Mycobacterium fortuitum infection: evidence of bactericidal defect due to hyperactive antigen-specific suppressor cells. Correction in vitro and in vivo by cholinergic agonist and indomethacin.

Immunologic studies in a patient with long-standing Mycobacterium fortuitum infection revealed normal numbers of T cells, T inducers, T suppressors, B cells, and monocytes, significant in vitro proliferative response to M. fortuitum antigen, and poor bactericidal activity against M. fortuitum but not against Escherhicia coli. M. fortuitum antigen-activated suppressor cells contributed to the bactericidal defect. The activity of these suppressor cells could be eliminated by the in vitro treatment of blood mononuclear cells with a combination of a cholinergic agonist and indomethacin, but not with either alone. Administration of the two drugs to the patient resulted in reversal of the bactericidal defect and dramatic clinical improvement. Systemic atypical (nontuberculous) mycobacterial infection may activate specific suppressor cells that could compromise the host's phagocytic cell function. Modulation of those suppressor cells by a combination of a cholinergic agonist and prostaglandin synthetase inhibitor could reverse this abnormality and may be beneficial to the patient.