MRSA gets piggyback from livestock to humans

Blogging on Peer-Reviewed ResearchMRSA gets piggyback from livestock to humansI’ve written an article for the Economist about a new strain of the antibiotic-resistant “superbug” MRSA (methicillin-resistant Staphylococcus aureus) that infects large numbers of farm pigs and can jump into humans.

The strain was first found in pig farms in the Netherlands and may be picking up new resistances from their porcine hosts because of the large amounts of antibiotics used to medicate livestock.

The piece is in the Science and Technology section of the November 29th issue of the Economist (out in the UK tomorrow) but you can already read it online. I’m pretty excited about this – it’s certainly the most prestigious magazine I’ve had the opportunity to write for.

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Drugs that work against each other could fight resistant germs

Using combinations of drugs that work poorly together could be the key to fighting strains of germs resistant to those same drugs. Drugs that block each other could actually switch off the evolutionary driving force that leads to drug-resistant bacteria.

When normal bacteria are exposed to a drug, those that gain a resistance gene also gain the huge and obvious advantage of invincibility. Bacteria are notoriously quick to seize upon such evolutionary advantages and resistant strains rapidly outgrow the normal ones.

Tuberculosis is developing increasingly resistant strains.Drug resistance poses an enormous potential threat to public health and their numbers are increasing. MRSA for example, has become a bit of a media darling in Britain’s scare-mongering tabloids.

More worryingly, researchers have recently discovered a strain of tuberculosis resistant to all the drugs used to treat the disease. New antibiotics are difficult to develop and bacteria are quick to evolve, so there is a very real danger of losing the medical arms race against these ‘super-bugs’.

Even combinations of drugs won’t do the trick, as resistant strains would still flourish at the expense of non-resistant ones. Antibiotic combos could even speed up the rise of super-bugs by providing a larger incentive for evolving resistance.

Clearly, fighting the rapidly evolving nature of bacteria is a dead end. So Remy Chait, Allison Craney and Roy Kishoni from Harvard Medical School used a different strategy – they changed the battle-ground so that non-resistant bacteria have the advantage.

Doxycycline works better against drug-resistant bacteria when given with a drug that it blocks!The trio looked at two strains of the common bacteria Escherichia coli – one that was normal, and another that was resistant to doxycycline.

Doxycycline is widely used to fight off a variety of bacterial invaders, but resistant E.coli use a specialised molecular pump to remove the drug. It can withstand 100 times more doxycycline than its normal counterparts.

First, the team hit the two strains with doxycycline and erythromycin, a combination of drugs that work particularly well together and enhance each other’s effects

The resistant strain was certainly more vulnerable to this double-whammy, but as expected, it always outperformed the normal bugs. With that advantage and enough time, it would inevitably evolve resistance to both drugs.

But Chait managed to remove this evolutionary impetus by combining doxycycline with a third drug, ciprofloxacin, a combination that would normally be useless. Doxycycline actually blocks the effects of ciprofloxacin, to the two drugs together are weaker than either alone.

To fight bacteria like MRSA, we need new strategiesPredictably, the resistant bug did what it had evolved to do – it pumped out doxycycline. But in doing so, it also unwittingly removed the block on ciprofloxacin, restoring this second drug to its full killing power.

The normal strain encountered no such problem. By leaving the drugs alone, it never faced the full effects of either, and out-competed their more heavily-pummelled resistant cousins.

Chait cautions that it’s too early to transfer his findings across to hospital beds. The experiment used non-lethal antibiotic concentrations in a very controlled environment. But they have certainly pointed other researchers down a new and interesting path.

Combinations of drugs that block each other have previously been dismissed by doctors because they would require higher doses. But Chait’s study suggests that they could be the key to controlling bacterial drug resistance.

We clearly can’t stop bacteria from evolving, but we can certainly steer the course of that evolution in our favour.

Reference: Chait, Craney & Kishony. 2007. Antibiotic interactions that select against resistance. Nature 446: 668-671.

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The secret of drug-resistant bubonic plague

The bacterium that causes bubonic plague can pick up drug resistance from common bacteria responsible for food poisoning.

Yersinia pestis causes bubonic plague.The plague, or the Black Death, is caused by a microbe called Yersinia pestis (right). In the 14th century, this microscopic enemy killed off a third of Europe’s population.

While many people consign the plague to centuries past, this attitude is a complacent one. Outbreaks have happened in Asia and Africa over the last decade and the plague is now recognised as a re-emerging disease.

In 1996, two drug-resistant strains of plague were isolated from Madagascar. One of these, was completely resistant to all the drugs that are used to control outbreaks.

Any scientist currently studying tuberculosis can attest to the ability of bacteria to evolve resistance to drugs. In the case of drug-resistant plague, the secret to its powers is a plasmid – a small free-floating ring of DNA, that carries drug resistance genes.

Bacteria can trade plasmids across individuals, transferring genes between each other in ways that humans can only achieve with technology.

The worry is that common and less harmful bacteria could transfer drug-resistance plasmids over to Yersinia, resulting in new resistant strains.

Plague bacteria could pick up drug resistance from Salmonellla like this. Timothy Welch and colleagues from the United States Department of Agriculture showed that this concern is well-founded. They found that the plague plasmid is virtually identical in parts to plasmids from an increasingly common strain of Salmonella (left) that is also resistant to multiple drugs.

They even found related plasmids were in other drug-resistant bacteria isolated from meat samples across the USA during quality control checks.

A word of caution – this doesn’t mean that people risk contracting plague from eating meat. Even though the plasmids are strikingly similar, the bacteria involved are very different.

But it does mean that the plague bacterium could potentially gain drug resistance from other common resistant bacteria, if they should both find themselves in the same human or flea host.

Despite this scary scenario, Welch’s study also provides us with a silver lining. We are aware of the threat and we know how to monitor for it, by searching for the plasmid.

Monitoring is especially important because the plague has all the qualities you would look for in a potential biological weapon – a high fatality rate, no vaccine and possible air-borne transmission.

If the worst happens, we will want to be prepared.

 

Reference: Welch, Fricke, McDermott, White, Rosso, Rasko, Mammel, Eppinger, Rosovitz, Wagner, Rahalison, LeClerc, Hinshaw, Lindler, Cebula, Carniel& Ravel. 2007. Multiple antimicrobial resistance in plague: an emerging public health risk. PLOS ONE.

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