As described above the parasite causes several pathological changes. The majority of the clinical features of trichinellosis are observed during the origin of infection. These features can be related to the capacity of Trichinella to induce allergic responses, a property shared by many species of worm parasites. The molecular basis of this allergenicity is still undefined, although clearly it must reflect particular characteristics of worm antigens and the manner in which they are presented to the host. Studies in mouse models show that Trichinella infections preferentially stimulate cells of the T helper 2 (Th2) subset of CD4+T lymphocytes (Grencis et al. 1991). These cells release the cytokines necessary for the development of many of the allergic components of the disease, and it can reasonably be assumed that a similar situation exists during human infections. During the intestinal phase there is a marked infiltration of inflammatory cells, including neutrophils, eosinophils, and mast cells into the gut mucosa. Significant changes take place in mucosal architecture (e.g. villous atrophy); fluid flux across the mucosa is disturbed, mucus production is increased, and intestinal transit time is decreased. All of these changes are the result of T cell activity and all can be related to the symptoms appearing during the intestinal phase of infection, of which diarrhoea is the most characteristic. Eosinophilia is a consequence of T cell response to both the intestinal adult worms and to the muscle larvae and is dependent upon release of the cytokine IL-5 (Herndon and Kayes 1992). It has been shown in rodents that infection stimulates both parasite-specific IgE and total IgE antibodies as well as IgG isotypes (IgG1) that are involved in hypersensitivity reactions (e.g. Gabriel and Justus 1979), and this is consistent with the dominance of the T cell response by the Th2 subset. Although Trichinella-specific IgE responses have been detected in humans by some workers (e.g. Bruschi et al. 1990) others have not been able to find such responses (Ljunstrom et al. 1988). This may be due to different assays used and/or time elapsed after infection when measured. It does seem probable that many of the systemic allergic symptoms of the disease do reflect type-1 hypersensitivity responses.

Invasion of the muscles and formation of the characteristic cysts are accompanied by the development of intense inflammatory responses. These are again T cell-dependent, involve accumulation of eosinophils and other leucocytes, and are maintained by continuous release of antigenic material from the larvae. This inflammation is the direct cause of the myositis that occurs at this stage of infection and which contributes, together with the physical disruption of muscle fibres, to the mechanical and electrophysiological disturbances associated with severe trichinellosis.

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