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Probable transmission of meningococcal disease on a school bus

MJA 2006; 184 (2): 90

Frank H Beard,* Jeremy M McAnulty, John W Tapsall, Angelo M Zaia§

* Senior Medical Officer, Communicable Diseases Unit, Queensland Health, 147-163 Charlotte Street, Brisbane, QLD 4001; Director, Communicable Diseases Branch, NSW Health, Sydney, NSW; Senior Specialist in Microbiology, SEALS, Prince of Wales Hospital, Sydney, NSW; § Molecular Biologist, University of Melbourne, VIC. Frank_BeardAThealth.qld.gov.au

To the Editor: We report two cases of serogroup B meningococcal disease, caused by genotypically indistinguishable organisms, where transmission is likely to have occurred on a school bus. To our knowledge, transmission of meningococcal disease on a bus has been reported only once before.1

In June 2005, two cases of serogroup B meningococcal disease in teenagers from the same school were reported to the Northern Sydney Public Health Unit. Patient 1 had symptoms of fever, headache, vomiting, and an erythematous rash. Two days after onset of this patient’s symptoms, Patient 2 also developed fever, headache and vomiting.

In both cases, diagnosis of meningococcal disease was confirmed by polymerase chain reaction (PCR) testing of cerebrospinal fluid (CSF). CSF cell counts were consistent with bacterial meningitis, but blood and CSF culture were negative, despite lack of prior antibiotic administration.

The patients were in different school years. No obvious links, such as common classes, sporting teams, or mutual friends, could be found. However, they reported travelling on the same buses to and from school each day. These buses carry up to 78 students (53 seated and 25 standing) from the patients’ school and other nearby schools. The patients reported that the buses were usually crowded.

Chemoprophylaxis was provided 8–9 days after symptom onset in Patient 2 to 132 students who claimed to have travelled on these buses during the exposure period.

The two patients recovered fully and returned to school. No subsequent cases of meningococcal disease have occurred at the school.

In the absence of meningococcal isolates, porA/porB genotyping2,3 was conducted on the meningococcal DNA contained in the CSF samples, and yielded identical sequences. While genotyping is not routinely conducted, porA/porB sequence nomenclature can be equated with serotype/subserotype (phenotypic expression of porA/porB). All 38 serogroup B isolates to date in NSW in 2005 have had serotyping/subserotyping performed, with no other cases having a serotype/subserotype equivalent to that of the two cases reported here. This supports the school bus as the most likely setting of transmission, given the lack of mutual friends and activities identified between the two cases.

Asymptomatic nasopharyngeal carriage of meningococci is common, with about 10% of individuals being carriers at any one time.4 While crowding and close contact increase transmission of meningococci, factors leading to invasive disease are poorly understood.5 Antibiotic chemoprophylaxis is given to close contacts to eradicate nasopharyngeal carriage and limit disease spread.5 However, the absence of further cases among the 132 fellow travellers in this setting does not provide evidence of effectiveness of the chemoprophylaxis, given that the secondary attack rate, even in close household contacts, has been estimated at 2–4 per 1000 people.6

Current Australian guidelines recommend that, in school-based outbreaks, chemoprophylaxis be considered for a wider group than solely close contacts of a household nature.7 This report provides evidence to support chemoprophylaxis in similar circumstances, where linked cases are identified in school bus co-travellers, and no other, more specific natural grouping makes epidemiological sense.

  1. Harrison LH, Armstrong CW, Jenkins SR, et al. A cluster of meningococcal disease on a school bus following epidemic influenza. Arch Intern Med 1991; 151: 1005-1009. <PubMed>
  2. Sacchi CT, Lemos AP, Brandt ME, et al. Proposed standardization of Neisseria meningitidis PorA variable-region typing nomenclature. Clin Diagn Lab Immunol 1998; 5: 845-855. <PubMed>
  3. Sacchi CT, Lemos AP, Whitney AM, et al. Correlation between serological and sequencing analyses of the PorB outer membrane protein in the Neisseria meningitidis serotyping system. Clin Diagn Lab Immunol 1998; 5: 348-354. <PubMed>
  4. Yazdankhah SP, Caugant DA. Neisseria meningitidis: an overview of the carriage state. J Med Microbiol 2004; 53: 821-832. <PubMed>
  5. Tzeng YL, Stephens DS. Epidemiology and pathogenesis of Neisseria meningitidis. Microbes Infect 2000; 2: 687-700. <PubMed>
  6. Raghunathan PL, Bernhardt SA, Rosenstein NE. Opportunities for control of meningococcal disease in the United States. Annu Rev Med 2004; 55: 333-353. <PubMed>
  7. Communicable Diseases Network Australia. Guidelines for the early clinical and public health management of meningococcal disease in Australia. Canberra: Commonwealth of Australia, 2001.

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