Leishmania amastigotes in the central nervous system of a naturally infected dog

Abstract

Canine leishmaniasis (CL) is a cutaneous, mucocutaneous, or visceral disease caused by intracellular Leishmania protozoan parasites that are transmitted by the bite of female sand flies. Domestic dogs are the main reservoir hosts. The clinical signs are very variable, ranging from subclinical infections to generalized disorders characterized by hyperthermia, anemia, weight loss, polydipsia, hepatomegaly, splenomegaly, hypergammaglobulinemia, generalized lymphadenopathy, cutaneous lesions, and other lesions. 2,4 In visceral CL, parasites and their lesions are found throughout the host organism, producing proliferative inflammatory reactions causing an immune imbalance. Among the inflammatory infiltrates, macrophages predominate, and occasionally amastigotes are found within them. Many organs have been observed to be affected, especially the lymph nodes, liver, spleen, and skin.2 It is thought that a humoral response and deposition of immune complexes are likely responsible for the pathogenesis 2,4 including the systemic necrotizing vasculitis that has been described in affected dogs. 17 Occasionally, neurological signs and/or histopathological lesions have been observed affecting the central nervous system (CNS) in CL, 2,9,11 giving rise to the term cerebral leishmaniasis. 8 However, except for the choroid plexuses 13 and meninges, 19 Leishmania amastigotes, to the authors' knowledge, have not been observed in either the CNS parenchyma or peripheral nerves in CL. The current study described a dog with radiculoneuritis, myelitis, and mild meningoencephalitis associated with Leishmania spp. amastigotes in the peripheral and central nervous systems.A 4-year-old male Labrador Retriever suffered an episode of left hemiparesis 9 months before presentation. Blood analysis at that time showed thrombocytopenia and mild hyperglobulinemia. Enzyme-linked immunosorbent assay (ELISA) a for anti-Leishmania antibodies and indirect fluorescent antibody test (IFAT) b for Leishmania were negative. The animal responded favorably to chronic treatment with prednisolone.c Seven months later the animal relapsed, and blood analysis revealed anemia, hyperproteinemia, hypoalbuminemia, and hyperglobulinemia. A second ELISA a test was performed and the result was again negative. Serology for Toxoplasma and Neospora was negative. At that time, treatment was begun with clindamycin, d and an improvement in the clinical signs was noted.Forty-five days later, the dog was referred to the Al Sur Veterinary Hospital with a 10-day evolution of tetraplegia. Clinical examination showed hypothermia, dehydration, tachypnea, and cachexia. The animal was depressed, and postural reactions were absent. Carporadialis and flexor reflexes in the forelimbs were absent; bilateral Horner syndrome was also observed. Atrophy of the supra and left spinal nerves. Microscopically, nerve fiber destruction together with mixed inflammatory infiltration was observed in the spinal nerves. Cervical spinal cord sections showed multifocal, diffuse granulomatous inflammation ...

Occurrence of Leishmania infantum in the central nervous system of naturally infected dogs: Parasite load, viability, co-infections and histological alterations

“…In addition, there was no evidence of co-infection with other pathogens in the CNS of this dog. Granulomatous inflammatory infiltration of the parasitized CNS by amastigote forms of Leishmania has also been reported by other authors [11, 15, 16, 35, 40]. Although amastigote forms were not detected in the CNS of the other dogs of this study, the participation of L .…”

“…The detection of amastigote forms of L . infantum in the CNS of dogs had only been described in Europe in rare reports of cases in the meninges [16], choroid plexus [11, 15], thalamus [11], spinal nerves [11], spinal canal granuloma [35], and spinal cord parenchyma [11]. …”

“…The sensitivity of parasitological culture of CSF would have been even higher if an enrichment method consisting of gentle centrifugation (500–800 rpm) and collection and seeding of pellets in culture medium were used. Immunosuppression triggered by the long-term use of corticosteroids in a tetraplegic dog [11] and parasite escape from the action of an anti- Leishmania drug in a child with neurological signs [36] have been indicated as possible causes for the invasion of viable forms of Leishmania into the CNS. In contrast to these hypotheses, in the present study in which the dogs were not treated with anti- Leishmania drugs or corticosteroids, 25% of the animals exhibited viable forms of L .…”

“…infantum [7, 9, 11, 12, 15–19, 39]. However, these alterations are not specific for infection with L .…”

“…infantum revealed the presence of anti- Leishmania antibodies in cerebrospinal fluid (CSF) [6, 8, 14, 16, 18, 20] and of L . infantum DNA in the brain [13, 20–22] and CSF [11]. However, only few surveys exist on the occurrence and load of L .…”