Mycobacterium avium enters a state of metabolic dormancy in response to starvation.

Members of the Mycobacterium avium complex (MAC) exhibit a highly effective and biphasic response to starvation, losing less than 90% viability after 2 years in deionized water. During the first adaptive phase of 4-7 days, the bacilli exhibit a burst of lipid catabolism, alteration of mycolate modifications, loss of catalase and urease activities, and a decline in sensitivity to antibiotics. There is also a decline in the protein level of alanine tRNA synthetase (AlaS), and an increase in ribonuclease E (Rne) levels. During the following persistence phase, the bacilli become metabolically dormant. However, with return of nutrients, the cells rapidly respond with increased activity, as determined by reduction of a tetrazolium dye. The primary reservoir for MAC is natural and municipal water, and the metabolic dormancy may be analogous to that of other aquatic organisms, such as vibrio. The organized metabolic shutdown that environmental mycobacteria utilize to survive starvation may have evolved into the host-specific dormancy mechanisms of Mycobacterium tuberculosis.