Emergence of short-lived meningococci causing focal epidemics can be associated with gene transfer from carriage-associated Neisseria
- 1University of Oxford
Abstract
In March 2026, an unusually large outbreak of invasive meningococcal disease (IMD) in Kent, UK, was linked to attendance at one nightclub over a single weekend. The outbreak organism was a Neisseria meningitidis variant belonging to the longstanding hyperinvasive genotype, cc41/44. Using genome analysis of six isolates from patients, alongside >48,000 meningococcal genomes, we investigated whether the outbreak variant had acquired traits potentially contributing to the highly invasive phenotype. The six isolates were capsular group B, sequence type (ST-)485, and essentially indistinguishable, consistent with the focal nature of the outbreak. Compared with their closest available relatives, we found changes mediated by phase variation, nucleotide variation, and horizontal gene transfer (HGT) involving adhesins, iron-acquisition systems (including Transferrin and Lactoferrin binding proteins, and FetA), and Type IV pili (Tfp), factors which affect bacteria-bacteria and bacteria-host interactions. These changes occurred in a ST-485 sub-lineage that expressed capsule at high levels and a PorA porin with a truncated surface-exposed epitope, both of which are predicted to reduce immune recognition. Donors for the HGT events were predominantly carriage-associated N. meningitidis and Neisseria cinerea. We show that meningococcal variants responsible for previous focal outbreaks have not been seen subsequently. We propose that focal outbreaks of IMD are caused by meningococcal variants that may have acquired traits from non- or less invasive organisms, but subsequently these variants disappear, as their highly invasive phenotype is inconsistent with sustained transmission. Ongoing disease surveillance alongside carriage studies are therefore essential to inform public health risk and manage epidemic IMD.
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BibTeX
@misc{rodrigues2026emergence,
title = {{Emergence of short-lived meningococci causing focal epidemics can be associated with gene transfer from carriage-associated Neisseria}},
author = {C. M. Rodrigues and J. Lucidarme and R. M. Exley and J. L. Clark and X. Bai and C. Bayliss and M. Chand and S. A. Clark and C. N. Cornelissen and J. Derrick and L. R. Green and N. Groves and Y. Gutierrez Vazquez and O. B. Harrison and K. A. Jolley and S. A. McKeand and R. Myers and N. Noinaj and K. Parfitt and P. Ribeca and R. Borrow and M. C. Maiden and C. M. Tang},
howpublished = {bioRxiv},
year = {2026},
month = sep,
doi = {10.64898/2026.09.17.752363},
url = {https://www.biorxiv.org/content/10.64898/2026.09.17.752363v1},
note = {CC BY},
}
RIS
TY - UNPB
TI - Emergence of short-lived meningococci causing focal epidemics can be associated with gene transfer from carriage-associated Neisseria
AU - C. M. Rodrigues
AU - J. Lucidarme
AU - R. M. Exley
AU - J. L. Clark
AU - X. Bai
AU - C. Bayliss
AU - M. Chand
AU - S. A. Clark
AU - C. N. Cornelissen
AU - J. Derrick
AU - L. R. Green
AU - N. Groves
AU - Y. Gutierrez Vazquez
AU - O. B. Harrison
AU - K. A. Jolley
AU - S. A. McKeand
AU - R. Myers
AU - N. Noinaj
AU - K. Parfitt
AU - P. Ribeca
AU - R. Borrow
AU - M. C. Maiden
AU - C. M. Tang
PY - 2026
DA - 2026/09/17
PB - bioRxiv
DO - 10.64898/2026.09.17.752363
UR - https://www.biorxiv.org/content/10.64898/2026.09.17.752363v1
AB - In March 2026, an unusually large outbreak of invasive meningococcal disease (IMD) in Kent, UK, was linked to attendance at one nightclub over a single weekend. The outbreak organism was a Neisseria meningitidis variant belonging to the longstanding hyperinvasive genotype, cc41/44. Using genome analysis of six isolates from patients, alongside >48,000 meningococcal genomes, we investigated whether the outbreak variant had acquired traits potentially contributing to the highly invasive phenotype. The six isolates were capsular group B, sequence type (ST-)485, and essentially indistinguishable, consistent with the focal nature of the outbreak. Compared with their closest available relatives, we found changes mediated by phase variation, nucleotide variation, and horizontal gene transfer (HGT) involving adhesins, iron-acquisition systems (including Transferrin and Lactoferrin binding proteins, and FetA), and Type IV pili (Tfp), factors which affect bacteria-bacteria and bacteria-host interactions. These changes occurred in a ST-485 sub-lineage that expressed capsule at high levels and a PorA porin with a truncated surface-exposed epitope, both of which are predicted to reduce immune recognition. Donors for the HGT events were predominantly carriage-associated N. meningitidis and Neisseria cinerea. We show that meningococcal variants responsible for previous focal outbreaks have not been seen subsequently. We propose that focal outbreaks of IMD are caused by meningococcal variants that may have acquired traits from non- or less invasive organisms, but subsequently these variants disappear, as their highly invasive phenotype is inconsistent with sustained transmission. Ongoing disease surveillance alongside carriage studies are therefore essential to inform public health risk and manage epidemic IMD.
ER -