L13- GI Infections V (inflam. diarrhea, bacteria) Flashcards
define acute inflammatory diarrhea
- Sxs
- infected site
- main cause
- *key feature in comparison to non-inflam. diarrhea
- <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)
list the general complication of acute inflammatory diarrhea (not specific to any bacteria)
- *dehydration (main target Sx for Tx)
- electrolyte disturbances
- acidosis
- malnutrition
- dissemination (–> osteomyelitis, meningitis, pneumonia, peritonitis, septicemia)
Listeria: describe microbial features
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)
Listeria grows in (1) temperature range and (2) pH range- indicate the significance of each
1- 1C-45C, survives refrigeration
2- pH 4-9.6, survives stomach acid
Listeria clinical manifestations (general disorders)
- febrile gastroenteritis
- endocarditis
- CNS infections
- sepsis
- perinatal infections
- miscarriages
- still birth
list the high risk groups for Listeria infections
- pregnancy, newborns
- elderly
- transplant patients + other immuno-compromised
Listeria:
- unique Gram(+) feature
- (2) found in environment
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
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
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)
discuss mortality in relation to Listeria
~20%
-~25% of pregnancy cases result in death of fetus or newborn
describe diagnosis of Listeria
Direct microscopy: Gram(+) rods
Culture: 2-3 day incubation / enrichment at 4C
PCR
list the bacterial agents of inflammatory diarrhea
YES PECKSS
Y- yersina
E- *escherichia (EIEC)
S- Serratia
P- proteus E- enterobacter C- citrobacter K- klebsiella S- *shigella
Enterobacteriae spp.:
- (1) important species (for enteric system)
- (2) microbial features
1- Shigella, Klebsiella
2- Gram(-) rods
motile except for (1) species
Shigella:
- (1) microbial features
- (2) transmission
- serotyping is based on (3)
- (4) is rare effect
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
list the shigella spp.
Group: A- S. dysenteriae B- S. flexneri C- S. boydii D- S. sonnei
list the main Shigellosis Sxs:
- (1) S. sonnei
- (2) S. flexneri
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%)
describe Shigella spp. transmission
4 F’s: Food, Flies, Feces, Fingers
- acid stable —> low infectious dose sufficient
- *no animal reservoirs
Shigella:
- (1) at risk populations
- (2) geographic / seasonal distribution
- (3) prevention / control
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
Shigella virulence factors:
- (1) system is important for invasiveness
- (2) endotoxin
- (3) exotoxin
- (4) location of replication
- (5) disrupts cell metabolism
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
briefly describe Shigella pathogenesis
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
Bacillary dysentery refers to infection by…..
Shigella dysenteriae type 1 (shiga bacillus) => producess Shiga Toxin
Shiga toxin:
- (1) type
- (2) encoded on what part of genome
- (3) structure
- (4) brief pathogenesis
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
Shiga Toxin effects:
- (1) enterotoxic
- (2) cytotoxic
- (3) neurotoxic
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
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
1- S. flexneri (MSM- men who have sex with men)
2- **S. sonnei
3- S. boydii
describe the main possible complication of Shigella infection
Reactive Arthritis: can’t see, can’t pee, can’t climb a tree
- conjunctivitis
- urethritis
- arthritis
Shigella Dx:
- (1) appearance on initial agar
- then (2) is differentiating agat
- (3) is unique / special agar
- Lactose (+/-), citric acid use (+/-), H2S production (+/-)
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(-)
list the Lactose fermenting bacteria (GI infections)
CEEK: Citrobacter Enterobacter *Escherichia *Klebsiella
list the non-lactose fermenting bacteria (GI infections) and how to differentiate them
ShYPS:
1) nonmotile, non-H2S producers:
- Shigella
- Yersina
2) motile, H2S producers
- proteus
- salmonella
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
1- enteroinvasive E. coli 2- SE Asia, S. America 3- colon 4- Shigellosis 5- absent Shiga toxin 6- small, 10 organisms
EIEC = (1):
- utilizes (2) genes a lot, which encode for (3)
- (3) will cause (4) in the colon and lead to (5) overall
1- enteroinvasive E. coli 2- plasmid associated genes 3- outer protein for invasion 4- tissue destruction, inflammation, necrosis, ulceration 5- blood, mucus in stool
briefly describe EIEC pathogenesis
(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
EAEC = (1):
- (2) is the key / unique feature with (3) as its main function
- (4) is important to note with pathogenesis with this bacteria
1- enteroaggregative E. coli
2- aggregative adherence fimbriae (AAF)
3- mediates attachement to intestinal mucosa –> triggers inflammatory response
4- non-invasive
briefly describe EAEC pathogenesis
(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
STEC = (1), (2) are alternate names:
- important produces (3)
- (4) are reservoirs
1- shiga toxin producing E. coli
2- EHEC, VTEC
3- Shigella Like Toxin (SLT): Stx-1, Stx-2
4- cattle, sheep
list the conditions STEC may cause
1) hemorrhagic colitis
2) hemolytic uremic syndrome
3) thrombotic thrombocytopenia purpura
STEC life threatening conditions, hemorrhagic colitis:
- (1) days after ingestion
- (2) affected population
- (3) Sxs
1- 3 days post-ingestion
2- adults/elderly mainly
3- bloody diarrhea (begins as watery), abdominal pain
STEC life threatening conditions, HUS:
- (1) days after diarrhea
- (2) affected population
- (3) Sxs
1- 5-13 days post-diarrhea
2- children <5y/o (90% cases)
3- microangiopathic hemolytic anemia, thrombocytopenia, acute renal failure
STEC life threatening conditions, TTP:
- (1) affected population
- (2) Sxs
1- elderly (mainly)
2- HUS, fever, neurological involvement
describe STEC pathogenesis
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
E. coli Dx, specifically STEC:
- (1) appearance on main agar
- list the other 4 steps (2), (3), (4), (5)
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
