Chagas disease is zoonotic illness or an anthropozoonosis caused by flagellated protozoan parasite Trypanosoma cruzi. This infection presents alarming rates of incidence/prevalence, for this reason, is recognized worldwide as one of the 13 most neglected tropical diseases 1. Numerous studies have demonstrated the existence of domestic dogs infected with T. cruzi across endemic areas ranging from southern United States of America to Argentina 2. The reported prevalence varies widely (1.42-92%), depending on ecoepidemiological and sociocultural factors 3. It is important to emphasize that the natural infection in dogs with T. cruzi occurs in the same way as in humans, that is to say, through active transmission by vectors, contamination by feces infected with the parasite through wounds or the conjunctiva, can also occur by ingestion of infected vectors or tissues of wild animals present in the peridomicile or home 4. The transplacental transmission is also an important mode of transmission in dogs 5. Nevertheless, the main mode of transmission in canine species seems to be the ingestion of infected vectors 6. During the life cycle of T. cruzi the trypomastigotes present in the heces of the triatomines are introduced in the mammalian host by contamination of the insect bite or mucosal membranes. The metacyclic form can penetrate a variety of phagocytic and nonphagocytic nucleated cells. Once inside the cells the parasite becomes in amastigote, which are multiplicative forms that divide into cells. Due to the high parasitic load they produce the lysis of the cells and escapes into the cytoplasm. The amastigotes transform to slender trypomastigotes which can invade adjacent cells, this forms can be ingested by triatomines and they transform into epimastigotes Finally, after migration to the bug's hindgut, the epimastigotes differentiate into infectious metacyclic trypomastigotes, in this way the life cycle of this microorganism is completed 7.
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Copyright © 2018 María Elizabeth Márquez Contreras, et al.
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Chagas disease is a zoonotic disease caused by flagellated protozoan parasite T. cruzi. The infection is recognized worldwide as one of the 13 most neglected tropical diseases 1. Numerous studies have demonstrated the existence of domestic dogs infected with T. cruzi across endemic areas ranging from southern United States of America to Argentina 2. The reported prevalence varies widely ranging from 1.42 to 92% depending on ecoepidemiological and sociocultural factors 3.
In both humans and dogs the mode of transmission of T. cruzi natural infection is through vectors, wound and conjunctiva contamination by feces of contaminated animals, and ingestion of infected vectors or tissues of wild animals living in the peridomicile or home 4. Transplacental transmission is also an important mode of transmission in dogs 5. The major mode of transmission in canine species, however, appears to be the ingestion of infected vectors 6.
Life Cycle of T. Cruzi
In the life cycle of T. cruzi the trypomastigotes present in the heces of the triatomines are introduced into the mammalian host by contamination of the insect bite or mucosal membranes. The metacyclic form can penetrate a variety of phagocytic and nonphagocytic nucleated cells. Once inside the cells the parasite becomes an amastigote, which are multiplicative forms that divide into cells. The high parasitic load produces lysis of infected cells and escapes into the cytoplasm. The amastigotes transform to slender trypomastigotes which invade adjacent cells. The trypomastigotes are ingested by triatomines before transforming into epimastigotes, which migrate to the triatomine bug’s hindgut and differentiation into infectious forms of metacyclic trypomastigotes completes the life cycle 7.
Clinical manifestations in dogs range from asymptomatic, acute myocarditis, chronic progressive cardiac disease to sudden death 8, 3. The clinical signs such as the development of diffuse chronic myocarditis with histological and electrocardiographic changes in Chagas-infected dogs during both the chronic and acute stages closely resemble the symptoms of human disease 4. This is the reason why canine species are considered the experimental model of choice for human Chagas disease study 2. Acute illness has been reported more frequently in very young dogs (less than 1 year old) and generally involves myocarditis and cardiac arrhythmias 3. The chronic phase of Chagas' disease in canine species chagasic, can cause severe cardiac damage involving dilated cardiomyopathy, electrocardiogram (ECG) abnormalities, and cardiac failure 9. This clinical presentation is highly variable and depends on the type of strain, route of infection, and parasite burden 10.
Diagnosis of Chagas Disease Canine
The diagnosis is based on serology 11, direct or indirect parasitological tests, and molecular tests 12. Parasitological diagnosis is made by microscopic examination of either the lymph node aspirates of blood, or cerebrospinal fluid (CSF) of infected dogs 13. Polymerase chain reaction (PCR) technique could be used on any patient sample that contains trypanosome DNA 14.
Epidemiology of Chagas Disease in Canines
Canine species are considered an important reservoir of T. cruzi in the domestic cycle carrying a risk for human population; because, these animals living in close proximity to humans are within the transmission and maintenance cycles of the parasite and serve as a source of food for insect vectors 2, 15. Reservoirs may be considered as a complex ecological system consisting of one or more species responsible for maintaining a given parasite species in nature. The infestation of houses and peridomestic areas is considered to be a major risk factor for Chagas disease transmission. Dog infection with T. cruzi is an important veterinary health concern in many countries of South America and more recently in the United States, in which the seroprevalence of specific anti-T. cruzi antibodies has also been reported 16, 17. Infected vectors have been reported in Texas military kennels, where some dogs showed clinical signs compatible with Chagas disease infection 18. From the veterinary point of view, it is also important to consider that dogs are susceptible to acquire American trypanosomiasis characterized by heart conditions, such as electrical conduction disturbances, and ventricular and supraventricular arrhythmias, as well as secondary signs such as ascites, respiratory distress, thoracic effusion, and cyanosis. Texas is a high-risk state for transmission of the parasite to dogs, considering the diversity of triatomine vectors, reservoir hosts, and previous documentation of canine disease 19. A high seroprevalence of canine infection with T. cruzi has been detected from southeastern USA States of Louisiana, Oklahoma, Georgia, and Texas; showing the epidemiological role of the domestic dog 20. In canines from countries in Latin American, various reports showed seroprevalences from 24% to 65% 21, 22. The presence of infected canine species increases the risk of transmission of parasites to vectors, and thus the probability of infection in humans. Generally, canine infections are more prevalent than human infections, a fact likely related to oral T. cruzi transmission, a more efficient route of infection and apparently common to many mammals 23, and also the fact that dogs often sleep near houses and may come in greater contact with peridomiciliary vectors.
It has been considered that separating domestic animals, mainly dogs, from people can significantly reduce transmission to humans 24. The fact that there is a high prevalence of canine infections represents a warning signal that should lead to the planning and execution of effective vector control strategies, i.e. it is essential to carry out fumigation strategies of areas infested with triatomines, to exterminate them and thus eliminate transmission 25.
In studies carried out by Meyer et al. (2017) 26 in along border Texas-México, the dogs showed an overall apparent seroprevalence of 7.4-18.9%. This values are similars to that described in dogs of endemic populations for Chagas in Peru (12.3%) 27, Argentina (45.6%) 11, Panama (11.1%) 28, Costa Rica (27.7%) 29, Yucatan State, Mexico (9.8%-14.4%) 30 and Mexico State, Mexico (10%-15.8%) 31.
The dogs are targeted in a Chagas’ disease control strategy, because they are considered natural sentinels 26. These animals generally inhabit a defined territory; are accessible, easy to enumerate and capture, and their population allows representative sampling 31.
Control measures to prevent transmission of Chagas' disease in endemic areas include: removing litter from the surroundings of the house, keeping clean areas where dogs stayed longer, and conduct periodic assessments to ensure the animals are free of insects. Placing meshes on doors and windows, and covering cracks in the whole house helps prevent the entry of triatomines to the home and minimizes their contact with humans or canine species.
- 1.Hotez P, Molyneux D, Fenwick A, Kumaresan J, Sachs S et al. (2007) Control of neglected tropical diseases. , N Engl J Med 357(10), 1018-1027.
- 2.Gurtler R, Cecere M, Lauricella M, Cardinal M, Kitron U et al. (2007) Domestic dogs and cats as source ofTrypanosomacruziinfection in rural northwestern Argentina. , Parasitology 134, 69-82.
- 3.Kjos S, Snowden K, Craig T, Lewis B, Ronald N et al. (2008) Distribution and characterization of canine Chagas disease in Texas. Vet Parasitol 152(3-4):. 249-256.
- 4.Barr S. (2009) Canine Chagas’ disease (American Trypanosomiasis) in North America. , Vet Clin North Am Small Anim Pract 39(6), 1055-1064.
- 5.Castañera M, Lauricella M, Chuit R, Gürtler R. (1998) Evaluation of dogs as sentinels of the transmission ofTrypanosomacruziin a rural area of north-western Argentina. , Ann Trop Med Parasitol 92(6), 671-683.
- 6.Eloy L, Lucheis S. (2009) Canine trypanosomiasis: etiology of infection and implications for public health. , J Venom Anim Toxins Incl Trop Dis 15(4), 589-611.
- 7.Tyler K, Engman D. (2001) The life cycle ofTrypanosomacruzirevisited. , Int J Parasitol 31(5), 472-481.
- 8.Barr S. (2009) Canine Chagas’ disease (American trypanosomiasis) in North America. , Vet Clin North Am Small Anim Pract 39(6), 1055-1064.
- 9.Barr S, Simpson R, Schmidt S, Bunge M, Authement J et al. (1989) Chronic dilatative myocarditis caused byTrypanosomacruziin two dogs. , J Am Vet Med Assoc 195(9), 1237-1241.
- 10.González-Vieyra S, Ramírez-Durán N, Sandoval-Trujillo Á, Vázquez-Chagoyán J, Monroy-Salazar H.Barbabosa-Pliego A (2011)Trypanosomacruziin dogs: electrocardiographic and echocardiographic evaluation, in Malinalco. , State of Mexico. Res Rep Trop Med 2, 155-161.
- 11.Enriquez G, Cardinal M, Orozco M, Schijman A, Gürtler R. (2013) Detection ofTrypanosomacruziinfection in naturally-infected dogs and cats using serological, parasitological and molecular methods. , Acta Trop 126(3), 211-217.
- 12.Lizundia R, Picado A, Cordero M, Calderón A, Deborggraeve S et al. (2014) Molecular and serological rapid tests as markers ofTrypanosomacruziinfection in dogs in Costa Rica Trop Parasitol. 4(2), 111-114.
- 13.Fujita O, Sanabria L, Inchausti A, A De, Tomizawa Y et al. (1994) Animal reservoirs forTrypanosomacruziinfection in an endemic area in Paraguay. , J Vet Med Sci 56(2), 305-308.
- 14.Araújo F, Bahia M, Magalhães N, Martins-Filho O, Veloso V et al. (2002) Follow-up of experimental chronic Chagas’ disease in dogs: use of polymerase chain reaction (PCR) compared with parasitological and serological methods. , Acta Trop 81(1), 21-31.
- 15.Ortega-Pacheco A, Guzmán-Marín E, Acosta-Viana K, Vado-Solís I, Jiménez-Delgadillo B et al. (2017) Serological survey ofLeptospirainterrogans,Toxoplasma gondiiandTrypanosomacruziin free roaming domestic dogs and cats from a marginated rural area of Yucatan Mexico. , Vet Med Sci 3(1), 40-47.
- 16.Villalobos G, Martínez-Hernández F, P de la Torre, Laclette J, Espinoza B. (2011) Entomological indices, feeding sources, and molecular identification ofTriatomaphyllosoma(Hemiptera:. Reduviidae) one of the main vectors of Chagas disease in the Istmo de , Tehuantepec, Oaxaca, Mexico, Am J Trop Med Hyg 85(3), 490-497.
- 17.Bern C, Kjos S, Yabsley M, Montgomery.S (2011)Trypanosomacruziand Chagas´Disease in the United States. Clinical Microbiology Reviews. 24(4), 655-681.
- 18.Arce-Fonseca M, Carrillo-Sánchez S, Molina-Barrios R, Martínez-Cruz M, Cedillo-Cobián J et al. (2017) Seropositivity forTrypanosomacruziin domestic dogs from Sonora. , Mexico, Infect Dis Poverty 6(1), 120.
- 19.Tenney T, Curtis-Robles R, Snowden K, Hamer S. (2014) Shelter dogs as sentinels forTrypanosomacruzitransmission across Texas. Emerg Infect Dis. 20(8), 1323-1326.
- 20.Mc Phatter L, Roachell W, Mahmood F, Hoffman L, Lockwood N et al. (2012) Vector surveillance to determine species composition and occurrence ofTrypanosomacruziat three military installations in San Antonio. , Texas, US Army Med Dep J 3, 12-21.
- 21.Kjos S, Snowden K, Olson J. (2009) Biogeography andTrypanosomacruziinfection prevalence of Chagas disease vectors in Texas. , USA. Vector Borne Zoonotic Dis 9(1), 41-50.
- 22.Curtis-Robles R, Snowden K, Dominguez B, Dinges L, Rodgers S et al. (2017) Epidemiology and molecular typing ofTrypanosomacruziin naturally-infected hound dogs and associated triatomine vectors in Texas. , USA. Plos Negl Trop Dis 11(1), 0005298.
- 23.Beard C, Pye G, Steurer F, Rodriguez R, Campman R et al. (2003) Chagas disease in a domestic transmission cycle. , southern Texas, USA, Emerg Infect Dis 9(1), 103-105.
- 24.Estrada-Franco J, Bhatia V, Diaz-Albiter H, Ochoa-Garcia L, Barbabosa A et al. (2006) HumanTrypanosomacruziinfection and seropositivity in dogs. , Mexico. Emerg Infect Dis 12(4), 624-630.
- 25.Barbabosa-Pliego A, Gil P, Hernández D, Aparicio-Burgos J, R de Oca-Jiménez et al. (2011) Prevalence ofTrypanosomacruziin dogs (Canisfamiliaris) and triatomines during2008in a sanitary region of the state of Mexico, Mexico. Vector Borne Zoonotic Dis. 11(2), 151-156.
- 26.Meyers A, Meinders M, Hamer S. (2017) WidespreadTrypanosomacruziinfection in government working dogs along the Texas-Mexico border: Discordant serology, parasite genotyping and associated vectors. , PLoS Negl Trop Dis 11(8), 0005819.
- 27.Castillo-Neyra R, Chou Chu L, Quispe-Machaca V, Ancca-Juarez J, Malaga Chavez F et al. (2015) The potential of canine sentinels for reemergingTrypanosomacruzitransmission. Prev Vet Med 120(3-4):. 349-356.
- 28.Pineda V, Saldaña A, Monfante I, Santamaría A, Gottdenker N et al. (2011) Prevalence of trypanosome infections in dogs from Chagas disease endemic regions in Panama, Central America. Vet Parasitol 178(3-4):. 360-363.
- 29.Montenegro V, Jimenez M, Dias J, Zeledon R. (2002) Chagas disease in dogs from endemic areas of Costa Rica. Mem Inst Oswaldo Cruz. 97(4), 491-494.
- 30.Jimenez-Coello M, Poot-Cob M, Ortega-Pacheco A, Guzmán-Marín E, Ramos-Ligonio A et al. (2008) American trypanosomiasis in dogs from an urban and rural area of Yucatan, Mexico. Vector Borne Zoonotic Dis. 8(6), 755-761.