L9- GI Infections III (non-inflam. diarrhea, bacteria) Flashcards
define acute diarrhea and the types
- <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
most cases of acute diarrhea are caused by…..
infections, 90%
what are the five high-risk American groups for developing acute diarrhea
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
Non-Inflammatory diarrhea (acute):
- (1) stool description
- (2) GIT wall changes
- (3) other Sxs
- (4) causes
- (5) typical affected segment
- (6) fecal leukocytes present?
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
Inflammatory diarrhea (acute):
- (1) stool description
- (2) GIT wall changes
- (3) causes
- (4) other Sxs
- (5) typical affected segments
- (6) fecal leukocytes present
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
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
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)
Eschericha Coli:
- (1) location / found in
- (2) bacterial family
- (3) classic microbial features
- (4) traditional agar
1- normal gut flora
2- enterbacteriaceae
3- Gram(-) rod, facultative anaerobes, catalase(+), oxidase(-), rapid lactose fermenter, motile (multiple flagella)
4- MacConkey agar (pink colonies)
list the important (diarrheal causing) Enterobacteriaceae spp.
- *Escherichia
- *Shigella
- *Salmonella
- *Yersinia
Klebsiella
Proteus
list the important antigenic structures of E. coli
- O Ag, lipopolysaccharide O side chains
- H Ag, flagella
- K Ag, capsule
- cell envelope (cytoplasmic membrane, peptidoglycan, outer membrane)
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
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
E. coli key virulence factors:
- (1) for adhesion
- (2) toxins
1- pili to attach to mucosa (colonization factor)
2- Exotoxin: heat-labile (LT) and or heat-stable (ST) toxins
ETEC = (1):
- (2) transmission, include dose
- primary cause of (3)
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)
describe ETEC pathogenesis
(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)
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.
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)
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
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
EPEC = (1), mainly causes (2)
1- enteropathogenic E. coli
2- infantile diarrhea (childhood diarrhea) –> 50% mortality in developing countries
EPEC pathogenesis (Note what is importantly absent)
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
most of the fluid absorbed in the GIT occurs in…..
small intestines
Vibrio Cholerae:
- (1) family
- (2) shape and size
- (3) important microbial features
1- vibronaceae
2- single curved rods, 2-4 µm long
3- Gram(-) bacillus, motile (single flagella), non-spore forming, facultative anaerobes, oxidase(+)
Vibrio Cholerae:
- (1) are important Ags
- (2) fermenters
- (3) sensitive
- (4) tolerant
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)
Tx for _____ inc risk for cholera infections (explain)
- people on antacids
- V. cholera is acid sensitive
V. cholera pathogenesis
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
Cholera toxin is encoded on (DNA/bacteriophage/plasmid) and functions to activate (2) in order to increase (3) and cause (4)
1- phage (AB toxin)
2- adenylate cyclase (like LT toxin)
3- inc cAMP
4- water / electrolyte efflux => watery diarrhea
V. cholera Sxs
- dehydration: isotonic fluid loss
- hypokalemia: K+ ion loss
- metabolic acidosis: HCO3- loss
- hypovolemic shock, acidosis, muscle cramps
- n/v/d
describe diarrhea caused by V. cholera
Rice Water Stool
- 20-30L per day
- white lumps contain bacteria and toxin
V. cholera Dx:
- (1) is necessary from patient history
- (2) screening is useful
- (3) agar is required with (4) as a differentiating agent
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.
describe cholera vaccine (type of vaccine and target population)
Vaxchora
- live-attenuated
- for travelers
- not for people <18y/o
Clostridium perfringens: microbial features (include normal location)
Gram(+), large, anerobic, non-motile, bacillus, *spore-forming
apart of intestinal microflora, ubiquitous in nature
list the diseases caused by C. perfringens
- myonecrosis (gas gangrene)
- Type A* food-bourne infection = diarrhea
describe C. perfringens pathogenesis
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
describe C. perfringens toxin(s)
CPE: clostrdium perfringens enterotoxin is similar to Heat-labile enterotoxin in ETEC (LT)
=> pore formation rather than inc cAMP
-*probably encoded on plasmid
C. perfringens:
- (1) incubation period
- (2) Sxs
- (3) Dx
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)
Bacillus cereus microbial features (include location)
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
Bacillus cereous causes the following… (explain by Sxs, incubation period, duration, associated foods)
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
Diarrheal Bacillus cereous pathogenesis
1) ingestion of pathogen
2) colonization in SI
3) LT enterotoxin production
4) activates adenylate cyclase –> inc cAMP –> inc water/electrolyte efflux => diarrhea
Emetic Baccillus cereous pathogenesis
ingestion of pathogen with toxin: ST neurotoxin (peptide)
Assign to emetic or diarrheal Bacillus cereous:
- (1) short incubation
- (2) enterotoxin
- (3) ST toxin
- (4) LT toxin
1- emetic, 4hrs (diarrheal 8-16hrs)
2- diarrheal (emetic has emetic toxin)
3- emetic (neurotoxin)
4- diarrheal
