Guillain-Barre Syndrome Outbreak in Pune, India

“Man is his own worst enemy.”                                                                                                         Marcus Tullius Cicero, Roman statesman (106 BCE-43 BCE)

“At least 21 people have died and nearly 300 have been affected by Guillain-Barre syndrome in India, marking the country’s largest ever outbreak of the rare neurological illness.”

Samaan Lateef, India-based UK Daily Telegraph journalist

Named after Georges Guillain and Jean Barre, the two French neurologists who first described the condition in 1916, Guillain-Barre Syndrome (GBS) is an autoimmune disorder involving the peripheral nervous system. In March 2025, an outbreak of GBS exploded in Pune, India.

A common theme in Germ Gems is the concept that the immune system behaves like a “double-edged sword,” that is, one side of the blade protecting us against a wide variety of pathogens but the other causing tissue damage, and, in some instances, even killing us. In this week’s post, I focus on GBS and the self-destructive side of the immune system.

Autoimmune diseases (a recap). Molecular mimicry is a phenomenon in which the immune system mistakenly recognizes similarities between foreign antigens (bacteria, viruses, or parasites) and self-antigens (molecules present in the body). This recognition leads to an immune response that targets both the foreign antigen and the self-antigen. Simply put, your immune system attacks your body instead of protecting it resulting in an autoimmune disorder. Type 1 diabetes, rheumatoid arthritis, systemic lupus erythematosus, multiple sclerosis, celiac disease, and GBS are all examples of autoimmune diseases (disorders).

What is GBS? GBS is an autoimmune neurological disorder caused by an activated immune system that mis-targets parts of the peripheral nerves (myelin sheaths or axons) in the wake of an infectious disease. (It doesn’t involve the central nervous system, i.e., brain or spinal cord.) It is a rare disorder—affecting about 100,000 people worldwide each year—but it can be life threatening.

The syndrome often begins suddenly with tingling in the toes or fingers followed by progressive weakness of the limbs and face, nerve pain (especially at night), autonomic nervous system dysfunction (blood pressure and heart rate irregularity). During the acute phase, the disorder can be life-threatening, with about 15% of people developing respiratory muscle weakness requiring mechanical ventilation. Globally, death occurs in about 7.5% of the patients. And while most patients gradually improve over time, approximately 10-15% of people with GBS are left with a permanent disability.

The cause of GBS is often unknown, but many of the key factors in its pathogenesis are established. The disease is usually triggered by an acute infectious disease. Microbes are the most common triggers of GBS. A variety of pathogens, including cytomegalovirus, influenza virus, tropical flaviviruses, and rarely, SARS-Cov-2, as well as the COVID-19 vaccine have been linked to GBS outbreaks. In the case of the Pune outbreak, gastrointestinal infections caused by Campylobacter jejuni and norovirus were responsible.

Treatment. The two main treatments for GBS are immunotherapy (plasmapheresis) and intravenous immunoglobulin (IVIG). Both aim to reduce immune attack on nerves. Plasmapheresis attempts to remove antibodies out of the bloodstream that may be attacking nerves, and IVIG neutralizes harmful antibodies and inflammation.

Respiratory failure may require hospitalization and mechanical ventilation. Moreover, rehabilitation following the acute phase of illness is needed in around 40% of people.

The blood complement system is another component of the immune system that is involved in the pathogenesis of GBS. Recently, researchers scored a big clinical win for complement-targeting therapy with a monoclonal antibody called ANX005/tanruprubart. (Jeffery, S.,  “Targeted Treatment Improves Disability in Guillain-Barre Syndrome,” MedPage Today, April 12, 2025).

Tanruprubart “is a C1q complement inhibitor that shuts down the complement cascade, blocking both neuroinflammation and edema, as well as nerve damage.” According to the lead researcher Jeffery Allen, M.D. of the University of Minnesota, by blocking C1q with tanruprubart, “the hope is that we can prevent and immediately stop that neuroinflammation, leading to more rapid improvement and then also stop that nerve damage and nerve destruction, which hopefully will lead to better long-term outcomes.” 

Prevention. While it is highly encouraging to see continued advances in the treatment of GBS, prevention is “worth a pound of cure.” Within this context, it appears an important public health approach— providing clean water—would have staved off the GBS outbreak in Pune. (Ramakrishnan, L., “India’s Guillain-Barre Syndrome outbreak lays bare the dangers of water contamination,” Nature India, March 20, 2025).

Such a public health measure could have eliminated the two pathogens that triggered the outbreak, C. jejuni and norovirus. In a March 29, 2025, letter to Lancet, “Guillain-Barre syndrome outbreak in Pune: a health emergency,” the authors suggest that “New laws should be enacted to enforce the supply of safe and clean water by responsible government bodies. By implementing…public health measures future risk of disease outbreaks can be minimized.”