Abstract

Rangeliosis is a condition transmitted by the tick Amblyomma aureolatum and caused by the protozoan parasite Rangelia vitalii in canids. In domestic dogs, the disease causes a severe hemolytic disease, while in wild canids the piroplasm is often detected without any clinical abnormality. This study aimed to detect and quantify the number of copies of the R. vitalii Hsp70 gene (indirect parasite burden) in several organs of domestic and South American wild canids (Cerdocyon thous and Lycalopex gymnocercus) to elucidate distinct clinical presentations of rangeliosis in these species. A total of seven domestic dogs that died due to rangeliosis and 38 wild foxes were initially included, with all dogs presenting histological and molecular features of rangeliosis, while eight C. thous were positive at the molecular analysis for R. vitalii. Fragments of 22 organs collected from domestic (n = 7) and wild foxes (n = 8) were employed for histological and molecular quantification using real-time polymerase chain reaction aiming at the Hsp70 gene. Histologically, parasitophorous vacuoles were constantly detected in the dogs, while these were detected only in two C. thous. Parasitic burden was significantly higher in the digestive, cardiorespiratory, endocrine, genitourinary, and skeletal-muscle systems of domestic dogs when compared to wild foxes. In the hematopoietic system of wild canids, some organs, such as the lymph nodes and tonsils, presented significantly lower amounts of R. vitalii, while other organs (spleen, bone marrow, and blood) had results similar to those of domestic dogs. Additionally, the central nervous system of both domestic and wild canids presented a similar quantity of R. vitalii. The etiological agent is possibly maintained through an asexual reproductive process (merogony) in both domestic and wild species. Nonetheless, a limited or short-duration schizogony phase occurs in C. thous, which would designate this species as a possible reservoir host for the agent. Dogs, in contrast, would most likely act as accidental hosts, presenting a severe and more pathogenic schizogony phase, resulting in characteristic clinical and pathological rangeliosis.

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