Molecular insights of melioidosis causing Burkholderia pseudomallei strains in Sri Lanka

Year 2020, Volume: 10 Issue: 04, 215 - 221, 15.12.2020

A. W. A. Chathura Wikumpriya Gunasekara Lgtg Rajapaksha

https://doi.org/10.5799/jmid.839461

Abstract

Objectives: Objectives: Gram-negative pathogenic bacterium Burkholderia pseudomallei is the causative organism of melioidosis, predominantly reported in Southeast Asia. The infections in humans can be recurrent, and sometimes difficult to cure. Studying the genome of B. pseudomallei is the key to understand origins, transmission routes, and phylogenetic relationships.
Methods: We compared all available B. pseudomallei genomes from the NCBI database representing Sri Lanka to 15 previously reported genomes in Asia. The analysis involved in silico MLST, wgMLST, single nucleotide polymorphism (SNP), average nucleotide identity (ANI), clonal complexes (CC), virulence, and antibiotic resistance profiles.
Results: The MLST analyses of 24 strains revealed, 6 Sri Lankan and 1 Indian strain formed CC594*, a novel single locus variant clonal complex, and 3 strains from Malaysia, Vietnam, Thailand formed another clonal complex named CC70*. From 9 Sri Lankan strains, BPs122 and BPs133 had ancestral origins tied to BPs114 with 114/99.6% and 140/99.6% for SNPs/ANIs. In CC70*, Thailand and Vietnam strains had 1196/99.95% for SNPs/ANIs, respectively. Among the Sri Lankan strains, actin-based motility gene bimA detected in BPs110 only, whereas LPS antigen was presented in BPs112, BPs115, and BPs116 genomes. A total of 67 genes related to antibiotic resistance (22 multidrug efflux systems, 10 regulators modulating/expression of antibiotic resistance, and 11 antibiotic inactivation enzymes related genes) were identified.
Conclusion: The B. pseudomallei strains in Sri Lanka represent a highly diverse nature and some of them had clonal relationships with other Asian strains. The present study concludes B. pseudomallei strains in Sri Lanka have probably risen from different ancestral origins. J Microbiol Infect Dis 2020; 10(4): 215-221.

Keywords

Burkholderia pseudomallei, Sri Lanka, SNPs, ANIs, clonal relation

References

• 1. Titball RW, Russell P, Cuccui J, et al. Burkholderia pseudomallei: Animal models of infection. Trans R Soc Trop Med Hyg 2008; 102: S111–116.
• 2. Chewapreecha C, Mather AE, Harris SR, et al. Genetic variation associated with infection and the environment in the accidental pathogen Burkholderia pseudomallei. Commun Biol 2019; 22(1):1–11.
• 3. Cheng AC, Currie BJ. Melioidosis: epidemiology, pathophysiology, and management. Clin Microbiol Rev 2005;18(2):383–416.
• 4. Mukhopadhyay C, Shaw T, Varghese G, Dance D. Melioidosis in South Asia (India, Nepal, Pakistan, Bhutan and Afghanistan). TropicalMed 2018;22(2):51.
• 5. Laws TR, Taylor AW, Russell P, Williamson D. The treatment of melioidosis: is there a role for repurposed drugs? A proposal and review. Expert Review of Anti-infective Therapy 2019;17(12):957–967.
• 6. Massey S, Yeager LA, et al. Comparative Burkholderia pseudomallei natural history virulence studies using an aerosol murine model of infection. Sci Rep 2014;7(1):4305.
• 7. Larsen JC, Johnson NH. Pathogenesis of Burkholderia pseudomallei and Burkholderia mallei. Military Medicine 2009;174(6):647–651.
• 8. Corea E, Thevanesam V, et al. Melioidosis in Sri Lanka: an emerging infection. Sri Lankan J Infec Dis 2012;31(1):2.
• 9. Corea EM, de Silva AD, Thevanesam V. Melioidosis in Sri Lanka. Trop Med Infect Dis 2018;21(1): PMC6136624.
• 10. Didelot X, Pang B, Zhou Z, McCann A, Ni P, Li D, et al. The role of china in the global spread of the current cholera pandemic. Casadesús J, editor. PLoS Genet 2015;13(3): e1005072.
• 11. Fu S, Tian H, Wei D, Zhang X, Liu Y. Delineating the origins of Vibrio parahaemolyticus isolated from outbreaks of acute hepatopancreatic necrosis disease in Asia by the use of whole genome sequencing. Front Microbiol 2017;28(8):2354.
• 12. Jayasinghearachchi HS, Corea EM, et al. Whole-genome sequences of eight clinical isolates of Burkholderia pseudomallei from melioidosis patients in Eastern Sri Lanka. Maresca JA, editor. Microbiol Resour Announc 2019;8(33): MRA.00645-19, e00645-19
• 13. Larsen MV, Cosentino S, et al. Multilocus sequence typing of total-genome-sequenced bacteria. J Clin Microbiol 2012;50(4):1355–1361.
• 14. Francisco AP, Bugalho M, Ramirez M, Carriço JA. Global optimal eBURST analysis of multilocus typing data using a graphic matroid approach. BMC Bioinformatics 2009;10(1):152.
• 15. Stoneking M. Single nucleotide polymorphisms. From the evolutionary past. Nature 2001;409(6822):821–822.
• 16. Richter M, Rosselló-Móra R, Oliver Glöckner F, Peplies J. JSpeciesWS: a web server for prokaryotic species circumscription based on pairwise genome comparison. Bioinformatics 2016;32(6):929–931.
• 17. Jolley KA, Bray JE, Maiden MCJ. Open-access bacterial population genomics: BIGSdb software, the PubMLST.org website and their applications. Wellcome Open Res 2018;3: PMC6192448.
• 18. Kaas RS, Leekitcharoenphon P, Aarestrup FM, Lund O. Solving the problem of comparing whole bacterial genomes across different sequencing platforms. PLoS ONE 2014;9(8): e104984.
• 19. Wattam AR, Abraham D, et al. PATRIC, the bacterial bioinformatics database and analysis resource. Nucleic Acids Res. 2014;42(Database issue): D581–D591.
• 20. Chen L, Zheng D, Liu B, Yang J, Jin Q. VFDB 2016: hierarchical and refined dataset for big data analysis—10 years on. Nucleic Acids Res 2016;44(D1): D694–D697.
• 21. Pearson T, Giffard P, et al. Phylogeographic reconstruction of a bacterial species with high levels of lateral gene transfer. BMC Biol 2009;18(7):78.
• 22. Chirakul S, Norris MH, et al. Transcriptional and post-transcriptional regulation of PenA β-lactamase in acquired Burkholderia pseudomallei β-lactam resistance. Sci Rep 2018;13(8):1. PMC6045580.
• 23. Schweizer HP. Mechanisms of antibiotic resistance in Burkholderia pseudomallei: implications for treatment of melioidosis. Future Microbiology 2012;7(12):1389–1399.
• 24. Bugrysheva JV, Sue D, et al. Antibiotic resistance markers in Burkholderia pseudomallei strain Bp1651 Identified by genome sequence analysis. Antimicrob Agents Chemother 2017;61(6): e00010-17, e00010-17.
• 25. Schell MA, Ulrich RL, et al. Type VI secretion is a major virulence determinant in Burkholderia mallei: Type VI secretion in B. mallei virulence. Mol Microbiol 2007;64(6):1466–1485.
• 26. Stone JK, DeShazer D, Brett PJ, Burtnick MN. Melioidosis: molecular aspects of pathogenesis. Expert Rev Anti Infect Ther 2014;12(12):1487–1499.
• 27. Woodman ME, Worth RG, Wooten RM. Capsule influences the deposition of critical complement C3 levels required for the killing of Burkholderia pseudomallei via NADPH-oxidase induction by human neutrophils. PLoS ONE 2012;7(12): e52276.
• 28. Burtnick MN, Brett PJ, Nair V, Warawa JM, Woods DE, Gherardini FC. Burkholderia pseudomallei Type III secretion system mutants exhibit delayed vacuolar escape phenotypes in raw 264.7 murine macrophages. Infect Immun 2008;76(7):2991–3000.
• 29. Balder R, Lipski S, et al. Identification of Burkholderia mallei and Burkholderia pseudomallei adhesins for human respiratory epithelial cells. BMC Microbiol 2010;10(1):250.
• 30. Saikh KU, Mott TM. Innate immune response to Burkholderia mallei. Curr Opin Infect Dis 2017;30(3):297–302.