Hidden spread of rifampicin-resistant TB in Addis Ababa

Tuberculosis remains a major public health threat in Ethiopia, especially because drug-resistant strains make the disease harder to control. Resistance to rifampicin (RR) is particularly important because RR is an accepted surrogate for multidrug-resistant TB (MDR-TB). More than 95% of RR comes from changes in an 81base pair segment of the rpoB gene, and these changes are now detectable by rapid molecular tests. Despite this, detailed molecular epidemiological information from Ethiopia has been limited. To fill that gap, Zerihun Woldesenbet and colleagues carried out a cross-sectional, hospital-based study in Addis Ababa to characterize specific rpoB gene mutation patterns and to look for factors associated with resistance. The team analyzed 753 Mycobacterium tuberculosis complex ( MTBC) clinical samples that had been confirmed positive for MTBC between 2020 and 2024. Alongside the genetic data, the researchers collected demographic and clinical information to test whether sex, age, HIV status or prior treatment history were linked to rifampicin resistance. The goal was to move beyond single-case clinical diagnosis and build a clearer picture of how resistant strains are spreading in the city.

For laboratory analysis the study used the Xpert MTB/RIF platform to generate probe mutation patterns for each of the 753 Mycobacterium tuberculosis complex ( MTBC) samples. Demographic and clinical variables were reviewed to identify potential risk factors for resistance. The overall rate of RR-TB detected was 2.3% (17 out of 753 samples). Molecular analysis revealed a distinct pattern of mutations within the rpoB gene: changes at codon 526 were the most common, accounting for 54.3% of the resistance mechanisms observed. Mutations at codon 531 were next most frequent at 21.7%, followed by codon 533 at 15.2%. A striking finding was that 100% of the RR-TB cases occurred in treatment-naïve patients, a result the authors interpret as clear evidence that primary transmission, not acquired resistance during treatment, is driving rifampicin resistance in this sample. Statistical testing found no significant links between RR-TB and sex, age, or HIV co-infection in this study population.

Taken together, the results point to a steady, low-grade epidemic of RR-TB in Addis Ababa that appears to be dominated by a strain with a characteristic mutation at rpoB codon 526. That pattern—combined with the fact that all resistant cases were in treatment-naïve people—suggests transmission in the community rather than resistance emerging during patient treatment. The authors argue this finding requires a shift from a reactive, clinically oriented model toward proactive public health measures to interrupt transmission. Specifically, the study recommends universal application of drug susceptibility testing so cases are identified quickly, enhanced and socially-directed contact tracing to find and protect people exposed to resistant strains, and integrating molecular surveillance into the TB control program to track how resistant strains move through the population. These steps are presented as essential if public health workers hope to break chains of transmission and prevent a rise in MDR-TB linked to rifampicin resistance.