Trichinosis

Trichinosis is a worldwide zoonotic disease closely related to cultural and dietary habits caused by a nematode Trichinella spp. Human infection is acquired through ingestion of undercooked meat containing infective encysted larvae. There are two cycles of transmission, one domestic and the other wi...

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Publicado: 1997
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Acceso en línea:https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_10156305_v7_n1_p663_Taratuto
http://hdl.handle.net/20.500.12110/paper_10156305_v7_n1_p663_Taratuto
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spelling paper:paper_10156305_v7_n1_p663_Taratuto2023-06-08T15:59:46Z Trichinosis albendazole levamisole mebendazole pyrantel tiabendazole central nervous system infection enzyme histochemistry human human tissue review Trichinella spiralis trichinosis Trichinosis is a worldwide zoonotic disease closely related to cultural and dietary habits caused by a nematode Trichinella spp. Human infection is acquired through ingestion of undercooked meat containing infective encysted larvae. There are two cycles of transmission, one domestic and the other wild. A complete life cycle develops in a single host harboring adult worms in the small intestine, from which newborn larvae migrate and finally encyst in striated muscle. Traumatic and immunological alterations are responsible for the main clinical features, including diarrhea, febrile syndrome, myalgias, oculopalpebral signs and eosinophilia. Cardiovascular, lung and CNS involvement characterize severe trichinosis. CNS inflammatory infiltration and damage may result from larval migration and vascular obstruction, or from the effect of toxic parasite antigens, or eosinophil infiltration. Humoral and cellular immune host response are relevant both to protect against re-infection and for immunodiagnosis. DNA probes and PCR technology may help to identify Trichinella spp. Muscle biopsy may disclose T spiralis larvae coiled within a muscle fibre host nurse cell surrounded by a capsule. Inflammatory infiltration includes monocytes, plasma cells, eosinophils and T lymphocytes mainly of the suppressor/cytotoxic phenotype. Histological appearance and histochemical profile of the host nurse cell differ from that of striated muscle fibre and are partly indicative of regeneration. Our own histological and histochemical findings in experimental studies of infected mouse muscle support the concept that changes induced by the larva encysting within a single host skeletal muscle fibre which becomes a nurse cell are unique of Trichinella infection. Interestingly, no dystrophin could be detected within the host nurse cell-capsule interface. It has been advanced that larva-induced host muscle fibre changes may be regulated at muscle gene transcription level whilst host regulatory pathways governed by cell cycle phase may also contribute to larval development. 1997 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_10156305_v7_n1_p663_Taratuto http://hdl.handle.net/20.500.12110/paper_10156305_v7_n1_p663_Taratuto
institution Universidad de Buenos Aires
institution_str I-28
repository_str R-134
collection Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA)
topic albendazole
levamisole
mebendazole
pyrantel
tiabendazole
central nervous system infection
enzyme histochemistry
human
human tissue
review
Trichinella spiralis
trichinosis
spellingShingle albendazole
levamisole
mebendazole
pyrantel
tiabendazole
central nervous system infection
enzyme histochemistry
human
human tissue
review
Trichinella spiralis
trichinosis
Trichinosis
topic_facet albendazole
levamisole
mebendazole
pyrantel
tiabendazole
central nervous system infection
enzyme histochemistry
human
human tissue
review
Trichinella spiralis
trichinosis
description Trichinosis is a worldwide zoonotic disease closely related to cultural and dietary habits caused by a nematode Trichinella spp. Human infection is acquired through ingestion of undercooked meat containing infective encysted larvae. There are two cycles of transmission, one domestic and the other wild. A complete life cycle develops in a single host harboring adult worms in the small intestine, from which newborn larvae migrate and finally encyst in striated muscle. Traumatic and immunological alterations are responsible for the main clinical features, including diarrhea, febrile syndrome, myalgias, oculopalpebral signs and eosinophilia. Cardiovascular, lung and CNS involvement characterize severe trichinosis. CNS inflammatory infiltration and damage may result from larval migration and vascular obstruction, or from the effect of toxic parasite antigens, or eosinophil infiltration. Humoral and cellular immune host response are relevant both to protect against re-infection and for immunodiagnosis. DNA probes and PCR technology may help to identify Trichinella spp. Muscle biopsy may disclose T spiralis larvae coiled within a muscle fibre host nurse cell surrounded by a capsule. Inflammatory infiltration includes monocytes, plasma cells, eosinophils and T lymphocytes mainly of the suppressor/cytotoxic phenotype. Histological appearance and histochemical profile of the host nurse cell differ from that of striated muscle fibre and are partly indicative of regeneration. Our own histological and histochemical findings in experimental studies of infected mouse muscle support the concept that changes induced by the larva encysting within a single host skeletal muscle fibre which becomes a nurse cell are unique of Trichinella infection. Interestingly, no dystrophin could be detected within the host nurse cell-capsule interface. It has been advanced that larva-induced host muscle fibre changes may be regulated at muscle gene transcription level whilst host regulatory pathways governed by cell cycle phase may also contribute to larval development.
title Trichinosis
title_short Trichinosis
title_full Trichinosis
title_fullStr Trichinosis
title_full_unstemmed Trichinosis
title_sort trichinosis
publishDate 1997
url https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_10156305_v7_n1_p663_Taratuto
http://hdl.handle.net/20.500.12110/paper_10156305_v7_n1_p663_Taratuto
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