Abstract

Environmental mycobacteria are capable of forming biofilms in low-nutrient environments, and these biofilms may act as reservoirs for opportunistic infections. The purpose of this study was to determine if bacteriophages could disrupt existing biofilms of acid-fast staining Mycobacterium smegmatis. Using the MBEC 96-well plastic peg assay system, M. smegmatis biofilms were created and then tested for their stability in the presence of mycobacteriophages isolated from a Minnesota sphagnum peat bog. All phages tested were lytic and were observed to have weak, intermediate, and strong abilities to disrupt M. smegmatis biofilms. The formation of biofilms was severely impaired in the presence of mycobacteriophages. Phage treatment was also shown to augment M. smegmatis biofilm disruption by mechanical forces of sonication or water flow. Our study shows that, as with biofilms of Gram-positive and Gram-negative bacteria, mycobacterial biofilms are also susceptible to destruction by bacteriophages.

Highlights

  • The genus Mycobacterium contains over 120 species, including saprophytic and pathogenic bacteria [1]

  • We first determined if MBEC plates can be used to generate M. smegmatis biofilms that can be exposed to antibiotics or mycobacteriophages

  • To determine if the sonication of bacterial biofilms was detrimental to M. smegmatis survival, aliquots of planktonic M. smegmatis were sonicated in a water bath and surviving cells enumerated using dilution plate counting

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Summary

Introduction

The genus Mycobacterium contains over 120 species, including saprophytic and pathogenic bacteria [1]. Mycobacteria can be classified into two groups: obligate pathogens such as Mycobacterium tuberculosis and Mycobacterium leprae, and environmental mycobacteria (EM), such as Mycobacterium avium complex. How to cite this paper: Kiefer, B. and Dahl, J.L. (2015) Disruption of Mycobacterium smegmatis Biofilms Using Bacteriophages Alone or in Combination with Mechanical Stress. L. Dahl majority of human infections are attributed to the tuberculosis complex of mycobacteria, EM are increasingly relevant in clinical settings as the cause of opportunistic infections that include skin lesions, pulmonary infections, lymphadenitis in children, endocarditis, meningitis, and disseminated disease [2]-[4]. EM infections are expected to increase due to expanding groups of the elderly, HIV-infected individuals, and those on immunosuppressive therapy [5]. EM are transmitted from aquatic and environmental sources primarily by ingestion, inhalation, and inoculation [6]

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