Q&A: The perspective from the point of CA-MRSA spear
Editor's note: Henry F. "Chip" Chambers, MD, chief of the division of infectious diseases at San Francisco General Hospital (SFG), works at the proverbial "point of the spear" in terms of emerging community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA). As previously reported in Hospital Infection Control, seven out of nine San Francisco hospitals reported last year that MRSA rates were rising higher than 50%, meaning that between 50% and 75% of all staph infections were caused by resistant strains. In five of those hospitals, the USA300 community strain was responsible for an average of 68% of all infections. With emergency departments becoming crowded with these patients, SFG established a skin and soft-tissue infection clinic to deal with the onslaught.HIC interviewed Chambers recently after he spoke at an MRSA meeting in Atlanta held by the Association for Professionals in Infection Control and Epidemiology.
Q. Could you elaborate on your statement during your presentation that "in 15 years, all staph would be resistant?"
A. "When I say, 'All,' I mean operationally we will have to act like it is. So what is that number [of resistant staph]? Is it 90%? Is it 50%? Operationally, we are already somewhere in that range. You have to — until you know — assume that it is MRSA. It already affects practice. I guess if you don't know you can still hope that it is susceptible. In the future, you will know it's resistant at a high proportion. But if you came into me right now and you had what I thought was a staph infection, you would be on vancomycin. I would cover for it. "
Q. But what about the old "use-it-and-lose-it" axiom in infection control? Is it too late to hold back antibiotics to preserve their efficacy?
A. "This is a great debate in medicine, but what makes great social policy may be bad for your patient. As a doctor, I take care of patients, not social policy. That's how we are trained."
Q. Do you think that the USA300 strain of CA-MRSA will eventually become the predominant nosocomial staph strain?
A. "I do, because it has all the tools it needs to survive in the hospital. It's more virulent, [meaning it can cause] more disease and it can survive in the community. Its ascendancy occurred in the community, competing against perfectly fine methicillin-susceptible staph strains. There were only a few other MRSA strains out there to compete with."
Q. You mentioned USA300 had the combination of being more virulent and more resistant. Does that translate to it being more transmissible?
A. "I think this strain is more transmissible. I don't really understand why. It may be very contextual, but there are a lot of indicators that it is. The burden of disease goes up when the strain becomes prevalent in the community. You find you have more skin and soft-tissue infections. In a couple of studies that have looked at it, there are reasons to think that it might be spread more easily. "
Q. The first reported case of a USA300 CA-MRSA strain with intermediate resistance to vancomycin (VISA) was reported by you and your colleagues last year.1 That sounds kind of ominous. Do you expect we will see more cases like that?
A. "I think as the burden of disease increases for that strain, we will start seeing more of those. Fortunately, there is a big cost in terms of biology if the strain is vancomycin-resistant. It tends not to be as virulent and tends not to transmit as well. It has mutations in important regulatory genes. They will occur, but when you talk about 18,000 people dying a year of MRSA — and there are many more than that, we are probably off by an order a magnitude – VISA cases are a drop in the bucket."
Q. Given the USA300 threat to hospitals and the continuing rise of staph in the community is a vaccine against this bug going to be the ultimate answer?
A. "A vaccine would be good, but the vaccine paradigm is tricky. Most vaccines are directed toward pathogens that if you get the natural infection you acquire immunity as a consequence of that. [A third of people] are colonized with Staph aureus, but if they get a Staph aureus infection then [colonization] doesn't help them you one bit as far as we know. In fact colonized people are at higher risk of having staph infections. In designing a vaccine, you would need something probably that had multiple components. There is a paper in [the Proceedings of the Natural Academy of Sciences] by an investigator named Schneewind.2 He deconstructed a group of staph strains and said, 'OK, what do 90% of Staph aureus strains have that I count on being the antigen?' But that's the thing, not all Staph aureus strains have all the same factors. But even with those that were 100% [comparable] across the board, when he picked those that made the best antibody, he found if you only used one [component] it wasn't good enough. But when he made a four-component vaccine then he got somewhere. So maybe something like that [would eventually work]."
- Graber CJ, Wong MK, Carleton HA, et al. Intermediate vancomycin susceptibility in a community-associated MRSA clone. Emerg Infect Dis [serial on the Internet]. 2007 Mar. Available from www.cdc.gov.
- Stranger-Jones YK, Taeok Bae, et al. Vaccine assembly from surface proteins of Staphylococcus aureus. Proc Natl Acad Sci USA 2006; 103:16,942-16,947.