GBS: How your body’s immune war turns deadly

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GBS: How your body’s immune war turns deadly

It begins like a shadow war — unseen, unfelt, until suddenly the damage is done.

In the crowded streets of Maharashtra, Andhra Pradesh, Karnataka and many other states, a battle rages not between armies, but within bodies. Twenty-one lives have already been claimed, with Maharashtra bearing the heaviest toll: Seventeen souls lost to Guillain-Barré Syndrome (GBS) that is neither foreign nor familiar, but rather, the body’s own defenses gone rogue.

GBS, a rare but serious condition where the body’s immune system — designed to be its greatest protector — becomes its most deadly adversary.

It is like watching your own security force burn down your house. The very system meant to keep you safe suddenly can’t tell friend from foe.

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The city under siege 

Imagine a prosperous city protected by an elite security force. For years, they successfully defended against countless invaders — viruses, bacteria, foreign bodies that threatened to disrupt the peace. The citizens sleep soundly, knowing these guardians stand watch.

But one day, something changes.

An enemy — perhaps a respiratory virus causing fever and cough or a gastrointestinal infection bringing stomach pain and diarrhea — launches an attack. The security force responds with practiced efficiency, eliminating the threat and restoring order.

Only this time, something goes terribly wrong.

Instead of standing down after victory, the security force becomes paranoid. They begin seeing enemies everywhere — even in the city’s own infrastructure. They attack the roads and communication lines, mistaking them for infiltrators. Without functional pathways, people struggle to move, businesses halt, and slowly, the city begins to collapse.

This is exactly what happens in Guillain-Barré Syndrome. The body’s defense system, having fought off an infection, misfires catastrophically and starts attacking the very nerves that allow movement, leading to a cascade of devastating symptoms: Weakness, paralysis, and in the worst cases, death.

“So essentially, GBS is a post-infectious immune-mediated neurological disorder. The antibodies, which are meant to fight infections, mistakenly identify the nervous system as foreign and start attacking it. In GBS, the peripheral nervous system is affected. There is typically a gap of one to two weeks between the initial infection and the onset of neurological symptoms,” Hyderabad based Neurologist Dr Sudhir Kumar told South First.

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The numbers: A growing crisis 

Since early January, over 250 cases of GBS have been documented across India, with the majority concentrated in Pune.

The health system groans under the pressure — 48 patients remain in intensive care, with 21 requiring ventilators to breathe.

While most people recover with timely treatment, GBS can be life-threatening. Mortality rates range from 3% to 13% depending on how quickly medical care is provided.

The suspected cause in Pune was sewage contamination of a drinking water source. Municipal authorities acknowledged that water from this well was distributed without proper chlorination. Water sample testing later revealed that 30-40 percent of the collected samples lacked chlorine. Thus, it is likely that people consuming this contaminated water became infected.

Dr Kumar said that in Pune, approximately 200 people developed GBS, meaning thousands more were likely infected but did not progress to GBS.

Since most cases of mild diarrhea do not result in hospital visits, we do not have an exact number of total infections. But based on past outbreaks, we estimate that for every one person who develops GBS, around 1000 were infected with Campylobacter jejuni.

Amid growing concern, health officials emphasise a critical fact: Guillain-Barré Syndrome is not contagious and cannot spread from person to person like a respiratory illness.

Unlike Covid-19, influenza, or the common cold, GBS cannot be transmitted through coughing, sneezing, or close contact.

“This is not an epidemic in the traditional sense,” clarifies Dr. Kumar. “GBS itself does not spread directly. Rather, it is a rare complication that occurs after certain infections. Those original infections — like food poisoning from Campylobacter — can spread, but GBS is a secondary immune response that happens in very few people.”

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When protection becomes destruction: The mechanism of GBS 

To understand how a defense mechanism can backfire so catastrophically, we must journey inside the human body — a complex ecosystem where balance means life and disruption can mean death.

Two common types of infections typically trigger GBS: Respiratory infections (usually viral, causing fever, cough, and runny nose) and gastrointestinal infections (presenting with stomach pain, cramps, diarrhea, and sometimes blood in stools).

When a threat enters — like a virus infiltrating the lungs or bacteria invading the stomach — the immune system mobilises rapidly.

It is a sophisticated response, evolved over millennia to protect the body from harm. Normally, once the battle is won, the soldiers stand down.

But in GBS, something goes disastrously wrong.

“These symptoms usually last three to four days, and the infection itself resolves,” explains Dr. Kumar.

“However, for GBS to develop, the person’s immune system must be strong enough to fight the infection first.”

It’s a cruel irony — only those with robust immune systems develop GBS. The very strength that helps them survive the initial infection becomes their downfall.

After defeating the original threat, the immune system becomes confused. It starts attacking the protective layer (myelin sheath) surrounding nerves — the body’s communication highways. Signals from the brain can no longer reach their destinations properly, leading to a progressive cascade of symptoms:

  • First, subtle traffic delays: tingling and numbness in hands and feet
  • Then, concerning road closures: Weakness in muscles
  • Finally, catastrophic shutdown: Paralysis in severe cases

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The hidden invader: Campylobacter Jejuni 

Behind many GBS cases lurks a particularly insidious culprit: Campylobacter jejuni, a stealthy bacterium that infiltrates the body through contaminated food and water.

Imagine this bacterium as a master spy, slipping through the body’s defenses disguised as a harmless visitor. Once inside, it does not attack immediately. Instead, it establishes a base in the intestines, waiting patiently for the perfect moment to strike.

Like any effective infiltrator, C. jejuni comes equipped with specialised tools:

  • Camouflage: Its curved rod shape makes it difficult to detect, like a spy blending seamlessly into a crowd.
  • Stealthy Movement: It propels itself using a corkscrew-like motion, powered by tiny whip-like tails called flagella, allowing it to navigate the gut undetected.
  • Strategic Positioning: It thrives in low-oxygen environments, particularly favouring the warm, dark conditions of the human intestines.
  • Sabotage Capabilities: Once established, it releases toxins and disrupts cell walls, triggering painful inflammation and diarrhea, sometimes accompanied by blood.

Within days of this covert invasion, the body realises something is amiss. The immune system dispatches its forces — white blood cells — to counter the threat, resulting in fever, stomach cramps, and fatigue. For most people, this battle concludes within a week.
But for some, this is merely the prelude to a far more dangerous confrontation.

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The case of mistaken identity: Molecular Mimicry 

C. jejuni, in its evolutionary cunning, wears a disguise.

Certain molecules on its surface bear a striking resemblance to gangliosides —important components found on human nerve cells. This resemblance is not coincidental; it is a sophisticated evolutionary strategy that helped the bacterium evade detection for millennia.

When the immune system produces antibodies to fight C. jejuni, these antibodies cannot distinguish between the bacterial components and the body’s own nerve structures. Like soldiers who can’t tell civilians from enemies, these antibodies attack indiscriminately, damaging the protective coating of nerves.

“It’s like friendly fire in warfare,” explains a neurologist. “The immune system thinks it is targeting the enemy, but it is actually shooting at its own troops.”

This case of mistaken identity explains why GBS typically emerges not during an infection, but in its aftermath — usually 1-2 weeks after recovery, when the immune system has already cleared the bacteria but mistakenly continues its assault on the nerves.

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Ground Zero 

Maharashtra remains at the epicenter of the crisis, with 17 deaths reported, including the latest cases from Pune and Nagpur.

Other states — Andhra Pradesh, Assam, Tamil Nadu, and West Bengal — have each reported one fatality.

For GBS patients, time is the most precious commodity. The condition progresses rapidly, sometimes leading to complete paralysis within days or even hours of the first symptoms.

Treatment typically involves two main approaches:

  • Plasma exchange (plasmapheresis): This procedure removes the blood’s plasma — which contains the harmful antibodies — and replaces it with new plasma, effectively removing the soldiers that have turned against the body.
  • Intravenous immunoglobulin therapy: In this treatment, healthy antibodies from blood donors are administered intravenously, helping to block the damaging effects of the rogue antibodies. This costs as least as Rs 2 lakh at private centres.

Both treatments show the best results when started within two weeks of symptom onset, underscoring the critical importance of early recognition and medical intervention.

(Rosamma Thomas)

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