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Journal of Clinical Microbiology, December 2004, p. 5689-5697, Vol. 42, No. 12
0095-1137/04/$08.00+0     DOI: 10.1128/JCM.42.12.5689-5697.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Clinical and Laboratory Features of Mycobacterium porcinum

Richard J. Wallace Jr.,^1* Barbara A. Brown-Elliott,¹ Rebecca W. Wilson,¹ Linda Mann,¹ Leslie Hall,² Yansheng Zhang,¹ Kenneth C. Jost Jr.,³ June M. Brown,⁴ Amin Kabani,⁵ Mark F. Schinsky,^4, Arnold G. Steigerwalt,⁴ Christopher J. Crist,¹ Glenn D. Roberts,² Zeta Blacklock,⁶ Michio Tsukamura,⁷ Vella Silcox,⁴ and Christine Turenne⁵

The Mycobacteria/Nocardia Research Laboratory, The University of Texas Health Center, Tyler,¹ Texas Department of Health, Austin, Texas,³ Mayo Clinic, Rochester, Minnesota,² Meningitis and Special Pathogens Branch, Division of Bacterial and Mycotic Diseases, National Center for Infectious Disease, Centers for Disease Control and Prevention, Atlanta, Georgia,⁴ National Reference Center for Mycobacteriology, National Microbiology Laboratory, Health Canada, Winnipeg, Manitoba, Canada,⁵ Queensland State Laboratory, Brisbane, Australia,⁶ National Chubu Hospital, Obu, Aichi, Japan⁷

Received 16 March 2004/ Returned for modification 22 April 2004/ Accepted 25 August 2004

Recent molecular studies have shown Mycobacterium porcinum, recovered from cases of lymphadenitis in swine, to have complete 16S rDNA sequence identity and >70% DNA-DNA homology with human isolates within the M. fortuitum third biovariant complex. We identified 67 clinical and two environmental isolates of the M. fortuitum third biovariant sorbitol-negative group, of which 48 (70%) had the same PCR restriction enzyme analysis (PRA) profile as the hsp65 gene of M. porcinum (ATCC 33776^T) and were studied in more detail. Most U.S. patient isolates were from Texas (44%), Florida (19%), or other southern coastal states (15%). Clinical infections included wound infections (62%), central catheter infections and/or bacteremia (16%), and possible pneumonitis (18%). Sequencing of the 16S rRNA gene (1,463 bp) showed 100% identity with M. porcinum ATCC 33776^T. Sequencing of 441 bp of the hsp65 gene showed four sequevars that differed by 2 to 3 bp from the porcine strains. Clinical isolates were positive for arylsulfatase activity at 3 days, nitrate, iron uptake, D-mannitol, i-myo-inositol, and catalase at 68°C. They were negative for L-rhamnose and D-glucitol (sorbitol). Clinical isolates were susceptible to ciprofloxacin, sulfamethoxazole, and linezolid and susceptible or intermediate to cefoxitin, clarithromycin, imipenem, and amikacin. M. porcinum ATCC 33776^T gave similar results except for being nitrate negative. These studies showed almost complete phenotypic and molecular identity between clinical isolates of the M. fortuitum third biovariant D-sorbitol-negative group and porcine strains of M. porcinum and confirmed that they belong to the same species. Identification of M. porcinum presently requires hsp65 gene PRA or 16S rRNA or hsp65 gene sequencing.

This paper is dedicated to the three coauthors Vella Silcox, Zeta Blacklock, and Michio Tsukamura, early investigators who contributed greatly to the present study but who retired before the present taxonomic status of isolates of the third biovariant complex was established. Both Zeta Blacklock and Michio Tsukamura passed away prior to submission of this study.

Present address: Washington University School of Medicine, Barnes-Jewish Hospital, St. Louis, MO 63140.

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