Abstract
Orally transmitted Chagas disease has become a matter of concern due to outbreaks reported in four Latin American countries. Although several mechanisms for orally transmitted Chagas disease transmission have been proposed, food and beverages contaminated with whole infected triatomines or their faeces, which contain metacyclic trypomastigotes of Trypanosoma cruzi, seems to be the primary vehicle. In 2007, the first recognised outbreak of orally transmitted Chagas disease occurred in Venezuela and largest recorded outbreak at that time. Since then, 10 outbreaks (four in Caracas) with 249 cases (73.5% children) and 4% mortality have occurred. The absence of contact with the vector and of traditional cutaneous and Romana’s signs, together with a florid spectrum of clinical manifestations during the acute phase, confuse the diagnosis of orally transmitted Chagas disease with other infectious diseases. The simultaneous detection of IgG and IgM by ELISA and the search for parasites in all individuals at risk have been valuable diagnostic tools for detecting acute cases. Follow-up studies regarding the microepidemics primarily affecting children has resulted in 70% infection persistence six years after anti-parasitic treatment. Panstrongylus geniculatus has been the incriminating vector in most cases. As a food-borne disease, this entity requires epidemiological, clinical, diagnostic and therapeutic approaches that differ from those approaches used for traditional direct or cutaneous vector transmission.
Highlights
The following possible mechanisms for orally transmitted Chagas disease have been postulated. (i) Contamination of food, drinks, fruits and juices with the faeces of infected triatomines prepared in areas where humans have invaded the ecological niche and where the enzootic vector-reservoir cycle occurs
Diaz-Ungría (1965) demonstrated this mechanism in laboratory animals through biological vectors such as triatomines and mechanic vectors such as Musca domestica. (iii) Consumption of food contaminated with urine or marsupial scent gland secretions containing metacyclic trypomastigotes of T. cruzi (Jansen & Deane 1985). (iv) Ingestion of raw or undercooked hunting meat
A clinical approach - Traditional cutaneous and/or ocular inflammatory signs are not present and the clinical manifestations in the acute phase tend to be more severe compared to Chagas disease acquired by direct dermal or mucosal contact with the vector
Summary
Transmitted Chagas disease cases have occurred in the north-central coastal and western regions of Venezuela (Fig. 2). The link to the first microepidemic known in the country was made by the appearance of a second case, a teacher that worked at the same school where the girl studied (Alarcón de Noya et al 2010b). One hundred and two individuals were infected, as well as the lady who prepared the breakfast in a neighbourhood 6 km away from the school, where T. cruzi-infected P. geniculatus, rodents and dogs were demonstrated
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