A variant of the deadly MRSA bacteria has rapidly evolved into what is potentially one of the most dangerous superbugs on the planet.
A scanning electron micrograph of the highly-antibiotic resistant Staphylococcus aureus bacteria (gold), also known as MRSA, outside a white blood cell (blue). A cousin to this bacteria, Staphylococcus epidermidis, is proving to be resistant to almost every antibiotic treatment as well. Photo: National Institute of Allergy and Infectious Diseases (NIAID), CC
As routine use of antibiotics has become a kind of epidemic in itself, so-called ‘superbugs’, bacteria which spread quickly, have the potential to cause serious harm and even death if not stopped, and are resistant to most treatments, have evolved to become a serious concern for health professionals around the world.
Methicillin-resistant Staphylococcus aureus (MRSA), also known as golden staph, had for many years held the crown as one of the most terrifying. Discovered first in hospitals and now showing up in infections from people who never came into a medical facility, it continues to thrive, change, and fight most medical treatments. It still responds to Cipro as an antibiotic treatment and can be killed in the presence of iodine, but its rapid spread from what looks like a bug bite with a yellowish bump in the center to a potentially life-threatening attack on the flesh still drives fear when health professionals diagnose the disease.
Now a biological cousin of MRSA is proving potentially even more dangerous. The new threat comes from Staphylococcus epidermidis (S. epidermidis). It is found on human skin. It has also been for some time one of the most common causes of infections within hospitals. It also used to be easily dispensed with using conventional antibiotics. Medical professionals could protect themselves and others from accidentally spreading the bacteria by handwashing or wiping with alcohol cleaning solutions.
According to a just-published report in Nature Microbiology, the days of easy treatment for this potentially severe infection are over.
The new study was conducted by Dr. Jean Lee, a former infectious diseases registrar at a hospital in Melbourne, Australia, with the aid of Professor Ben Howden, her consultant and PhD supervisor. Howden is the Director of the Microbiological Diagnostic Unit Public Health Laboratory at the Doherty Institute., at the University of Melbourne (Australia).
Dr. Lee’s investigation into this began in 2012, when in her role as the infectious diseases registrar she learned of a patient who was generally healthy but came down with an infection contracted in the hospital. The patient had come in for a simple elective procedure but developed an infection which would not heal. As Dr. Lee noted in an interview on the subject, “He should have been in and out of hospital quickly. But instead he contracted a very resistant infection and had to stay in hospital for over two months, followed by rehab.”
The infection the patient had contracted was Straphylococcus epidermidis. It turned out to be resistant to almost any kind of antibiotic treatment – and was very difficult to isolate and treat.
As Dr. Howden explained further, “Current guidelines for these kinds of infections recommend a combination treatment of rifampicin and vancomycin, which are completely unrelated and should protect against one another.” What he and Dr. Lee discovered in this case was instead that “resistance to one antibiotic is causing resistance in the other, raising concerns about current treatment guidelines.”
While worrisome, that the bacteria could respond to one antibiotic by evolving resistance to it over time was not a surprise. That the response also rendered it resistant to an entirely different one was a far more serious concern.
As Professor Howden noted further, “[The bacteria] has also managed to spread despite the good infection control now in place in hospitals in developed countries, which has helped manage golden staph [MRSA].”
As the researchers investigated further, they discovered the resistant versions of S. epidermidis were already showing up in hospitals in Victoria. They then checked references for S. epidermidis cases seen in ten separate countries and 78 different institutions. The bad news was the bacteria had already spread globally. Europe, the UK and the United States have all reported the presence of the superbug.
Howden and Lee then brought in help from the Doherty Institute’s whole genome sequencing technology, to understand how the antibiotic-resistant bacteria were related. That ended up revealing the same mutations were present in every country’s antibiotic resistant strains of S. epidermidis.
As further data was gathered, it was determined that the infection often occurred when there was a unique ‘entry portal’ into the body to allow the bacteria to get underneath the skin. In hospitals, these include catheters and joint replacements.
According to Professor Howden in an interview on the topic, these kinds of “implanted devices are frequently impregnated with antibiotics as a strategy to prevent infection, however, this approach may be promoting the development of resistance.” S. epidermidis, like some other antibiotic-resistant bacteria, produces its own protective layer around whatever has been inserted into the body. That protective layer, per Howden, “allows it to avoid antibiotics and the body’s immune response”. The layer being more or less generic is part of why this evolutionary trick of the bacteria in response to one antibiotic also renders it resistant to others.
Another complication is that those patients with catheters and other implanted devices are also often in intensive care. The patients themselves are often routinely provided with strong antibiotics as a disease-prevention measure. That, together with the presence of antibiotics essentially built into implantation devices creates a ready laboratory for the harmful bacteria to build up further resistance.
Currently the researchers are looking into understanding more about how the bug is being passed on to patients. How that happens and why the bacteria has spread so rapidly around the world remains a mystery. That is why they are focusing on understanding where the bacteria is and to continue to track the various strains of the bacteria as they emerge.
In the short term, the even more serious concern is, as Professor Howden pointed out in recent comments, that “what we’re doing is just leading to more resistance. So, we urgently need to think about what we should be recommending instead.”