Molecular Epidemiologic Source Tracking of Orally Transmitted Chagas Disease, Venezuela - Vol. 19 No. 7 - July 2013 - Emerging Infectious Disease journal - CDC
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Volume 19, Number 7—July 2013
Molecular Epidemiologic Source Tracking of Orally Transmitted Chagas Disease, Venezuela
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Rapid urbanization presents new challenges for Chagas disease control in Latin America. Foci of disease are now reported in slums surrounding several Andean cities (1–3). Oral transmission is believed responsible for recent outbreaks of Chagas disease, most of which were characterized by atypically severe symptoms (4,5). Many cases have occurred in urban settings (5,6), amplifying the size and effect of the outbreaks.
AbstractOral outbreaks of Chagas disease are increasingly reported in Latin America. The transitory presence of Trypanosoma cruzi parasites within contaminated foods, and the rapid consumption of those foods, precludes precise identification of outbreak origin. We report source attribution for 2 peri-urban oral outbreaks of Chagas disease in Venezuela via high resolution microsatellite typing.
Sources of orally transmitted disease outbreaks vary, but contaminated food and juices are often blamed. However, after a contaminated food is eaten, it may take weeks for the onset of clinical signs and symptoms, and direct molecular and cytological incrimination of a particular batch of food/beverage has not been possible (5). Thus, evidence pointing to particular foodstuffs is often circumstantial.
Molecular epidemiologic analyses of human and environmental isolates are routinely used to track the source of outbreaks caused by foodborne pathogens. High-resolution molecular markers have been developed and validated for Trypanosoma cruzi, the parasite that causes Chagas disease (7,8). These markers, used in conjunction with careful sampling, can identify the source of foodborne outbreaks.
We studied 2 outbreaks of orally transmitted Chagas disease (120 cases, 5 deaths). The first occurred in Chichiriviche, Vargas State, a coastal community (population ≈800 persons) ≈50 km northwest of Caracas, Venezuela. The outbreak occurred at a primary school where food was prepared on site. In early April 2009, a total of 71 children (6–13 years of age) who attended the morning school shift and 14 adults became ill. Exposure of these persons to T. cruzi was established by use of IgM and IgG ELISA. Parasitemia was observed in 33 of the patients with serologic results positive for T. cruzi infection (9,10).
The second outbreak occurred in Antimano, a peri-urban slum southwest of central Caracas (Technical Appendix [PDF - 463 KB - 3 pages] Figure 1). In May 2010, 35 patients with suspected T. cruzi infection were examined at Hospital Miguel Perez Carreno in Caracas. Patients reported that they regularly ate at the same local communal canteen. Among the patients tested, 15 were positive for T. cruzi IgM and IgG (9). Parasitemia in 14 patients was confirmed indirectly by hemoculture. Of the 35 patients, 21 (2 adults, 19 children) were hospitalized.
To enable outbreak source attribution, we undertook intensive additional sampling of contemporary, nonhuman sources local to each outbreak and of human and nonhuman sources from more distant localities throughout Venezuela. In total, 246 T. cruzi strains and clones were typed for 23 microsatellite markers (Technical Appendix 1 [PDF - 463 KB - 3 pages] Table) (8). A list of the samples and their sites of origin is in Technical Appendix 2 [PDF - 463 KB - 3 pages]).