ArticleBrain pathology (Zurich, Switzerland)1997
Trichinosis.
Article in Brain pathology (Zurich, Switzerland), 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 35 citations in OpenAlex.
- Bafilomycin A1 is a promising therapeutic agent against T. spiralis infection by inhibiting the heme-transporting ATP6V0C/HRG-1 complex.PLoS pathogens · 2026Article
- Aspartic protease 2 from Trichinella spiralis excretion/secretion products hydrolyzes tight junctions of intestinal epithelial cells.PLoS neglected tropical diseases · 2025Article
- The high larval burden ofHelminthologia · 2025Article
- Pleural effusion caused by Trichinella spiralis infection: two case reports.BMC infectious diseases · 2023Article
- From the immune system to mood disorders especially induced byFrontiers in cellular and infection microbiology · 2023Review
- Ts-Hsp70 induces protective immunity against Trichinella spiralis infection in mouse by activating dendritic cells through TLR2 and TLR4.PLoS neglected tropical diseases · 2018Article
- Serum IgE and IgG4 against muscle larva excretory-secretory products during the early and late phases of human trichinellosis.Parasitology research · 2017Article
- Molecular cloning and phylogenetic analysis of small GTPase protein Tscdc42 from Trichinella spiralis.Parasitology research · 2010Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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 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.
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Registered trials
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