Populations of the common bed bug, Cimex lectularius, have recently undergone explosive growth. Bed bugs share many important traits with triatomine insects, but it remains unclear whether these similarities include the ability to transmit Trypanosoma cruzi, the etiologic agent of Chagas disease. Here, we show efficient and bidirectional transmission of T. cruzi between hosts and bed bugs in a laboratory environment. Most bed bugs that fed on experimentally infected mice acquired the parasite. A majority of previously uninfected mice became infected after a period of cohabitation with exposed bed bugs. T. cruzi was also transmitted to mice after the feces of infected bed bugs were applied directly to broken host skin. Quantitative bed bug defecation measures were similar to those of important triatomine vectors. Our findings suggest that the common bed bug may be a competent vector of T. cruzi and could pose a risk for vector-borne transmission of Chagas disease.
Modern cities represent one of the fastest growing ecosystems on the planet. Urbanization occurs in stages; each stage characterized by a distinct habitat that may be more or less susceptible to the establishment of disease vector populations and the transmission of vector-borne pathogens. We performed longitudinal entomological and epidemiological surveys in households along a 1900 Â 125 m transect of Arequipa, Peru, a major city of nearly one million inhabitants, in which the transmission of Trypanosoma cruzi, the aetiological agent of Chagas disease, by the insect vector Triatoma infestans, is an ongoing problem. The transect spans a cline of urban development from established communities to land invasions. We find that the vector is tracking the development of the city, and the parasite, in turn, is tracking the dispersal of the vector. New urbanizations are free of vector infestation for decades. T. cruzi transmission is very recent and concentrated in more established communities. The increase in land tenure security during the course of urbanization, if not accompanied by reasonable and enforceable zoning codes, initiates an influx of construction materials, people and animals that creates fertile conditions for epidemics of some vector-borne diseases.
Background Sexual reproduction provides an evolutionary advantageous mechanism that combines favorable mutations that have arisen in separate lineages into the same individual. This advantage is especially pronounced in microparasites as allelic reassortment among individuals caused by sexual reproduction promotes allelic diversity at immune evasion genes within individuals which is often essential to evade host immune systems. Despite these advantages, many eukaryotic microparasites exhibit highly-clonal population structures suggesting that genetic exchange through sexual reproduction is rare. Evidence supporting clonality is particularly convincing in the causative agent of Chagas disease, Trypanosoma cruzi , despite equally convincing evidence of the capacity to engage in sexual reproduction. Methodology/ Principle Findings In the present study, we investigated two hypotheses that can reconcile the apparent contradiction between the observed clonal population structure and the capacity to engage in sexual reproduction by analyzing the genome sequences of 123 T . cruzi isolates from a natural population in Arequipa, Peru. The distribution of polymorphic markers within and among isolates provides clear evidence of the occurrence of sexual reproduction. Large genetic segments are rearranged among chromosomes due to crossing over during meiosis leading to a decay in the genetic linkage among polymorphic markers compared to the expectations from a purely asexually-reproducing population. Nevertheless, the population structure appears clonal due to a high level of inbreeding during sexual reproduction which increases homozygosity, and thus reduces diversity, within each inbreeding lineage. Conclusions/ Significance These results effectively reconcile the apparent contradiction by demonstrating that the clonal population structure is derived not from infrequent sex in natural populations but from high levels of inbreeding. We discuss epidemiological consequences of this reproductive strategy on genome evolution, population structure, and phenotypic diversity of this medically important parasite.
We used sentinel animal enclosures to measure the rate of infestation by the Chagas disease vector, Triatoma infestans, in an urban community of Arequipa, Peru, and to evaluate the effect of deltamethrin-impregnated netting on that rate. Impregnated netting decreased the rate of infestation of sentinel enclosures (rate ratio, 0.23; 95% confidence interval, 0.13-0.38; P < 0.001), controlling for the density of surrounding vector populations and the distance of these to the sentinel enclosures. Most migrant insects were early-stage nymphs, which are less likely to carry the parasitic agent of Chagas disease, Trypanosoma cruzi. Spread of the vector in the city therefore likely precedes spread of the parasite. Netting was particularly effective against adult insects and late-stage nymphs; taking into account population structure, netting decreased the reproductive value of migrant populations from 443.6 to 40.5. Impregnated netting can slow the spread of T. infestans and is a potentially valuable tool in the control of Chagas disease.
ObjectiveTo assess the efficacy of strategies informed by behavioural economics for increasing participation in a vector control campaign, compared with current practice.DesignPragmatic cluster randomised controlled trial.SettingArequipa, Peru.Participants4922 households.InterventionsHouseholds were randomised to one of four arms: advanced planning, leader recruitment, contingent group lotteries, or control.Main outcome measuresParticipation (allowing the house to be sprayed with insecticide) during the vector control campaign.ResultsIn intent-to-treat analyses, none of the interventions increased participation compared with control (advanced planning adjusted OR (aOR) 1.07 (95% CI 0.87 to 1.32); leader recruitment aOR 0.95 (95% CI 0.78 to 1.15); group lotteries aOR 1.12 (95% CI 0.89 to 1.39)). The interventions did not improve the efficiency of the campaign (additional minutes needed to spray house from generalised estimating equation regressions: advanced planning 1.08 (95% CI −1.02 to 3.17); leader recruitment 3.91 (95% CI 1.85 to 5.97); group lotteries 3.51 (95% CI 1.38 to 5.64)) nor did it increase the odds that houses would be sprayed in an earlier versus a later stage of the campaign cycle (advanced planning aOR 0.94 (95% CI 0.76 to 1.25); leader recruitment aOR 0.68 (95% CI 0.55 to 0.83); group lotteries aOR 1.19 (95% CI 0.96 to 1.47)). A post hoc analysis suggested that advanced planning increased odds of participation compared with control among households who had declined to participate previously (aOR 2.50 (95% CI 1.41 to 4.43)).ConclusionsAchieving high levels of household participation is crucial for many disease prevention efforts. Our trial was not successful in improving participation compared with the existing campaign. The trial highlights persistent challenges to field experiments as well as lessons about the intervention design process, particularly understanding barriers to participation through a behavioural lens.Trial registration numberAmerican Economic Association AEARCTR-0000620.
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