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DERS (GIT) > L13- GI Infections V (inflam. diarrhea, bacteria) > Flashcards

L13- GI Infections V (inflam. diarrhea, bacteria) Flashcards

1
Q

define acute inflammatory diarrhea

  • Sxs
  • infected site
  • main cause
  • *key feature in comparison to non-inflam. diarrhea
A
  • <2 wk duration
  • blood, pus diarrhea (may progress from watery diarrhea)
  • fever
  • mainly colon
  • mainly invasive bacteria, toxin-producing bacteria
  • *mucosal invasion => inflammation (also more common in immuno-compromised)
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2
Q

list the general complication of acute inflammatory diarrhea (not specific to any bacteria)

A
  • *dehydration (main target Sx for Tx)
  • electrolyte disturbances
  • acidosis
  • malnutrition
  • dissemination (–> osteomyelitis, meningitis, pneumonia, peritonitis, septicemia)
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3
Q

Listeria: describe microbial features

A 
Gram(+)
coccobacilli (short rods)
facultative intracellular
motile (at <30C = tumbling motility)
non-spore forming
halophilic
β-hemolytic (β-hemolysin)

Grows in 1C-45C (survive refrigeration), pH 4-9.6 (survives stomach acid)

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4
Q

Listeria grows in (1) temperature range and (2) pH range- indicate the significance of each

A

1- 1C-45C, survives refrigeration

2- pH 4-9.6, survives stomach acid

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5
Q

Listeria clinical manifestations (general disorders)

A
  • febrile gastroenteritis
  • endocarditis
  • CNS infections
  • sepsis
  • perinatal infections
  • miscarriages
  • still birth
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6
Q

list the high risk groups for Listeria infections

A
  • pregnancy, newborns
  • elderly
  • transplant patients + other immuno-compromised
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7
Q

Listeria:

  • unique Gram(+) feature
  • (2) found in environment
A

1- only one with an endotoxin although it is not a true endotoxin

2- soil, water, vegetation, feces (some animals) //// contaminates food (dairy, raw meat, salads) during processing / distribution / in retail environments

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8
Q

Listeria pathogenesis:

  • entry occurs via (1) proteins, within vacuole
  • vacuole lysis occurs via (2) proteins
  • (3) follows lysis, then (4) protein initiates aggregation / polymerization
  • viral exiting occurs through (5) process
A

1- (epithelial cell binding) Internalin A/B = InlA, InlB

2- listeriolysin O (pore-forming) + phospholipase A/B (LLO + PlcA, PlcB)

3- replication
4- ActA (actin polymerization)

5- actin-based motility (–> to other cell, now in double membrane vacuole)

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9
Q

discuss mortality in relation to Listeria

A

~20%

-~25% of pregnancy cases result in death of fetus or newborn

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10
Q

describe diagnosis of Listeria

A

Direct microscopy: Gram(+) rods

Culture: 2-3 day incubation / enrichment at 4C

PCR

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11
Q

list the bacterial agents of inflammatory diarrhea

A

YES PECKSS
Y- yersina
E- *escherichia (EIEC)
S- Serratia

P- proteus
E- enterobacter
C- citrobacter
K- klebsiella
S- *shigella
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12
Q

Enterobacteriae spp.:

  • (1) important species (for enteric system)
  • (2) microbial features
A

1- Shigella, Klebsiella

2- Gram(-) rods
motile except for (1) species

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13
Q

Shigella:

  • (1) microbial features
  • (2) transmission
  • serotyping is based on (3)
  • (4) is rare effect
A

1- Gram(-) rod, non-motile, non-encapsulated

2- (low-infectious dose) fecal-oral (no animal reservoirs)

3- O-Ag (group A-D)

4- dissemination into blood

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14
Q

list the shigella spp.

A 
Group:
A- S. dysenteriae
B- S. flexneri
C- S. boydii
D- S. sonnei
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15
Q

list the main Shigellosis Sxs:

  • (1) S. sonnei
  • (2) S. flexneri
A

1- watery diarrhea (75%), vomiting (60%), mucus in stool (50%), abdominal pain (50%)

2- (more severe) mucus in stool (75%), abdominal pain (70%), bloody stool (50%)

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16
Q

describe Shigella spp. transmission

A

4 F’s: Food, Flies, Feces, Fingers

  • acid stable —> low infectious dose sufficient
  • *no animal reservoirs
17
Q

Shigella:

  • (1) at risk populations
  • (2) geographic / seasonal distribution
  • (3) prevention / control
A

1- carrier exposure: young children or those in daycare centers, nurseries + communities with poor sanitation and hygiene

2- worldwide, no seasonal incidence

3- hand washing, disposal of soiled linens

18
Q

Shigella virulence factors:

  • (1) system is important for invasiveness
  • (2) endotoxin
  • (3) exotoxin
  • (4) location of replication
  • (5) disrupts cell metabolism
A

1- type 3 secretion system
2- O Ag (LPS)
3- Shiga toxin
4- intracellular survival and multiplication
5- NAD glycohydrolase –> destroys NAD –> shuts down metabolism –> cell death

19
Q

briefly describe Shigella pathogenesis

A

1) ingestion
2) **M-cell transcytosis
3) phagosomal lysis
4) *cytoplasmic replication
5) induces cell apoptosis and release of ILs
6) actin filaments propel move from host cell to host cell

20
Q

Bacillary dysentery refers to infection by…..

A

Shigella dysenteriae type 1 (shiga bacillus) => producess Shiga Toxin

21
Q

Shiga toxin:

  • (1) type
  • (2) encoded on what part of genome
  • (3) structure
  • (4) brief pathogenesis
A

1- enterotoxic, neurotoxic, cytotoxic

2- chromosomal genes

3- one A subunit, five B subunits
4- B subunit binds surface glycoprotein and A toxin is internalized into cytoplasm

22
Q

Shiga Toxin effects:

  • (1) enterotoxic
  • (2) cytotoxic
  • (3) neurotoxic
A

1- (SI epithelium adherence) blocks absorption of electrolytes, glucose, AAs

2- B binds glycoprotein for adherence and A entry –> A domain irreversibly inhibits 60S ribosomal subunit => no protein synthesis, cell death, microvascular damage, hemorrhage

3- abdominal cramping

23
Q

Shigellosis, indicate the species associated with the following:

  • (1) MSM population (hint- most severe type)
  • (2) children <5y/o (day-care, most common type)
  • (3) rare infection
A

1- S. flexneri (MSM- men who have sex with men)

2- **S. sonnei

3- S. boydii

24
Q

describe the main possible complication of Shigella infection

A

Reactive Arthritis: can’t see, can’t pee, can’t climb a tree

  • conjunctivitis
  • urethritis
  • arthritis
25
Q

Shigella Dx:

  • (1) appearance on initial agar
  • then (2) is differentiating agat
  • (3) is unique / special agar
  • Lactose (+/-), citric acid use (+/-), H2S production (+/-)
A

1- pale/colorless on MacConkey agar
2- S-S agar, Salmonella-Shigella agar
3- EMB, eosin methylene blue agar

4- lactose(-), citric acid use(-), H2S production(-)

26
Q

list the Lactose fermenting bacteria (GI infections)

A 
CEEK:
Citrobacter
Enterobacter
*Escherichia
*Klebsiella
27
Q

list the non-lactose fermenting bacteria (GI infections) and how to differentiate them

A

ShYPS:

1) nonmotile, non-H2S producers:
- Shigella
- Yersina

2) motile, H2S producers
- proteus
- salmonella

28
Q

EIEC = (1):

  • (2) common geographic area
  • infects (3) part of GIT
  • often mistaken for (4) infection, where (5) is distinguishing feature
  • requires (large/small) inoculating dose
A 
1- enteroinvasive E. coli
2- SE Asia, S. America
3- colon
4- Shigellosis
5- absent Shiga toxin
6- small, 10 organisms
29
Q

EIEC = (1):

  • utilizes (2) genes a lot, which encode for (3)
  • (3) will cause (4) in the colon and lead to (5) overall
A 
1- enteroinvasive E. coli
2- plasmid associated genes
3- outer protein for invasion
4- tissue destruction, inflammation, necrosis, ulceration
5- blood, mucus in stool
30
Q

briefly describe EIEC pathogenesis

A

(enteroinvasive E. coli)

1) ingestion
2) colon invasion
3) phagosomal lysis
4) cytoplasmic replication
5) spreads host cell to host cell
6) destroys colonic cells

31
Q

EAEC = (1):

  • (2) is the key / unique feature with (3) as its main function
  • (4) is important to note with pathogenesis with this bacteria
A

1- enteroaggregative E. coli

2- aggregative adherence fimbriae (AAF)

3- mediates attachement to intestinal mucosa –> triggers inflammatory response

4- non-invasive

32
Q

briefly describe EAEC pathogenesis

A

(enteroaggregative E. coli- pathogenesis not fully understood)

1) AAF binding to MUC1 on colon epithelium
2) enhanced mucus production –> thick mucus biofilm
3) ?cytotoxin production? –> intestinal cell damage

33
Q

STEC = (1), (2) are alternate names:

  • important produces (3)
  • (4) are reservoirs
A

1- shiga toxin producing E. coli
2- EHEC, VTEC
3- Shigella Like Toxin (SLT): Stx-1, Stx-2
4- cattle, sheep

34
Q

list the conditions STEC may cause

A

1) hemorrhagic colitis
2) hemolytic uremic syndrome
3) thrombotic thrombocytopenia purpura

35
Q

STEC life threatening conditions, hemorrhagic colitis:

  • (1) days after ingestion
  • (2) affected population
  • (3) Sxs
A

1- 3 days post-ingestion
2- adults/elderly mainly
3- bloody diarrhea (begins as watery), abdominal pain

36
Q

STEC life threatening conditions, HUS:

  • (1) days after diarrhea
  • (2) affected population
  • (3) Sxs
A

1- 5-13 days post-diarrhea
2- children <5y/o (90% cases)
3- microangiopathic hemolytic anemia, thrombocytopenia, acute renal failure

37
Q

STEC life threatening conditions, TTP:

  • (1) affected population
  • (2) Sxs
A

1- elderly (mainly)

2- HUS, fever, neurological involvement

38
Q

describe STEC pathogenesis

A

1) ingestion
2) attachment (similar to EPEC)
3) production of phage encoded cytotoxin: Stx-1/2 (block protein synthesis)
4) hemorrhagic colitis
5) toxin enters circulation binding to glomerular epithelium
6) hemolytic anemia, renal damage => renal failure

39
Q

E. coli Dx, specifically STEC:

  • (1) appearance on main agar
  • list the other 4 steps (2), (3), (4), (5)
A

1- red-pink colonies on MacConkey’s agar (all E. coli spp.)
2- sorbitol MacConkey’s agar: no fermentation STEC => colorless
3- ELISA on toxin bound to AB
4- DNA probe to detect toxin genes
5- schistocytes for STEC

DERS (GIT) (21 decks)

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