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      Rhodnius prolixus Colonization and Trypanosoma cruzi Transmission in Oil Palm ( Elaeis guineensis) Plantations in the Orinoco Basin, Colombia

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          Abstract.

          Trypanosoma cruzi is the etiological agent of Chagas disease that infects more than seven million people in Latin America. The parasite is transmitted by triatomine insects, of which some species are often associated with palms. The establishment of oil palm plantations ( Elaeis guineensis) in the Orinoco region (Colombia) has been rapidly growing, possibly constituting a new environment for the establishment and increase in triatomine populations. In this study, the potential of Rhodnius prolixus to colonize E. guineensis plantations and maintain T. cruzi transmission was assessed. Fieldwork was conducted in two areas located in the department of Casanare for sampling E. guineensis and Attalea butyracea palms, sampling for triatomines to determine their abundance and prevalence of T. cruzi infection. To assess T. cruzi transmission potential in the area, sylvatic and domestic mammals were sampled. Results showed that palm infestation with triatomines was higher in A. butyracea than in E. guineensis palms and T. cruzi infection in triatomines varied between habitats for one study area, but was constant in the other site. Trypanosoma cruzi–infected mammals in the E. guineensis plantations were mainly generalist rodents, suggesting that these mammals could have an important role in T. cruzi transmission in plantations. In conclusion, E. guineensis plantations in the Orinoco region are suitable habitats for R. prolixus and T. cruzi transmission.

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          Anthropogenic land use change and infectious diseases: a review of the evidence.

          Humans have altered ecosystems worldwide, and it is important to understand how this land use change impacts infectious disease transmission in humans and animals. We conducted a systematic review 305 scientific articles investigating how specific types of anthropogenic land use change influence infectious disease dynamics. We summarized findings, highlighted common themes, and drew attention to neglected areas of research. There was an increase in publications on this topic over the last 30 years spanning diseases of humans, livestock, and wildlife, including a large number of zoonotic pathogens. Most papers (66.9%) were observational, 30.8% were review or concept papers, and few studies (2.3%) were experimental in nature, with most studies focusing on vector-borne and/or multi-host pathogens. Common land use change types related to disease transmission were deforestation/forest fragmentation/habitat fragmentation, agricultural development/irrigation, and urbanization/suburbanization. In response to anthropogenic change, more than half of the studies (56.9%) documented increased pathogen transmission, 10.4% of studies observed decreased pathogen transmission, 30.4% had variable and complex pathogen responses, and 2.4% showed no detectable changes. Commonly reported mechanisms by which land use change altered infectious disease transmission included alteration of the vector, host, and pathogen niche, changes in host and vector community composition, changes in behavior or movement of vectors and/or hosts, altered spatial distribution of hosts and/or vectors, and socioeconomic factors, and environmental contamination. We discussed observed patterns in the literature and make suggestions for future research directions, emphasizing the importance of ecological and evolutionary theory to understand pathogen responses in changing landscapes.
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            Current epidemiological trends for Chagas disease in Latin America and future challenges in epidemiology, surveillance and health policy.

            Chagas disease, named after Carlos Chagas, who first described it in 1909, exists only on the American Continent. It is caused by a parasite, Trypanosoma cruzi, which is transmitted to humans by blood-sucking triatomine bugs and via blood transfusion. Chagas disease has two successive phases: acute and chronic. The acute phase lasts six-eight weeks. Several years after entering the chronic phase, 20-35% of infected individuals, depending on the geographical area, will develop irreversible lesions of the autonomous nervous system in the heart, oesophagus and colon, and of the peripheral nervous system. Data on the prevalence and distribution of Chagas disease improved in quality during the 1980s as a result of the demographically representative cross-sectional studies in countries where accurate information was not previously available. A group of experts met in Brasilia in 1979 and devised standard protocols to carry out countrywide prevalence studies on human T. cruzi infection and triatomine house infestation. Thanks to a coordinated multi-country programme in the Southern Cone countries, the transmission of Chagas disease by vectors and via blood transfusion was interrupted in Uruguay in 1997, in Chile in 1999 and in Brazil in 2006; thus, the incidence of new infections by T. cruzi across the South American continent has decreased by 70%. Similar multi-country initiatives have been launched in the Andean countries and in Central America and rapid progress has been reported towards the goal of interrupting the transmission of Chagas disease, as requested by a 1998 Resolution of the World Health Assembly. The cost-benefit analysis of investment in the vector control programme in Brazil indicates that there are savings of US$17 in medical care and disabilities for each dollar spent on prevention, showing that the programme is a health investment with very high return. Many well-known research institutions in Latin America were key elements of a worldwide network of laboratories that carried out basic and applied research supporting the planning and evaluation of national Chagas disease control programmes. The present article reviews the current epidemiological trends for Chagas disease in Latin America and the future challenges in terms of epidemiology, surveillance and health policy.
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              Adaptive strategies of Yersinia pestis to persist during inter-epizootic and epizootic periods

              Plague is a flea-borne zoonotic bacterial disease caused by Yersinia pestis. It has caused three historical pandemics, including the Black Death which killed nearly a third of Europe's population in the 14th century. In modern times, plague epizootics can extirpate entire susceptible wildlife populations and then disappear for long time periods. Understanding how Y. pestis is maintained during inter-epizootic periods and the factors responsible for transitioning to epizootics is important for preventing and controlling pathogen transmission and ultimately reducing the burden of human disease. In this review, we focus primarily on plague in North American foci and discuss the potential adaptive strategies Y. pestis might employ to ensure not only its survival during inter-epizootic periods but also the rapid epizootic spread and invasion of new territories that are so characteristic of plague and have resulted in major pandemics and establishment of plague foci throughout much of the world.
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                Author and article information

                Journal
                Am J Trop Med Hyg
                Am. J. Trop. Med. Hyg
                tpmd
                tropmed
                The American Journal of Tropical Medicine and Hygiene
                The American Society of Tropical Medicine and Hygiene
                0002-9637
                1476-1645
                July 2020
                26 May 2020
                26 May 2020
                : 103
                : 1
                : 428-436
                Affiliations
                [1 ]Grupo de Investigación en Biología Matemática y Computacional (BIOMAC), Universidad de los Andes, Bogotá, Colombia;
                [2 ]Centro de Investigaciones en Microbiología y Parasitología Tropical (CIMPAT), Facultad de Ciencias, Universidad de los Andes, Bogotá, Colombia
                Author notes
                [* ]Address correspondence to Diana Erazo or Juan Cordovez, Universidad de los Andes, Cra 1 Este #19a–40, Bogota 111711, Colombia. E-mails: erazodiana1@ 123456gmail.com or jucordov@ 123456uniandes.edu.co

                Financial support: The research was funded by Vicerrectoria de Investigaciones, Universidad de los Andes, and Colciencias (call 617 of 2013).

                Authors’ addresses: Diana Erazo, Juan Daniel Umaña, and Juan Cordovez, Grupo de Investigación en Biología Matemática y Computacional (BIOMAC), Universidad de los Andes, Bogotá, Colombia, E-mails: erazodiana1@ 123456gmail.com , jd.umana10@ 123456uniandes.edu.co , and jucordov@ 123456uniandes.edu.co . Camila González, Felipe Guhl and Juan Alejandro Morales-Betancourt, Centro de Investigaciones en Microbiología y Parasitología Tropical (CIMPAT), Facultad de Ciencias, Universidad de los Andes, Bogotá, Colombia, E-mails: c.gonzalez2592@ 123456uniandes.edu.co , fguhl@ 123456uniandes.edu.co , and ja.morales12@ 123456uniandes.edu.co .

                Article
                tpmd190331
                10.4269/ajtmh.19-0331
                7356441
                32458775
                9093bf53-d722-47dc-a65c-517944dffdef
                © The American Society of Tropical Medicine and Hygiene

                This is an open-access article distributed under the terms of the Creative Commons Attribution (CC-BY) License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

                History
                : 29 April 2019
                : 06 November 2019
                Page count
                Pages: 9
                Categories
                Articles

                Infectious disease & Microbiology
                Infectious disease & Microbiology

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