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Background <p>This study included tuberculosis (TB) patients from high-burden Russian regions of Siberia and Far East. We aimed to assess the impact of the COVID-19 pandemic on the genotypic structure of <i>Mycobacterium tuberculosis</i> population and on epidemiology and clinical course of tuberculosis in TB and TB/COVID-19 coinfected patients.</p> Methods <p>A total of 456&#xa0;M<i>. tuberculosis</i> isolates were studied and submitted to drug susceptibility testing and genotyping. The modern Beijing genotype and its main Russian epidemic and endemic clusters (B0/W148 and Central Asian/Russian), and ancient Beijing sublineage were detected by PCR assays targeting specific molecular markers. Non-Beijing isolates were spoligotyped and compared to SITVIT2 database.</p> Results <p>More than 80% of strains belonged to the Beijing genotype. Among Beijing strains, genetic clusters B0/W148 and Central-Asian/Russian (94–32) accounted for 94.2% in the pre-pandemic period and 96.6% during the pandemic in the TB group, and 81.5% of TB/COVID-19 group. Moreover, in the pre-pandemic TB group, the ratio of B0/W148 and 94–32 was almost 1:1 (49.7:44.4%), during the pandemic—1.5:1.0 (57.9:38.8%), while in the TB/COVID-19 group, the ratio shifted in favor of the 94–32 cluster and became 1:2 (31.8:65.9%). In TB/COVID patients, the structure of clinical forms shifted from chronic forms (fibrous cavernous TB, tuberculoma) to forms with more active inflammatory and destructive-inflammatory reactions (infiltration, dissemination, cavernous TB). In TB (without COVID-19-coinfection) group, the effectiveness of TB treatment during the pandemic decreased by 20.6% (<i>p</i> = 0.002). In the TB/COVID-19 group, the effectiveness of treatment increased, likely due to the predominance of the less frequently MDR Beijing 94–32 cluster in this group. A statistically significant positive correlation was shown between the detection of the&#xa0;94–32-cluster and the effectiveness of treatment of patients with TB/COVID-19 (Q = 0.56, <i>p</i> = 0.006).</p> Conclusions <p>Our results are consistent with the reportedly higher ability of Beijing B0/W148 strains (compared to Beijing 94–32) to acquire resistance to anti-TB drugs, their increased virulence and transmissibility. Thus, the seemingly paradoxical, milder clinical course of TB in patients who further developed COVID-19 is explained by a shift in the ratio of <i>M. tuberculosis</i> subtypes due to syndemic interaction between the two epidemics.</p>

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Impact of the COVID-19 pandemic on the epidemiology and clinical course of tuberculosis: expected and paradoxical consequences

  • 期刊论文

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  • 发表日期：

    2025年3月26日

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  • Yakov Schwartz,
  • Anna Vyazovaya,
  • Natalya Tursunova,
  • Igor Mokrousov

摘要

Background

This study included tuberculosis (TB) patients from high-burden Russian regions of Siberia and Far East. We aimed to assess the impact of the COVID-19 pandemic on the genotypic structure of Mycobacterium tuberculosis population and on epidemiology and clinical course of tuberculosis in TB and TB/COVID-19 coinfected patients.

Methods

A total of 456 M. tuberculosis isolates were studied and submitted to drug susceptibility testing and genotyping. The modern Beijing genotype and its main Russian epidemic and endemic clusters (B0/W148 and Central Asian/Russian), and ancient Beijing sublineage were detected by PCR assays targeting specific molecular markers. Non-Beijing isolates were spoligotyped and compared to SITVIT2 database.

Results

More than 80% of strains belonged to the Beijing genotype. Among Beijing strains, genetic clusters B0/W148 and Central-Asian/Russian (94–32) accounted for 94.2% in the pre-pandemic period and 96.6% during the pandemic in the TB group, and 81.5% of TB/COVID-19 group. Moreover, in the pre-pandemic TB group, the ratio of B0/W148 and 94–32 was almost 1:1 (49.7:44.4%), during the pandemic—1.5:1.0 (57.9:38.8%), while in the TB/COVID-19 group, the ratio shifted in favor of the 94–32 cluster and became 1:2 (31.8:65.9%). In TB/COVID patients, the structure of clinical forms shifted from chronic forms (fibrous cavernous TB, tuberculoma) to forms with more active inflammatory and destructive-inflammatory reactions (infiltration, dissemination, cavernous TB). In TB (without COVID-19-coinfection) group, the effectiveness of TB treatment during the pandemic decreased by 20.6% (p = 0.002). In the TB/COVID-19 group, the effectiveness of treatment increased, likely due to the predominance of the less frequently MDR Beijing 94–32 cluster in this group. A statistically significant positive correlation was shown between the detection of the 94–32-cluster and the effectiveness of treatment of patients with TB/COVID-19 (Q = 0.56, p = 0.006).

Conclusions

Our results are consistent with the reportedly higher ability of Beijing B0/W148 strains (compared to Beijing 94–32) to acquire resistance to anti-TB drugs, their increased virulence and transmissibility. Thus, the seemingly paradoxical, milder clinical course of TB in patients who further developed COVID-19 is explained by a shift in the ratio of M. tuberculosis subtypes due to syndemic interaction between the two epidemics.