Work

Temperature variability increases Trypanosoma cruzi load but not the extrinsic incubation period in Triatoma infestans

Year: 2026

Type: article

Abstract: BACKGROUND: Trypanosoma cruzi, the etiologic agent of Chagas disease, is transmitted via the dejections of triatomine insects such as Triatoma infestans. Parasite development inside the vector depends on temperature, which determines the extrinsic incubation period (EIP) and modulates the parasite load. As global warming is expected to increase mean temperatures and thermal variability, these shifts may influence vector competence. METHODS: Triatoma infestans individuals were experimentally infected with T. cruzi Dm28c strain and then exposed to four thermal regimes: two constant (18 °C and 27 °C) and two fluctuating (18 ± 5 °C and 27 ± 5 °C). Parasite load in the dejection samples was quantified by quantitative PCR over 42 days and the time to the first positive dejection determined to estimate the EIP. RESULTS: Higher temperatures significantly shortened the EIP, with mean values of 18.6 days at 18 ± 0 °C, 17.3 days at 18 ± 5 °C, 9.6 days at 27 ± 0 °C and 11.0 days at 27 ± 5 °C. Temperature variability did not affect the EIP but it did increase parasite load under cold conditions. Parasite load showed a bell-shaped curve, peaking earlier and at higher levels at warmer temperatures. A larger volume of ingested blood also reduced the EIP, especially under cold treatments. CONCLUSIONS: Rising temperatures accelerate T. cruzi development within T. infestans, potentially enhancing vector competence under climate change scenarios. Although temperature variability did not affect the EIP, it increased parasite load, particularly under cold conditions, which is a relevant result considering that low temperatures have historically limited the vector and Chagas disease transmission. Temperature variability-not only mean warming-can modulate parasite development. Our results therefore provide novel and relevant insights into how climate change may alter vector-borne disease dynamics.

Source: Parasites & Vectors

DOI: 10.1186/s13071-026-07270-y