Hospital superbugs can make poison like a rattlesnake

September 8th, 2008 - 11:13 am ICT by IANS  

London, Sep 8 (IANS) Hospital superbugs can make poisons similar to that of rattlesnake venom to beat our natural defences, according to a new study. The toxins are produced by communities of the hospital superbug Pseudomonas aeruginosa called biofilms, which are up to a thousand times more resistant to antibiotics than free-floating single bacterial cells.

Scientists also discovered that the biofilm bacteria can produce a protein similar to an active ingredient in rattlesnake venom - a protein that causes the host cells to commit suicide and die. The research team is currently studying the protein to see if it functions in the same way.

“This is the first time that anyone has successfully proved that the way the bacteria grow - either as a biofilm, or living as individuals - affects the type of proteins they can secrete, and therefore how dangerous they can potentially be to our health,” said Martin Welch of Cambridge University.

“Acute diseases caused by bacteria can advance at an astonishing rate and tests have associated these types of disease with free-floating bacteria. Such bugs often secrete tissue-damaging poisons and enzymes to break down our cells, contributing to the way the disease develops, so it is natural to blame them,” said Welch.

“By contrast, chronic or long-term infections seem to be associated with biofilms, which were thought to be much less aggressive,” he added.

“For example, these chronic infections by bacteria are now the major cause of death and serious disability in cystic fibrosis patients - which is the most common lethal inherited disease in the UK and affects about 8,000 people.”

In cystic fibrosis, a gene defect means that people are very susceptible to a particular group of opportunistic bacteria including Pseudomonas aeruginosa - one of the three major hospital superbugs.

Aggressive antibiotic treatment can usually control the infection in cystic fibrosis sufferers but eventually the strain becomes completely resistant to antibiotics, leading to respiratory failure and death, often while patients are still in their thirties.

“We think that the bacteria in a cystic fibrosis sufferer’s lungs are partly living in communities called biofilms, and although medical scientists have investigated their strongly antibiotic-resistant properties, very little research has been done to investigate any active contribution the biofilms might have in causing diseases in the first place,” said Welch.

A widely-held view is that biofilms serve as reservoirs of bacteria that do relatively little harm; they just sit there. The main danger is thought to be from ‘blooms’ of free living cells which occasionally break away from the biofilm and cause periods of poor lung function in the cystic fibrosis patients.

“In this scenario, it follows that bacteria in a biofilm will produce fewer disease-causing chemicals than free-living cells of the same type of bacteria, which is a prediction that we can test,” said Welch.

“We found that biofilms do indeed produce harmful chemicals. However, the type of tissue-degrading enzymes and toxins made by the biofilm bacteria differ from those produced by free-floating bugs, which may help them to survive attacks by our immune systems,” he added.

These findings were presented Monday at the Society for General Microbiology’s Autumn meeting being held this week at Trinity College, Dublin.

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