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Volume 356:524-526 February 1, 2007 Number 5
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Prevention of Meningococcal Disease

 

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To the Editor: In his article on the prevention of meningococcal disease, Gardner (Oct. 5 issue)1 notes that both active and passive smoking may be risk factors for the disease but does not address the issue of exposure to smokers as differentiated from exposure to smoke. Contact with smokers rather than smoke is now recognized as a critical risk factor, most likely owing to higher rates of carriage and coughing among smokers.2,3,4 The case–control study by Coen et al. of 144 teenage survivors of meningococcal disease showed that older teens are more at risk from exposure to smokers than to smoke.4 In two studies, significant odds ratios for meningococcal disease (3.8 and 9.1) were reported for children whose mothers smoked.2,3 A remarkable 37% of cases were reported as being attributable to exposure to smokers in one of the studies,2 and we estimate that 60% of cases were attributable to exposure to smokers in the other study.3 Public health messages should underscore the need to stop smoking, not merely the need to limit smoking to outside the home.

Gardner also mentions that deficiency in the terminal complement pathway is responsible for increased risk but does not mention the much more common deficiency of mannose-binding lectin. Recent work has demonstrated that a deficiency of this protein, which is responsible for activation of the alternative complement pathway, is a critical factor. The frequency of homozygous variants was significantly higher among 194 children with meningococcal disease than among control subjects (odds ratio, 6.5; 95% confidence interval, 2.0 to 27.2). The fraction of cases attributed to mannose-binding lectin variants was 32%.5


Robert Booy, M.D.
Mary Iskander, M.B., B.S.
National Centre for Immunisation Research and Surveillance
Westmead 2145, Australia
robertb2{at}chw.edu.au


Russell Viner, M.D.
University College London Hospitals
London NW1 2PG, United Kingdom

Dr. Booy reports receiving research support from CSL, Sanofi, Roche, and Wyeth.

References

  1. Gardner P. Prevention of meningococcal disease. N Engl J Med 2006;355:1466-1473. [Free Full Text]
  2. Fischer M, Hedberg K, Cardosi P, et al. Tobacco smoke as a risk factor for meningococcal disease. Pediatr Infect Dis J 1997;16:979-983. [CrossRef][Web of Science][Medline]
  3. McCall BJ, Neill AS, Young MM. Risk factors for invasive meningococcal disease in southern Queensland, 2000-2001. Intern Med J 2004;34:464-468. [CrossRef][Web of Science][Medline]
  4. Coen PG, Tully J, Stuart JM, Ashby D, Viner RM, Booy R. Is it exposure to cigarette smoke or to smokers which increases the risk of meningococcal disease in teenagers? Int J Epidemiol 2006;35:330-336. [Free Full Text]
  5. Hibberd ML, Sumiya M, Summerfield JA, Booy R, Levin M. Association of variants of the gene for mannose binding lectin with susceptibility to meningococcal disease. Lancet 1999;353:1049-1053. [CrossRef][Web of Science][Medline]

 
To the Editor: The article by Gardner identifies close contacts of an index patient with meningococcal disease who would need chemoprophylaxis. These contacts include people who have been directly exposed to the patient's oral secretions, including through kissing. However, saliva itself is thought to have an inhibitory effect on meningococcus, probably owing to the presence of other oropharyngeal flora.1 This has been supported by a study of 258 college students in the United Kingdom, in which meningococcal carriage in the tonsils, nasopharynx, and saliva was examined. The overall carriage rate was 34.9% (90 of 258 students), but only one swab from saliva (0.4%) was positive for meningococcus.1 The Australian national guidelines now recommend that chemoprophylaxis not be used purely on the basis of activities such as nonintimate kissing (even on the mouth) or sharing of food, drinks, cigarettes, or bongs.2 However, intimate kissing, especially with multiple partners, is a risk factor for meningococcal disease.3 Certainly, as Gardner suggests, endotracheal intubation and mouth-to-mouth resuscitation would constitute sufficient exposure to warrant chemoprophylaxis; however, the risk associated with these activities is probably related to aerosolization of meningococci rather than exposure to saliva.


Sanjaya N. Senanayake, M.B., B.S.
Canberra Hospital
Canberra 2606, Australia
sanjaya.senanayake{at}act.gov.au

References

  1. Orr HJ, Gray SJ, Macdonald M, Stuart JM. Saliva and meningococcal transmission. Emerg Infect Dis 2003;9:1314-1315. [Web of Science][Medline]
  2. Changes to the management of meningococcal disease in Australia. Commun Dis Intell 2004;28:278-279. [Medline]
  3. Tully J, Viner RM, Coen PG, et al. Risk and protective factors for meningococcal disease in adolescents: matched cohort study. BMJ 2006;332:445-450. [Free Full Text]

 
The author replies: Clinical Practice articles in the Journal focus on management considerations, and space constraints allow for only a limited discussion of basic science and public health issues. Dr. Booy and colleagues provide additional insights in both areas. First, they note that in addition to the long-recognized increased risk of invasive meningococcal disease from active and passive smoking, there is an increased risk from exposure to people who smoke (presumably because these people have increased colonization with Neisseria meningitidis). It is notable that, despite the recognition of smoking as a risk factor for both invasive meningococcal disease1 and invasive pneumococcal disease,2 the Advisory Committee on Immunization Practices of the Centers for Disease Control and Prevention has failed to include smokers among the high-risk groups for which immunization against these diseases is recommended.1,3 Second, their mention of a deficiency of mannose-binding lectin in the pathophysiology of invasive meningococcal disease is welcome.

Dr. Senanayake discusses the Australian guidelines for chemoprophylaxis, which define persons considered to be close contacts of a patient with meningococcal disease more specifically than do the U.S. guidelines. Noting that saliva is a much less likely source of N. meningitidis than material taken from the nasopharynx or tonsils, the Australians do not consider "nonintimate kissing" or shared ingested or smoked materials to constitute significant exposure. Accordingly, the Australian recommendations for chemoprophylaxis are more restrictive than the U.S recommendations.1 I applaud the effort to define the at-risk contacts more precisely but anticipate that parsing the definition too finely will result in many gray areas and may make the guidelines difficult to implement.


Pierce Gardner, M.D.
Stony Brook University School of Medicine
Stony Brook, NY 11794

References

  1. Prevention and control of meningococcal disease: recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR Recomm Rep 2005;54:1-121. [Medline]
  2. Nuorti JP, Butler JC, Farley MM, et al. Cigarette smoking and invasive pneumococcal disease. N Engl J Med 2000;342:681-689. [Free Full Text]
  3. Prevention of pneumococcal disease: recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR Recomm Rep 1997;46:1-24. [Medline]

 

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