Introduction 

At first glance, Campylobacter and Guillain-Barré Syndrome (GBS) may seem unrelated to each other. Consider these differences:

• Campylobacter is a type of bacteria often responsible for gastrointestinal and diarrhoeal infections, while GBS is a neurodegenerative autoimmune disease^1,2
• Campylobacter is relatively common with about 500,000 cases per year in the UK, while GBS is a very rare condition with an estimated 100,000 cases per year worldwide^3,4

However, a strong link between the two has been established, as many cases of Campylobacter infections lead to the occurrence of GBS. In fact, one source estimated that people suffering with a gastrointestinal Campylobacter infection were “38 times more likely to be diagnosed with GBS in the subsequent two months”.⁵ 

Campylobacter: a small summary

Campylobacter is a group of similar bacterial species known to be the “leading cause of bacterial-derived foodborne illnesses worldwide”.⁶ Of the many Campylobacter species, it is Campylobacter jejuni ( C. jejuni) and Campylobacter coli (C. coli) which are the most common causes of gastrointestinal infections in humans.⁷ 

There are many other observable symptoms of disease which present with Campylobacter infections; these range from Barrett’s esophagitis and blood infections to various abscesses, endocarditis and many more.⁸

Sources and symptoms

Usual sources of human infection with Campylobacter include but are not limited to:^6,8

• contaminated poultry
• unpasteurised milk
• contaminated water sources

Symptoms typically last from a few days up to a week and these include:⁶

• severe abdominal pain
• diarrhoea (can be bloody)
• fever
• nausea

Guillain-Barré syndrome: an overview

As described above, Guillain-Barré Syndrome is a neurodegenerative autoimmune disease, which means that GBS is a disease where your own body is responsible for damaging parts of your nervous system.

To be specific, GBS affects the Peripheral Nervous System (PNS)⁹; the PNS is composed of nerve fibres and nerve cell bodies that exist outside of the spinal cord and the brain.¹⁰ 

The way in which GBS impacts the nervous system depends on the specific subtype afflicting the person affected. The 4 main subtypes are:¹¹

• Acute inflammatory demyelinating polyradiculoneuropathy (AIDP)
• Acute motor axonal neuropathy (AMAN) 
• Acute motor and sensory axonal neuropathy (AMSAN)
• Miller Fisher syndrome (MFS)

Some subtypes solely affect motor neurons while others also affect sensory neurons:

• Motor neurons are nerves that carry messages/orders out from the brain and spinal cord to muscles. Therefore, damage to motor neurons give rise to symptoms such as weakness and paralysis
• Sensory neurons send signals received from skin and muscles (such as pain) back to the brain and spinal cord. When damaged, symptoms such as numbness may arise

Symptoms 

There are a number of symptoms which can indicate the onset of GBS:^12,13,14

• Growing weakness and/or tingling sensations in the legs and, sometimes, the arms. This normally ascends upwards (i.e. beginning in the toes or fingers and moving upwards towards the thighs or shoulders)
• Numbness (not present in AMAN GBS)
• Weak or absent tendon reflex
• Pins and needles in the extremities 
• Loss of balance/coordination and/or tripping
• Pain
• Difficulty breathing
• Difficulty chewing, swallowing or breathing
• Troubles with eye movement (very likely to be an indication of Miller-Fisher Syndrome)

Progression

GBS “is a typical post-infectious disorder” with “several microorganisms […] associated with [it], most notably Campylobacter jejuni, Zika virus, and in 2020, the severe acute respiratory syndrome coronavirus 2”.^14,15 Other analyses showed evidence that GBS patients had previously been infected with Mycoplasma pneumoniae, hepatitis E virus, cytomegalovirus, and Epstein-Barr virus.^16,17

Having said this, GBS patients do not always report having had a recent infection; one paper from 2016 suggested that up to 40% (<40%) of patients do not report “antecedent infectious symptoms”¹⁸.

Following the onset of GBS there are four key consecutive phases which often succeed to describe the changes to the severity of the disease in patients:¹⁴

• Progression - this immediately occurs with the onset of GBS and signifies that symptoms get progressively worse, usually at a fast rate
• Plateau - a period when no (or very limited) change in the disease severity is observed. It can last from a few days, to a few weeks or even months. This phase can result in patients struggling with symptoms such as muscle weakness and/or balance problems for a substantial period of time after treatment
• Recovery - gradually certain symptoms begin to subside over a period of months and years. The extent and speed of recovery may be affected by various factors such as age, diet, genetics and engagement with physiotherapy 
• Disability - most patients recover to an extent that they can function normally in day to day life, however, some residual symptoms may linger for large portions - if not the rest - of their lives

There is, generally, strong consensus regarding the nature of the initial progression phase. One paper stated that GBS reaches its “maximal severity within 4 weeks”; another described a study showing “that 80% of patients with GBS reach the [maximum severity of their symptoms] within 2 weeks after onset of weakness, and 97% reach the [maximum severity of their symptoms] within 4 weeks.”^20,19 In up to 20% of patients, this phase of the disease may even result in them requiring mechanical ventilation.²¹ 

The plateau is also variable, “ranging from 2 days to 6 months”; however, “most patients start recovering within less than a week” of having reached the maximum severity of their symptoms.^20,22 

“Although most people have an uneventful recovery, 15 to 20% of GBS patients are left with severe neurologic deficits.”²¹ “In mild cases, complete recovery may occur over a few weeks [..] although other residual effects may persist permanently.”²³ A few examples of residual effects include:²³

• Neuropathic pain
• Fatigue
• Residual muscle weakness resulting in pain from overuse
• Tremors

The link between campylobacter and GBS

Cases of infection with C. jejuni leading to GBS have been thoroughly documented so the association is well established.²¹ In fact, it is “responsible for about a third of GBS cases.”⁴

The proposed mechanism that causes Campylobacter to initiate GBS is known as molecular mimicry.²⁴ In this case, what it means is that antibodies (a class of weapon made by your immune system in order to fight any specific species of germ), made in response to infection with Campylobacter, end up accidentally targeting harmless structures in your nerves. 

This accident occurs since the specific structure on C. jejuni, which is targeted by your antibodies, is similar to a surface structure found on your nerves.¹⁴ It should be noted that the precise detail behind this is complicated and not fully understood in certain GBS subtypes which undergo other mechanisms.

Risk factors

Aside from implementing basic food and water safety practices to avoid exposure to Campylobacter, there are a number of risk factors which may also:

• increase the chance of suffering certain subtypes
• increase the chance of being diagnosed
• increase the severity and/or increase the time taken to recover

Global impact and variations in risk

The area of the world you’re from can have a huge bearing on the probability of suffering any one of the subtypes of GBS:²⁵

• 90% of GBS cases in Europe and North America AIDP; less than 10% are AMAN 
• “22-46% of cases in China, Japan, India, Southeast Asia, and Mexico” are AIDP, while AMAN accounts for 30-65% of cases in these countries

Furthermore, the Miller Fisher Syndrome subtype of GBS, “makes up about 5 percent of the cases of GBS in most countries, but about 25 percent in Japan”.²³ 

Genetic factors

The inference of genetic factors in GBS is very likely. There are in fact, documented incidents of GBS affecting multiple family members.^26,27

There are many ways in which genetics may play into GBS. Genes are like code which programme the structures of various components in our bodies. In the context of GBS this means that genes can affect whether we produce antibodies which target nerve cells post-infection.²⁰ There are other aspects which genes may affect, however, more research is needed to reach definitive conclusions.²⁸ 

Diet

Diet may also affect GBS in numerous ways and this topic warrants an article of its own. However, in many neuropathic conditions the benefits of a high-fibre diet can not be understated. Evidence suggests that consumption of fibre increases short-chain fatty acids (SCFAs), which can cause healthy regulation of autophagy (the process by which your body gets rid of sick and dead cells and cell components).²⁹ On the other hand, low levels of these SCFAs may result in neurodegeneration.³⁰ 

FAQs

What is the likelihood of developing GBS after a Campylobacter infection? 

One source claims that patients are “38 times more likely to be diagnosed with GBS” within two months after a Campylobacter infection.⁵

Can I get Campylobacter from properly cooked chicken?

Unless cooked chicken is incorrectly stored (i.e. not put in a fridge), then it is very unlikely to cause a Campylobacter infection.

How long does it take for GBS to develop after a Campylobacter infection?

Usually this takes 1-3 weeks after an infection.

Can I get Campylobacter more than once?

Yes.

Summary

 Campylobacter, a common bacterial infection, is linked to Guillain-Barré Syndrome (GBS), a rare neurodegenerative autoimmune disease. Campylobacter infections, often from contaminated food or water, can increase the risk of developing GBS by 38 times. GBS affects the peripheral nervous system, causing various symptoms like weakness, numbness, and paralysis. The disease progresses through four phases: progression, plateau, recovery, and potential disability. While most patients recover, some may experience lasting effects. The link between Campylobacter and GBS is attributed to molecular mimicry, where antibodies mistakenly target nerve structures. Risk factors include geography, genetics, and diet.​​​​​​​​​​​​​​​​