Fig 1.
Lifecycle of T. cruzi demonstrating the predominant infection routes of people via vector-borne and foodborne transmission.
In this illustration, food is contaminated either via an infected triatomine (reduviid bug) or via secretions from an infected reservoir host. Note: Fig 1 was initially created in BioRender (www.biorender.com) and then modified. Less frequent transmission routes (not included in this figure) are: transplacental/congenital infection, blood transfusion and organ/bone marrow transplant infection, and laboratory accidents. In addition, consumption of inadequately cooked meat or blood from infected animals may act as a transmission route. An infected triatomine vector takes a blood meal from a person and infects them by defecating in or near to the wound with trypomastigotes in its feces (A). The trypomastigotes (B) invade cells and differentiate into intracellular amastigotes (C) that multiply by binary fission. These differentiate into trypomastigotes that are released into the circulation (D) and infect further cells (E) from various tissues, where they again transform into intracellular amastigotes and replicate (C). The triatomine vector becomes infected by feeding on an infected person (F). Inside the midgut of the vector (G), the ingested trypomastigotes (H) transform into epimastigotes (I). Here they multiply, before differentiating into infective metacyclic trypomastigotes in the hindgut (K) that may then be defecated into a feeding wound (A). Food, particularly fruit, may also be contaminated by being colonized by infected triatomines (L). In addition, reservoir hosts (such as opossums) can also be infected from trypomastigotes in the feces of feeding vectors (M). The circulating trypomastigote-intracellular amastigote cycle (N, O) then occurs. Food may be contaminated by trypomastigotes in the secretions of the opossums (P). Food, particularly fruit juices, contaminated by trypomastigotes (Q), either via infected triatomines (L) or secretions from infected opossums (P), may act as a vehicle for oral infection.
Table 1.
Summary of Chagas disease manifestation differences following vector-borne or foodborne transmission (references and greater detail included in the text below).
Table 2.
Estimates of DALYs associated with foodborne Chagas disease using older and newer global data, but not taking into account the greater disease severity associated with foodborne transmission.
Fig 2.
Change in rate of YLL due to ChD for children 0–14 years in 3 different regions of Latin America (shaded areas indicate uncertainty): data from IHME and graph created in Global Health Data Exchange GBD 2019 website (http://ghdx.healthdata.org/gbd-results-tool) [62].
In the absence of systematically sourced data on the proportion of foodborne ChD, whether these declines are associated with all potential exposures to ChD or primarily due to declining vector-borne disease cannot be estimated, particularly given the limited interventions to address the burden of foodborne ChD.