Diarrhoea outbreak after a village feast: attack rates and control
On 18 June the medical officer of your PHC is told that many people in Rampura village (population 2,400) have had watery stools since the night of 13 June. A marriage feast was held on the evening of 12 June and was attended by 300 villagers; the food was cooked the previous afternoon, kept overnight in open metal vessels and served cold. Drinking water comes from a hand pump 8 metres from a soak pit, and about 60% of households have no toilet. Your team finds 96 people who attended the feast and 6 people who did not attend who have had three or more loose watery stools in 24 hours since 13 June. Two children aged 2 and 4 have died. Stool samples from four patients have been sent for culture and the report is awaited. The sarpanch says the illness is "just heat" and refuses to stop the weekly village market on 20 June.
1. Write a working case definition, calculate the attack rates in attenders and non-attenders, interpret the result, and state two hypotheses for transmission.
Read the worked answer
Case definition (working): a resident of Rampura with three or more loose or watery stools in 24 hours, with or without vomiting, with onset on or after 13 June.
Attack rate, attenders: 96 ÷ 300 × 100 = 32%.
Attack rate, non-attenders: the population at risk is 2,400 − 300 = 2,100; 6 ÷ 2,100 × 100 = 0.29%.
Interpretation: relative risk ≈ 32 ÷ 0.29 ≈ 112. Attenders were more than a hundred times more likely to fall ill. That is far too strong to be chance, and the shape of the epidemic - many cases after one shared meal, with onset within 12–48 hours - is a point-source outbreak from the feast, not "heat". The six non-attender cases are important: they suggest either a continuing common exposure (the hand pump) or secondary person-to-person spread in households.
Hypotheses: (1) cooked food held overnight at ambient temperature in open vessels and served cold allowed massive bacterial multiplication; (2) drinking water from the hand pump contaminated by soakage from the soak pit, or food washed or vessels rinsed with it. Most likely agents: Vibrio cholerae or enterotoxigenic E. coli; the culture report will decide. Both hypotheses can be tested by food-specific attack rates and by water sampling (H2S vials).
2. List your control measures in priority order with the rationale, and describe how you would handle the sarpanch's refusal.
Read the worked answer
1. Treat and find cases. Set up ORS corners, do house-to-house case search, give low-osmolarity ORS and zinc to every case, and refer severe dehydration on a stretcher. Rationale: two children have already died; deaths are preventable within hours.
2. Safe water now. Stop use of the hand pump, superchlorinate the source, chlorinate household storage, and supply tanker water or advise boiling. Rationale: if water is the continuing source, cases will keep appearing regardless of food advice.
3. Sanitation. Stop open defecation near the pump, provide temporary latrines, and disinfect spillage. Rationale: breaks the faecal-oral cycle and protects the aquifer.
4. Food safety education and no further community feasts until the source is identified.
5. Notify the district surveillance unit (IDSP) immediately and send stool and water samples. Rationale: an outbreak is a statutory notification, and culture confirmation guides antibiotics for severe cases.
Handling the sarpanch: do not argue in front of the village. Show him the numbers in one line - "3 out of every 10 people who ate at the feast are ill, against 3 in 1,000 who did not" - and ask him to help with chlorination and latrine siting, which are visible and popular. Explain that the market itself is not the danger; unsafe water sold at it is. Cancelling the market is the district administration's decision, not yours; your duty is to notify and to give the sarpanch the written advice. Record his response.
3. Why did the two young children die, and what treatment should have been given?
Read the worked answer
Why children die: young children have a higher body-water turnover, a smaller reserve and a greater surface area relative to weight, so they dehydrate faster than adults. They also cannot ask for water or reach it. Death in acute diarrhoea is from dehydration and electrolyte loss (hypovolaemic shock, hypokalaemia, acidosis), and sometimes from hypoglycaemia, which is common in malnourished children and can cause convulsions and coma. Parents often do not recognise the signs - sunken eyes, no tears, dry mouth, reduced urine, lethargy - until shock is established.
What should have been done:
- No dehydration (Plan A): extra fluids at home and ORS 50–100 mL after each loose stool for under-2s, 100–200 mL for older children, plus zinc 20 mg daily for 14 days (10 mg for infants under 6 months), which shortens the episode and prevents recurrence.
- Some dehydration (Plan B): ORS 75 mL/kg over 4 hours under observation, then reassess.
- Severe dehydration (Plan C): intravenous Ringer's lactate 100 mL/kg - for infants 30 mL/kg in the first hour then 70 mL/kg over 5 hours; for children over 1 year, 30 mL/kg in 30 minutes then 70 mL/kg over 2.5 hours - switching to ORS as soon as the child can drink. Treat hypoglycaemia and give zinc.
- Refer any child with convulsions, lethargy, inability to drink, or persistent vomiting.
The lesson to record: both deaths were preventable, and the village needs ORS available in every household before the next outbreak.