Pulmonary Tb With Concomitant Mycobacteriosis in Patients With Late-Stage Hiv Infection

Abstract

We studied social status, clinical and radiological manifestations, microbiological and immunological peculiarities in 26 latestage HIV infection patients with pulmonary TB and concomitant mycobacteriosis. They all had CD4+ lymphocyte counts less than 30 cells/μL of blood, did not receive antiretroviral therapy, and excreted both M. tuberculosis and nontuberculous mycobacteria (NTM). Identification of NTM species was based on molecular genetic methods. We found M. avium complex in 84,6%, M. kansasii — in 7,7%, M. fortuitum — in 3,8% and M. xenopi — in 3,8% of the patients. The disease manifested 6–9 years after diagnosing HIV infection; it had pronounced intoxication syndrome, bronchopulmonary and extrapulmonary presentations and was accompanied by other opportunistic infections. Radiological studies revealed intrathoracic adenopathy, dissemination with predominant localization in the middle and lower lung departments, foci and small infiltrates with cavities; injury of interlobar and visceral pleura.

Compensatory evolution drives multidrug-resistant tuberculosis in Central Asia

“…The frequencies of fluoroquinolone resistance, mediated by gyrA and gyrB mutations, remained low among the Karakalpakstan MDR-MTBC strains, which is consistent with the notion that such drugs were rarely used for treating TB in former Soviet Union countries (see discussion (13), (27–29)). This observation explains the generally favorable MDR-TB treatment outcomes observed with the use of individualized second-line regimens, including a fluoroquinolone, in the latter MDR-TB treatment program in the Karakalpakstan patient population (14, 32).…”

“…in Karakalpakstan, can be explained by past, largely empirical treatment decisions or self-medication. For instance, high frequencies of mutations in the ribD promoter region, and folC among Beijing-CAO strains, associated with para-aminosalicylic acid resistance (25, 26), are a likely consequence of the use of para-aminosalicylic acid in failing treatment regimens in the late 1970s to the early 1980s in the Soviet Union (27–29). Likewise, the frequent independent emergence of mutations in the eis promoter and of rare variants in the upstream region of whiB7 , both linked to resistance to aminoglycosides (mainly streptomycin and kanamycin) (30, 31), probably reflects self-administration of kanamycin that was available in local pharmacies.…”