Triquinelosis humana

Archivos de medicina, Vol. 2, Nº. 4, 2006 01/2006;
Source: OAI


La triquinelosis es una enfermedad zoonotica causada por diferentes especies, subespecies y cepas de nematodos del género Trichinella. La infección humana más prevalente es causada por T. spiralis la cual tiene amplia distribución en todo el mundo, constituyendo un problema de salud pública y es seguida de T. nativa y T. britovi. T. spiralis es de forma cilíndrica y de vela delgada, se pueden identificar tres estadios; estado adulto (hembras y machos), larva recién nacida (LRN) y larva de músculo enquistada o larva infectante (LI). El ciclo biológico de T. spiralis, se puede encontrar en un huésped intermediario y un definitivo. En este ciclo, el hombre aparece como huésped accidental. Para la infección del hombre, el huésped definitivo que trasmite al parásito es el cerdo. En el caso de la infección del cerdo, el huésped intermedio es la rata, lo que es posible cuando es criado en malas condicione higiénicas o simplemente, cuando debe buscar su propia fuente de alimentación en basurales

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    ABSTRACT: Genetic influences upon host variation in eosinophilia and resistance to helminth infection, and the relationship between these parameters, were investigated in 7 inbred and 1 hybrid strains of mice infected with Trichinella spiralis. Clear strain-dependent variations were observed in the maximum peripheral blood, bone marrow and spleen eosinophilia attained in infected animals. SWR, NIH and SJL strains of mice all gave high responses to infection; four congenic strains sharing the B10 background (C57BL10 [B10], B10.S, B10.G and B10.BR) were low responders. Some of the genes for high responsiveness appeared to be dominant, as F1 hybrids from high- and low-response phenotype parental strains showed intermediate to high responses to infection. Intestinal eosinophilia showed no correlation with either peripheral blood or bone marrow responses (NIH and B10 strains having similar levels of eosinophil response in gut tissue) and was unrelated to the level of resistance to infection. Whereas NIH were highly resistant, with adult worm burdens at 13 days post-infection and muscle larval burdens at 35 days post-infection significantly lower than all other strains, B10 were quite susceptible, retaining substantial worm burdens at day 13 and harbouring large numbers of muscle larvae. Measurements of the level of the eosinophilopoietic cytokine IL-5 in sera during infection showed that the two strains differed in the kinetics of release but not in their absolute capacity to produce this cytokine. NIH mice released high levels during a primary infection, B10 released high levels during a secondary infection.(ABSTRACT TRUNCATED AT 250 WORDS)
    Parasitology 09/1992; 105 ( Pt 1)(01):117-24. DOI:10.1017/S0031182000073765 · 2.56 Impact Factor
  • Journal of Zoology 07/2010; 1(4):315 - 324. DOI:10.1111/j.1096-3642.1835.tb00631.x · 1.88 Impact Factor
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    ABSTRACT: The differential induction of cytokines associated with Th1 and Th2 subsets has recently been described during Trichinella spiralis infection. Increased levels of resistance appear to correlate with elevated levels of the Th1-associated cytokines, IFN-gamma and IL-2. In the present report, a filter immunoplaque assay is used to quantify the actual numbers of cells that secrete IFN-gamma and IL-5. It is demonstrated that, in T. spiralis-infected B10.Q mice, Th1- and Th2-associated responses are compartmentalized to different lymphoid organs. Thus, Ag-induced IFN-gamma-producing cells predominate in the spleen, whereas IL-5-producing cells prevail in the mesenteric lymph nodes (MLN). A corresponding compartmentalization of Ag-specific IgA and IgG1 antibody-secreting cells to the MLN is also noted. The virtual absence of Th1-associated responses in the MLN appears to be an Ag-associated phenomenon. MLN from either naive or T. spiralis-infected mice do have the capacity to secrete IFN-gamma if stimulated with Con A. The striking compartmentalization of Ag-driven cytokine responses seen in this parasite system may facilitate study of the mechanisms that regulate the induction of Th1 and Th2 subsets.
    The Journal of Immunology 08/1991; 147(1):306-11. · 4.92 Impact Factor
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