Exogenous Reinfection as a Cause of Recurrent Tuberculosis after Curative Treatment
Annelies van Rie, M.D., Robin Warren, Ph.D., Madeleine Richardson, M.Sc., Thomas C. Victor, Ph.D., Robert P. Gie, M.D., Donald A. Enarson, M.D., Nulda Beyers, Ph.D., and Paul D. van Helden, Ph.D.
Background For decades it has been assumed that postprimarytuberculosis is usually caused by reactivation of endogenousinfection rather than by a new, exogenous infection.
Methods We performed DNA fingerprinting with restriction-fragmentlengthpolymorphism analysis on pairs of isolates of Mycobacteriumtuberculosis from 16 compliant patients who had a relapse ofpulmonary tuberculosis after curative treatment of postprimarytuberculosis. The patients lived in areas of South Africa wheretuberculosis is endemic. Medical records were reviewed for clinicaldata.
Results For 12 of the 16 patients, the restriction-fragmentlengthpolymorphism banding patterns for the isolates obtained afterthe relapse were different from those for the isolates fromthe initial tuberculous disease. This finding indicates thatreinfection was the cause of the recurrence of tuberculosisafter curative treatment. Two patients had reinfections witha multidrug-resistant strain. All 15 patients who were testedfor the human immunodeficiency virus were seronegative.
Conclusions Exogenous reinfection appears to be a major causeof postprimary tuberculosis after a previous cure in an areawith a high incidence of this disease. This finding emphasizesthe importance of achieving cures and of preventing anyone withinfectious tuberculosis from exposing others to the disease.
Source Information
From the Department of Pediatrics and Child Health (A.V.R., R.P.G., N.B.) and the Medical Research Council Center for Molecular and Cellular Biology and the Department of Medical Biochemistry (R.W., M.R., T.C.V., P.D.V.H.), University of Stellenbosch, Tygerberg, South Africa; the Department of Pediatrics, Catholic University Leuven, Leuven, Belgium (A.V.R.); and the International Union against Tuberculosis and Lung Disease, Paris (D.A.E.).
Address reprint requests to Dr. van Helden at the Department of Medical Biochemistry, University of Stellenbosch, P.O. Box 19063, Tygerberg 7505, South Africa, or at pvh{at}gerga.sun.ac.za.
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