Astrocytic and microglial response and histopathological changes in the brain of horses with experimental chronic Trypanosoma evansi infection

Abstract

SUMMARYThis study aimed to characterize astrocytic and microglial response in the central nervous system (CNS) of equines experimentally infected with T. evansi. The experimental group comprised males and females with various degrees of crossbreeding, ages between four and seven years. The animals were inoculated intravenously with 10 6 trypomastigotes of T. evansi originally isolated from a naturally infected dog. All equines inoculated with T. evansi were observed until they presented symptoms of CNS disturbance, characterized by motor incoordination of the pelvic limbs, which occurred 67 days after inoculation (DAI) and 124 DAI. The animals in the control group did not present any clinical symptom and were observed up to the 125 th DAI. For this purpose the HE histochemical stain and the avidin biotin peroxidase method was used. Lesions in the CNS of experimentally infected horses were those of a wide spread non suppurative meningoencephalomyelitis.The severity of lesions varied in different parts of the nervous system, reflecting an irregular distribution of inflammatory vascular changes. The infiltration of mononuclear cells was associated with anisomorphic gliosis and reactive microglia was identified. The intensity of the astrocytic response in the CNS of the equines infected by T. evansi characterizes the importance of the performance of these cells in this trypanosomiasis. The characteristic gliosis observed in the animals in this experiment suggests the ability of these cells as mediators of immune response. The parasite, T. evansi, was not identified in the nervous tissues.

­Immunohistochemistry for the detection of neural and inflammatory cells in equine brain tissue

“…Identification of equine-reactive antibodies can be challenging due to limited knowledge of commercial antibodies' reactivity with veterinary tissues and lack of development of multiple species-specific reagents. Evaluation of cross-species reactivity of commercially available antibodies, particularly CD antigens, has been largely performed in equine tissues prepared for whole-cell analysis like flow-cytometry (Johne et al, 1997, Mérant et al, 2003, Terio et al, 2003, Kunisch et al, 2004, and Ibrahim et al, 2007 or on fresh or frozen specimens (Bilzer et al, 1995, Zeng et al, 1996, Lemos et al, 2008, and Härtig et al, 2009. Large screenings of non-equine derived antibodies have often resulted in limited identification of equine reactive reagents (Ibrahim et al, 2007, Schnabel et al, 2013, and Szabo and Gulya, 2013.…”

Histopathology of Trypanosoma (Trypanozoon) evansi infection in Bandicoot rat. II. Brain and choroid plexus

“…Cerebral trypanosomiasis in surra is less studied in naturally infected and experimental animals including horse (Kalra et al, 1981;Seiler et al, 1981;Patel et al, 1982;Suryanarayana et al, 1986;Lemos et al, 2008). Some characteristic features of the brain in T. evansi infected camel, donkey, horses and laboratory animals include lymphocytic perivascular cuffing, meningeal congestion, neuronal necrosis and occasionally patchy gliosis.…”

“…Multiple sclerosis, neuronophagia, necrosis, focal haemorrhage, cerebellar hyperplasia, oedema, oligodendrocytoma, astrocytoma and fatty degeneration of brain tissue are noticed in the brain of bandicoot during the last phase of T. (T.) evansi infection. Lemos et al (2008) recorded astrocytic and microglial response in the CNS of experimentally T. evansi infected horses. Recently, Rodrigues et al (2009) studied the neuropathology of naturally occurring T. evansi infection in horses and recorded necrotizing encephalitis in white matter, oedema, demyelination, meningoencephalitis, lymphoplasmacytic perivascular cuffs, etc.…”

“…Trypanosoma brucei brucei is able to cross BBB and is frequently found in the brain parenchyma from 12-22 days post infection in rat (Philip et al, 1994;Mulenga et al, 2001). Recently, Lemos et al (2008) observed that chronic infection of T. evansi in horse causes lesions in CNS and wide spread nonsupportive meningoencephalomyelitis.…”

An Overview of Trypanosoma brucei Infections: An Intense Host–Parasite Interaction

“…T. evansi (monomorphic) and T. equiperdum (monomorphic but occasionally pleomorphic) are morphologically similar to the slender forms of T. b. brucei , as well as of T. b. rhodesiense and T. b. gambiense (Blacklock and Yorke, 1993; Brun et al, 1998). The information about the host response in infections produced by these veterinarian parasites is limited (Lemos et al, 2008; Camargo et al, 2015); therefore, the present review deals mostly with the human infecting trypanosomes that cause HAT.…”