Lack of Association between Group B Meningococcal Disease and Autoimmune Disease

• Published in: Clinical infectious diseases 2007-11, Vol.45 (10), p.1327-1334
• Main Authors: Howitz, Michael, Krause, Tyra Grove, Simonsen, Jacob Brunbjerg, Hoffmann, Steen, Frisch, Morten, Nielsen, Nete Munk, Robbins, John, Schneerson, Rachel, Molbak, Kare, Miller, Mark A.
• Format: Article
• Language: English
• Subjects: Addison disease; Adolescent; Adult; Aged; Aged, 80 and over; Articles and Commentaries; Autoimmune diseases; Autoimmune Diseases - epidemiology; Autoimmune diseases of the nervous system; Bacterial diseases; Bacterial diseases of the nervous system. Bacterial myositis; Biological and medical sciences; Cell adhesion & migration; Child; Child, Preschool; Correlation analysis; Denmark - epidemiology; Diabetes; Disease risk; Epidemiology; Female; Human bacterial diseases; Humans; Incidence; Infant; Infant, Newborn; Infectious diseases; Male; Medical sciences; Meningitis; Meningitis, Meningococcal - complications; Middle Aged; Musculoskeletal diseases; Neisseria meningitidis; Neisseria meningitidis, Serogroup B - immunology; Nervous system diseases; Polysaccharides; Risk factors; Systemic lupus erythematosus; Vaccines
• ISSN: 1058-4838; 1537-6591
• DOI: 10.1086/522190

Background. The capsular polysaccharide of group B meningococci (GBM) is structurally identical to a polysaccharide found on neural cell adhesion molecules in humans. This structural identity has raised concern that a vaccine based on the GBM capsular polysaccharide might induce autoimmune disease in vaccinated persons. Because systemic infection with GBM induces serum antibody in adults, we investigated whether persons with a history of GBM disease are at increased risk of developing autoimmune diseases. Methods. The entire Danish population constituted our study cohort of 7,467,001 individuals, who were observed for autoimmune diseases from 1977 through 2004. At-risk years were counted as the number of uninfected years prior to the first recorded diagnosis of meningococcal disease but changed to person-years at risk at the diagnosis of GBM disease (2984 subjects) or group C meningococcal disease (914 patients). Ratios of incidence rates of autoimmune disease served as measures of the relative risk. Results. Persons with a history of GBM disease experienced a total of 37,290 person-years at risk, ranging from 11 days to 31 years at risk after the onset of GBM disease, during which 49 cases of autoimmune disease occurred. Persons with GBM disease had no increased risk of autoimmune diseases, either compared with persons with a history of group C meningococcal disease (incidence rate ratio, 0.9; 95% confidence interval, 0.5–1.4) or compared with persons without a history of meningococcal disease (incidence rate ratio, 1.1; 95% confidence interval, 0.8–1.5). Conclusions. Our findings suggest that invasive disease caused by GBM is not associated with autoimmune diseases in humans for up to 31 years after meningococcal disease and should lessen concerns regarding the development of a capsular-based GBM vaccine.