Outbreak of serogroup C meningococcal disease associated with campus bar patronage.

Between February 1991 and April 1992, eight undergraduates at a US residential university and one at a nearby 2-year college contracted serogroup C meningococcal disease. A case-control investigation with 20 controls per case, oropharyngeal carriage surveys, and multilocus enzyme electrophoresis (MEE) of serogroup C isolates were used to identify factors contributing to the outbreak. All eight sterile-site isolates from cases were closely related by MEE and were similar (though not identical) to the strain associated with the 1991-1992 epidemic of meningococcal disease in eastern Canada. Disease was associated with cigarette smoking (p = 0.012), recent patronage of campus-area bars (p = 0.034), estimated amount of time spent in campus-area bars (p = 0.0003), and, especially, recent patronage of one specific bar, bar A (p = 0.0006; odds ratio = 23.1, 95% confidence interval 3.0-571.5). In carriage surveys, 1,528 throat cultures taken from (primarily student) noncases yielded only five (0.3%) strains that were identical by MEE to those from cases. Two of these were found among 22 cultures obtained from bar A employees in spring 1992. Some cases in this outbreak may have followed transmission of the epidemic strain in bar A. Campus bar environments may facilitate the spread of meningococcal disease among teenagers and young adults.

Meningococcal carriage, alcohol consumption, and campus bar patronage in a serogroup C meningococcal disease outbreak.

Community outbreaks of serogroup C invasive meningococcal disease are increasing in North America (L. H. Harrison, JAMA 273:419-421, 1995; L. A. Jackson, A. Schuchat, M. W. Reeves, and J. D. Wenger, JAMA 273:382-389, 1995; C. M. Whalen, J. C. Hockin, A. Ryan, and F. Ashton, JAMA 273:390-394). In a recent 15-month university outbreak, disease was linked to patronage of a specific campus-area bar, suggesting that aspects of a campus bar environment might promote meningococcal transmission (P. B. Imrey, L. A. Jackson, P. H. Ludwinski, et al., Am. J. Epidemiol., in press). To investigate this hypothesis, oropharyngeal carriage results from samples taken from 867 university health service clients and 85 campus-area bar employees during the last 3 months of the outbreak were analyzed to determine factors correlated with carriage of any strain of Neisseria meningitidis. Results were validated with data from samples from 344 health center clients and 211 campus bar employees taken 8 months after the last outbreak case. Recent alcohol consumption (adjusted prevalence odds ratio = 3.8 for > 15 versus 0 drinks in last week [P = 0.0012]) and campus bar patronage (adjusted odds ratio = 1.9 for any versus no patronage in last 2 weeks [P = 0.0122]) showed separate effects in both univariate and multiple logistic regression analyses of data from the 1992 health center clients. Prevalence of meningococcal carriage among 1992 campus bar workers was 3.8 times that among health center clients; this prevalence ratio was roughly 2.5 after adjustment for alcohol consumption and bar patronage. Recent antibiotic usage was protective (prevalence odds ratio = 0.3) among health center clients and bar workers. These findings were generally supported by the validation samples. If alcohol consumption and other aspects of the campus bar environment facilitate transmission of and/or colonization by N. meningitidis, then the introduction of a highly pathogenic substrain into the campus bar environment may provide an unusual opportunity for invasive meningococcal disease within a campus community.

Amplification of rDNA loci to detect and type Neisseria meningitidis and other eubacteria.

In 1991-92, Neisseria meningitidis group C was isolated from the blood of eight students in Urbana, Illinois, USA, and from the cerebrospinal fluid of one student from a nearby community, Decatur, Illinois. These and other bacterial species were analysed by PCR fingerprinting using primers selected from the ribosomal (r)DNA loci. A rDNA primer pair spanning a region within the 16S rDNA amplified a predicted 280 base pair (bp) DNA fragment from Neisseria spp. and fragments of different sizes for other genera. This primer pair specifically detected a carrier of N. meningitidis in a small clinical battery. Identity of the fragment was confirmed by restriction endonuclease analysis. A 600 bp fragment was also amplified from the 16S-23S internal transcribed spacer (ITS) of N. meningitidis; amplification from six other genera yielded different-sized fragments. Digestion of the ITS fragment from N. meningitidis with Alu I revealed three patterns; pattern I was found only for serogroup C isolates, and it was the dominant pattern among recent isolates with the exception of the one from Decatur. The isolate from Decatur yielded pattern III which suggested a non-clonal relationship to the seven isolates from Urbana. Patterns II and III were more prevalent in isolates from the 1960's and 1980's. PCR-based analysis of these loci can complement the techniques which are currently used for the detection and typing of these and other eubacteria.