Abstract
Mycobacterium avium complex (MAC) organisms are waterborne, opportunistic pathogens whose source is natural waters and soils and proliferates and persists in premise plumbing, for example household and hospital plumbing. M. avium complex and other environmental mycobacteria grow slowly, not because their metabolism is slow, but because they synthesize long chain (C(60)-C(80)) fatty acids that make up its hydrophobic and impermeable outer membrane. There are costs and benefits to the presence of that lipid-rich outer membrane. One benefit is that cell-surface hydrophobicity drives M. avium complex cells to adhere to surfaces to reduce their interaction with charged ions in suspension; they are likely "biofilm pioneers", adhering to a wide variety of surface materials. The result is that the slow-growing M. avium complex cells (1 gen/day at 37 °C) will not be washed out of any flowing system, whether a stream or plumbing in the built environment. Although the slow permeation of nutrients in M. avium complex organisms limits growth, they are also resistant to disinfectants, thus increasing their survival in water distribution systems, premise plumbing, and medical equipment. There are three components to the antimicrobial resistance of M. avium complex in biofilms: (1) innate resistance due to the hydrophobic, impermeable outer membrane, (2) residence in a matrix of extracellular polysaccharide, lipid, DNA, and protein that prevents access of antimicrobials to M. avium cells, and (3) an adaptive and transient increased resistance of biofilm-grown M. avium cells grown in biofilms. As expected M. avium in biofilms will display neutral, antagonistic, or beneficial interactions with other biofilm inhabitants. Methylobacterium spp., the common pink-pigmented, waterborne bacteria compete with M. avium for surface binding, suggested an approach to reducing M. avium biofilm formation and hence persistence in premise plumbing.