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Published on: November 5, 2019
Metabolic shift in the emergence of hyperinvasive pandemic meningococcal lineages
Eleanor R Watkins1, Martin C J Maiden1
1Department of Zoology, University of Oxford, South Parks Road, Oxford, OX1 3PS, UK.
Abstract:
Hyperinvasive lineages of Neisseria meningitidis, which persist despite extensive horizontal genetic exchange, are a major cause of meningitis and septicaemia worldwide. Over the past 50 years one such lineage of meningococci, known as serogroup A, clonal complex 5 (A:cc5), has caused three successive pandemics, including epidemics in sub-Saharan Africa. Although the principal antigens that invoke effective immunity have remained unchanged, distinct A:cc5 epidemic clones have nevertheless emerged. An analysis of whole genome sequence diversity among 153 A:cc5 isolates identified eleven genetic introgression events in the emergence of the epidemic clones, which primarily involved variants of core genes encoding metabolic processes. The acquired DNA was identical to that found over many years in other, unrelated, hyperinvasive meningococci, suggesting that the epidemic clones emerged by acquisition of pre-existing metabolic gene variants, rather than 'virulence' associated or antigen-encoding genes. This is consistent with mathematical models which predict the association of transmission fitness with the emergence and maintenance of virulence in recombining commensal organisms.
Insights
Hyperinvasive meningococci, serogroup A clonal complex 5, cause pandemics. New epidemic clones emerged by acquiring metabolic genes, not virulence factors, from other bacteria.
Area of Science:
- Microbiology
- Genetics
- Epidemiology
Background:
- Hyperinvasive lineages of *Neisseria meningitidis* cause global meningitis and septicaemia.
- Serogroup A, clonal complex 5 (A:cc5) has caused three pandemics in the last 50 years, particularly in sub-Saharan Africa.
- Distinct A:cc5 epidemic clones have emerged despite unchanged principal antigens.
Purpose of the Study:
- To investigate the genetic basis for the emergence of distinct A:cc5 epidemic clones.
- To identify the source and type of genetic material acquired by these epidemic clones.
Main Methods:
- Whole genome sequencing of 153 A:cc5 isolates.
- Analysis of genetic diversity and introgression events.
Main Results:
- Eleven genetic introgression events were identified in the emergence of A:cc5 epidemic clones.
- Acquired DNA primarily involved variants of core genes encoding metabolic processes.
- The acquired DNA originated from pre-existing variants in other unrelated hyperinvasive meningococci.
Conclusions:
- A:cc5 epidemic clones emerged through the acquisition of pre-existing metabolic gene variants, not virulence or antigen-encoding genes.
- This acquisition mechanism is consistent with models linking transmission fitness to virulence in recombining organisms.
