A typhoid fever outbreak in a slum of South Dumdum municipality, West Bengal, India, 2007: Evidence for foodborne and waterborne transmission

Typhoid fever is an acute febrile illness caused by Salmonella (enterica) Typhi [1, 2]. The incubation period ranges from three days to one month [3]. Early symptoms include progressive onset of fever, headache, abdominal discomfort, loss of appetite, constipation followed by diarrhea, dry cough, malaise and rash along with relative bradycardia [2, 3]. The case fatality ratio is 10% in the absence of treatment and less than 1% with antibiotics [1]. Human beings are the only natural reservoir. It is transmitted through ingestion of water or food that have been contaminated by feces or urine of patients and carriers [2, 3]. Prevention is based on access to safe water and hygienic food handling practices [4]. In 2000, typhoid fever affected 21,650,974 million people worldwide and caused 216,510 deaths [5].

It is estimated that In Asia, the crude annual typhoid incidence rate was 274 per 100,000 persons in 2000 [5]. In India, typhoid incidence rates declined between 1974 and 1996 [5]. However, typhoid fever outbreaks continue to be reported in the country [6, 7]. In 2004, the estimated incidence of typhoid was 104 per 100,000 populations in West Bengal [8].

In 2006, in the "North 24 Parganas" district of the Indian state of West Bengal, the incidence of typhoid fever was 124 per 100,000, three times more than in 2001. It was unclear whether this rise was real (increased incidence) or artefactual (increased reporting). In the Darjeeling district of the same state, improvement of reporting between 2000 and 2004 led to a 10 fold increase in five years [8]. On 12 April 2007, health authorities of the South Dumdum municipality in the North 24 Paraganas district (2001 population: 392,150, divided in 35 wards, [9]) noted and reported an increase in the number of fever cases reported passively from a slum. This municipality is in the suburban area of Kolkata, the Capital of West Bengal. We investigated this cluster to identify the causative agent, identify the source, control the outbreak and propose recommendations to prevent future occurrences.

A number of elements suggested that part of this outbreak was foodborne. First, there was an association between eating food from the sweet shop and illness, and that exposure explained about half of the cases. Second, there was an infected source patient working in the sweet shop who engaged in unsafe food handling practices three weeks before the occurrence of the outbreak. The distribution of the suspected case-patients with exposure to the food from the shop over time suggested that this exposure explained the first part of the outbreak. Among typhoid outbreaks, food borne episodes are common in several countries [11–18]. Following contamination by an infected patient, milk-based sweets would have constituted good growth media for the bacterium.

The second part of the outbreak suggested waterborne transmission. Several studies reported typhoid fever outbreak as waterborne [19–22]. A number of elements suggested that the piped water accounted for a number of cases during this outbreak. First, suspected cases clustered in a location that was consistent with a contamination of the piped water. Second, there was an association between exclusive consumption of piped water and illness that explained about half of the cases. Third, analysis of the water specimen supported the hypothesis of contamination. The distribution of the suspected cases over time suggested that the piped water supply explained the second part of the outbreak. While there was no direct evidence to explain the sequence between the two parts of the outbreak, the environmental assessment suggested a possible scenario. The patients affected during the first phase of the outbreak excreted the pathogen in the environment. In a context of a poor sanitation system where water pipelines with negative pressure on account of intermittent water supply, ran closely to the open drainage system, the contaminated sewage may have been sucked in the piped water distribution system. Once the bacteria were transmitted in the community, unsafe water handling practices may also have led to a number of cases. Stored water was significantly associated with the disease when in uncovered or wide mouthed container and stored water was contaminated with fecal coliform. Narrow mouthed containers have been shown to prevent secondary transmission of typhoid [21, 22]. Water storage in a covered container (that helps prevent contaminations) may be associated with a lower risk of disease [21]. Other findings of our case control study were consistent with reported risk factors for typhoid fever, including high attack rates among children [23–25], large households [25] and families living in poor sanitation environment [26–29].

This study had one main limitation. We had only one positive blood culture for Salmonella (enterica) Typhi. Thus, we cannot exclude the possibility that a number of the 103 suspected cases had other forms of infections and we may have overestimated the size the outbreak. In the case control study, we included only probable cases that had a Widal test >= 1;80. The use of a single Widal agglutination test for the diagnosis of typhoid is controversial, particularly when the reagents are not standards and when there are no data on the local sensitivity and specificity for a given dilution [30]. However, in the context of India, it is still used as (1) a 1:80 titre provides acceptable sensitivity and specificity in the absence of other diagnostic options and (2) the positive predictive value is higher in a context of high frequency of the disease [31]. The clinical symptoms were compatible with the diagnosis of typhoid fever and did not change during the two phases of the outbreak. Furthermore, if we included patients with other infections in the case control study, this would have led to non-differential misclassification that would not prevent our ability to conclude with respect to the sources of infection identified.

This probable typhoid fever outbreak presented with a unique sequence with a first phase associated with eating food from a sweet shop and a second phase secondary to a contamination of the piped water supply. Unsafe water handling practices might also have contributed to the spread. On the basis of these conclusions, we formulated a number of recommendations. First, we educated the food handler of the shop regarding use of soap before sweet preparation and use of spoon to serve food. Second, we recommended daily chlorination of the piped water. We ensured the implementation of this recommendation through several meetings with the local authorities and engineers. After chlorination of the piped water supply, the outbreak came to an end. Third, we conducted health education with the community regarding safe water handling practices. For the long-term control of typhoid, both food safety and water safety will be needed, and adequate sanitation should be achieved to prevent the type of environmental contaminations that triggered a waterborne outbreak after a foodborne one. Epidemiologists investigating typhoid and other outbreaks transmitted through the fecal-oral route must always keep in mind the possibility of combined mixed modes of transmission during outbreaks. Finally, efforts must be made to evaluate newer innovative strategies for the diagnosis of typhoid fever in India so that the common use of the Widal test may be replaced with a better option, possibly with the use of rapid tests (e.g., Typhi-Dot) that have been proposed in the context of the new national surveillance programme.