Trichinella infection and clinical disease

Trichinellosis is caused by ingestion of insufficiently cooked meat contaminated with infective larvae of <it>Trichinella</it> species. The clinical course is highly variable, ranging from no apparent infection to severe and even fatal disease. We report two illustrative cases of trichinellosis. Returning to Denmark a few days after having eaten roasted pork in the Republic of Serbia, a female patient suffered from severe vomiting, epigastric pain, diarrhoea, and later myalgia, generalized oedema, and prostration. A biopsy showed heavy infestation with <it>Trichinella spiralis</it>, 2000 larvae/g of muscle. Life-threatening cardiopulmonary, renal and central nervous system complications developed. The patient recovered after several months. Her husband, who also ate the pork, did not have clinical symptoms, but an increased eosinophil count and a single larva in a muscle biopsy confirmed infection. The epidemiology, clinical manifestations, diagnosis, treatment and prevention of trichinellosis are reviewed.      

Chronic mucocutaneous candidiasis with macrophage dysfunction, a plasma inhibitor, and co-existent aplastic anemia.

A 56-year-old man developed chronic mucocutaneous candidiasis (MCC) and pernicious anemia. Nine years later he developed aplastic anemia which ultimately was fatal. A small thymoma was found at autopsy. He was anergic and his mononuclear leukocytes (MNL) failed to undergo a proliferative response in culture to soluble antigens. His monocytes did not mediate a proliferative response by lymphocytes from sensitized control donors when stimulated with Monilia albicans antigen but did mediate a mixed leukocyte reaction normally. His plasma contained a poten inhibitor of -3H-thymidine incorporation by sensitized control MNL when stimulated with soluble antigens but was not inhibitory of the mixed leukocyte reaction, lymphoproliferative responses to plant mitogens, and was not shown either in vivo or in vitro to depress hematopoiesis. Patient lymphocytes were responsive to plant mitogens, Monilia antigen, in the mixed leukocyte reaction, and produced macrophage migration inhibitory factor in response to Monilia antigen. After plasmapheresis, delayed hypersensitivity and lymphoproliferative responses to soluble antigens were temporarily restored. This case implicates the macrophage in the pathogenesis of MCC and demonstrates some consequences of chronic monocyte dysfunction. The inhibitor of some expressions of cell-mediated immunity was removed by plasmapheresis.     

Patients with neoplastic and nonneoplastic hematologic diseases acquire CTLA-4 antibodies after blood transfusion

BACKGROUND: The presence of antibodies to CTLA-4, a negative regulator of T-cell activation, was investigated in multiply transfused patients with malignant and non- malignant hematologic diseases. A previous study showed that, in multiply transfused patients, an immune response against nuclear matrix proteins can be induced by WBCs undergoing apoptosis during RBC unit storage. This study evaluated whether the same phenomenon could be involved in the induction of CTLA-4 antibodies in the patients analyzed. STUDY DESIGN AND METHODS: Patient sera were tested for binding to the recombinant full-length CTLA-4 beta-galactosidase fusion protein by an ELISA. Immuno-fluorescence stainings were performed to analyze the CTLA-4 epitopes recognized by the antibodies and to detect such epitopes in the apoptotic cells present in the RBC units. RESULTS: CTLA-4 antibodies were found in multiply transfused patients with beta-thalassemia (40%) and with other hemolytic diseases (33%) including leukemias (42%). A higher incidence of CTLA-4 antibodies was found in patients receiving non-WBC-reduced blood (88%) than in those receiving WBC-reduced blood (26%). Immunofluorescence staining showed that WBCs undergoing apoptosis in the RBC unit expressed CTLA-4 epitopes. CONCLUSIONS: The apoptotic WBCs present in the RBC units, after cold storage, express CTLA-4 epitopes. These epitopes can be released and induce formation of CTLA-4 antibodies with profound implications in the development of autoimmune disorders and in facilitating tumor dissemination and metastasis.