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No, it's not 1976 all over again

In February 1976, a new, more severe, and highly transmissible strain of H1N1 influenza virus, believed to be closely related to the one responsible for the 1918 influenza pandemic, was first identified at Fort Dix, an army post in New Jersey. The Advisory Committee on Immunization Practices (ACIP) of the United States Public Health Service, reviewed the findings and ultimately suggested a broad immunization program. The administration of President Gerald Ford with the support of Congress, pursued an aggressive campaign to rapidly immunize the US population and a National Swine Flu Immunization Program, was put into action, with the expectation that without such a program, the winter of 1977 could see the development of a catastrophic pandemic. The World Health Organization took a more cautious wait-and-see approach and ultimately decided to not endorse this concern with any global directives. Over the next several months, approximately 45 million Americans (approximately 25% of the US population at the time) were vaccinated. The vaccine was a live, attenuated form of the virus that was hurriedly developed and tested. Although the feared pandemic never emerged, it was gradually recognized that there was an increased incidence of Guillain Barre Syndrome (GBS) in those who had received the vaccine. Ultimately, it was determined that about 450 people who received the vaccine developed GBS, but given uncertainty in the baseline frequency of GBS, an increased incidence of approximately 1 per 100,000, though this relationship continues to be questioned. It is with knowledge of this history that we publish in this issue two reports of patients who received the AstraZeneca ChAdOx1-S adenovirus vector vaccine for COVID-19 and who developed GBS within the next 3 weeks, one set of four patients in the United Kingdom and one set of seven in India. While the data support that this is GBS both clinically, serologically, and electrophysiologically (when such data was obtained), this form of GBS was characterized by a disproportionately frequent and severe bilateral facial paresis. Though facial weakness is hardly atypical in GBS, it is not usually a predominant finding, as compared to severe appendicular weakness and respiratory dysfunction. Critically, we recognize that association does not necessarily imply causation. Thus, both sets of authors attempted to determine the relative number of cases in comparison to the expected “natural” incidence of the disease, and indeed, as best as we can judge, the incidence is higher than for the populations of people these institutions serve. In the Indian report, the authors estimated this incidence to be 1.4-10 higher than the baseline rate for their population served. In the UK report, they reported a likely higher frequency as well. Although we cannot know that the GBS was truly due to the vaccine, the greater-than-anticipated number, the unusual severe bilateral facial paresis, and the close temporal association makes it difficult to ignore a potential causal association. Coincidentally, shortly before our editorial office received these two manuscripts, our neurology service at Beth Israel Deaconess Medical Center in Boston admitted a 58-year-old man without significant past medical history who presented with marked bilateral facial weakness and modest appendicular weakness approximately 2 weeks after receiving the J&J/Janssen COVID-19 vaccine, which like the AstraZeneca vaccine, is also adenovirus based with embedded spike proteins. However, his case was also complicated by the presence of unexplained small subarachnoid hemorrhages. His evaluation included a lumbar puncture which demonstrated prototypical albuminocytological dissociation with a protein of 188 mg/dL, glucose of 63 mg/dL, and two nucleated cells and 1,025 red cells/mm. Nerve conduction studies and needle electromyography confirmed the presence of a demyelinating polyradiculoneuropathy with markedly prolonged F responses in multiple nerves. Facial nerve studies revealed relatively intact motor responses but absent blink reflexes, also supporting a demyelinating process impacting cranial nerve VII bilaterally. There has been at least one other recent report of GBS characterized by marked bilateral facial paresis following the AstraZeneca vaccine and another following the J&J vaccine. As the authors of the latter article warn, we have to be careful of simply assuming that these cases of GBS are due to the vaccine. Accordingly, we also queried the Vaccine Adverse Effects Reporting System (VAERS) on June 6, 2021. Importantly, this system records reports from recipients of the vaccines only in the United States, and thus