We're in serious trouble

We’ve only been able to treat bacterial infections for the past 70 years or so. Other than our natural defences, which will be the subject of my next blog, we had no means to fight off these infections. None of our medicines were effective against bacteria. Then came the discovery and use of penicillin, first widely used by Allied troops during WW2. This discovery led to a class of drugs we refer to as antibiotics and these have revolutionised how we treat disease. Before this, what we see as minor, easily treated infections could often be fatal.

Penicillin and antibiotics were seen as a panacea. Until chinks began to appear in our medical armour. Let me start this with the story of syphilis. That is syphilis the sexually transmitted infection, not Sisyphus, the man from Greek mythology. Apart from sounding similar these two have a lot in common as we shall soon see. Bear with me. Soon after the use of penicillin to treat syphilis in hospitals, doctors noticed a strain of syphilis had emerged that was resistant to treatment by penicillin. The new uber-medicine was not as effective as thought. Now, not all bacteria were as susceptible as when treatment with penicillin was first used. Why? Bacteria reproduce rapidly via binary fission. One becomes two, then four, then eight. Like this. You get the picture. And due to binary fission they are all clones. Except for the occasional, rare, genetic mutant. As we will discover in Unit 4, which is just around the corner, often these mutations lead to death or suboptimal functioning but sometimes the mutation causes the organism to have an advantage. The competitive edge in the case of this bacterium was resistance to penicillin. When hit with a dose that killed all its non-mutant siblings, this bacterium survived. And reproduced passing that trait for resistance on to its daughter cells. And soon a strain had evolved that was resistant to treatment. But here comes the interesting part. While bacteria reproduce asexually, they also perform an incredible evolutionary act, they swap genes in an act called conjunction. Two bacterium can come together and exchange genetic information. It’s like a brunette going up to a red-head and taking a copy of the red-head’s gene for hair colour, while the donating a gene for lactose tolerance. The brunette now expresses the red-hair phenotype and the red head can now tolerate lactose. A resistant bacterium could, did and still does come in contact with non-resistant bacteria and swap genetic information, passing on this gene for resistance. New mutations can rapidly spread throughout populations. The drugs we use became less effective, so we would use a different antibiotic. Successfully at first, then, over time, less so. Hmmmm, a strain now resistant to two treatments. That’s OK, we have another drug...

Then humans come along and start over using and misusing antibiotics. Prescribing antibiotics for viral infections, using them at the wrong dosage level, or not for long enough. Placing antibiotics into the food we give farm animals. How many of you have started a course of antibiotics and not finished them? Every time you do this you are establishing the perfect evolutionary pressures for drug resistance to evolve. And it has. Rapidly. Each year nearly 500,000 cases of multi-drug resistant tuberculosis are diagnosed. Half a million cases that are resistant to all known treatments. 150,000 fatalities occur as a result. According to WHO extensively drug-resistant tuberculosis has been reported in 64 countries to date.
Many articles in the mainstream media refer to the 'superbug NDM-1'. A bacteria that is resistant to all of our medicines. This is pretty scary but it is also wrong. NDM-1 isn't a bacterium, it's a gene. And this gene is readily passed from one species of bacteria to another, through bacterial conjunction termed horizontal gene transfer (the passing of genetic information to an organism that is not a decendant). The media do have it right about one thing though. Bacteria that have the NDM-1 gene are resistant to all treatments we have available.

But it is not just bacteria. Plasmodium, the protozoan that causes malaria, is also developing resistance to many forms of treatment. Areas of Thailand, Burma, Laos and Cambodia now have malaria with resistance to some of the most effective treatments and preventatives. As do other regions in the world.

Anti-viral treatments for disease such as HIV/AIDS have been shown to be losing their efficacy as these viral strains evolve into new types as a direct response to the drug treatment. In a recent article I read, which I have attached, the idea of a world in the not-too-distant future where disease is resistant to our treatments is suggested by WHO. We will potentially be in a situation where ‘minor’ disease become fatal again. Scary shit.

I mentioned a Greek guy at the start with a name similar to a sexually transmitted disease, Sisyphus. Sisyphus was cursed to spend his life pushing a bolder up a hill and just when he would near the top the bolder would roll to the bottom and he would be back where he started. As we look at drug resistant syphilis taking us back to where we were 70 years ago I think syphilis and Sisyphus have more in common than similar sounding names.

http://www.abc.net.au/news/stories/2011/04/07/3185138.htm

UPDATE 15/5:
Todays's RadioTherapy program on 3RRR had an interesting discussion on NDM-1 and other bacterial infections. Listen to it here while studying