Tissue (re)distribution of Trypanosoma equiperdum in venereal infected and blood transfused horses.

Dourine, caused by Trypanosoma equiperdum, is a life-threatening venereal disease in equidae. So far, there is no clear evidence on how and when stallions become infectious, nor which tissues are affected by the parasite in diseased animals. Post-infection, after a transient, temporary phase of parasitaemia, the parasite disperses to different tissues in an unknown distribution pattern. This study describes the distribution of the parasite after infection by artificial insemination (AI) or blood transfusion. Mares (N = 4) were artificially inseminated with T. equiperdum spiked semen whereas stallions (N = 4) were infected by blood transfusion. The course of the disease was monitored by parasitological (Woo) and molecular (PCR) tests and clinical signs and haematological parameters were recorded. At 120 days post infection, horses had a full necropsy, histopathology and PCR. A similar pattern of parasitaemia, disease progression and tissue distribution were seen in all horses. Ejaculated semen in the preclinical stage and epididymal semen in the chronic stage of the disease was positive on PCR and caused infection in mice. Cymelarsan® treatment in the chronic stage did not result in a clinico-haematological or histopathological improvement. At necropsy, lesions were observed in the nervous and reproductive system. Histopathological lesions were most severe in the peripheral nerves and associated ganglia, the testicles and genital mucosae with multifocal infiltration of lymphocytes, plasma cells and histocytes. The parasites disseminated to several tissues including the nervous system, testicles and semen. The results indicate that transmission of T. equiperdum is possible through semen even from symptomless stallions post-treatment.

[Guillain-Barré syndrome revealing visceral leishmaniasis in an immunocompetent woman]. / Syndrome de Guillain-Barré révélateur d'une leishmaniose viscérale chez une patiente non immunodéprimée.

Visceral leishmaniasis is an endemic parasitic infection rarely observed in association with Guillain-Barré syndrome in immunocompetent patients. A 40-year-old immunocompetent woman was admitted to our unit with recent onset difficulty in walking. The neurological examination and electrophysiological study led to the diagnosis of Guillain-Barré syndrome. During hospitalization, she developed cytopenia involving all three lines revealing visceral leishmaniasis. A few cases of visceral leishmaniasis with neuropathy have been reported, mainly in tropical regions. Neuropathological manifestations of visceral leishmaniasis are probably underestimated. The question is whether Guillain-Barré syndrome and visceral leishmaniasis are causally related.

Neurotropic behaviour of Trichobilharzia regenti in ducks and mice.

The bird nasal schistosome Trichobilharzia regenti is a new agent of cercarial dermatitis. Cercariae are able to penetrate the skin of birds and mammals including man. The parasite then attacks the central nervous system. The present study has shown that schistosomula avoid penetration of blood capillaries and enter the peripheral nerves of the legs of mice and ducks as early as 1 day post-infection (p.i.) and 1.5 days p.i., respectively. These peripheral nerves are used as a route to the spinal cord. In the specific host (duck) schistosomula were found in the spinal cord from 2 days p.i. until 15 days p.i. and in the brain from 12 days p.i. until 18 days p.i. In non-specific hosts (mice; inbred strains BALB/c, hr/hr, SCID) living schistosomula were found in the spinal cord from 2 days p.i. until 21 or 24 days p.i. (depending on the mouse strain) and in the brain of two (BALB/c, SCID) of three inbred strains from 3 days p.i. until 24 days p.i. No correlation was found between the infection dose and clinical status of the experimental hosts. A high affinity of schistosomula for the peripheral nerves was also proved in vitro, suggesting a new type of migratory behaviour in schistosomatids.

Neuroesquistossomose em Alagoas / Neuroschistosomiasis in Alagoas

Este trabalho foi realizado no Hospital do Açúcar e Hospital do SESI, em Maceió. Estudamos aproximadamente 100 pacientes que chegaram aos nossos Serviços com manifestaçöes clínicas sugestivas de neuropatias periféricas, discopatias ou comprometimento do sistema nervoso autônomo, com vistas a estabelecer a etiologia das referidas alteraçöes. Identificamos neste grupo 18 pacientes com neuroesquistossomose, confirmados com análise do líquor cefalorraquiano (L.C.R.), exame parasitológico de fezes (E.P.F.) ou biópsia retal (B.R.). Encontramos, além dos quadros já descritos na literatura, casos com diagnóstico prévio de hérnia discal, hiperplasia prostática ou histeria. A evoluçäo clínica e sobretudo liquórica com o tratamento específico (praziquantel ou oxaminiquine) foi mais favorável do que os relatos prévios da literatura. Houve um caso com história pregressa de mielite transversa alguns anos antes, com remissäo total, porém os estudos de potenciais evocados afastaram a possibilidade de esclerose múltipla. Dentre os trabalhos já descritos o nosso se destaca pela alta incidência de esquistossomose como etiologia dos quadros acima descritos

Neuropathy associated with experimental Chagas' disease.

Mice were acutely and chronically infected with Trypanosoma cruzi and then examined histologically for the presence of lesions in the peripheral nervous system. In acutely infected animals, small lymphocytic and macrophagic infiltrates were found in the nerves in association with intracellular parasites. Little or no nerve damage was present at this stage. In chronically infected animals, large perivascular granulomatous infiltrates were found in association with multifocal, predominantly demyelinative lesions of neighboring nerve fibers. Similar inflammatory infiltrates were present in muscles and were frequently associated with vasculitis and destruction of muscle fibers. Our pathological findings and the negative results produced by intraneural injections of sera from chronically infected animals and the positive results following injections of small numbers of live trypanosomes suggest that the demyelination is not due to circulating serum factors such as antibodies cross-reacting with peripheral myelin. Delayed-type hypersensitivity may be induced by the presence of the parasites, a notion supported by the development of granulomas in naive mice injected intravenously with helper T cells from chronically infected animals.