Chapter 3 provides a detailed discussion of the historical and scientific evidence establishing the biologic plausibility of a relation between vaccines and the development of GBS. In summary, it is biologically plausible that injection of an inactivated virus, bacterium, or live attenuated virus might induce an autoimmune response to peripheral nerve and root in the susceptible host, either by deregulation of the immune response, by nonspecific activation of T cells directed against myelin proteins, or by autoimmunity triggered by sequence similarities to host proteins such as those of myelin. The latter mechanism might evoke a response to a self-antigen, so-called molecular mimicry (Fujinami and Oldstone, 1989).
In surveying the medical literature, 29 instances of adverse events labeled as either GBS or polyneuritis were found in association with diphtheria or tetanus toxoids (Dittmann, 1981b; Holliday and Bauer, 1983; Hopf, 1980; Newton and Janati, 1987; Onisawa et al., 1985; Pollard and Selby, 1978; Quast et al., 1979; Reinstein et al., 1982; Robinson, 1981; Rutledge and Snead, 1986; Schlenska, 1977). These occurred primarily in the European literature. The majority of reported cases were in adults who had received either tetanus toxoid alone (21 individuals) or who had received tetanus toxoid and anti-tetanus toxin serum (4 individuals). Anti-tetanus toxin serum is known to induce GBS in its own right (Miller and Stanton, 1954). In most of the case reports describing what was labeled as GBS or polyneuritis, clinical details are lacking or, when present, are inconsistent with the diagnostic criteria for GBS. Three of the 25 cases following receipt of tetanus toxoid are described in enough detail and fall within the diagnostic criteria to be acceptable as documented cases of GBS with an appropriate latency (5 days to 6 weeks) following vaccination (Hopf, 1980; Newton and Janati, 1987; Pollard and Selby, 1978). One patient (Newton and Janati, 1987) received tetanus toxoid made by a U.S.-licensed manufacturer. All these patients were adults.
One particular case reported by Pollard and Selby (1978) is particularly relevant for a possible causal relation between tetanus toxoid and GBS for that case. A 42-year-old male laborer received tetanus toxoid on three separate occasions over a period of 13 years, and following each vaccination a self-limited episode of clear-cut, well-documented polyneuropathy of the GBS variety ensued. The latencies for each episode were 21, 14, and 10 days, respectively. He had minimal residual neurologic signs following the