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

Question 1

define acute inflammatory diarrhea

• Sxs
• infected site
• main cause
• *key feature in comparison to non-inflam. diarrhea

Answer 1

• <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)

Question 2

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

Answer 2

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

Question 3

Listeria: describe microbial features

Answer 3

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)

Question 4

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

Answer 4

1- 1C-45C, survives refrigeration

2- pH 4-9.6, survives stomach acid

Question 5

Listeria clinical manifestations (general disorders)

Answer 5

• febrile gastroenteritis
• endocarditis
• CNS infections
• sepsis
• perinatal infections
• miscarriages
• still birth

Question 6

list the high risk groups for Listeria infections

Answer 6

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

Question 7

Listeria:

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

Answer 7

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

Question 8

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

Answer 8

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)

Question 9

discuss mortality in relation to Listeria

Answer 9

~20%

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

Question 10

describe diagnosis of Listeria

Answer 10

Direct microscopy: Gram(+) rods

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

PCR

Question 11

list the bacterial agents of inflammatory diarrhea

Answer 11

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

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

Question 12

Enterobacteriae spp.:

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

Answer 12

1- Shigella, Klebsiella

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

Question 13

Shigella:

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

Answer 13

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

Question 14

list the shigella spp.

Answer 14

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

Question 15

list the main Shigellosis Sxs:

• (1) S. sonnei
• (2) S. flexneri

Answer 15

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%)

Question 16

describe Shigella spp. transmission

Answer 16

4 F’s: Food, Flies, Feces, Fingers

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

Question 17

Shigella:

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

Answer 17

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

Question 18

Shigella virulence factors:

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

Answer 18

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

Question 19

briefly describe Shigella pathogenesis

Answer 19

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

Question 20

Bacillary dysentery refers to infection by…..

Answer 20

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

Question 21

Shiga toxin:

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

Answer 21

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

Question 22

Shiga Toxin effects:

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

Answer 22

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

Question 23

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

Answer 23

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

2- **S. sonnei

3- S. boydii

Question 24

describe the main possible complication of Shigella infection

Answer 24

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

• conjunctivitis
• urethritis
• arthritis

Question 25

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

Answer 25

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(-)

Question 26

list the Lactose fermenting bacteria (GI infections)

Answer 26

``` CEEK: Citrobacter Enterobacter *Escherichia *Klebsiella ```

Question 27

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

Answer 27

ShYPS: 1) nonmotile, non-H2S producers: - Shigella - Yersina 2) motile, H2S producers - proteus - salmonella

Question 28

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

Answer 28

``` 1- enteroinvasive E. coli 2- SE Asia, S. America 3- colon 4- Shigellosis 5- absent Shiga toxin 6- small, 10 organisms ```

Question 29

EIEC = (1): - utilizes (2) genes a lot, which encode for (3) - (3) will cause (4) in the colon and lead to (5) overall

Answer 29

``` 1- enteroinvasive E. coli 2- plasmid associated genes 3- outer protein for invasion 4- tissue destruction, inflammation, necrosis, ulceration 5- blood, mucus in stool ```

Question 30

briefly describe EIEC pathogenesis

Answer 30

(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

Question 31

EAEC = (1): - (2) is the key / unique feature with (3) as its main function - (4) is important to note with pathogenesis with this bacteria

Answer 31

1- enteroaggregative E. coli 2- aggregative adherence fimbriae (AAF) 3- mediates attachement to intestinal mucosa --> triggers inflammatory response 4- non-invasive

Question 32

briefly describe EAEC pathogenesis

Answer 32

(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

Question 33

STEC = (1), (2) are alternate names: - important produces (3) - (4) are reservoirs

Answer 33

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

Question 34

list the conditions STEC may cause

Answer 34

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

Question 35

STEC life threatening conditions, hemorrhagic colitis: - (1) days after ingestion - (2) affected population - (3) Sxs

Answer 35

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

Question 36

STEC life threatening conditions, HUS: - (1) days after diarrhea - (2) affected population - (3) Sxs

Answer 36

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

Question 37

STEC life threatening conditions, TTP: - (1) affected population - (2) Sxs

Answer 37

1- elderly (mainly) | 2- HUS, fever, neurological involvement

Question 38

describe STEC pathogenesis

Answer 38

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

Question 39

E. coli Dx, specifically STEC: - (1) appearance on main agar - list the other 4 steps (2), (3), (4), (5)

Answer 39

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