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Microbiology Yr3 > Bacterial gastroenteritis > Flashcards

Bacterial gastroenteritis Flashcards

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1
Q

What are the 2 mechanisms of diarrhoea and dystentry?

A
  1. 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
  2. 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
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2
Q

What diseases does B. cereus cause?

A
  • 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

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3
Q

Salmonella media can include:

A

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
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4
Q

what colour is salmonella on XLD and DCA?

A

most strains produce hydrogen sulphide so black colour colonies- acid butt (yellow) red slant, black in TSI, urea slope NEG (yellow)

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5
Q

how can we differentiate salmonella serotypes?

A

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

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6
Q

What serotype antigens used for salmonella serology?

A

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

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7
Q

Lab characteristics of shigella

A

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

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8
Q

Which is the most pathogenic sp of shigella and why?

A

S. dysentariae has shiga toxin

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9
Q

yellow on xld and urea pos

A

Klebsiella and enterobacter

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10
Q

Genera - all are:
* GNB
* Oxidase POS
* Motile - polar flagellar
* Ferment glucose
* Indole POS (most of the medically important species)

A

Vibrio, Aeromonas, Plesiomonas

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11
Q

What does vibrio look like in gram stain
Which sp are the main human pathogens and which can also cause wound and GIT

A

Slightly curved GN rods- comma shaped
Main human GIT pathogens
- Vibrio cholerae
- Vibrio parahaemolyticus
* Others: GIT and wounds
- Vibrio vulnificus
- Vibrio alginolyticus
- Vibrio fluvialis

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12
Q

What is cholera and what is the infective dose (also what for people with impaired gastic acid production)

A

Severe diarrhoeal diseases caused by the bacterium Vibrio cholerae
Infective dose 10^10 orgs/ml (<100 in people with impaired gastric acid production)

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13
Q

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

A

10%, painless, K+, <50-100ml/day, acidosis, Rice water

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14
Q

How can cholera be transmitted?

A

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

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15
Q

How many vibrio cholera serotypes are there and which 2 are toxigenic and cause epidemic cholera?

A

139 V. cholerae serogroups, O1 and O139 are the 2 toxigenic ones, cause epidemic cholera

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16
Q

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

A

Separated into Classical and El Tor biotype based on their phenotypic features (not genetic)

El Tor compared to classical:

17
Q

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

A

– Ogawa (A,B antigens)
– Inaba (A,C)
– Hikojima (A,B,C) – rare

18
Q

What are the other cholera serotypes of importance (not O1)

A

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)
19
Q

Vibrio cholerae – virulence factors/pathogenesis
what infectious dose is needed?
what is the main virulence factor

A
  • 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

20
Q

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)
A

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

21
Q

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 ⇧_______

A

GM1 receptor
* pore, A1-A2 unit passes
* A1, reduction , A2
* ⇧ production of adenyl cyclase leading to ⇧ cAMP

22
Q
A
23
Q

what are v. cholerae lab characteristics?

A

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)

24
Q

What does v. parahaemolyticus cause? how is it treated? where is it found and how is it transmitted?

what are its lab characteristics?

A

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

25
Q

Where is v alginolyticus found? what is it associated with?
What does it cause?
What are its lab characteristics?

A

In sea water (salt loving) NG on low salt MAC
Associated with the marine environment and industries
* Causes septic wound infections and ear infections
* TCBS agar - sucrose positive (yellow) and mucoid
- Colour can fade with time
* Resistant to 10μg O129 compound (disk test)
* Can ID with API20E

26
Q

Where can you find v. vulnificus?
what infection does it cause? (like vulture=vulnificus)

what are its lab characteristics?

A

Can be found in warm brackish sea water
* Avoid exposure of wounds to this kind of water
* Wound infections including necrotising fasciitis
- Tissue destruction and septic shock (1/5 fatality rate)
- May require amputation
* Septicaemia following ingestion of contaminated seafood

  • TCBS agar - sucrose negative (green)
  • Sensitive to 10μg O129 compound (disk test)
27
Q

Vibrio, Plesiomonas and aeromonas chart
how to diff between v cholerae and v alginolyticus which are both yellow on TCBS?
What about v parahaemolyticus and vulnifirus which are both blue-green?

how can we diff between plesiomonas and aeromonas? both don’t grow on TCBS and R to O129 (10microgram disc)

A

ALL genus are oxidase and indole POS
4 sp of vibrio= cholerae, parahaemolyticus, alginolyticus vulnifirus

V cholerae and alginolyticus- V cholerae is S to O129 (10 microgram disc) and v alginolyticus is R. Although both are yellow, alginolyticus is MUCOID.

Plesiomonas is S to O129 150microgram disc while aeromonas is R. the 4 vibrio sp are ALL S to O129 150ug

28
Q

Where is aeromonas natural habitat, what does it cause?
what is the main pathogen?
Other potentially clinically significant species - A. caviae complex including A. media
- A. veronii complex
- A. salmonicida
* All are oxidase POS and most indole POS
* Nil growth on TCBS, most are B-haemolytic except __ ______

A

fresh water and sea water, can be recovered from sink traps, drainpipes, dH2O supplies
causes
Cellulitis and wound infections
- Acute diarrhoea* 20% dysentery-like stool
- Septicaemia (hepatobiliary disease, malignancies)
- Occasionally UTI, meningitis, ear infections, endocarditis
Aeromonas hydrophila- main pathogen and water loving
A. caviae non b haemolytic

29
Q

what are aeromonas virulence factors?
for antimicrobial R which 2 types of B lactamases for A1 and A2 are produced?

A

Not well understood
* Adherence factors
* Toxin production
- Cytotoxins
* Mucosal invasion - ? Motility a factor

A1 - inducible Type 1 cephalosporinase (ESCHAPM)
- R to all B-lactams & cephalosporins except carbapenems (flattening of CTX)- Test aztreonam (monobactam)
* A2 - inducible penicillinase/carbapenemase
- R to penicillins and imipenem/meropenem (carbapenems)- reduced inhibitory zone around IMP- Test cephalosporins
* Fluoroquinolones, SXT, AMG are alternatives

30
Q

GNB - straight* ß haemolytic* Oxidase positive* Indole Pos* DNAse Pos* Very motile
* Selective media
- BAMP agar (BA with ampicillin) – set up if diarrhoea for >2 weeks * Large, oxidase positive and indole pos colonies
- Alkaline PW (pH 8.6) enrichment broth =BAMP
* can improved isolation rate from 1.5% to 5%
- Grows on CIN agar (Yersinia)
- ? Only some strains of A. hydrophila will grow on TCBS (yellow) – Oxoid manual
* Nil species grow on TCBS according to Bailey and Scott 13th Edition, 2014
* 10μg O129 Resistant
* ? Use of plain BA to screen for oxidase pos, indole pos colonies in faeces
- Can ID with API20E

A

Aeromonas sp

31
Q

Whats special about P shigelloides? where is it found what animals it infects and how it infects humans

what can it cause?

A

Only species in genus

  • Ubiquitous in soil and water
  • Infects frogs, snakes, lizards, turtles
  • Human infection is mainly through ingestion of contaminated food
  • Mild watery diarrhoea
  • More prevalent in tropical/subtropical areas
  • Occasional extraintestinal infections
  • Cellulitis
  • Septicaemia * Meningitis
32
Q
  • Short GNB, Motile
  • Non-haemolytic * OxidasePos, IndolePos
  • Ferments glucose* Inhibited on BAMP(Aeromonas sp.) * Inhibited on TCBS(Vibriosp.)
  • Lactose neg on MAC,DCA,XLD
  • Resistant to 10μgO129, Sensitiveto150μgO129 * CanIDwithAPI20E
  • Resistant to Pc
  • Sensitive to AMG,C,TE,SXT,CIP
A

Plesiomonas shigelloides

33
Q

Yersinia sp main pathogen is? which one is rare?
what do they both cause?

What about yersinia pestis?

A

Both cause:
- Severe enterocolitis - Fever, diarrhoea, abdominal pain
- May mimic appendicitis- Can lead to systemic infection
- Reservoir is animals and with poor hygiene
* Preparation of chitterlings – pig”s intestines* Can be found in Raw Milk* High incidence in children (adults transfer)

Yersinia pestis
- bubonic, pneumonic, septicaemic plague
- found in rodents including squirrels

34
Q

Member of the Enterobacteriaceae
* Non-motile 37 ̊C, motile at 22 ̊C
* Isolated from raw food, faeces and milk
* Best recovered from stool specimens at 25 ̊C
* Biochemical reactions best tested at room temperature
* Grows at 4 ̊C (can use cold enrichment for isolation)
* Use CIN media for isolation
- Cefsulodin, irgasan, novobiocin agar
- Classic bull’s eye colony
* Dark pink in middle, clear on the outside (fermentation of mannitol)

A

Yersinia enterolitica

35
Q
  • Used to be a member of the Enterobacteriaceae (now Hafniaceace)
  • Found in brackish water as well as fish/sea food
  • 2015 review found 77 human cases reported globally (45.5% in Japan)
  • Overall mortality rate 44.6%
  • Usually causes diarrhoea but can cause bacteraemia/septicaemia
  • Zoonosis in fish, reptiles, amphibians, mammals
  • Laboratory ID
  • H2S+ colonies on DCA/XLD etc (screen with TSI and urea)
  • Alkaline slope with H2S in TSI, negative urea. TSI - Looks like a Salmonella (red/black/yellow) but with possible gas in the bottom of the tube
  • Salmonella serology negative
  • API20E+ or MALDI-TOF
A

Edwardsiella tarda

36
Q

For GIT infections the good thing is? when do you need to have antimicrobial treatment?

A

Most are self-limiting = no treatment
* Sensitivities may be set up but not reported or
* Sensitivities may only be set up on certain pathogens
Some situations may warrant antimicrobial treatment
* Severe infection or chronic infection in babies
* Elderly and immunocompromised

Microbiology Yr3 (13 decks)

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