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. 2008 Jun 28;7(1):663–672. doi: 10.1111/j.1750-3639.1997.tb01081.x

Trichinosis

Ana Lia Taratuto 1,✉, Stella M Venturiello 2
PMCID: PMC8098547  PMID: 9034572

Abstract

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 immun‐odiagnosis. 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.

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