Population genetics of Triatominae
L. Stevens1 and PL. Dorn2
''University of Vermont, Burlington, VT, United States, 2Loyola University New Orleans, New Orleans, LA, United States
Chapter Outline
Introduction 169
The importance of population genetics in Chagas disease epidemiology and control 169 Why study the population genetics of insect disease vectors? 170 Vector population structure directs Chagas disease epidemiology and control 171 Genetic variation, population structure, and implications for vector control 171
Evolutionary forces and genetic variation 171 Hardy-Weinberg equilibrium 175 The neutral theory and statistical tests 178 Spatial scale 179
Genetic variation and population structure of T. infestans, T. dimidiata, R. prolixus and other significant vectors of human Chagas disease 180
T. infestans 180 T. dimidiata 184 R. prolixus 187 Other species of Triatoma 189 Perspective and future directions 190 Acknowledgments 190 References 191
Introduction
The importance of population genetics in Chagas disease epidemiology and control
Launched in 1991, the “Southern Cone Initiative” was the first multicountry control program designed to eliminate domestic populations of Triatoma infestans, arguably the main vector of Chagas disease worldwide at the time and certainly in the Southern Cone of South America. This initiative was followed by Andean and Central American initiatives in 1997. Although implementation of control activities in the Andean subregion has been slow and coverage incomplete,1 these three initiatives have been highly successful in eliminating domestic vector populations, thus interrupting disease transmission throughout much of Latin America.2,3 However,
American Trypanosomiasis Chagas Disease. DOI: http://dx.doi.org/10.1016/B978-0-12-801029-7.00008-3
Copyright © 2017 Elsevier Inc. All rights reserved.
less success has been realized in the Gran Chaco region (northern Argentina, Bolivia, and Paraguay), partially due to high levels of insect reinfestation after spraying.4 A key question is whether recurrent infestations are due to residual domestic populations that survive insecticide spraying, or to reinvasion of insects from external sources (either from unsprayed communities or from sylvatic [wild] foci).
In the Southern Cone, 10 years of coordinated control actions reduced disease incidence by 94%.5 Nonetheless, recent estimates show that infection prevalence remains at 6 million, with 12,000 deaths annually.6 What epidemiological factors contribute to new cases? Current hypotheses include: residual insects—perhaps from inadequate insecticide application or insecticide resistance; reinfestation from nearby houses or villages; and invasion of sylvatic vectors. Historically passive transport by humans expanded the geographic range of many vector species including two major vectors, Triatoma infestans and Rhodnius prolixus. In many cases, the vector species were exclusively domestic in the extended range and once eliminated, disease transmission was greatly reduced. However, over their native range, species are distributed across extensive sylvatic ecotopes, making the recolonization of treated villages a recurrent problem. In their own respective “home” areas in the Bolivian highlands and Venezuelan plains, T. infestans and R. prolixus reinfestation from sylvatic foci requires continued vigilance.7,8 New epidemiological scenarios are also a matter of concern. For example, in Amazonia, foci of relatively intense transmission related to large-scale harvesting or consumption of forest products (such as acal fruits and pia- cava fibers) are overlaid onto a background of low-intensity, widespread, continuous vector-borne transmission.9 Insecticide resistance is also an increasing problem.10
Why study the population genetics of insect disease vectors?
Population genetics can provide insight into ecological and evolutionary processes (i.e., mutation, genetic drift, natural selection, and migration) relevant to vector-borne disease transmission by examining spatial and temporal patterns of genetic variation in insect vectors (Fig. 8.1). How much migration and interbreeding occur among nearby
Figure 8.1 Examples of (A) random population genetic structure and (B) distinct subpopulations with different amounts of gene flow (migration) among them.
populations? What barriers limit gene flow (e.g., deforestation, mountain ranges, biogeographical limits)? When insects reappear following insecticide treatment, do they represent recrudescent domestic populations, sylvatic colonizers, or migrants from nearby houses or villages? Do genetically different subpopulations also differ in vectorial competence or capacity? How fast might insecticide-resistance alleles spread throughout a population? The answers to these population genetics questions are of fundamental importance to the epidemiology and control of vector-borne diseases.
