Over-dispersed Trypanosoma cruzi parasite load in sylvatic and domestic mammals and humans from northeastern Argentina

Abstract

Background The distribution of parasite load across hosts may modify the transmission dynamics of infectious diseases. Chagas disease is caused by a multi-host protozoan, Trypanosoma cruzi, but the association between host parasitemia and infectiousness to the vector has not been studied in sylvatic mammalian hosts. We quantified T. cruzi parasite load in sylvatic mammals, modeled the association of the parasite load with infectiousness to the vector and compared these results with previous ones for local domestic hosts. Methods The bloodstream parasite load in each of 28 naturally infected sylvatic mammals from six species captured in northern Argentina was assessed by quantitative PCR, and its association with infectiousness to the triatomine Triatoma infestans was evaluated, as determined by natural or artificial xenodiagnosis. These results were compared with our previous results for 88 humans, 70 dogs and 13 cats, and the degree of parasite over-dispersion was quantified and non-linear models fitted to data on host infectiousness and bloodstream parasite load. Results The parasite loads of Didelphis albiventris (white-eared opossum) and Dasypus novemcinctus (nine-banded armadillo) were directly and significantly associated with infectiousness of the host and were up to 190-fold higher than those in domestic hosts. Parasite load was aggregated across host species, as measured by the negative binomial parameter, k, and found to be substantially higher in white-eared opossums, cats, dogs and nine-banded armadillos (range: k = 0.3–0.5) than in humans (k = 5.1). The distribution of bloodstream parasite load closely followed the “80–20 rule” in every host species examined. However, the 20% of human hosts, domestic mammals or sylvatic mammals exhibiting the highest parasite load accounted for 49, 25 and 33% of the infected triatomines, respectively. Conclusions Our results support the use of bloodstream parasite load as a proxy of reservoir host competence and individual transmissibility. The over-dispersed distribution of T. cruzi bloodstream load implies the existence of a fraction of highly infectious hosts that could be targeted to improve vector-borne transmission control efforts toward interruption transmission. Combined strategies that decrease the parasitemia and/or host–vector contact with these hosts would disproportionally contribute to T. cruzi transmission control. Graphical Abstract

Geographic Distribution of the Genus Panstrongylus Berg, 1879 in the Neotropic with Emphasis on Trypanosoma cruzi Vectors

“…Modelling showed that Panstrongylus species richness overlapped with high Dasypus/Didelphis (potential blood source for this vector) areas, all coinciding with CD cases (latest 2014). This scenario of overlap would be a potential risk factor for an increase in the incidence of this anthroponotic disease ( Figure 3 C,D) [ 11 , 72 , 73 , 74 ]…”

Trypanosoma cruzi parasitemia in chronic Chagas disease: Insights from hierarchical modeling

“…It is my view that estimates like the ones discussed here, and especially those presented in Fig 1 , are far more informative than measures of bloodstream parasite availability that disregard imperfect (<100%) test sensitivity or measures of test sensitivity that disregard imperfect (<100%) parasite availability [ 1 ]. The former are often presented as estimates of the “infectiousness” of pathogen-carrying hosts to blood-feeding vectors (e.g., [ 13 ]), and the latter as estimates of the “clinical sensitivity” of diagnostic procedures (cf. [ 14 ]); as a rule, a formal assessment of how test sensitivity affects measures of “infectiousness”, and of how pathogen availability affects measures of “clinical sensitivity”, is lacking in these kinds of studies.…”