To do a do a really good study of this, that avoids problems with confounders etc, you would need to randomly intervene in different communities (add or remove guns). Otherwise, we are in the realm of quasi-experimentation. Good quasiexperimental studies can be done, but they hard, and most are done very badly and highly vulnerable to spurious results. I haven't read the book, but I would be surprised if stands up to scrutiny: most quasi-experiments don't.
Anyone thinking of doing a study would do well to read the classic text: Quasiexperimentation, but Cook and Campbell.
Following on from that book, the
Campbell Collaboration was set up to objectively evaluate exactly this sort of question using the best available evidence. There doesn't seem to much there that's relevant to the original question so far, though. My guess is that there just haven't been any decent studies.
This story is a big deal because until recently vancomycin has been the one antibiotic microbiologists could reliably fall back on to treat MRSA. Resistance to all other antibiotics has been seen in S.aureus . It's also a big deal because Staphylococcus aureus (the SA in MRSA) is a pretty aggressive bug, unlike say VRE, which, though also effectively untreatable in some cases due to drug-resistance, are pertty weedy bugs that only affect a few very ill patients.
MRSA strains with intermediate resistance to vancomycin have been seen in many parts of the world since 1996, and patients certainly have died as as result of vancomycin treatment failure. However, these perhaps weren't so scary as the resistance mechanism was a very thick cell wall which made these strains very slow growing and not so viable in the absence of vancomycin.
What's new is that MRSA strains have now emerged with high-level vancomycin-resistance and this happened by acquistion of the vancomycin-resistance gene (vanA) from VRE.
That this was possible was shown in the lab in 1992, but the first time it's been seen in patients was this year. The two reports of Vancomycin-resistant MRSA in the U.S. can be found in the CDC's newsletter:
MMWR Morb Mortal Wkly Rep 2002 Oct 11;51(40):902
MMWR Morb Mortal Wkly Rep 2002 Jul 5;51(26):565-7
How scary is it? Until recently MRSA has been almost exclusively a hospital pathogen, so it's pretty scary if you're a hospital patient with a lot of tubes sticking into you which alow the bugs to get in and cause infections, but if you're well it's not a big threat (doctors and nurses can carry MRSA, but generally they don't develop infections despite a lot of exposure). There have been reports recently of strains of MRSA that do spread well in the community, and that can cause serious infections amongst essentially healthy people. However, these have not been multiply-resistant strains, and really these are no worse than virulent strains of normal S. aureus which have been round for millions of years. The message is, if you're well, don't rush out and buy cipro (this will only helps MSRA as the bugs are resistant to it), and if you're ill, keep away from hospitals.
Just to rebut a few other comments: over-prescribing of antibiotics probably is very important for encouraging drug-resistantce, but even correct of use of antibiotics will lead to some resistance. Use of antibiotics in animal feed can't really be blamed in this case, as drugs of the same class as vancomycin (glycopeptides) have not been used in animal feed in the US, though they have in Europe. They've probably played a significant role in VRE transmission in humans in some European countries, but in the U.S. hospital prescribing of this and other antibiotics have probably been the driving force.
Crazy question for microbiologists: Is it possible that resistance to a specific antibiotic costs an organism enough that it could no longer out-compete it's non-resistant cousins? Would it be worth infecting someone who has a resistant strain with a non-resistant strain in the hope that the non-resistant one will 'win'? Then, (if the patient still lives), treat that with antibiotics?
Similar things have been done. Since most staph usually just colonize patients' noses rather than causing infections, you can block transmission by deliberately implanting relatively a-virulent strains in patients' noses. This was done buy a microbiologist called Shinefield in a series of experiments in neonatal units in the 50s and 60s.
Another approach is to use viruses that target bacteria but not human cells. This has been used a lot in the former Soviet Union, and there's a good bit of research now going on into such methods in the West.
It is certainly possibly that resistance costs will lead to drug-sensitive strains winning out in the long run if the antibiotic selective pressure is withdrawn. However, it really would be pretty crazy to deliberately cause an infection (rather than just colonization) in a patient with a second virulent bug.
Slashdot Mirror
Yep, catastrophe theory
Anyone thinking of doing a study would do well to read the classic text: Quasiexperimentation, but Cook and Campbell.
Following on from that book, the Campbell Collaboration was set up to objectively evaluate exactly this sort of question using the best available evidence. There doesn't seem to much there that's relevant to the original question so far, though. My guess is that there just haven't been any decent studies.
MRSA strains with intermediate resistance to vancomycin have been seen in many parts of the world since 1996, and patients certainly have died as as result of vancomycin treatment failure. However, these perhaps weren't so scary as the resistance mechanism was a very thick cell wall which made these strains very slow growing and not so viable in the absence of vancomycin.
What's new is that MRSA strains have now emerged with high-level vancomycin-resistance and this happened by acquistion of the vancomycin-resistance gene (vanA) from VRE. That this was possible was shown in the lab in 1992, but the first time it's been seen in patients was this year. The two reports of Vancomycin-resistant MRSA in the U.S. can be found in the CDC's newsletter:
MMWR Morb Mortal Wkly Rep 2002 Oct 11;51(40):902
MMWR Morb Mortal Wkly Rep 2002 Jul 5;51(26):565-7
How scary is it? Until recently MRSA has been almost exclusively a hospital pathogen, so it's pretty scary if you're a hospital patient with a lot of tubes sticking into you which alow the bugs to get in and cause infections, but if you're well it's not a big threat (doctors and nurses can carry MRSA, but generally they don't develop infections despite a lot of exposure). There have been reports recently of strains of MRSA that do spread well in the community, and that can cause serious infections amongst essentially healthy people. However, these have not been multiply-resistant strains, and really these are no worse than virulent strains of normal S. aureus which have been round for millions of years. The message is, if you're well, don't rush out and buy cipro (this will only helps MSRA as the bugs are resistant to it), and if you're ill, keep away from hospitals.
Just to rebut a few other comments: over-prescribing of antibiotics probably is very important for encouraging drug-resistantce, but even correct of use of antibiotics will lead to some resistance. Use of antibiotics in animal feed can't really be blamed in this case, as drugs of the same class as vancomycin (glycopeptides) have not been used in animal feed in the US, though they have in Europe. They've probably played a significant role in VRE transmission in humans in some European countries, but in the U.S. hospital prescribing of this and other antibiotics have probably been the driving force.
Similar things have been done. Since most staph usually just colonize patients' noses rather than causing infections, you can block transmission by deliberately implanting relatively a-virulent strains in patients' noses. This was done buy a microbiologist called Shinefield in a series of experiments in neonatal units in the 50s and 60s. Another approach is to use viruses that target bacteria but not human cells. This has been used a lot in the former Soviet Union, and there's a good bit of research now going on into such methods in the West. It is certainly possibly that resistance costs will lead to drug-sensitive strains winning out in the long run if the antibiotic selective pressure is withdrawn. However, it really would be pretty crazy to deliberately cause an infection (rather than just colonization) in a patient with a second virulent bug.