Cholera and Bacillary Dysentery Flashcards
Which of cholera and bacillary dystentery are notifiable?
Both are!!
Cholera: Microbiology, source, epidemiology
Vibrio cholerae
- serogroups based on O antigen
- O1 and O139 responsible for pandemics; O1 El Tor in 7th pandemic (1960), O139 in 8th pandemic (1992)
- Non-agglutinating vibrios (non-O1/O139) = self limiting GE and wound infections
Source: marine environments
Cholera: transmission, infective dose, invasive?
Transmission: Faecal-oral route (contaminated food/water)
Non-acid resistant: survive gastric acid by large inoculum size (high infectious dose) and protection by food
–> use of antacids or PPI increases risk of infection and lowers infectious dose
Multiply in small intestine
Attach to intestinal mucosa by pili
NON-INVASIVE
Cholera: pathogenesis of toxin
Cholera toxin (enterotoxin)
- binds to enterocyte surface receptor (GM1)
- activation adenylate cyclase and increase cAMP
- increase Cl- secretion (create osmotic gradient with Na, K and water lost passively) and decrease Na/Cl reabsorption
==> massive secretion of isotonic fluid into intestinal lumen
Cholera: clinical presentations
Most are asymptomatic
Acute onset of watery diarrhoea
(incubation hours - 5 days)
Severe cases (10%): vomiting, rice-like stool (mucus), dehydration –> hypovolemic shock and electrolyte imbalance –> death within 12 hrs
NO HIGH FEVER,
Little abdominal pain
Ileus and muscle cramps common
Cholera: investigations
STOOL: MICROSCOPY AND CULTURE
- gram -ve curved rods
- yellow TCBS due to sucrose fermentation
(recall other characteristics: halophilic, tolerate 6% NaCl, oxidase positive, motile)
Cholera: treatment
REHYDRATION
- ORS or IVF replacement if severe or can’t tolerate oral
Antibiotics (tetra/doxycycline, erythromycin/azithromycin, ciprofloxacin) NOT ESSENTIAL
- reduce volume of diarrhoea
- decrease vibrio excretion by 1 day as infection control measures in outbreak
Cholera: prevention
WASH (water sanitation, hygiene)
Proper waste disposal
Surveillance
Vaccines - generally not indicated
- -> 2 oral-killed doses for travellers to endemic areas
- -> but limited efficacy and short duration
Dysentery definition
Frequent passing of stool with blood and mucus, along with painful defecation
Can be amoebic or bacillary
Bacillary can be shigella or invasive strains of E. coli (generally refers to shigella)
Shigella dysentery: microbiology
Shigella species (47 seroptypes in 4 groups)
S. dysenteriae - most pathogenic
S. flexneri
S. boydii
S. sonnei - least pathogenic
Enterobacteriaceae, non-motile (c.f. E. coli and salmonella, non-lactose fermenter c.f. E. coli)
Shigella dysentery: pathogenesis - transmission, infective dose, invasive?, toxin
Transmission: faecal-oral route (contaminated food/water, human-to-human)
Gastric acid resistant: low infective dose of 10-100 bacteria
INVADES enterocytes, multiplies and destroys intestinal mucosa –> colonic ulceration and mucosal abscesses
Shiga toxin (enterotoxin and cytotoxic) --> binds to GB3 receptor on intestinal mucosa --> cause cell death and vascular injury
Rarely invades systemically
Shigella dysentery: clinical presentations
Incubation period: 1-7 days
Diarrhea with blood and mucus (50-80%)
Fever, abdominal pain, vomiting
DISEASE OF CHILDREN (<5yrs)
Shigella dysentery: investigation
STOOL CULTURE
rarely require blood culture
Shigella dysentery: treatment
Rehydration
ANTIBIOTICS INDICATED – lower excretion and decrease duration of symptoms (as there is high risk of spread with low infective dose c.f. cholera)
–> fluoroquinolone, 3rd gen cephalosporin (ceftriaxone), azithromycin, septrin
Shigella dysentery: prevention
No vaccine
Clean food and water, proper waste disposal, sanitation
Infection Control
Escherichia coli infections: strains, source
Only certain strains cause diarrhoea
- EPEC, ETEC (traveller’s diarrhoea), EIEC (can also cause dysentery), EHEC
O157:H7 EHEC/ verotoxigenic E. coli
- found in GIT on CATTLE - GROUND BEEF
- hamburgers as common source
O104:H4 recent outbreak in Germany due to sprouts
E. coli diarrhoea: pathogenesis
Human-to-human transmission
EHEC
- bloody diarrhoea by Shiga-like toxin (verotoxin) with similar mechanism as shigella – toxigenic and haemorrhagic
ETEC
- traveller’s diarrhoea with heat labile toxin similar to that of cholera toxin (mild to severe diarrhoea)
EHEC: clinical presentations
Watery diarrhoea, fever, vomiting
Haemorrhagic colitis in elderly (bloody diarrhoea)
HUS in children: triad of HA, thrombocytopenia (thrombotic microangiopathy) and AKI; mortality 3-5%
EHEC: treatment
Supportive: rehydration
ANTIBIOTICS CONTRAINDICATED - increase the release of verotoxin and shedding period –> precipitate HUS
General investigations and management of Dysentery
STOOL
- microscopy for ova, cysts, RBC, WBC
- culture on selective media
- modified acid-fast stain for parasites
Blood
- rarely culture in severe cases e.g. shigella in HIV patients
NOTIFICATION OF DOH
Outbreak:
- identify source and travel history
- culture suspected food
- contact precautions (enteric isolation - prevent spread by contact with faeces or vomit e.g. room, cohort, PPE, disinfection)
Treatment:
- FLUID AND ELECTROLYTE replacement (ORT, IV if severe or vomiting)
- Antibiotics not routine (only with systemic involvement, in shigella infection or for control in outbreaks in non-endemic countries; C/I in EHEC!!)