Thursday February 2 2012
The UK is not under siege from a 'flesh-eating bug'
Britain is in the grip of a new “flesh-eating bug spread by sneezes and coughs”, according to The Sun.
The basis of this news was a laboratory study that investigated why healthcare-acquired meticillin-resistant staphylococcus aureus (MRSA) bacteria rarely cause infections in healthy individuals. The study found that healthcare-acquired MRSA has a high level of antibiotic resistance, but that this property comes at a cost of reduced virulence (being less able to cause infection). Conversely, the study found that the type of MRSA that is usually caught in a community setting is more virulent, but weaker against treatment with antibiotics.
This study has not investigated the transmission, effects or number of cases of community-acquired MRSA in the UK, the discussion of which formed the basis of many news reports on the research. The researchers state that MRSA outside the healthcare system and in the community is a growing concern, but cases are still very rare. This interesting research contributes to our knowledge of MRSA, rather than warning us of an invasion of airborne superbugs.
Where did the story come from?
The study was carried out by researchers from the University of Bath and the University of Nottingham in the UK; University College Dublin in Ireland; and Texas A&M Health Science Centre and the University of Texas in the US. It was funded by the UK Medical Research Council and a Biotechnology and Biological Sciences Research Council Studentship. The study was published in the peer-reviewed Journal of Infectious Diseases.
This story was widely covered. Most reports were alarmist, concentrating on the supposed emergence of a dangerous, highly infectious new form of community-acquired MRSA. Many newspapers suggested that transmission is easy, that it can lead to a “flesh-eating form of pneumonia”, and that cases are on the increase. These claims seem to be based on the press release for the research rather than the research paper itself. The study was actually laboratory-based research that had investigated why healthcare-acquired MRSA bacteria rarely cause infections in healthy individuals. Although there was some investigation of community-acquired MRSA, the results do not justify the news coverage.
What kind of research was this?
This was a laboratory-based study. It aimed to examine why healthcare-acquired MRSA bacteria rarely cause infections in healthy individuals. Healthcare-acquired, or hospital-acquired, means that the bacteria cause infections that mostly occur in healthcare environments.
The researchers initially covered the nature of MRSA and how it resists certain types of antibiotics. It is already known that MRSA is resistant to the antibiotics meticillin and oxacillin because it has acquired a piece of DNA called a ‘mobile genetic element’. Meticillin is an old antibiotic that is now no longer used and has been replaced by flucloxacillin.
Many staphylococcus aureus bacteria have now also developed resistance to the penicillin group of antibiotics (because they produce enzymes that can make penicillin inactive), but they are usually still susceptible to the antibiotic flucloxacillin. MRSA, however, does not have this susceptibility to flucloxacillin, and is, therefore, harder to treat than most staphylococci bacteria, needing stronger antibiotics still.
One particular genetic element that is key for deciding the properties of MRSA is called the ‘staphylococcal cassette chromosome mec’ (SCCmec). There are several different versions of this cassette, which each provide bacteria with slightly different properties. The researchers state that healthcare-acquired MRSA have type I, II or III SCCmec elements, whereas community-acquired MRSA have type IV and V elements. These different cassettes all contain a gene (mecA) that codes for a protein called PBP2a, located in the cell wall of the bacteria. PBPs (penicillin binding proteins) are a normal part of the cell wall of many bacteria. Many antibiotics work by inactivating PBPs, which cause the bacteria to die. However, the version of PBP encoded by mecA, PBP2a, is less sensitive to antibiotics, allowing the bacteria to survive.
What did the research involve?
The researchers initially determined whether deleting the mecA gene, which encodes the PBP2a cell wall protein, affects the toxicity of MRSA. They then took a healthcare-acquired MRSA strain and a version of this strain that they genetically modified to delete the mecA gene, and performed tests to see how each was able to break up a type of immune cell called a T cell in the laboratory.
The researchers then investigated the ability of the different strains to respond to ‘signalling molecules’, which normally cause the bacteria to activate their production of toxins. The virulence of these strains was confirmed using mouse experiments.
The researchers then compared the production of the PBP2a cell wall protein, T-cell toxicity and the resistance of healthcare-acquired MRSA to antibiotics, compared with community-acquired MRSA.
What were the basic results?
The researchers found that deleting the mecA gene caused the MRSA to become more toxic. This was because the expression of mecA results in cell wall changes that interfere with MRSA’s ability to detect or respond to signals to switch on toxin expression. MRSA with mecA deleted was also more virulent in a mouse model, causing mice to lose weight or die.
The researchers then compared MRSA strains with different SCCmec elements: those with type II elements (typical of healthcare-acquired MRSA) and those with type IV elements (typical of community-acquired MRSA). They found that typical community-acquired MRSAs had lower resistance to the antibiotic oxacillin, were more toxic to the immune system’s T-cells and expressed less PBP2a.
How did the researchers interpret the results?
“As a direct result of its high level of antibiotic resistance, healthcare-acquired MRSA is impaired in its ability to cause infection, which can explain its inability to cause infection in community settings, where antibiotic usage and the prevalence of susceptible patients are low.” In other words, healthcare-acquired MRSA makes a trade-off, sacrificing its ability to spread to healthy individuals in order to fight off a greater range of antibiotics.
This interesting study helps explain why healthcare-acquired MRSA infections are rarely found in healthy individuals. It found that expression of a gene that produces one of the proteins responsible for MRSA’s antibiotic resistance caused it to be less toxic. It also showed that typical community-acquired MRSA strains express less of this antibiotic-resistance protein, but are more toxic.
However, this intriguing lab study did not investigate the transmission, effects or number of cases of community-acquired MRSA in the UK, the discussion of which formed the majority of the news reports. On this basis, the research itself does not support the claims that we are under siege from an ‘airborne, bacteria-resistant, flesh-eating superbug’, as newspapers have today suggested.