GBS is an acute, immune-mediated, demyelinating peripheral neuropathy characterized by progressive symmetric weakness. Most cases occur after an infectious event, most notably Campylobacter jejuni enteritis. In 1976, a new H1N1 influenza strain caused severe respiratory illness in 13 soldiers at Fort Dix, New Jersey; ultimately, approximately 230 soldiers were infected. The virus, dubbed A/New Jersey/76 (Hsw1N1) and known to be closely related to the deadly 1918 pandemic strain, had circulated in pigs for years and had apparently jumped to humans. Fearing the start of a new pandemic, the US government responded with a mass immunization campaign. In retrospect, this event may have been an anomaly—an animal virus introduced into a stressed, crowded, closed population that actually had little potential to spread in normal communities.

In fact, the virus never spread beyond the military installation. Unfortunately, the mass immunization campaign was not benign. Over 45 million people were immunized over a 3-month period of time, resulting in more than 500 cases of GBS; the attributable risk of GBS to swine flu vaccination was estimated at around 1 in 100,000. The mechanism may have involved some form of molecular mimicry, supported by the observation that mice receiving the vaccine develop anti-ganglioside antibodies.While some studies have suggested a possible causal relationship between influenza vaccine and GBS, most have not.

One, for example, looked at two influenza seasons in the United States in the early 1990s and found an RR of 1.7 (95% CI 1.0, 2.8), corresponding to approximately one additional case of GBS per million people vaccinated.125 It is important to keep a perspective here: in any given 6 week period of time, somewhere between 1 in 220,000 and 1 in 1.4 million people will develop GBS—vaccine or no vaccine. Another study in the United Kingdom spanning the years 1992 to 2000 found 228 incident cases of GBS; seven cases occurred within 42 days of any immunization (three were after influenza immunization) and 221 were not associated with immunization, for a RR of 1.03 (95% CI 0.48, 2.18). A study from Canada published in 2006 demonstrated no seasonality of GBS and no increase in hospital admissions for GBS after the introduction of a universal influenza immunization program. Finally, as of early 2010, there were no reports linking 2009 H1N1 vaccine to GBS.

By September 2006, 17 cases of GBS associated with MCV4-D administration had been reported to VAERS (the vaccine was licensed in January 2005). Most of the cases occurred within 2 weeks of vaccination, a time frame that would fit with a causal relationship. The rate of GBS among immunized teenagers, calculated based on doses distributed, was estimated to be about 0.20 per 100,000 person-months. This rate was similar to the background rate of GBS calculated from the VSD database, but it was slightly higher than that seen in the Healthcare Cost and Utilization Project, a multistate hospital discharge database. It was estimated that if GBS is truly caused by MCV4-D, there would be 1 extra case for every 800,000 teenagers vaccinated. Data are not available to evaluate the potential risk of GBS following administration of MCV4-CRM.

—Marshall, Gary S. “Addressing Concerns About Vaccines.” The Vaccine Handbook: A Practical Guide for Clinicians. 3rd ed. New York: Professional Communications, Inc., 2010. 231-232. Print.

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