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Flesh eating bacteria ‘thrive on their victim’s pain’

The germ that causes strep throat is also responsible for the devastating flesh-eating disease, known as necrotizing fasciitis, which affects as many as 200,000 people worldwide each year.

The bacterium, Streptococcus pyogenes, emits a toxin that causes excruciating pain. As it does this, it burrows deep under the skin and eats into connective tissue and muscle.

It is known for being hard to diagnose and can quickly become fatal.


New research from Harvard Medical School has discovered that ‘flesh-eating’ bacteria actually hijacks a victim’s pain receptors for their own benefit. Pictured: The bacterium, Streptococcus pyogenes

New research from Harvard Medical School has discovered that S. pyogenes hijacks neurons and exploits the normal communication that occurs between the nervous and immune systems during injury or infection, essentially ‘thriving’ off its hosts pain. 

‘Necrotizing fasciitis is a devastating condition that remains extremely challenging to treat and has a mortality rate that’s unacceptably high,’ said study senior investigator Isaac Chiu, assistant professor of microbiology and immunobiology at Harvard Medical School. 

‘Our findings reveal a surprising new role of neurons in the development of this disease and point to promising countermeasures that warrant further exploration.’

By experimenting on mice, the researchers realized the bacteria produced a toxin called streptolysin S (SLS) that caused pain-sensing neurons to fire, causing agony for the host.

As many as three in 10 humans who get the disease die.

The scientists also discovered that the toxin emitted a peptide that disrupted communication with the immune system, essentially preventing the body from fighting back against the infection.

This stopped immune cells from releasing an enzyme that would kill the invasive bacteria, like bleach would. It also left the bacteria free to multiply and continue eating through healthy tissue.

‘Effectively, this neuronal signal silences the alarm system that normally calls on the body’s infection fighters to curb infection,’ Chiu said.

The absence of inflammation-inducing white blood cells at the site infection, the researchers say, may explain why, in the early stages of necrotizing fasciitis, patients tend to experience intense pain but without the heavy swelling, redness and overall inflammation that develop when the defense system rushes to the wound.


Necrotizing fasciitis is a bacterial infection that quickly kills surrounding tissue.

S. pyogenes hijacks neurons and exploits the normal communication that occurs between the nervous and immune system

S. pyogenes hijacks neurons and exploits the normal communication that occurs between the nervous and immune system

Once the bacteria enters the body, it can spread to the muscles, nerves, fat and blood cells around the infected site causing damage.

Death can occur if it is not stopped quickly enough.


  • Pain or soreness
  • Swelling near wound
  • Ulcers, blisters or black spots 
  • Fever
  • Chills 
  • Fatigue 
  • Vomiting


Strong antibiotics are imperative to treating the disease and are typically administrated through an IV.

Surgery is recommended when the antibiotics are unable to reach the tissue that has already been infected.

This happens when the bacteria has prevented blood flow to those areas.

If any of the infection is left in the body after surgery, it can cause organ failure and the patient will die. 

The researchers theorized that by blocking the neuron’s signals, the immune system could fight off the bacteria, thus creating a potential treatment for S. pyogenes infections. 

They injected mice with the bacteria, as well as the protein botulinum neurotoxin A, used in Botox, which works by blocking nerve signals. One group of mice got the Botox injection a week before the S. pyogenes, the other immediately after. 

The mice only developed minor wounds that never progressed to a full-blown disease, regardless of when the rodents received the nerve-blocking agent.

In a third group, the mice received a Botox injection two days after the bacterial injection, when they had already developed a wound. 

The injection essentially stopped the disease in its tracks and prevented further damage.

In the last experiment, the scientists used another compound which blocked the release of the neurotransmitter that disrupted the immune system. 

The immune cells were able to rapidly respond and prevent the spread of necrotizing fasciitis.

The study has shown how important neurons are in the spread of flesh-eating bacteria, as well as offer a potential solution to treating the disease.

‘Our findings provide a striking example of how closely intertwined the nervous and immune systems are and how intricate their interaction can be in the setting of infection,’ Chiu said in the statement.

‘Our study also underscores the therapeutic potential of modulating one system to affect the other as a way to treat infection.’  



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