Cellular immunity in Peyer's patches of rats infected with Trichinella spiralis.
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A rat model of Trichinella spiralis gut infection was used to observe the sequence of developing cellular immunity in Peyer's patches and other lymphoid tissues. Whereas cellular reactivity (lymphocyte blastogenesis) for worm antigens was evident in mesenteric lymph nodes draining the gastrointestinal tract within 3 days after infection, Peyer's patch lymphocytes developed maximal reactivity 2 to 3 weeks later at the same time as the spleen and other lymphoid tissues. Furthermore, the immune reactivity found in Peyer's patches was only transient. Thus, in this parasitic gut infection, the Peyer's patch lymphoid tissue does not appear to be the first site of cellular responsiveness but rather to acquire cellular reactivity only when other lymphoid elements in the infected host have also acquired similar antigen-induced reactivity. (+info)
Leucoagglutination and cytotoxicity of the serum of infected mice and of extracts of Trichinella spiralis larvae and the capacity of infected mouse sera to prolong skin allografts.
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The sera of mice infected with the nematode Trichinella spiralis agglutinate and kill homologous lymphoid cells in vitro. The agglutinating activity is present in the sera of infected animals on the 7th day following inoculation with the parasite, rises to a maximum on the 30th day of the infection and then decreases. The leucoagglutinating titre of these sera is related neither to the level of the inoculating dose of parasites nor to the intensity of muscle infection. The agglutinating and leucotoxic activity of the sera of infected mice is probably due to the same factor(s), but target cells require sensitization before cytotoxicity becomes apparent. Skin allografts were prolonged in infected animals or in animals treated with the serum of infected animals. Saline extracts of T. spiralis larvae also have leucoagglutinating and leucotoxic activity. (+info)
Trichinella pseudospiralis outbreak in France.
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Four persons became ill with trichinellosis after eating meat from a wild boar hunted in Camargue, France. Nonencapsulated larvae of Trichinella pseudospiralis were detected in meat and muscle biopsy specimens. The diagnoses were confirmed by molecular typing. Surveillance for the emerging T. pseudospiralis should be expanded. (+info)
Detection and identification of eight Trichinella genotypes by reverse line blot hybridization.
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A reverse line blot (RLB) assay was developed to identify different Trichinella genotypes. The RLB assay accomplishes detection and specific identification of the different Trichinella genotypes and relies on hybridization of the amplified 5S ribosomal DNA intergenic spacer regions to specific, membrane-bound oligonucleotide probes. After one single amplification, we were able to detect and genetically identify six sibling species, i.e., T. spiralis, T. britovi, T. nativa, T. murrelli, T. nelsoni, and T. pseudospiralis, and two additional Trichinella genotypes, T6 and T8. Twenty-four Trichinella strains of different genotypes were unequivocally identified evaluated using one simple PCR-based assay based on single larvae. This assay allows the specific identification of Trichinella species without the need to passage larvae in laboratory animals. (+info)
An evaluation of low temperature sterilization of trichinae infected park.
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Twenty-four refrigeration trials at temperatures ranging from minus 13 degrees C to minus 195.8 degrees C were carried out on trichinous porcine meat samples ranging in size from 120 gm to 11 kg. The findings reaffirmed that Canadian regulations regarding refrigeration treatment of pork and pork products to destroy trichinae are satisfactory. Results also demonstrated the presence of a critical temperature about minus 30 degrees C below which trichinae in meat do not survive for any appreciable period of time. (+info)
Neural change in Trichinella-infected mice is MHC II independent and involves M-CSF-derived macrophages.
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Intestinal inflammation due to nematode infection impairs enteric cholinergic nerve function and induces hypercontractility of intestinal muscle. Macrophages have been implicated in the neural changes, but the subpopulation and mechanism involved are unknown. We examined whether macrophages alter nerves by virtue of their ability to activate lymphocytes via major histocompatibility complex (MHC) II-restricted antigen presentation. We also attempted to evaluate the role of macrophage subsets using op/op mice deficient in macrophage colony-stimulating factor (M-CSF). ACh release from the myenteric plexus was measured in MHC II- and M-CSF-deficient (op/op) mice infected with Trichinella spiralis. F4/80-positive macrophages and interleukin-1 beta were constitutively present in op/op and op/? mice but increased only in op/? mice postinfection. After infection, a marked suppression of ACh release occurred only in infected MHC II-deficient and op/? mice. Muscle hypercontractility remained evident in infected op/? mice. Treatment with M-CSF restored macrophage number, and this was accompanied by suppression of cholinergic nerve function during infection. Thus M-CSF plays a critical role in this model by recruiting a subset of macrophages that selectively suppresses enteric neural function. (+info)
Differential effects of homocytotropic antibodies on the mast cell and anaphylactic responses in actively and passively sensitized mice.
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The relationship between mast cell degranulation, anaphylaxis, and the production of homocytotropic antibodies was examined in ICR mice after trichinella infection. It was found that the active cutaneous response to trichinella antigen had a rapid onset (within 2 weeks) and the sensitivity increased over a 9-week period after infection. Two types of mast cell degranulation were observed: (i) moderate, with few extracellular, deep-blue-staining granules (May-Grunwald-Giemsa), and (ii) "explosive," with many extracellular reddish-staining, swollen granules, indicating an apparent breakdown of cell membrane. The moderate type was observed primarily during the first 4 weeks after infection, whereas the explosive type predominated during 5 to 8 weeks. Homocytotropic antibody of the immunoglubulin G(1) type appears responsible for moderate type degranulation, and mouse immunoglobulin E appears responsible for the explosive degranulation. No correlation was evident between the active cutaneous anaphylactic response and either type of degranulation or between active cutaneous anaphylaxis and circulating levels of homocytotropic antibody. A proposed role of immunoglobulin G(1) and mouse immunoglobulin E in immunity is discussed. (+info)
The first host record of trichinosis in a red fox, Vulpes vulpes japonica, from Aomori Prefecture, northern Honshu, Japan.
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A case of wildlife trichinosis was found in a red fox (Vulpes vulpes japonica) captured at Rokkasho, Aomori Prefecture on November 27, 1998. Trichinella larvae were obtained from almost all of the muscle tissues except for the masseter. The highest number of larvae per gram of tissue was found in the muscles of the gluteal region and throat. The lowest number was found in the diaphragm and tongue. Trichina cysts within the muscle fibers had groups of fatty cells at the poles, and minimal tissue reaction was observed around the cyst. No calcification was found in the cyst. These morphological findings suggested that the considerable time had elapsed since the invasion. This is the first case of trichinosis in a red fox in Japan. (+info)