VACCINE

J Neurology, Neurosurgery And Psychiatry • 2012
Contamination with gangliosides
in brain-derived rabies vaccine
may trigger Guillain–Barré syndrome
Author Information
Hiromichi Sakai1, Faqeehah Mohamed Harun1,
Naoki Yamamoto1,2, Nobuhiro Yuki1,2
1. Department of Microbiology, National University of Singapore, Singapore
2. Department of Medicine, National University of Singapore, Singapore
Abstract
Guillain–Barré syndrome (GBS) is an autoimmune-mediated peripheral neuropathy
typically occurring after microbial infections such as Campylobacter jejuni
enteritis. It can also occur following vaccinations such as the 1976 swine flu vaccine
in the USA.1 GBS is divided into demyelinating and axonal subtypes. There
is now good evidence that gangliosides or similar components trigger the development
of axonal GBS.2 Axonal GBS associated with IgG anti-GM1 or anti-GD1a
antibodies after bovine brain ganglioside administration have been recorded in
several patients. Sensitisation of rabbits with bovine brain gangliosides or isolated
GM1 produced a replica of axonal GBS. Based on these findings, it has
been suggested that C jejuni components mimic human gangliosides GM1 and
GD1a, and C jejuni infection induces the production of autoantibodies against
the gangliosides that are expressed in the peripheral nerves, resulting in the limb
weakness seen in GBS. By contrast, the mechanism by which certain vaccines
elicit the development of GBS remains unresolved, although there have been studies
to suggest that the 1976 swine flu vaccine could elicit anti-GM1 antibodies in
mice and that the GM1 epitope was present in the influenza haemagglutinin.3 It is
important to understand the pathogenesis of postvaccination GBS to allow safer
vaccines to be developed.
“There is now good evidence that
gangliosides or similar components
trigger the development of axonal
Guillain–Barré syndrome (GBS).”
http://jnnp.bmj.com/content/83/4/467.extract