Six months on, scientists say they know why the Canterbury meningitis outbreak was so severe

In the second week of March, a meningococcal outbreak unlike any seen in Britain for decades hit Canterbury. Within 48 hours of the first case being reported, 15 people were ill, a pace the UK Health Security Agency said it never sees in a typical cluster of two to four cases. By the end of the month there were 21 confirmed cases, all of them in hospital, nine in intensive care, and two young people were dead: a 21-year-old student at the University of Kent and an 18-year-old school pupil. Every case linked back to one nightclub, Club Chemistry, over the weekend of 5 to 7 March.⁶⁷¹

Six months later, the scientists who sequenced the bacteria say they can explain why. In a preprint posted to bioRxiv and presented to the UKHSA conference this week, researchers from UKHSA's Meningococcal Reference Unit, the University of Oxford and partner institutions report that the outbreak strain had acquired stretches of DNA from other, harmless bacteria that live in the human throat, and that those borrowed genes made it unusually good at causing disease.³²

What the genomes showed

The team compared six isolates from Canterbury patients against more than 48,000 meningococcal genomes in the PubMLST database. The strain was serogroup B, sequence type 485, part of a long-established hyperinvasive lineage known as cc41/44 that already circulates in the UK and that existing MenB vaccines cover. What set it apart was a set of genes it had taken on by horizontal gene transfer, mostly from non-disease-causing meningococci and from a related species, Neisseria cinerea. The changes affected the systems the bacterium uses to scavenge iron from its host, the surface proteins it uses to stick to human cells, its type IV pili, and a key surface antigen, PorA, which was truncated in a way that would make it harder for antibodies to recognise.⁵³

"This investigation shows just how quickly and dramatically these bacteria can change, sometimes acquiring new traits from harmless bacteria circulating nearby, that make them more likely to cause disease," said Dr Charlene Rodrigues of UKHSA, who led the analysis. Professor Martin Maiden, professor of molecular epidemiology at Oxford, said genomic studies had "played a crucial role in defining, managing, and understanding" the outbreak.¹²

Why it burned out

The finding that will interest public health planners most is a trade-off. Meningococci spread by living quietly in the throats of healthy carriers, and only occasionally invade the bloodstream. The genes that made the Canterbury strain so invasive appear to have made it a poor carrier, and the authors note that strains behind previous intense clusters, including one at the University of Southampton in 1997, have not been seen again afterwards. "The very same genetic changes that made this strain so dangerous may also explain why it hasn't continued to spread," Dr Rodrigues said.¹⁵

Professor Robert Heyderman, professor of infectious diseases at University College London, who was not involved in the work, told the Science Media Centre that the study identified "multiple genetic changes that could explain why this particular MenB strain has an increased disease-causing potential", but cautioned that increased virulence does not mean increased transmissibility, and that "only ongoing genetic surveillance of carriage and disease MenB strains" would show whether the authors are right about the risk of further outbreaks.⁴

How the outbreak unfolded

The response was fast and large. Antibiotics were offered to close contacts, to everyone living on the University of Kent's Canterbury campus, to sixth-formers at affected schools and to anyone who had been at Club Chemistry between 5 and 15 March; more than 10,500 doses had been given by 20 March. The MenB vaccine was offered to the same groups, more than 4,500 doses in the first week, and the university cancelled a week of in-person exams. Schools in Faversham, Ashford and Canterbury were drawn in as contacts were traced. The European Centre for Disease Prevention and Control assessed the risk to the rest of Europe as very low.⁷⁶⁹

What it means for vaccination and surveillance

Two points in the preprint are less comfortable. Genomic surveillance, however good, cannot forecast an outbreak like this one, because the bacteria that matter live in healthy throats and are barely sampled until someone falls ill. And the MenB vaccine, given to babies in the UK since 2015, offers protection that wanes before the late-teenage years when the risk of meningococcal disease, and of nightclubs, peaks. Teenagers are offered the MenACWY vaccine, which covers other serogroups but not B. The authors do not call for a change in policy, but they do say symptom awareness has to sit alongside vaccination.⁵

UKHSA's advice is unchanged: a high fever, severe headache, stiff neck, vomiting, a rash that does not fade under a glass, sensitivity to light, cold hands and feet, confusion or extreme sleepiness need urgent medical attention, and not everyone gets the rash. The preprint has not been through peer review, and its authors describe it as a first analysis. The two families who lost children in March are unlikely to find much comfort in learning that the bacterium that killed them was, in evolutionary terms, a dead end. But it is the first real explanation of why one weekend in one club did what it did.⁶¹⁰