Arbovirus infection inAedes aegyptihas historically been quantified from a sample of the adult population by pooling collected mosquitoes to increase detectability. However, there is a significant knowledge gap about the magnitude of natural arbovirus infection within areas of active transmission, as well as the sensitivity of detection of such an approach. We used indoorAe. aegyptisequential sampling with Prokopack aspirators to collect all mosquitoes inside 200 houses with suspected active ABV transmission from the city of Mérida, Mexico, and tested all collected specimens by RT-PCR to quantify: a) the absolute arbovirus infection rate in individually testedAe. aegyptifemales; b) the sensitivity of using Prokopack aspirators in detecting ABV-infected mosquitoes; and c) the sensitivity of entomological inoculation rate (EIR) and vectorial capacity (VC), two measures ABV transmission potential, to different estimates of indoorAe.aegyptiabundance. The total number ofAe.aegypti(total catch, the sum of allAe.aegyptiacross all collection intervals) as well as the number on the first 10-min of collection (sample, equivalent to a routine adult aspiration session) were calculated. We individually tested by RT-PCR 2,161Aedes aegyptifemales and found that 7.7% of them were positive to any ABV. Most infections were CHIKV (77.7%), followed by DENV (11.4%) and ZIKV (9.0%). The distribution of infectedAedes aegyptiwas overdispersed; 33% houses contributed 81% of the infected mosquitoes. A significant association between ABV infection andAe.aegyptitotal catch indoors was found (binomial GLMM, Odds Ratio > 1). A 10-min indoor Prokopack collection led to a low sensitivity of detecting ABV infection (16.3% for detecting infected mosquitoes and 23.4% for detecting infected houses). When averaged across all infested houses, mean EIR ranged between 0.04 and 0.06 infective bites per person per day, and mean VC was 0.6 infectious vectors generated from a population feeding on a single infected host per house/day. Both measures were significantly and positively associated withAe.aegyptitotal catch indoors. Our findings provide evidence that the accurate estimation and quantification of arbovirus infection rate and transmission risk is a function of the sampling effort, the local abundance ofAedes aegyptiand the intensity of arbovirus circulation.

Chagas disease is caused by Trypanosoma cruzi Chagas, a parasite with a life cycle involving hematophagous triatomines and vertebrate mammals as hosts. The parasite’s metapopulation is nested within its biological habitat patches, or hosts. In anthropogenic landscapes, the hierarchical arrangement of territorial units (locality, block, property) complicates the identification of an appropriate geographic patch size to assess parasite and host persistence. In this study, we evaluated local spatial co-occurrence patterns among Triatoma dimidiata (sensu lato) (Latreille), Didelphis virginiana Allen, and T. cruzi using 3 distinct patch sizes: (i) property area (x¯=3115 ± 1.01 m2), (ii) perceptual range of D. virginiana (x¯=16241 ± 5.29 m2), and (3) urban block area (x¯=36473 ± 4.89 m2) averages, replicated across 10 localities in Yucatán, Mexico. A total of 1,437 host individuals were sampled, with infection prevalence reaching 12% in triatomines and 50.1% in opossums. We delineated over 13,000 spatial patches for assessing parasite–host dynamics. Our results showed that block-sized patches had a higher density of hosts and stronger host–parasite interactions, resulting in increased parasite occupancy in a smaller number of patches. While interactions varied more across localities in these patches, most localities exhibited significant spatial autocorrelation in patches defined by the perceptual range of D. virginiana. Co-occurrence patterns were best captured at the urban block scale. Increasing patch size led to a higher probability of non-random spatial co-occurrence, indicating that geographic patch size is a key factor in understanding how the spatial ecology of its hosts affects the distribution and persistence of T. cruzi.