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Journal of Clinical Microbiology, February 2001, p. 647-650, Vol. 39, No. 2
0095-1137/01/$04.00+0   DOI: 10.1128/JCM.39.2.647-650.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Pyrazinamide-Monoresistant Mycobacterium tuberculosis in the United States

Margaret M. Hannan,1,2,* Edward P. Desmond,3 Glenn P. Morlock,4 Gerald H. Mazurek,1 and Jack T. Crawford4

Division of Tuberculosis Elimination, National Center for HIV, STD, and TB Prevention,1 and National Center for Infectious Diseases,4 Centers for Disease Control and Prevention, Atlanta, Georgia 30333; California Department of Health Services, Berkeley, California 947043; and Department of Infectious Diseases and Microbiology, Imperial College School of Medicine, London W2 1PG, United Kingdom2

Received 30 June 2000/Returned for modification 9 October 2000/Accepted 15 November 2000

Mycobacterium bovis is naturally resistant to the antituberculosis drug pyrazinamide (PZA). To determine whether all Mycobacterium tuberculosis complex isolates demonstrating PZA monoresistance were truly M. bovis, we examined the phenotype and genotype of isolates reported as PZA monoresistant in five counties in California from January 1996 through June 1999. Isolates reported by local laboratories to be PZA monoresistant were sent to the state reference laboratory for repeat susceptibility testing using the BACTEC radiometric method and to the Centers for Disease Control and Prevention for pncA sequencing and PCR-restriction fragment length polymorphism (RFLP) analysis of the oxyR gene. Of 1,916 isolates, 14 were reported as PZA monoresistant and 11 were available for retesting. On repeat testing, 6 of the 11 isolates were identified as PZA-susceptible M. tuberculosis, 1 was identified as PZA-monoresistant M. bovis, and 1 was identified as M. bovis BCG. The three remaining isolates were identified as PZA-monoresistant M. tuberculosis. Sequencing of the pncA and oxyR genes genotypically confirmed the two M. bovis and the six susceptible M. tuberculosis species. Each of the three PZA-monoresistant M. tuberculosis isolates had different, previously unreported, pncA gene mutations: a 24-bp deletion in frame after codon 88, a base substitution at codon 104 (Ser104Cys), and a base substitution at codon 90 (Ile90Ser). This study demonstrates that PZA monoresistance is not an absolute marker of M. bovis species but may also occur in M. tuberculosis, associated with a number of different mutational events in the pncA gene. It is the first report of PZA-monoresistant M. tuberculosis in the United States.

* Corresponding author. Mailing address: Surveillance and Epidemiology Branch, Division of Tuberculosis Elimination, 1600 Clifton Rd., Mailstop E-10, Atlanta, GA 30333. Phone: (404) 639-5485. Fax: (404) 639-1287. E-mail: mhannan{at}cdc.gov.

Journal of Clinical Microbiology, February 2001, p. 647-650, Vol. 39, No. 2
0095-1137/01/$04.00+0   DOI: 10.1128/JCM.39.2.647-650.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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