Chagas' disease: an emergent urban zoonosis. The caracas valley (Venezuela) as an epidemiological model.

The unprecedented emergence of important public health and veterinary zoonoses is usually a result of exponential population growth and globalization of human activities. I characterized Chagas' disease as an emergent zoonosis in the Caracas Valley (Venezuela) due to the following findings: the presence of reservoirs (Didelphis marsupialis, Rattus rattus) and vectors (Panstrongylus geniculatus, Panstrongylus rufotuberculatus) infected with Trypanosoma cruzi in urbanized or marginalized areas; the elevated contact between P. geniculatus and human beings detected by parasitological and molecular examinations of triatomine feces demonstrated the possibility of transmission risks; a study of outbreaks of urban Chagas' disease reported the first proven case of oral transmission of T. cruzi to human beings; the risk of transmission of glandular metacyclic stages from marsupials by experimental ocular and oral instillation; mice genitalia infected with T. cruzi contaminated blood resulted in the formation of amastigotes very close to the lumen suggesting that there may be a possibility of infection via their release into the urine and thence to the exterior; the ubiquitous histotropism and histopathology of T. cruzi was demonstrated using a mouse model; the presence of experimental T. cruzi pseudocysts in adipose, bone-cartilage, and eye tissue indicated a potential risk for transplants. Socio-sanitary programs that include improvements in housing, vector control, and access to medical treatment, as well as strategies aimed at combating social inequalities, poverty, and underdevelopment should be undertaken in those areas where zoonoses are most prevalent. Disciplines, such as Ecology, Epidemiology, Medical Entomology, Human and Veterinary Medicine, Environmental Studies, Public Health, Social and Political Studies, Immunology, Microbiology, and Pharmacology could all provide important contributions that aim to reduce the occurrence of factors governing the spread of emergent diseases.

Achatina fulica Bowdich, 1822 (Mollusca, Gastropoda, Achatinidae) carrier of Helminthes, Protozoa and Bacteria in northeast Venezuela / Achatina fulica Bowdich, 1822 (Mollusca, Gastropoda, Achatinidae) hospedador de helmintos, protozoarios y bacterias en el noreste de Venezuela

Por cuanto el molusco Achatina fulica nativo del África es vector de helmintos, pero su relación con protozoarios y bacterias es poco conocida, decidimos estudiar las excretas de 1.200 ejemplares capturados en los estados Anzoátegui, Monagas, Sucre y Nueva Esparta, del noreste de Venezuela. Su moco pedal y heces mostraron infección por los protozoarios Chilomastix spp., Trichomonas spp., Giardia spp., Balantidium spp., Entamoeba spp., Iodamoeba spp., Blastocystis spp. Y por los helmintos de los grupos Ascarioidea, Trichuroidea, Ancylostomatidae y Cestoda. El moco céfalopodal mostró únicamente larvas de Rhabditida. Las bacterias Citrobacter freundii, Escherichia coli, Klebsiella pneumoniae, K. azaenae, Aeromonas hydrophila, Acinetobacter baumannii, Pseudomonas aeruginosa, Campylobacter spp. infectaron a las tres excretas. Los mecanismos de transmisión y la composición de las excretas, como nichos fisiológicamente apropiados para los organismos encontrados, son discutidos en relación con el riesgo epidemiológico que el molusco representa en salud pública y veterinaria.

The mollusk Achatina fulica, native to Eastern Equatorial Africa, has been incriminated as a carrier or vector of helminthes. Nevertheless, information in the literature as regards its status as a carrier for bacteria is scarce, and we could find no reference at all for its relation to protozoa. We studied microscopically the excreta from 1200 snails captured in Anzoátegui, Monagas, Sucre and Nueva Esparta states, in northeast Venezuela. The pedal mucus and feces were infected by the protozoa Chilomastix spp., Trichomonas spp., Giardia spp., Balantidium spp., Entamoeba spp., Iodamoeba spp., Blastocystis spp., as well as helminthes of Ascarioidea, Trichuroidea, Ancylostomatidae and Cestoda groups. The only helminthes found in the cephalopodal mucus were Rhabditida larvae. The three excreta were also infected by the bacteria: Citrobacter freundii, Escherichia coli, Klebsiella pneumoniae, K. azaenae, Aeromonas hydrophila, Acinetobacter baumannii, Pseudomonas aeruginosa, Campylobacter spp. Risk of infection and transmission mechanisms as well as the composition of the excreta as appropriate physiological niches for the organisms mentioned, are discussed with regard to the epidemiological importance of this snail for in human and veterinary health.

Trypanosoma cruzi III from armadillos (Dasypus novemcinctus novemcinctus) from Northeastern Venezuela and its biological behavior in murine model. Risk of emergency of Chagas' disease.

Trypanosoma cruzi, etiological agent of Chagas' disease, was isolated from armadillos (Dasypus novemcinctus novemcinctus) captured in rural communities Northeastern Venezuela from Nueva Esparta State (no endemic for Chagas' disease), Monagas and Anzoátegui States (endemics). The isolates, genetically typed by PCR-RFLP as belonging to the TcIII DTU, have demonstrated in murine model heterogenic parasitemia, mortality and histotropism with marked parasitism in cardiac, skeletal, and smooth myocytes that showed correlation with lymphobasophilic inflammatory infiltrates. Our finding of T. cruzi infected armadillos in Isla Margarita (Nueva Esparta State), together with reports of triatomine vectors in this region, the accentuated synanthropy of armadillos, intense economic activity, migration due to tourism and the lack of environmental education programs all of them represent risks that could cause the emergence of Chagas' disease in this area. This is the first report of the TcIII DTU in Northeastern Venezuela, thus widening the geographic distribution of this DTU.

Trypanosoma cruzi: experimental parasitism in the central nervous system of albino mice.

Trypanosoma cruzi causes a pan-infection, Chagas disease, in American mammals through fecal transmission by triatomine insects, resulting in an acute phase parasitemia with intracellularity mainly in the myocells and cells of the central nervous system (CNS).The parasites, due to the immune response, then decrease in number, characteristic of the life-long chronicity of the disease. We infected a mouse model with isolates obtained from reservoirs and vectors from rural and urban endemic areas in Venezuela. Intracellular proliferation and differentiation of the parasite in astrocytes, microglia, neurons, endothelial cells of the piarachnoid, cells of the Purkinje layer, and spinal ganglion cells, as well as extracellularly in the neuropil, were evaluated during the acute phase. Damages were identified as meningoencephalitis, astrocytosis, reactive microglia, acute neuronal degeneration by central chromatolysis, endothelial cell hyperplasia, edema of the neuropil, and satellitosis. This is the first time that satellitosis has been reported from a mammal infected with T. cruzi. Intracellular T. cruzi and inflammatory infiltrates were found in cardiac and skeletal myocytes and liver cells. No parasitism or alterations to the CNS were observed in the chronic mice, although they did show myocarditis and myocitis with extensive infiltrates. Our results are discussed in relation to hypotheses that deny the importance of the presence of tissue parasites versus the direct relationship between these and the damages produced during the chronic phase of Chagas disease. We also review the mechanisms proposed as responsible for the nervous phase of this parasitosis.

Geographical distribution of Trypanosoma cruzi genotypes in Venezuela.

Chagas disease is an endemic zoonosis native to the Americas and is caused by the kinetoplastid protozoan parasite Trypanosoma cruzi. The parasite is also highly genetically diverse, with six discrete typing units (DTUs) reported TcI - TcVI. These DTUs broadly correlate with several epidemiogical, ecological and pathological features of Chagas disease. In this manuscript we report the most comprehensive evaluation to date of the genetic diversity of T. cruzi in Venezuela. The dataset includes 778 samples collected and genotyped over the last twelve years from multiple hosts and vectors, including nine wild and domestic mammalian host species, and seven species of triatomine bug, as well as from human sources. Most isolates (732) can be assigned to the TcI clade (94.1%); 24 to the TcIV group (3.1%) and 22 to TcIII (2.8%). Importantly, among the 95 isolates genotyped from human disease cases, 79% belonged to TcI - a DTU common in the Americas, however, 21% belonged to TcIV- a little known genotype previously thought to be rare in humans. Furthermore, were able to assign multiple oral Chagas diseases cases to TcI in the area around the capital, Caracas. We discuss our findings in the context of T. cruzi DTU distributions elsewhere in the Americas, and evaluate the impact they have on the future of Chagas disease control in Venezuela.

Eratyrus mucronatus (Stal, 1859) (Hemiptera, Reduviidae, Triatominae): primer registro para el estado Anzoátegui (Venezuela) / Eratyrus mucronatus (Stal, 1859): first report for Anzoátegui state (Venezuela)

Señalamos la presencia de Eratyrus mucronatus (Stal, 1859) (Hemiptera, Reduviidae, Triatominae) infectado con Trypanosoma cruzi, en un área urbana peridomiciliar (Universidad de Oriente, Núcleo de Anzoátegui, estado Anzoátegui, Venezuela) lo que representa, en nuestro conocimiento, el primer reporte de la especie para este estado. Se discute la importancia epidemiológica de este hallazgo.

The authors report the presence of Eratyrus mucronatus (Stal, 1859) (Hemiptera, Reduviidae, Triatominae) infected with Trypanosoma cruzi, in an urban peridomiciliar area (Universidad de Oriente, Núcleo de Anzoátegui, Anzoátegui state, Venezuela), what represents, to our knowledge, the first report of the species for this state. The epidemiological importance of this finding is emphasized.

Cornea as a tissue reservoir of Trypanosoma cruzi.

Trypanosoma cruzi causal agent of Chagas' disease is a paninfective parasite of mammals transmitted through skin fecal contamination by Triatominae vectors. Studies of alternative routes for infection are scarce; therefore, eye infection should be important, because of the eye's high blood irrigation and brain proximity, as port of entry of the parasite. Trypanosoma cruzi parasites and/or their genetic material in ocular and adjacent muscle tissues were studied in batches of six NMRI mice (15 g) and Trichomys apereoides, an ancient caviomorph (250 g) inoculated with T. cruzi metacyclics from Brazilian (2) and Venezuelan (3) isolates genetically typified as T. cruzi I and II. Two animals/batch in the acute or chronic phase were killed and necropsies of cardiac and skeletal muscles, eyeball, and surrounding ocular muscle were processed for hematoxylin-eosine staining. Tissue parasitism was determined. DNA of the digested sections of the eyeball (5-10 mum) was extracted for T. cruzi k-DNA amplification by PCR, with S35 and S36 primers. The PCR products were analyzed. The average of maximum values of parasitemia of all infected animals was of 10(5) trypomastigotes/ml blood. Skeletal muscle and heart were colonized in patent infection for all isolates. Amastigote nests were found in corneal tissue of 2/3 of the used isolates and adjacent ocular muscle and connective tissue were parasitized. Trypanosoma cruzi k-DNA (330-bp band) was observed in ocular tissue of 4/6 of the isolates studied in both animal models. Investigations concerning infection of the eye globe tissues by T. cruzi are extremely scarce. The presence of stages of T. cruzi and/or its genetic products in ocular tissues indicate a broad colonization from a systemic infection. The results show the ocular environment as a possible appropriate microniche for T. cruzi and emphasize the risk of transmitting T. cruzi by ocular fluids and by parasitized cornea through transplants.

Trypanosoma cruzi: experimental parasitism of bone and cartilage.

Trypanosoma cruzi causes Chagas' disease, a systemic infection that affects cells of meso-, endo-, and ectodermic origin. However, as far as we know, the presence of T. cruzi stages in bone has not been reported previously, and it has scarcely been investigated in cartilage. We inoculated 7- and 20-day-old (8 and 15 g) NMRI albino mice i.p. with metacyclic trypomastigotes from Rhodnius prolixus used for xenodiagnosis of mice previously infected with mammalian, human, and triatomines isolates, characterized by randomly amplified polymorphic DNA as zymodeme 1 (equivalent to T. cruzi I). Tissular parasitism (quantified according to the number of pseudocysts/50 fields 400x) showed amastigotes, intermediate forms, or trypomastigotes in sternum chondroblasts, osteoblasts, macrophages, and fibroblasts; chondrocyte and osteocyte invasion was rare. All isolates parasitized bone marrow macrophages, with few amastigotes. We observed marked associated myotropism, with or without inflammatory infiltration; there were small numbers of intensely parasitized mononuclear cells in perichondrium and periosteum. We discuss the results in relation to the marked differences of the T. cruzi tropism toward the different types of sternum cells, and, additionally, we outline the possibility of transmitting parasitized bone marrow through transplants. The fact of finding parasite stages in sternum bone and cartilage may be considered important due to the studies on Chagas' disease paleoparasitology that are based on histological and molecular analysis.

Trypanosoma cruzi in a caviomorph rodent: parasitological and pathological features of the experimental infection of Trichomys apereoides (Rodentia, Echimyidae).

To understand the interaction of Trypanosoma cruzi with caviomorph rodents, which supposedly have an ancient co-evolutionary history with this parasite, experimental infection of laboratory reared Trichomys apereoides with several isolates of both genotypes of the parasite was studied. Parasitemia, pattern of hematic cells, specific humoral immune response, histopathological features and parasite clearance were appraised. T. apereoides maintained stable infections independent of the T. cruzi genotype as demonstrated by positive PCR results in analyses of several tissues after a 5 months follow-up. The acute phase was characterized by abundant and disseminated presence of amastigotes, vacuolization and/or myocytolysis. Lymphocytosis was a common feature. The chronic phase was characterized mainly by lymphomacroeosinophilic infiltrates independent of the inoculated T. cruzi isolate. T. cruzi of different genotypes did not show any tissular preference in T. apereoides.

Trypanosoma cruzi: behavior of metatrypomastigotes from didelphis marsupialis and panstrongylus geniculatus

Trypanosoma cruzi coloniza las glándulas anales odoríferas de rabipelados o zarigüeyas donde se diferencia a metatripomastigotes que infectan a mamíferos por contaminación, en forma similar a los insectos vectores. Tripomastigotes metacíclicos obtenidos de las glándulas anales de Didelphis marsupialis y del intestino de Panstrongylus geniculatus, naturalmente infectados y capturados en áreas urbanas del valle de Caracas (Venezuela), fueron inoculados por vía intraperitoneal (i.p) en ratones NMRI para comparar su infectividad, tropismo tisular y virulencia. Metatripomastigotes de ambas fuentes produjeron 100 por ciento de infección y de mortalidad, con histotropismo en corazón, músculo esquelético, páncreas, colon, hígado y pulmón; sin embargo, tripomastigotes metacíclicos glandulares causaron niveles mas elevados de proliferación parasitaria en los tejidos. Ratones inoculados con metacíclicos de glándulas anales de rabipelados mostraron, adicionalmente, tropismo hacia la musculatura lisa de testículo, epidídimo, conducto deferente y vesícula seminal. Rabipelados controles inoculados i.p. con tripomastigotes luminales desarrollaron parásitos sanguíneos y glandulares; estos últimos inoculados i.p. en ratones produjeron parasitemias letales. Los resultados fueron discutidos en relación con la elevada variabilidad de las poblaciones de T. cruzi, la cual ha sido señalada como respuesta a diferentes y simultáneos ciclos de transmisión que se producen en ecótopos con particularidades propias. La importancia epidemiológica de la presencia de estadios metacíclicos de T. cruzi en las glándulas anales de rabipelados de áreas rurales y urbanas es enfatizada

Experimental transmission of Trypanosoma cruzi through the genitalia of albino mice

Trypanosoma cruzi is usually transmitted by contact with the excreta of infected Triatominae; among non-vectorial infections, direct transmission through coitus has been proposed. We investigated this possibility by instilling, through the external meatus of the vagina and the penis of previously anesthetized NMRI albino mice, blood of mice infected with strains isolated from Didelphis marsupialis (opossum, strain CO57), Rattus rattus (rat, strain CO22) and human (strain EP). Some animals were allowed to copulate the same day of the instillation. In other experiments, the strains were inoculated in the scrotum. To determine the effect of immunosuppression, some mice were treated with cyclophosphamide 30 days post-instillation. Controls were instilled orally and ocularly. Vaginal instillation with strain CO22 produced systemic infection with tropism to the heart, skeletal muscle, skin, duodenum, pancreas, ovary and sternum. Scrotal inoculation with strain EP likewise invaded liver, spleen, lung, lymph nodes and urogenital organs; while strain CO57 invaded skeletal and cardiac muscle, pancreas, testis, and vas deferens. Penile infection with strain CO22 was detected by xenodiagnosis. Immunosuppression did not increase parasitemia of vaginally infected mice or controls. Mating did not produce infection. Our results show that contact of blood trypomastigotes of T. cruzi with genital mucosa can produce blood and tissue infections. These results are discussed in relation to reports of frequent experimental tropism of T. cruzi toward urogenital organs

Synanthropic rodent reservoirs of Trypanosoma (Schizotrypanum) cruzi in the Valley of Caracas, Venezuela

Exame direto de sangue e xenodiagnostico de 47 roedores sinantropicos (Rattus rattus, R. norvegicus, Mus musculus) capturados no Vale de Caracas, Venezuela, revelaram infecçäo por tripanosoma em 12 R. rattus, 10 com T. lewisi e 2 com T. cruzi. Dos ultimos o curso de parasitemia, o pleomorfismo dos tripomastigotas na corrente sanguinea, tropismo tissular em ratos e camundongos natural e experimentalmente infectados, mortalidade dos hospedeiros, morfologia dos parasitas fecais em Rhodnius prolixus usados para xenodiagnóstico e infectividade das fezes do "barbeiro" para camundongos NMRI, foram todos caracteristicos de Trypanosoma (Schizotrypanum) cruzi...

Trypanosoma (Schizotrypanum) cruzi: histopathology in mice infected with strains isolated from Didelphis marsupialis from the Valley of Caracas (Venezuela)

The histopathological alterations produced in NMRI strain mice by isolates of Trypanosoma cruzi from Didelphis marsupialis captured near human dwellings in the valley of Caracas, Venezuela are described. The donor opossums showed pseudocysts and amastigotes and trypomastigotes only in the heart muscle, and few areas of discrete inflammations and lysis of some muscle cells. Mice were parasitized in the heart, skeletal muscle, jejunum, colon, liver, lung, urinary bladder, penis, seminal vesicle, prostate, pancreas, and brain. All the isolates produced histiolymphocyticinflammation, severe in cardiac and skeletal muscle, and light in the smooth muscle of the intestine and urinary bladder; certain of the isolates produced destruction of muscle fibers. These findings, together with the morphology and behavior reported in previous papers, suggest that the isolates from this mammal reservoir and from the local vector Panstrongylus geniculatus) belong to the same type. The possible venereal transmission through the parasitosis of the urogenital system is discussed. The necessity for characterization of strains of the parasite that have been isolated from areas of intense urbanization, where the ecological changes have reduced the number of host species, is emphasized; such studies may help to clarify the extreme heterogeneity of T. cruzi and the parasitoses it induces

Trypanosoma (Herpetosoma) Rangeli Tejera, 1920: study of the effects of the parasite on the vector

For evaluation of posible pathogenicity of Trypanosoma (Herpetosoma) rangeli Tejera, 1920 to the triatomid vector, first-stage nymphs of laboratory-bred insects were engorged upon albino mice showing average parasitemias of 2 x 10 a la 6 and 2 x 10 a la 5 trypanosomes/ml blood. The vector strains were: Rhodnius prolixus ("New" strain), Triatoma pallidipennis, and tritoma vitticeps. An "Old" strain of R. prolixus (maintained 30 years in the laboratory) was also employed to check the effects of laboratory breeding Other lots of nymphs of the same vector strains were fed on healthy mice as controls. T. rangeli produced intense infections in the gut and hemolymph of all the vector tested, with later differentiation in the salivary glands to metatrypomastigotes that couls be transmited by the bite of the inct and establish infections in healthy mice. No statistically significant differences whatever between enfected and control bugs were found for degree of engorgement, percentage or cause of mortality, molting time, oviposition/female, hatching time, percentage of hatching, or duration of life cycle. The possible role of experimental methodology in producing pathology in infected insect, and the epidemiological significance of a strain of T. rangeli non-pathogenic to the vector are discussed

Trypanosoma (Herpetosoma) rangeli tejera, 1920: influence of host weight, size of inoculum and route of infection upon experimental parasitemia

Para estudiar la influecia de la edad del hospedador, del tamaño del inóculo y su ruta de adminsitración sobre la infección por Trypanosoma (Herpetosoma) rangeli, fueron inoculados i.p. 12 lotes de ratones albinos (cepa NMRI) de 6.0 g de peso con 25.0 - 2.5x10**6 metatripomastigotes/g obtenidos del medio LIY. Los inóculos mas bajos produjeron parasitemias bajas pero persistentes; los inóculos mas elevados originaron níveles altos de parasitemias que cayeron prontamente, sugiriendo la mobilización de mecanismos de resistencia a níveles diferentes de actividad. En otros experimentos, la inoculación i.p. y el usodeem%de em de ratones de 6.0 g dieron parasitemias mas elevadas que cuando se usaron inoculaciones s.c. o animales de 16.0 y 26.0 g. Estos resultados indican la necesidad deemplear una metodologúa uniforme cuando se investigue el posible carácter heterogénico del complejo de T. rangeli

Trypanosoma (herpetosoma) rangeli Tejera, 1920: the course of infection in immunosuppressed mice

Las infecciones experimentales por Trypanosoma (Herpetosoma) rangeli Tejera, 1920 muestran típicamente un repentino aumento de la parasitemia la cual, igualmente, declina y desaparece de manera abrupta e irregular. La droga cyclofosfamida fue usada para inmunosuprimir ratones albinos de 6, 16 y 26g infectados i.p. con T. rangeli de cultivo LIT. Las curvas iniciales de parasitemia fueron similares en los animales tratados y controles, pero la droga extendió el período de parasitemia patente y la repetición del tratamiento reactivó la parasitemia críptica,. Por cuanto ha sido demostrado que T. rangeli realiza un ciclo intracelular mediante multiplicación de amastigotes, es sugerido que el aumento de la parasitemia y el mantenimiento de infecciones crípticas son debidos al ciclo tisular del parásito en el cual tripomastigotes "jóvenes" reinvaden los tejidos mientras que las formas "adultas", incapaces de penetrar, predominan en sangre durante los niveles más elevados de la parasitemia de donde pueden ser tomados por el insecto vector o eliminados más tarde por la respuesta inmune adquirida del hospedador; supresión mediada por drogas de esta respuesta podría prolongar la parasitemia

Trypanosoma (herpetosoma) rangeli Tejera, 1920: the course of infection in immunosuppressed mice

Las infecciones experimentales por Trypanosoma (Herpetosoma) rangeli Tejera, 1920 muestran típicamente un repentino aumento de la parasitemia la cual, igualmente, declina y desaparece de manera abrupta e irregular. La droga cyclofosfamida fue usada para inmunosuprimir ratones albinos de 6, 16 y 26g infectados i.p. con T. rangeli de cultivo LIT. Las curvas iniciales de parasitemia fueron similares en los animales tratados y controles, pero la droga extendió el período de parasitemia patente y la repetición del tratamiento reactivó la parasitemia críptica,. Por cuanto ha sido demostrado que T. rangeli realiza un ciclo intracelular mediante multiplicación de amastigotes, es sugerido que el aumento de la parasitemia y el mantenimiento de infecciones crípticas son debidos al ciclo tisular del parásito en el cual tripomastigotes "jóvenes" reinvaden los tejidos mientras que las formas "adultas", incapaces de penetrar, predominan en sangre durante los niveles más elevados de la parasitemia de donde pueden ser tomados por el insecto vector o eliminados más tarde por la respuesta inmune adquirida del hospedador; supresión mediada por drogas de esta respuesta podría prolongar la parasitemia (AU)

Trypanosoma (Herpetosoma) rangeli tejera, 1920: preliminary report on histopathology in experimentally infected mice

Ratones machos (cepa NMRI) de 3 y 5 gr, inoculados i.p. con 8 x 10**6 y 9 x 10**4 metatripomastigotes/gr cosechados de cultivo LIT de 12 días de repique de la cepa "Perro-82" de Trypanosoma rangeli fueron procesados, em determinados períodos postinoculación, para seccionar y teñir con hematoxilina-eosina y Giemsacolofonio trozos de corozón, hígado, bazo, pulmones, fémur, riñon, intestino, estómago, cerebro, cerebelo, esternón y columna vertebral. Se detallan los resultados preliminares sobre la histopatología provocada por el T. rangeli en los cinco primeiros órganos citados. Los tejidos conjuntivos subcutáneo, periosteal, intersticial y peribronquial, así como las miocélulas del corazón fueron altamente parasitados por amastigotes y tripomastigotes. Se discuten las posibles razones de la disminución del parasitismo tisular cuando la parasítemia se encontró en sus níveles máximos así como la escasa inflamación obtenida en los tejidos parasitados. Las observaciones de varios autores sobre el comportamiento del protozoario en humanos y en animales de laboratorio así como los resultados descritos en este trabajo, plantean la posibilidad de que determinadas cepas de T. rangeli, en condiciones particulares, podrían causar alteraciones patológicas en el mamífero

Trypanosoma (Herpetosoma) rangeli tejera, 1920: intracellular amastigote stages of reproduction in white mice

El método, sitio y estadio de multiplicación de Trypanosoma (Herpetosoma) rangeli Tejera, 1920 no había sido determinado hasta ahora. Nosotros hemos observado numerosos nidos o pseudoquistes intracelulares que contienen amastigotes y tripomastigotes de este parásito en el corazón, hígado y bazo de ratones albinos machos de 5,0 g de peso (cepa NMRI) inoculados por vía i.p. con 9,0 x 10**4 metatripomastigotes/g de repique de 12 días en medio LIT, cepa "Perro-82". En el pico de la parasitemia (1,9 x 10**6 tripomastigotes/ml de sangre, 3 días post-inoculación) fueron retirados varios órganos para seccionar y teñir con hematoxilina-eosina. El corazón fue el órgano mas intensamente parasitado. Los amastigotes son redondeados y ovalados, con núcleo redondeado y kinetoplasto en forma de barra recta o curva; el promedio del diámetro máximo de 50 amastigotes medidos fue de 4,2 micron. Fue observada fision binaria en el núcleo y kinetoplasto de algunos amastigotes; no fue vista división en los tripomastigotes sanguícolas. Las características anteriores, así como tambien la localización de los pseudoquistes en los tejidos, son similares a T. cruzi. La comparación de estos resultados con los reportados para otros Herpetosoma sugiere el estudio de la posición taxonómica de T. rangeli