To identify and characterize the pathogens responsible for meningitis outbreaks in Chad during 2024–2025 and determine whether emerging *Neisseria meningitidis* strains were involved.
Approach:
Surveillance and Specimens: Demographic data and 90 cerebrospinal fluid specimens from suspected bacterial meningitis cases were analyzed: 25 collected in 2024 and 65 collected in 2025.
Pathogen Detection: Real-time polymerase chain reaction testing was used to detect *N meningitidis*, *Streptococcus pneumoniae*, and *Haemophilus influenzae*. Meningococcal-positive specimens underwent capsule genogrouping.
Sequencing and Analysis: Sixteen meningococcal-positive specimens with RT-PCR cycle-threshold values of ≤33.8 underwent targeted enrichment using the SureSelectXT CD *N meningitidis* Community Design, followed by direct whole-genome sequencing and phylogenetic analysis.
Key Findings:
In 2024, 12 of 25 specimens were positive for *S pneumoniae*; none were positive for *N meningitidis*.
In 2025, 18 of 65 specimens were positive for *N meningitidis*, 12 for *S pneumoniae*, and 2 for *H influenzae*.
Sequencing identified non-groupable ST-5789 (n = 1), genogroup W ST-11 (n = 4), genogroup C ST-10217 (n = 10), and a newly assigned genogroup C sequence type, ST-18990 (n = 1), within clonal complex 10217.
CC10217, previously associated with ongoing epidemics in Nigeria and Niger since 2015, was responsible for the large serogroup C invasive meningococcal disease outbreak in Chad in 2025.
All ST-10217 and ST-18990 genomes carried *gyrA* mutations associated with reduced ciprofloxacin susceptibility; the ST-18990 genome also carried a *parC* mutation associated with reduced susceptibility.
Interpretation:
Direct whole-genome sequencing of culture-negative, RT-PCR–positive cerebrospinal fluid specimens enabled detailed characterization of the meningococcal strains circulating in Chad. The emergence of CC10217 with mutations associated with reduced ciprofloxacin susceptibility represents an important epidemiological change requiring close monitoring.
Limitations:
Cerebrospinal fluid specimens were collected from only a subset of patients with suspected meningitis.
Limited capacity to culture disease-causing bacterial isolates constrains genomic surveillance in many meningitis-belt countries.
Sequencing was performed on 16 of the 18 meningococcal-positive specimens; the 2 specimens with RT-PCR cycle-threshold values above 33.8 were not sequenced.
The serotype of the *S pneumoniae* strains responsible for the cases in Goundi had not yet been identified.
Conclusion:
CC10217 caused a large outbreak of serogroup C invasive meningococcal disease in Chad in 2025. Direct sequencing from clinical specimens can strengthen surveillance where culture rates are low, while the emergence of CC10217 carrying mutations linked to reduced ciprofloxacin susceptibility warrants enhanced genomic and epidemiological monitoring.
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