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Journal of Clinical Microbiology, October 1999, p. 3255-3259, Vol. 37, No. 10
0095-1137/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
Evidence from Molecular Fingerprinting of Limited
Spread of Drug-Resistant Tuberculosis in Texas
Rebecca W.
Wilson,1
Zhenhua
Yang,2,3
Michael
Kelley,4
M. Donald
Cave,2,5
Janice M.
Pogoda,6
Richard J.
Wallace Jr.,1,7
J. Peter
Cegielski,1,8
Denise F.
Dunbar,4
David
Bergmire-Sweat,4
L. Bruce
Elliott,4 and
Peter F.
Barnes1,8,9,*
Center for Pulmonary and Infectious Disease
Control,1 Departments of
Microbiology,7 Cell
Biology,9 and
Medicine,8 University of Texas Health
Center at Tyler, Tyler, and Texas Department of Health,
Austin,4 Texas; Regional
Tuberculosis Genotyping Laboratory2 and
Departments of Pathology3 and
Anatomy,5 University of Arkansas for
Medical Sciences, Little Rock, Arkansas; and Statotology,
Truckee, California6
Received 2 December 1998/Returned for modification 20 March
1999/Accepted 26 June 1999
To determine the contribution of recent transmission to spread of
drug-resistant tuberculosis in Texas, we performed
IS6110-based and pTBN12-based restriction fragment length
polymorphism (RFLP) analyses on Mycobacterium tuberculosis
isolates. Isolates collected from 201 patients in Texas between 1992 and 1994 were studied. The distribution of cases was strikingly focal.
All cases were reported from 35 of the 254 counties in Texas, and 74%
(148 of 201) were reported from only 9 counties. One hundred sixty-one (80%) of the patients had M. tuberculosis isolates with
unique RFLP patterns, and 41 (20%) patients were in 20 clusters, each comprising 2 to 3 patients. The largest number of cases of
drug-resistant tuberculosis were reported in counties bordering Mexico,
but the percentage of clustered cases was highest in northeast Texas
and in counties that included the cities of Dallas, Fort Worth, and Houston. Compared to nonclustered patients, clustered patients were
more likely to be African American and to have been born in the United
States. Clustered patients were significantly more likely to be from
the same geographic area, and clustered patients from the same
geographic area were more likely to have isolates with identical drug
susceptibility patterns, suggesting that they were linked by recent
transmission. In 11 of 20 clusters, clustered patients were from
geographically separate regions, and most isolates did not have
identical drug susceptibility patterns, suggesting that tuberculosis
was contracted from a common source in the remote past. Based on the
low percentage of clustered cases and the small cluster size, we
conclude that there is no evidence for the extensive transmission of
drug-resistant tuberculosis in Texas.
*
Corresponding author. Mailing address: Peter F. Barnes,
Center for Pulmonary and Infectious Disease Control, University of Texas Health Center at Tyler, 11937 U.S. Highway 271, Tyler, TX 75708-3154. Phone: (903) 877-5956. Fax: (903) 877-5516. E-mail: pbarnes{at}uthct.edu.
Journal of Clinical Microbiology, October 1999, p. 3255-3259, Vol. 37, No. 10
0095-1137/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
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