Health Stream Literature Summary - Issue 55 - September 2009

Massive outbreak of viral gastroenteritis associated with consumption of municipal drinking water in a European capital city.
Werber, D., Lausevic, D., Mugosa, B., Vratnica, Z., Ivanovic-Nikolic, L., Zizic, L., Alexandre-Bird, A., Fiore, L., Ruggeri, F.M., Di Bartolo, I., Battistone, A., Gassilloud, B., Perelle, S., Nitzan Kaluski, D., Kivi, M., Andraghetti, R. and Pollock, K.G.J. (2009) Epidemiology and Infection, 1-8.

On 24 August 2008, the Institute of Public Health (IPH) of Montenegro (formerly a state of Yugoslavia) was notified of an unusually high number of patients presenting with acute gastroenteritis at the Infectious Disease and Paediatric hospitals in the city of Podgorica. An outbreak investigation was undertaken by local health authorities with the assistance of the World Health Organisation regional office. A range of investigations were undertaken to identify the source and magnitude of the outbreak and to develop control and preventive measures.

An initial investigation was made of reported cases of acute gastroenteritis with onset dates from 23 August to 7 September (outbreak period). Interviews were conducted with a subset of these cases, available family members and the nearest available neighbours. These provided preliminary information on symptoms and possible exposures, the extent of the outbreak and potential sources of infection. Analysis of these data resulted in the hypothesis that contamination of municipal tap water was the probable cause of the outbreak.

From 18-24 September, an age- and neighbourhood-matched case-control study was performed to test this hypothesis. A case was defined as having ‘acute gastroenteritis with an onset date from 23 to 25 August (outbreak peak) who had the earliest onset date in their household and who lived in North-western districts of Podgorica’. This area was almost exclusively served by a water source (Mareza), which was deemed to be a potential source of contamination of the municipal water supply. Controls were neighbours of cases and three controls were selected for each case according to age grouping. Cases and controls were administered a questionnaire which collected information on drinking water habits (e.g. consumption of unboiled water at home or at work and consumption of bottled water).

Faecal samples were obtained from 200 cases with onset dates of illness from 24 to 26 August 2008, 2-4 days after the onset of symptoms. These samples were tested for pathogens including Salmonella, Campylobacter, Shigella or Yersinia spp., rotavirus and adenovirus. Additionally, 38 faecal samples from a subset of cases were sent for norovirus testing and genotyping.

The municipal water supply was assessed through field visits, interviews with responsible staff and review of routine microbiological sampling results (raw and final drinking water quality tested for coliforms and enterococci once every 2 weeks, at 18-19 fixed sampling points). The municipal water supply was hyperchlorinated on 25 August. From this date, daily samples from 8-9 of the fixed sampling points were taken. Four drinking water samples were collected from the municipal supply of Podgoria on 27 August and 22 September for molecular analyses (RT-PCR) of adenovirus, rotavirus, norovirus and hepatitis A virus.

There were 1699 reported cases of acute gastroenteritis during the 16-day outbreak period, compared to a usual number of 10-20 per week for this time of year. The median age of cases was 13 years and 48% were male. In the matched case-control study there were 83 cases and 89 controls. Some of the cases (40) had initially been contacted as potential controls (neighbours of reported cases) but were found have experienced gastroenteritis and were reclassified as cases. All of the 83 cases and 80 of the 89 controls reported drinking unboiled water from the municipal water supply during the week before the outbreak. Illness was found to have a positive association with drinking unboiled, municipal tap water [match odds ratio (mOR) 11.2, 95% CI 1.6-infinity). Controls were found to more frequently drink bottled water (mOR 0.3, 95% CI 0.1-0.8) than cases. Drinking only bottled water (8 controls) was highly protective (mOR 0.02, 95% CI 0.0-0.8). A significantly greater number of glasses of bottled water were consumed by controls than cases (0.9 vs. 0.7 glasses).

Analysis of the 200 faecal samples failed to detect any Salmonella, Campylobacter, Shigella or Yersinia spp. Samples from 16 people (all children) had a positive stool antigen result for rotavirus and two (1%) samples from adults tested positive for adenovirus. Norovirus was found in 23 (60%) of 38 faecal samples by one or both of the RT-PCR methods used. Norovirus genogroup II strains were recovered from 18 (47%) of 38 faecal samples. Of these 18, 7 strains were typed by sequence analysis and found to belong to genotypes GII.2 (three), GII.4-2006b (two) and GII.17 (two). In addition, norovirus genogroup I strains were found in the stools of 6 of the 38 patients including one patient also shedding GII norovirus and the strains were typed to GI.3 (one), GI.2 (three) and GI.13 (one).

The results of routine water tests prior to the outbreak (last sampling date 18 August) were negative for coliforms and enterococci. However, 3 of 8 samples taken from different points in the Mareza distribution system on 27 August were positive for coliforms. Also no chlorine could be detected in these water samples, although the system is normally chlorinated. Investigators found that two of the water treatment works at Mareza had reported electrical pump failures on 22 and 27 August. The four water samples collected on the 27 August and 22 September were negative for all viruses assayed.

It was estimated that this outbreak affected about 10,000 – 15,000 people. The population of the affected area is normally about 40,000 but many people had left the city during the summer holiday period, thus reducing the number potentially exposed. Norovirus was the probable causative agent however a contribution from other faecal pathogens can not be ruled out. The investigation revealed multiple weaknesses in the municipal water supply system. Although water was usually chlorinated, the contact time and chlorine residual level were unknown. A series of water pump failures occurred in the month before the outbreak, including the 22 August, the day before the number of cases began to increase. The subsequent drop in water pressure probably allowed ingress of faecally contaminated water or raw sewage into the drinking water distribution system, causing the outbreak. A multiple barrier approach adopting best practice criteria needs to be developed for source, treatment, efficient distribution, monitoring and responding appropriately to breaches in quality.

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