Rickettsial perimyocarditis—A follow-up study

Summary Sera and lymphocytes from a 37-year-old male patient with acute perimyocarditis during a Q-fever endemic were analyzed for antibody and cell-mediated immune reactions and followed up 28 months later. Circulating autoantibodies against myocardial tissue were assessed by indirect immunofluorescence. Cytolysis of vital contracting rat cardiocytes, by antimyolemmal antibodies and complement, and lymphocytotoxicity, with and without the patient's serum, were evaluated and compared with the results obtained in ten patients suffering from Q-fever without perimyocardial involvement and with 40 healthy subjects.Antimyolemmal antibodies (AMLA), a muscle-specific subtype of antisarcolemmal antibodies, were demonstrated by immunofluorescence in the one patient with Q-fever perimyocarditis in titers of up to 1 : 320 but not in the controls. AMLA induced cytolysis of myocytes in the presence of complement. Both AMLA and cytolytic serum activity could be absorbed in all sera of this patient by usingCoxiella burnetii. Only marginal lymphocytotoxicity against heterologous cardiocytes was detected in the early phase and again during the follow-up 2 years later in the Q-fever myocarditis patient but not in any of the noncarditic Q-fever cases nor in controls. It is postulated that cross-reacting, complement-fixing, cytolytic autoantibodies against the cardiac myolemma are operative either as a cause of cardiac damage or a consequence, pointing to a secondary immunopathogenesis of chronic Q-fever perimyocarditis.supported by grants of the Deutsche Forschungsgemeinschaft (Ma 780/1–5)