, ST: MW 1500-4000, activates guanylate cyclase (inc cGMP)

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15
Q

ETEC toxin MOA:

  • (A/B) subunit binds (2)
  • (A/B) subunit enters cell to activate (4), increasing (5) levels
  • (6) is the ultimate cell response leading to (7) symptom
A 
1- B subunit binds...(2)
2- GM1 receptor
3- A subunit enters
4- A activates adenylate/guanylate cyclase
5- inc cAMP/cGMP
6- H20 / electrolyte efflux (Na, Cl)
7- watery diarrhea
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16
Q

EPEC = (1), mainly causes (2)

A

1- enteropathogenic E. coli

2- infantile diarrhea (childhood diarrhea) –> 50% mortality in developing countries

17
Q

EPEC pathogenesis (Note what is importantly absent)

A

1) pathogen ingestion
2) colonization / adherence to SI via EPEC adherence factor plasmid encoding BFP (bundle forming pili)
3) micro-villi effacement (attachment-effacing lesion)
4) loss of villous SA => watery diarrhea

Note- no LT/ST toxins, or CFA (pili) as in ETEC

18
Q

most of the fluid absorbed in the GIT occurs in…..

A

small intestines

19
Q

Vibrio Cholerae:

  • (1) family
  • (2) shape and size
  • (3) important microbial features
A

1- vibronaceae
2- single curved rods, 2-4 µm long

3- Gram(-) bacillus, motile (single flagella), non-spore forming, facultative anaerobes, oxidase(+)

20
Q

Vibrio Cholerae:

  • (1) are important Ags
  • (2) fermenters
  • (3) sensitive
  • (4) tolerant
A

1- O / H (lipopolysaccharide, flagella): serogroup O1, O139

2- sucrose, mannose (NOT arabinose)

3- acid sensitive (often dies in stomach, therefore antacids inc risk)

4- halotolerant (high salinity)

21
Q

Tx for _____ inc risk for cholera infections (explain)

A
  • people on antacids

- V. cholera is acid sensitive

22
Q

V. cholera pathogenesis

A

1) ingestion (10^8-10^9 bacteria) via solid/liquid
2) colonization in SI
3) cholera toxin production
4) cholera toxin action is similar to LT (ETEC) –>
5) loss of H2O, NaCl, HCO3- =>
6) profuse watery diarrhea

23
Q

Cholera toxin is encoded on (DNA/bacteriophage/plasmid) and functions to activate (2) in order to increase (3) and cause (4)

A

1- phage (AB toxin)
2- adenylate cyclase (like LT toxin)
3- inc cAMP
4- water / electrolyte efflux => watery diarrhea

24
Q

V. cholera Sxs

A
  • dehydration: isotonic fluid loss
  • hypokalemia: K+ ion loss
  • metabolic acidosis: HCO3- loss
  • hypovolemic shock, acidosis, muscle cramps
  • n/v/d
25
Q

describe diarrhea caused by V. cholera

A

Rice Water Stool

  • 20-30L per day
  • white lumps contain bacteria and toxin
26
Q

V. cholera Dx:

  • (1) is necessary from patient history
  • (2) screening is useful
  • (3) agar is required with (4) as a differentiating agent
A

1- clinical presentation including cholera = mucoid blebs in stool

2- stool sample screening: oxidase activity

3- TCBS / thiosulphate-citrate-bile salt-sucrose agar

4- sucrose(+), otherwise a different Vibrio spp.

27
Q

describe cholera vaccine (type of vaccine and target population)

A

Vaxchora

  • live-attenuated
  • for travelers
  • not for people <18y/o
28
Q

Clostridium perfringens: microbial features (include normal location)

A

Gram(+), large, anerobic, non-motile, bacillus, *spore-forming

apart of intestinal microflora, ubiquitous in nature

29
Q

list the diseases caused by C. perfringens

A
  • myonecrosis (gas gangrene)

- Type A* food-bourne infection = diarrhea

30
Q

describe C. perfringens pathogenesis

A

1) ingestion via food, 10^6-10^7 bacteria
2) colonization in SI
3) sporulation in intestines
4) LT toxin production (CPE- C. perfringens enterotoxin)
5) cytotoxicity = pore formation in membrane –>
6) H2O, electrolyte efflux
7) watery diarrhea

31
Q

describe C. perfringens toxin(s)

A

CPE: clostrdium perfringens enterotoxin is similar to Heat-labile enterotoxin in ETEC (LT)

=> pore formation rather than inc cAMP

-*probably encoded on plasmid

32
Q

C. perfringens:

  • (1) incubation period
  • (2) Sxs
  • (3) Dx
A

1- 8-24hr

2- watery diarrhea (non-inflam.), severe abdominal pain [no fever, n/v]

3- stool / food testing for bacteria / toxin via culture or direct enterotoxin testing (present in feces)

33
Q

Bacillus cereus microbial features (include location)

A

Gram(+) bacillus (0.7µm x 3-10µm long)

  • arranged in chains
  • aerobic
  • spore formation
  • enteric toxin and enterotoxin
  • found in air, soil, water, dust (food)

Note- only need to ingest bacteria with toxin or just toxin

34
Q

Bacillus cereous causes the following… (explain by Sxs, incubation period, duration, associated foods)

A

1) Diarrheal (similar to C. perfringens)
- diarrhea, abdominal pain
- incubation 8-16hrs, lasts 12-24hrs
- meats, veggies, sauces, pasta, desserts, dairy

2) Emetic (similar to S. aureus)
- vomiting
- incubation 2-3hrs, lasts 6-24hrs
- rice and pulses

35
Q

Diarrheal Bacillus cereous pathogenesis

A

1) ingestion of pathogen
2) colonization in SI
3) LT enterotoxin production
4) activates adenylate cyclase –> inc cAMP –> inc water/electrolyte efflux => diarrhea

36
Q

Emetic Baccillus cereous pathogenesis

A

ingestion of pathogen with toxin: ST neurotoxin (peptide)

37
Q

Assign to emetic or diarrheal Bacillus cereous:

  • (1) short incubation
  • (2) enterotoxin
  • (3) ST toxin
  • (4) LT toxin
A

1- emetic, 4hrs (diarrheal 8-16hrs)
2- diarrheal (emetic has emetic toxin)
3- emetic (neurotoxin)
4- diarrheal

DERS (GIT) (21 decks)

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