Bacterial gastroenteritis Flashcards
(36 cards)
What are the 2 mechanisms of diarrhoea and dystentry?
- Intoxication (food poisoning)- ingest preformed toxin in food, occur w/in 30min-8hrs, not due to ingestion and colonisation/growth of organisms - s. aureus, bacillus, chlostridium
- colonisation of gut ingestion of organisms then multiplication 16-48hrs before symptoms normally, virulence factors include toxin production, adherence or attachment, invasion- shigella salmonella c. difficile
What diseases does B. cereus cause?
- food poisoning - short incubation of 1-6hrs
vomiting and abdominal cramps - Spores survive insufficient cooking, germinate in ‘warm’ food (i.e. RT to <50 ̊C)
- Consume preformed heat stable exotoxin in food (acts as an enterotoxin in the host)
- associated with fried rice, cream, milk products, pasta, infant formula
- Symptoms last for 10-14 hrs
Longer incubation (8-16 hours)
* profuse watery diarrhoea, nausea, lower abdominal pain, tenesmus
* Consumption of spores not killed by cooking
* in vivo enterotoxin production formation (heat labile)
- cAMP production = fluid loss (similar to V. cholerae)
* inadequate cooking of foods
* Meat, veg. dishes, dairy, cakes, sauces
* Symptoms last for 12-36 hours
In immunocompromised hosts may cause a range of other conditions - Bacteraemia, endocarditis, LRT, meningitis, wounds, burns
Salmonella media can include:
Solid media
- Hektoen enteric agar (HEK)
- Xylose lysine desoxycholate (XLD)
- Desoxycholate citrate agar (DCA)
- Salmonella Shigella media (SS) – similar to DCA
- Bismuth sulphite agar (BSA)
- Chromagar Salmonella and Salmonella plus
- Enrichment broths
- Strontium chloride
- Selenite F
- Tetrathionate
what colour is salmonella on XLD and DCA?
most strains produce hydrogen sulphide so black colour colonies- acid butt (yellow) red slant, black in TSI, urea slope NEG (yellow)
how can we differentiate salmonella serotypes?
S. Typhi weakly H2S + (could appear negative)
- S. Paratyphi B and C are H2S + (normal TSI colours)
- S. Paratyphi A is H2S Negative- if look like shigella but serology neg try with salmonella
confirm all pos serology with MALDI TOF
can do if potential salmonella- serology agglutination rxns
What serotype antigens used for salmonella serology?
O antigens (“poly O”) – polyclonal cell wall antisera: POS =Salmonella sp.
H antigens (“poly H”) – polyclonal flagella antisera: POS =Salmonella sp.
can also have capsular antigens Vi associated with S.Typhi, K associated with other Salmonellae
Lab characteristics of shigella
pale pink on XLD (NF= yellow), straw coloured on DCA (NF=pink)
TSI
- H2S NEG
- Acid butt, red slant
* Urea slope NEG
* Speciation performed by agglutination
with specific anti-sera
- Shigella Poly “O” antisera (NO flagella = NO ‘H’ antigen)
- Wellcolex latex aggltn. - reactions colour coded to groups
Which is the most pathogenic sp of shigella and why?
S. dysentariae has shiga toxin
yellow on xld and urea pos
Klebsiella and enterobacter
Genera - all are:
* GNB
* Oxidase POS
* Motile - polar flagellar
* Ferment glucose
* Indole POS (most of the medically important species)
Vibrio, Aeromonas, Plesiomonas
What does vibrio look like in gram stain
Which sp are the main human pathogens and which can also cause wound and GIT
Slightly curved GN rods- comma shaped
Main human GIT pathogens
- Vibrio cholerae
- Vibrio parahaemolyticus
* Others: GIT and wounds
- Vibrio vulnificus
- Vibrio alginolyticus
- Vibrio fluvialis
What is cholera and what is the infective dose (also what for people with impaired gastic acid production)
Severe diarrhoeal diseases caused by the bacterium Vibrio cholerae
Infective dose 10^10 orgs/ml (<100 in people with impaired gastric acid production)
Less than ___ of infected persons develop typical cholera
– Sudden onset of massive , _____ diarrhoea
* Dehydration (requires oral re-hydration or IV fluid)
– loss of __
– anuria(____________)
– metabolic _____ and shock
* ____ _______ stools (up to 24 litres per 24 hrs)
* Death (50-60% if untreated), <1% if treated
10%, painless, K+, <50-100ml/day, acidosis, Rice water
How can cholera be transmitted?
Contaminated water supplies (fresh and salt water)
* Fish and shellfish from contaminated water, eaten raw
* Contaminated foods (milk, eggs, chicken, lentils, rice, potato)
* Vegetables fertilised with human faeces/contaminated water
* Often associated with algal blooms in estuaries
* Asymptomatic carriers
How many vibrio cholera serotypes are there and which 2 are toxigenic and cause epidemic cholera?
139 V. cholerae serogroups, O1 and O139 are the 2 toxigenic ones, cause epidemic cholera
How is O1 epidemic cholera subdivided into two Biovars and what are they?
_____ compared to ________:
Produces less cholera enterotoxin, but
– Increased ability to colonise the intestinal epithelium
– More resistant to environmental factors
– Long duration of carriage after infection
Separated into Classical and El Tor biotype based on their phenotypic features (not genetic)
El Tor compared to classical:
Each O1 epidemic cholera biotype is further subdivided into serotypes based on the variable O antigen composition/fractions of their cell walls which are:
The designated cell wall “A” antigen is common to the cholera group
– Ogawa (A,B antigens)
– Inaba (A,C)
– Hikojima (A,B,C) – rare
What are the other cholera serotypes of importance (not O1)
0139 epidemic cholera “Bengal’’
* Re-emerged as a predominant strain in Bangladesh (2002)
* Mutation of El Tor biotype
* Not identified by O1 antisera which is more common
– O1 gene deleted
– O139 LPS and a capsule instead
* Has now spread to 11 countries in SE Asia
- Non-01 cholera-like disease (serogroups O2-138)
- Mild diarrhoea
- ? More commonly associated with extraintestinal infections
- Present in QLD waterways (only Australian source of V. cholerae)
Vibrio cholerae – virulence factors/pathogenesis
what infectious dose is needed?
what is the main virulence factor
- Susceptible to stomach acid, so a large infective dose required
Adherence to small GIT via pili (no epithelial invasion) - TCP pili help bacteria to aggregate, protecting them from IR and leads to an concentration of cholera toxin secretion
- Produce mucinolytic enzymes
Main virulence factor is Enterotoxin (cholera toxin)
* Encoded by a lysogenic bacteriophage called CTXf or CTXφ
How does the cholera toxin work?
Toxin binds to _______ ____ via GM1 (monosialosyl ganglioside) glycoprotein receptor (recognition event)
* The main part of the toxin molecules is composed of__ tubular proteins (Beta subunits)
* Comprised of a further____ subunits
– ___ subunit facilitates entry of __ subunit into the cell
– ___ component is _________ and stimulates ________ ______ production
- Leads to excretion of NA , Cl , K , HCO3 , H2O from cells
– ______ minutes from ingestion to onset of symptoms
– Large ___ loss - ______ loss ceases after ___days (mechanism unknown)
mucosal cells
* 5
* two
– A2 subunit facilitates entry of A1 subunit into the cell
– A1, internalised and stimulates intracellular cAMP production
– 15-60
– fluid
* Fluid, 5 days
Cholera toxin entry
-Toxin (5 x B subunits plus A1-A2 toxin molecule) binds to the _____ _______ on host cells
* 5 B subunits form a ____ in the host cell membrane through which the ____ unit passes
* The ___ subunit is released from the toxin by _________ of the disulphide bond that links it to ___
* A1 induces ___ production of _____ _____ leading to ⇧_______
GM1 receptor
* pore, A1-A2 unit passes
* A1, reduction , A2
* ⇧ production of adenyl cyclase leading to ⇧ cAMP
what are v. cholerae lab characteristics?
Selective and differential medium = Thiosulphate Citrate Bile Sucrose agar (TCBS) * V. cholerae sucrose + produce yellow colonies on TCBS
* Prefers pH > 7.0, optimal pH 8.2
* Can add faeces to alkaline peptone water, pH 8.4. 12-18 hrs, 37 ̊C, then sub-culture to a TCBS plate
* Set up a TCBS plate if Hx or specimen indicates
* Seafood, Overseas travel, Watery stool
* Hx: subcultured suspect colonies from TCBS ® NA for oxidase test ® if ox pos do API20E (or equiv.) & Gram
Other tests
* POS agglutination with O1 serogroup or O139 antisera
* S to pteridine compound O129 (10μg disk)
* PCR for toxin gene
* EIA for toxin in faeces
Any growth on TCBS should be subcultured and tested further (i.e. oxidase test)
What does v. parahaemolyticus cause? how is it treated? where is it found and how is it transmitted?
what are its lab characteristics?
Gastroenteritis which includes
- Watery, maybe bloody diarrhoea (japan 50%?) Abdominal pain, Nausea, Vomiting, Headache, Low grade temperature
Self-limiting after 2-3 days (not usually treated)
* Salt loving (halophilic) - found in sea water
- NG on low salt MAC
* Transmitted through eating raw or improperly cooked seafood
on TCBS sucrose neg= blue green colonies, R to O129 compound and ID w API20E
