N. Honoré | Semantic Scholar

Comparing the 3.27-megabase genome sequence of an armadillo-derived Indian isolate of the leprosy bacillus with that of Mycobacterium tuberculosis provides clear explanations for these properties and reveals an extreme case of reductive evolution.

Using comparative genomics, it is demonstrated that all extant cases of leprosy are attributable to a single clone whose dissemination worldwide can be retraced from analysis of very rare single-nucleotide polymorphisms.

Sixteen interrelated SNP subtypes were defined by genotyping both extant and extinct strains of M. leprae from around the world and showed a strong geographical association that reflects the migration patterns of early humans and trade routes, with the Silk Road linking Europe to China having contributed to the spread of leprosy.

Molecular detection of resistance to the two main antituberculous drugs, INH and RMP, can be accomplished accurately by using a strategy which limits analysis to four genetic regions, which may allow the expedient analysis of drug resistance by reference laboratories.

By cloning the ampC gene it was shown that a linked genetic locus, ampR, mediated the induction by beta‐lactams of cephalosporin hyper‐resistant Enterobacter cloacae strains and it is proposed that a homologous recombination event between these in an ancestral enteric bacterium may have led to the deletion of ampR from the E. coli genome.

It is proposed that one of the main features of ESAT-6 in the infection process of M. tuberculosis is the interaction with biomembranes that occurs after dissociation from its putative chaperone CFP-10 under acidic conditions typically encountered in the phagosome.

Study of a panel of INH‐resistant clinical isolates using a novel strategy based on the polymerase chain reaction and single‐strand‐conformation polymorphism analysis (PCR‐SSCP) to detect mutations in katG found that in most cases INH resistance was associated with missense mutations while in a small number of strains the gene had been completely, or partially, deleted.

It is shown here that streptomycin resistance in some clinical isolates of Mycobacterium tuberculosis is associated either with missense mutations in the rpsL gene, which encodes ribosomal protein S12, or with base substitutions at position 904 in the 16S rRNA.