Background
Neisseria meningitidis remains a leading cause of bacterial meningitis and invasive disease with high mortality despite antimicrobial therapy. Multi-regional surveillance is critical for understanding outbreak dynamics and guiding public health interventions. ST-35 complex meningococci have been emerging across regions with variable antimicrobial resistance profiles. This outbreak investigation documents the epidemiology, molecular characteristics, serotype distribution, and antimicrobial resistance patterns of N. meningitidis isolates collected over a three-year surveillance period in Sri Lanka.
Methods
Forty-nine N. meningitidis isolates were collected from clinical specimens - Blood (n=48) and CSF(n=1) between the years 2022 and 2025 from Sri Lanka. Isolate identification was confirmed using real-time PCR (sodC). Serogrouping was performed by multiplex PCR targeting serogroup-specific capsular genes (A,W135, X, B, C and Y). Whole genome sequencing was performed for all the isolates, followed by molecular characterization using PubMLST. Core genome MLST version-3 was used for outbreak strain differentiation and clonal lineage assignment.
Results
The 49 culture-confirmed cases originated from multiple provinces, presenting as meningitis (65.3%) and sepsis (34.6%), with a case fatality rate of 12.2% (6/49). Serogroup B predominated (91.8%, n=45), with minor contributions from serogroup W135 (6.1%, n=3) and serogroup C (2.0%, n=1). Geographical distribution shows cases in Western (63.3%) and Southern (30.6%) regions, with smaller clusters in the Northern region (4.1%) and Sabaragamuwa (2.0%). MLST analysis identified ST-35 complex as the predominant clonal complex (75.5%, n=37). cgMLST analysis revealed considerable genetic diversity within ST-35 complex isolates. Minor clusters belonged to ST-11, ST-41/44, ST-32, and ST-4821 Antimicrobial susceptibility profiling revealed reduced penicillin susceptibility: 61.2% (30/49) showed intermediate resistance and 32.7% (16/49) were fully resistant, with only 6.1% remaining fully susceptible. These phenotypes correlated with penA allelic variants (A510V, F504L, H541N, I515V, and I566V), indicating penA-mediated mechanisms as the predominant driver of reduced penicillin susceptibility. Cefotaxime susceptibility was retained across all 49 isolates. gyrA mutations were identified in 16.3% (8/49) of isolates.
Conclusions
This multi-regional outbreak investigation reveals sustained ST-35 complex meningococcal transmission with rising intermediate penicillin resistance. The predominance of serogroup B with a moderate case fatality rate highlights the need for continued enhanced surveillance and molecular epidemiology and evaluation of meningococcal B vaccination programs.