Mycobacterium fortuitum pulmonary infection associated with an antigen-selective defect in cellular immunity.
In this study we describe the first example of a well documented case of pulmonary infection caused by Mycobacterium fortuitum shown to be associated with an antigen-selective defect in cell-mediated immunity to this organism. Immunologic parameters were evaluated before, during and after antibiotic treatment with amikacin. A defect in cellular immunity to purified protein derivative from Myco. fortuitum, shown to be antigen-selective as indicated by normal responsiveness to purified protein derivative from Mycobacterium tuberculosis and several other common recall antigens, accompanied the prolonged infection by this organism. During the first three months of treatment with amikacin, the patient's clinical status improved coincident with the eradication of the organism from the sputum. During the next three months of therapy with amikacin, however, a generalized defect in cellular immunity developed, and the lung disease again progressed. The deteriorating clinical condition was presumably related to a generalized cellular immune anergy or hyporesponsiveness induced by the amikacin therapy. After three more months of treatment, the organism became resistant to the drug and reappeared in sputum cultures. Since amikacin therapy was discontinued, the patient's general immune responsiveness returned to normal. He did, however, remain unresponsive to purified protein derivative from Mycobacterium fortuitum.
D000583:Amikacin / Q000008:administration & dosage; D002464:Cell Migration Inhibition; D007111:Immunity, Cellular; D007961:Leukocyte Migration-Inhibitory Factors / Q000096:biosynthesis; D009165:Mycobacterium Infections, Nontuberculous / Q000188:drug therapy / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology; D014397:Tuberculosis, Pulmonary / Q000276:immunology*
D007961:Leukocyte Migration-Inhibitory Factors; D000583:Amikacin