VRSA and Clostridium difficile – The War on the superbugs’ has only just begun
You could be forgiven for thinking that MRSA is the worse thing lurking in our hospitals, but as far as superbugs go MRSA is only the support act for some deadly headliners.
In the last decade Methicillin-resistant Staphylococcus aureus (MRSA) has become as infamous with hospitals as pubs are to Glasgow. But how many of us worry about contracting more dangerous superbugs like Clostridium difficile or VRSA or even PVL associated infections?
In the UK it is estimated that around 40% of patients leave hospital with a hospital acquired infection and the number of community associated cases is also on the rise. But these figures are most likely grossly underestimated.
According to experts the best way to control these outbreaks would be “to screen and isolate all potential cases”, advises. But with the number of positive cases for MRSA now heading towards outnumbering those not infected, isolations appears to be impossible.
Like MRSA, the superbugs’ Clostridium difficile (C difficile) and Vancomycin resistant Staphylococcus aureus (VRSA), have proliferated as a result of the overuse and misuse of antibiotics.
C difficile kills nearly three times more people when compared to MRSA. The bacterium is found in small numbers amidst the normal gut bacteria found. But today, in patients treated with arrays of antibiotics, normal intestinal bacteria levels drop and C difficile advantageously multiplies producing toxins that damage the cells lining the intestine. The result is severe diarrhoea and in some cases ulceration and bleeding. In the UK from 2003 to 2005 the cases of C difficile increased by 29% and in 2006 some health boards recorded increases of another 20 per cent.
A deadly strain of MRSA that produces the necrotising toxin Panton-Valentine leukocidin (PVL) is also concerning health experts. Previously more common in Community associated cases (CA-MRSA) the bug is now becoming more prevalent in hospitals. The PVL toxin destroys leukocytes (white blood cells) that are core to our immune system and the effects can range from skin and soft tissue infections to pneumonia. Once in your lungs you could die in less than 24 hours.
For any of us unlucky enough to contract MRSA the treatment is Vancomycin; nicknamed the last resort drug’. It is the only antibiotic left that has any real effect on the superbug’. But its administration intravenously is not easy and it can be highly toxic.
Margaret Scott from Mayfield in Midlothian remembers being told that she had MRSA. In 2005 she was admitted to Edinburgh Royal Infirmary with an ongoing health issue; emphysema.
She said: “I wasn’t in long before a sore on my arm started to swell and the blood tests revealed I had MRSA”.
“I was isolated in a high dependency ward and given an antibiotic (most likely Vancomycin) intravenously”.
After leaving the hospital a visit from a nurse revealed that Margaret had actually contracted MRSA in 2000, when she had been admitted to hospital to have part of her lung removed. Today she is left with unanswered questions.
She added: “some doctors told me they can operate on my lungs while I have MRSA, others told me exactly the opposite”.
How can it be, that some patients testing positive for superbugs’, are still being left in the dark?
Margaret Scott’s infection was most likely cleared with the help of Vancomycin but there are bacteria that have now gained resistance to our last resort drug’. The increased use of Vancomycin, to treat infections caused by MRSA, has resulted in the emergence of a Vancomycin-resistant Staphylococcus aureus (VRSA). Unlike MRSA, these strains can be controlled by other FDA approved drugs but its increased prevalence means its only time before VRSA and MRSA swap information resulting in strains of S.aureus immune to all antibiotics, including the last resorts.
Professor Tom Evans, from the University of Glasgow’s Biomedical Research Centre points out that it’s only “natural that such a strain will evolve with the increased use of Vancomycin”.
He added “we can’t stop bacteria evolving. But it is our actions that are speeding up their evolution”.
But how did all these mutant bacteria arise? Is it as simple as we are oversubscribing antibiotics? The term superbug’ is used to describe any disease-causing bacterium that develops a resistance to the agents normally used to eradicate them. In 1928 Alexander Fleming discovered the first antibiotic and it was heralded as a medical miracle. But as early as the 1940s, only a few years after the first mass production of Penicillin, bacteria had already started to evolve resistance to our wonder drugs, beating us at our own game.
When Charles Darwin coined the phrase “natural selection” he suggested that all species, including bacteria, evolve via a process known as survival of the fittest.
“It is not the strongest of the species that survives, nor the most intelligent that survives. It is the one that is the most adaptable to change.”
Bacteria carry genes that protect them from a range of substances toxic to them. If bacteria are faced with a constant onslaught of antibiotics only those bacteria carrying genes providing resistance will survive, and in turn they will become more abundant. For decades doctors have enthusiastically and incorrectly prescribed antibiotics to patients, unknowingly creating the perfect environment for these superbugs’ to evolve. But the blame should not solely lie with the medical profession. In the community superbugs are also rife in old folk’s homes and farms where antibiotics are used in animal husbandry.
In comparison to humans microbes can evolve much quicker, taking only days to do what took us thousands of years. Bacteria can reproduce and exchange segments of DNA with bacteria in close proximity to themselves via a process known as horizontal gene transfer. In 2004 Julian Parkhill from the Sanger institute near Cambridge told Nature; “the resistance genes transfer very quickly between strains this is extremely bad news”. In our hospitals millions of bacteria live in close quarters, increasing the chances of these gene transfer events.
Antibiotics have the potential to kill bacteria by inhibiting either their ability to generate their protective membrane, or by inhibiting their metabolic activities. Today many of us still believe that antibiotics will help us get over the common cold or the flu, but they have no effect on viruses. Health professional may have proscribed you antibiotics for undiagnosed illnesses. Such acts were most likely fuelled by ignorance, and pressure; to please persistent patients who may not be happy to simply go home, rest and drink lots of fluids.
Today researchers are still fighting to create and discover new antibiotics but as Prof Evans explains “it can take up to ten years for any new drug to make it onto the market”. For the moment the drug Vancomycin is still the last line of defence’ against MRSA. But with the discovery of Vancomycin resistant Staphylococcus aureus (VRSA) it may be only a matter of time before the line breaks and we have to fall back.
So what do we do until then? Prof Evans, like many, believe that it could be as simple as cleaner hospitals and better screening, “measures like strict cleaning of door knobs, bed rails and staff uniforms would help minimise the spread of these bugs in hospitals”.
For now the future is uncertain. Could we see strains of C.difficile exhibiting the same antibiotic resistance as MRSA? Could we see PVL strains of VRSA? The truth is that we simply do not know but if we continue to encourage the indiscriminate use of antibiotics then we will only fuel the evolution of superbugs’.
