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Spontaneous reversion of Mycobacterium abscessus from a smooth to a rough morphotype is associated with reduced expression of glycopeptidolipid and reacquisition of an invasive phenotype

Judith Recht^3,

¹ Center for Pulmonary and Infectious Disease Control, University of Texas Health Center at Tyler, Tyler, TX 75708, USA
² C4 101 Veterinary Medical Center, Cornell University, Ithaca, NY 14850, USA
³ Department of Microbiology and Molecular Genetics, Harvard Medical School, Boston MA 02115, USA
⁴ The University of New Mexico School of Medicine, Albuquerque, NM87108, USA
⁵ Department of Medicine, Albuquerque Veterans Affairs Medical Center, 1501 San Pedro, SE, Albuquerque, NM 87108, USA

Correspondence
Thomas F. Byrd
tbyrd{at}salud.unm.edu

Mycobacterium abscessus is an increasingly important cause of human disease; however, virulence determinants are largely uncharacterized. Previously, it was demonstrated that a rough, wild-type human clinical isolate (390R) causes persistent, invasive infection, while a smooth isogenic mutant (390S) has lost this capability. During serial passage of 390S, a spontaneous rough revertant was obtained, which was named 390V. This revertant regained the ability to cause persistent, invasive infection in human monocytes and the lungs of mice. Glycopeptidolipid (GPL), which plays a role in environmental colonization, was present in abundance in the cell wall of 390S, and was associated with sliding motility and biofilm formation. In contrast, a marked reduction in the amount of GPL in the cell wall of 390R and 390V was correlated with cord formation, a property associated with mycobacterial virulence. These results indicate that the ability to switch between smooth and rough morphologies may allow M. abscessus to transition between a colonizing phenotype and a more virulent, invasive form.

Present address: Department of Oncological Sciences, Mount Sinai School of Medicine, NY 10029, USA.

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