Estudo histológico e imunoistoquímico do sistema nervoso central de cães naturalmente infectados por Leishmania (Leishmania) chagasi

Abstract

The present study aimed to characterize the histopathological alterations and to detect, by immunohistochemistry, the presence of amastigote forms of Leishmania in CNS tissue of dogs with and without neurological clinical signs of the disease. Two groups of animals were used: the first was composed of 18 dogs with visceral leishmaniasis without clinical evidence of neurological involvement, and the second, composed of 21 dogs with visceral leishmaniasis and neurological symptoms. The most frequent histopathological alterations found in the CNS of dogs of both groups were neuronal degeneration with neuronophagia, gliosis, leptomeningitis, vascular congestion, presence of perivascular lymphoplasmacytic infiltrate and areas of focal microhemorrhage. Antigen labeling for whole forms of Leishmania amastigotes was not observed in any fragment of the CNS of the dogs of either groups; however, most of them presented labeling of blood vessels walls, which suggests the presence of circulating parasite antigens.

Lymphocytic hypophysitis in dogs infected with Leishmania spp.

“…Similar to the findings of studies performed on the brains of dogs with CanL, inflammation was not related to the presence of amastigotes in the tissue ( 30 , 41 – 43 ). One hypothesis would be that chronic systemic inflammation resulting from L. infantum infection, with production of cytokines and chemokines, could alter barrier permeability ( 44 – 46 ).…”

Main lesions in the central nervous system of dogs due to Leishmania infantum infection

“…Inflammatory reaction during canine visceral leishmaniasis was also observed by Ikeda et al [11], who analyzed brains of dogs with and without neurological signs and described degenerative alterations with neuronophagia, gliosis, leptominingitis, vascular congestion and the presence of a perivascular lymphoplasmacytic infiltrate and areas of micro-hemorrhages.…”

“…Other studies, despite the observation of histopathological alterations in the CNS of dogs during visceral leishmaniasis, failed to verify the presence of Leishmania amastigotes [11, 19, 20, 23–25]. Some authors explain these contradictory findings by the chronicity of the disease, arguing that the presence of Leishmania in the CNS has generally been demonstrated in dogs with an earlier infection, either because of delayed diagnosis or by the choice of treatment for the infected dogs, as in two studies in the Mediterranean region [11, 24]. In fact, here we observed that animals that presented amastigote forms in the CNS had clinical signs such as cachexia and the presence of skin lesions, observed in the chronic phase.…”

“…However, in 1996, the presence of Leishmania donovani amastigote forms in the cerebrospinal fluid (CSF) was described for first the time in a human patient [6]. Since then, the central nervous system has become the subject of many studies seeking to confirm that Leishmania species cross the BBB and cause pathological alterations and clinical neurological signs [8, 10, 11, 20, 22]. …”

“…Many other neurological signs, suggesting the widespread involvement of the central nervous system, had already been observed through a rigorous clinical evaluation. These included convulsions, blindness, signs of vestibular and cerebellar involvement (tilted head, nystagmus, motor incoordination, and tremors), paraparesis, tetraparesis, tetraplegia and myoclonia [11]. …”