TRICHINOSIS

Trichinosis is a worldwide zoonotic disease closely related to cultura l and dietary habits caused by a nematode Trichinella spp. Human infec tion is acquired through ingestion of undercooked meat containing infe ctive encysted larvae. There are two cycles of transmission, one domes tic and the other wild. A complete life cycle develops in a single hos t harboring adult worms in the small intestine, from which newborn lar vae migrate and finally encyst in striated muscle. Traumatic and immun ological alterations are responsible for the main clinical features, i ncluding diarrhea, febrile syndrome, myalgias, oculopalpebral signs an d eosinophilia. Cardiovascular, lung and CNS involvement characterize severe trichinosis. CNS inflammatory infiltration and damage may resul t from larval migration and vascular obstruction, or from the effect o f toxic parasite antigens, or eosinophil infiltration. Humoral and cel lular immune host response are relevant both to protect against re-inf ection and for immunodiagnosis. DNA probes and PCR technology may help to identify Trichinella spp. Muscle biopsy may disclose T spiralis la rvae coiled within a muscle fibre host nurse cell surrounded by a caps ule. Inflammatory infiltration includes monocytes, plasma cells, eosin ophils and T lymphocytes mainly of the suppressor/cytotoxic phenotype. Histological appearance and histochemical profile of the host nurse c ell differ from that of striated muscle fibre and are partly indicativ e 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 infe ction. 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 transcriptio n level whilst host regulatory pathways governed by cell cycle phase m ay also contribute to larval development.