T and B lymphocytes in the brains of dogs with concomitant seropositivity to three pathogenic protozoans: Leishmania chagasi, Toxoplasma gondii and Neospora caninum

Background: Visceral leishmaniasis is a disease with great variability regarding the clinical manifestations in humans and dogs. Chronically infected dogs may develop neurological disorders, however, there are few reports that characterize the lesions and make clear the pathogenesis of the canine ce...

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Bibliographic Details
Authors: Sakamoto, Keila Priscilla [UNESP], De Melo, Guilherme Dias [UNESP], Machado, Gisele Fabrino [UNESP]
Format: article
Status:Published version
Publication Date:2013
Country:Brasil
Institution:Universidade Estadual Paulista (UNESP)
Repository:Repositório Institucional da UNESP
Language:English
OAI Identifier:oai:repositorio.unesp.br:11449/75634
Online Access:http://dx.doi.org/10.1186/1756-0500-6-226
http://hdl.handle.net/11449/75634
Access Level:Open access
Keyword:CD3
CD79α
Central Nervous System
Inflammation
Lymphocyte
Neosporosis
Toxoplasmosis
Visceral Leishmaniasis
Canis familiaris
Leishmania donovani chagasi
Neospora
Neospora caninum
Protozoa
Toxoplasma
Toxoplasma gondii
Description
Summary:Background: Visceral leishmaniasis is a disease with great variability regarding the clinical manifestations in humans and dogs. Chronically infected dogs may develop neurological disorders, however, there are few reports that characterize the lesions and make clear the pathogenesis of the canine cerebral leishmaniasis. Concomitant with Leishmania chagasi, dogs may be infected by opportunistic pathogens, such as Toxoplasma gondii and Neospora caninum, which may contribute to the occurrence of lesions in the central nervous system. Hence, we aimed to compare the T and B lymphocytes population in the brains of infected dogs with seropositivity to L. chagasi, T. gondii and N. caninum concurrently (n = 24), seropositivity only to L. chagasi (n = 31), and seropositivity to T. gondii and N. caninum (n = 16). Uninfected dogs were used as control (n = 10). Results: Inflammatory lesions, characterised by mononuclear cell accumulation, composed mainly of CD3+ T lymphocytes predominated in several encephalic regions of the dogs from all the three infected groups, with no difference among them (P = 0.0004), whereas CD79α+ B lymphocytes were detected in very small intensity and presented no difference among groups (P = 0.5313). Furthermore, no association among diseases was detected at the serological enquire. Conclusions: We demonstrate that the peripheral infection by L. chagasi per se can promote the influx of lymphocytes within the nervous milieu as occurs during Toxoplasma and Neospora infections, and the concomitant seropositivity against these pathogens does not exacerbate the inflammatory brain lesions. Therefore, these findings give additional support that the brain should be included in the list of organs affected by visceral leishmaniasis and that even asymptomatic infected dogs may develop brain lesions. © 2013 Sakamoto et al.; licensee BioMed Central Ltd.