Bifdobacterium adolescentis is intrinsically resistant to antitubercular drugs.

Multiple mutations in the β subunit of the RNA polymerase (rpoβ) of Mycobacterium tuberculosis
(Mtb) are the primary cause of resistance to rifamycin (RIF). In the present study, bifdobacterial rpoβ
sequences were analyzed to characterize the mutations that contribute to the development of intrinsic
resistance to RIF, isoniazid, streptomycin and pyrazinamide. Sequence variations, which mapped to
cassettes 1 and 2 of the rpoβ pocket, are also found in multidrug-resistant Mtb (MDR Mtb). Growth
curves in the presence of osmolytes and diferent concentrations of RIF showed that the bacteria
adapted rapidly by shortening the growth curve lag time. Insight into the adapted rpoβ DNA sequences
revealed that B. adolescentis harbored mutations both in the RIF pocket and in regions outside
the pocket. The minimum inhibitory concentrations (MICs) and mutant prevention concentrations
(MPCs) indicated that B. longum, B. adolescentis and B. animalis are resistant to antitubercular drugs.
3D-homology modeling and binding interaction studies using computational docking suggested that
mutants had reduced binding afnity towards RIF. RIF-exposed/resistant bacteria exhibited variant
protein profles along with morphological diferences, such as elongated and branched cells, surface
conversion from rough to smooth, and formation of a concentrating ring.