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Hospital cases of Vancomycin Resistant Enterococcus highlight a growing concern over drug resistant bacteria developing from antibiotics in animal feed and the misuse and overuse of antibiotics in the community.

GORDON TAYLOR: Doctors have often warned that we're squandering the benefits of antibiotics - the wonder drugs of modern medicine. The bacteria slowly become resistant to each new type of antibiotic and so far we've been only just ahead of them.

Hello, I'm Gordon Taylor - you're listening to Background Briefing.

Now the bugs are winning. A new bacteria, known as VRE, has turned up in Australia that is resistant to all known antibiotics. It has already infected six people here, and claimed two lives.

JOHN TURNIDGE: Six cases is just the tip of the iceberg. We do not want to get into the situation where, in the United States, where so many people that come to hospital have picked up the germ and become colonised. We don't want germs that are difficult to treat at any time; we don't want to go back to the bad old days. We have to find it, jump on it, and make it go away.

GORDON TAYLOR: But finding and jumping on VRE is very hard because the infection is not notifiable, and anyway the monitoring is not yet in place to find it. VRE stands for Vancomycin Resistant Enterococcus, and it's a killer. State health departments are reluctant to disclose what information they do have about the bug's appearance here. From the New South Wales Health Department, Dr Jeremy McAnulty.

JEREMY MCANULTY: Well, we've had four cases of people colonised or infected with VRE in 1996; those are the first cases that have been recognised in this State.

GORDON TAYLOR: And do we know where those cases are?

JEREMY MCANULTY: They're in New South Wales. We can't specify which facilities they are.

GORDON TAYLOR:And why is that?

JEREMY MCANULTY: Well, for a number of reasons: first, it's really irrelevant; we know VRE is common in other parts of the world and it's really a matter of chance which facilities or hospitals are affected in New South Wales, and we really are cooperating with hospitals to enable us to get a very accurate picture of how many cases there are, so we need to ensure that there's some confidentiality there.

GORDON TAYLOR: Background Briefing has been able to establish that the first hospital to have a case of VRE was Melbourne's Austin Hospital in 1994, and in the last few months four cases have occurred in New South Wales - at the Royal Prince Alfred Hospital in Sydney and the John Hunter Hospital in Newcastle. In Brisbane, there has been one case.

The first case in Victoria, in 1994, was a 21-year-old liver transplant patient. He was already seriously ill when he became infected with the virulent Golden Staph and the new superbug, VRE. These infections contributed to his death. In Sydney's Royal Prince Alfred Hospital, a woman died when Golden Staph and VRE entered her blood stream. The patient at Newcastle's John Hunter Hospital cross-infected two others in the intensive care ward. Cross-infection like this is frightening in hospital surgical wards. In the US, there is now a 14 per cent chance of catching VRE in some wards.

Jeremy McAnulty.

JEREMY MCANULTY: We know that overseas it's a big problem - in the United States, where they measure hospital infections, and the proportion of those that are related to VRE has really increased substantially in the last two years, to up to 14 per cent in some intensive care units. So it's a big problem overseas, and we're starting to see cases here in Australia.

GORDON TAYLOR: But that's the level of infection. How dangerous is it to a patient?

JEREMY MCANULTY: Well, it really depends on the patient's pre-existing condition. It's particularly a problem for people who are otherwise unwell either because of a problem with their immune system or because they've had operations and they've got lines or things sticking into them, and they're more likely to get very sick if infected.

GORDON TAYLOR: Could there be more cases in New South Wales that we don't know about?

JEREMY MCANULTY:People can carry this bug in their normal gut without having any problems at all. So we don't really know how common or if it exists at all in very many numbers in New South Wales. In overseas studies, where they find cases, they certainly have a lot of effort to look for other cases around them, so in Australia that's done as well; if there are cases found in the hospital, then the surrounding patients will be examined, and so far we haven't found any other cases.

GORDON TAYLOR: The reason VRE is so dangerous is because it is resistant to virtually all antibiotics. It usually lives harmlessly and passively in our gut, but let loose into the bloodstream of a weakened hospital patient, it can rapidly kill. VRE - Vancomycin Resistant Enterococcus - is a previously harmless Enterococcus bacterium that has developed resistance to our drug of last resort, the powerful antibiotic Vancomycin.

Dr Ken Harvey, a senior microbiologist in Melbourne, is one of the doctors here who are very concerned about VRE now turning up in Australia. Ken Harvey.

KEN HARVEY: In a hospital environment with lots of very sick people with tubes and catheters breaching their defences, with lots of antibiotics permeating the environment and killing off other germs, this has created an environment where this relatively harmless germ can actually now cause problems, especially as it's become antibiotic resistant. There is virtually nothing left to treat these infections, so we've not just got Vancomycin Resistant Enterococcus, we've got multi-drug-resistant enterococcus, and we've got nothing left with this particular germ.

GORDON TAYLOR: Elsewhere in the world, VRE is already well-known. At Tufts University, in Boston, world authority on antibiotics, Dr Stuart Levy, says we have to pay attention to what's happening.

STUART LEVY:It is extremely serious, for two reasons of course: one, the organism itself is a problem to patients undergoing what we think are curative therapies for cancer or even in the treatment of AIDS and other immunologic diseases. Secondly, the resistance in the enterococcus is unfortunately on a transferable trait. So it can transfer it to other bacterium and it has - it was transferred in the laboratory to the staphylococcus; it's been transferred to other bacteria; it's clearly transferable. So the enterococcus, being Vancomycin resistant, is a problem not only for itself, but for other diseases that might be caused by bacteria that could pick up that trait.

GORDON TAYLOR: Dr Levy is warning that resistance to antibiotics could be transferred to even more dangerous bacteria, creating what's been called a 'Doomsday Bug'. How does that kind of resistance transfer happen? In Britain, Dr Barry Cookson, interviewed for the BBC.

BARRY COOKSON: The bugs are extremely clever, particularly VRE. I mean, for it to become resistant to Vancomycin is the most amazing feat, and the way it's done it genetically is absolutely incredible. That, actually is - to use a popular word these days - fairly awesome. And I think they will become no less clever in the future. I think if new antibiotics are invented, I have no great confidence that they won't become resistant to those as well - I'd be stupid if I said anything else - and clearly the problems we have on a global basis are extremely serious. And I think, at the moment, I would say the bugs are winning.

GORDON TAYLOR: What happens is a single bacterium mutates and becomes resistant. That bacterium then multiplies and becomes dominant. In Melbourne, Dr Ken Harvey.

KEN HARVEY: It is basically Darwinian selection of the species. If you permeate an environment, be it an intensive care ward or a hospital with lots of antibiotics, you will kill off the sensitive germs, which is what we of course want, but if there just happens to be the odd mutation in a germ that has perhaps just slightly altered some chemical or enzyme, that it might have originally used for example for breaking down its foodstuff, and if a slight mutation in that then means that it can break down an antibiotic instead of its foodstuff, or as well as its food, then obviously that gives that one strain a selective advantage. So the sensitive ones will die off; that one strain will multiply and become dominant and will take over. And that's certainly what we saw, very rapidly, in the early days, with staph aureus and penicillin.

GORDON TAYLOR: So why is it able to happen so quickly? We're having resistance developing within years. It takes thousands, maybe millions of years for evolutionary change to happen in, say, humans.

KEN HARVEY: Yes, well, you see the germs multiply faster than us, that's the problem. We take 20 to 30 years to reproduce. These fellows can do it in 20 to 30 minutes. And that's an awful lot of generations in a very short time, and therefore it's evolution in rapid forward motion, basically.

GORDON TAYLOR:Evolution in rapid forward motion. Within 10 years, some say, resistance to antibiotics will be a major public health issue with hospital wards again filled with seriously sick people with bacterial infections. Another Australian doctor who is deeply concerned is Peter Collignon, from Canberra's Woden Valley Hospital.

PETER COLLIGNON: This is sort of a gradual bracket-creep thing. We are losing more and more of the little skirmishes, and eventually, unless things turn around and we, if you like, are much luckier with making dramatic new discoveries and complete new classes of drug, we're going to find a bigger and bigger percentages of infections are either more difficult to treat or, in some cases, impossible to treat because we don't have any available agents to treat them with.

GORDON TAYLOR: But that may mean that in 10, 20 years' time we turn around and diseases that previously were simply treatable by antibiotics are now no longer treatable by antibiotics, and someone who would have survived a disease earlier, would now die from it.

PETER COLLIGNON: Well, I think that's true. I mean, on current trends that's what our feeling is will happen in 10 years' time - not that they will all be non-treatable, but there will be a bigger percentage. But we don't have to wait for 10 years for that, that's actually happening now. I mean, germs like tuberculosis, which we thought we had under control 10 years ago, we now, both in Third World countries, but even modern countries such as Australia, but particularly the US, have multi-resistant strains of tuberculosis that aren't readily treatable, or some are not treatable, by current drugs, and people have died with these germs, and not being able to treat.

GORDON TAYLOR: And it's the microbe's unique ability to shift resistance to a different species that makes the problem even harder to fight. Dr Stuart Levy again.

STUART LEVY: One bacterium can transfer its resistance to another bacteria of a very different type. You look at an evolutionary scale, they're very, very distant, so much that you could imagine that it's a dog and a cat transferring information, which we know you can't get if you try to mix a dog and a cat. But bacteria can.

GORDON TAYLOR: Well, how dangerous is that, the fact that they can transfer resistance?

STUART LEVY: Well, I think that is underlying the reason that we're seeing so much resistance out there today in so many different bacteria. You look at the traits, they're the same, shared by hundreds of different types of bacteria that have somehow acquired the same resistance trait and, in doing so, they might change it just a little big so it works better in them, and then they transfer it to other bacteria of their same type, even though they may have picked it up from a bacteria of a very different type.

GORDON TAYLOR:That's Dr Stuart Levy. That transfer can even occur between bacteria that live in different species, between say the bugs in the gut of a dog and those in the gut of a cat, or even between animals and humans. That, say some Australian scientists, may be the source of the VRE occurring at the John Hunter Hospital and at Austin Hospital. Certainly, antibiotics are widely used in agriculture, both as a therapy for sick animals and at low levels as a growth promoter. An example is Australia's poultry industry. Head of the Chicken Meat Producers' Association, Dr Jeff Fairbrother.

JEFF FAIRBROTHER: Certainly, antimicrobials are used as growth promotants in the industry. Growth promotant is probably not the right word because it doesn't actually promote growth; what it does is make better utilisation of the feed, so a bird can use the feed better, and you make it 2 to 3 per cent efficiency in the utilisation of feed. It doesn't really mean that the birds will grow any quicker, they still take, say, 42 days to grow, but they eat less feed. And so the feed conversion is better and, in the long run, you're going to save a bit of money.

GORDON TAYLOR: So how important are growth promoters, or that class of drug, how important are they to the poultry industry?

JEFF FAIRBROTHER: Well, I think straight from an economic point of view, they're really very important. And you may save a cent a bird in a batch - it doesn't sound a lot, but if you put it over 320 to 350 million birds in a year, you're saving a lot of money.

GORDON TAYLOR: There are two almost identical antibiotics involved. Vancomycin and Avoparcin. Vancomycin is used to treat humans and Avoparcin is used in animal feed. It's the close similarity between these two antibiotics that's causing the problem. Each year, Australia uses 125,000 kilograms of Avoparcin in agriculture, mainly in pigs and poultry. It's used more to promote growth than to cure infections. But the animals still build up resistance, and it's possible that the animal resistance is being transferred to humans.

A study in Denmark has found just that. Resistance to Avoparcin in animals has been transferred to humans and becomes resistant to the human drug, Vancomycin, and so that previously unimportant bacterium, an enterococcus, now becomes VRE, Vancomycin Resistant Enterococcus. Prompted by the Danish scientific work, the Danish and German governments have sought to ban the use of Avoparcin, but have been overruled by the scientific body of the European Union.

Avoparcin, the animal antibiotic, is made by the multinational Roche company. Roche doesn't accept that Avoparcin use is a problem, and says the Danish findings are flawed. Background Briefing asked Roche for an interview for this program, but we were refused because 'it would give the issue an importance it doesn't deserve'. Roche says anything they said would only stir up an emotional response from opponents. However, Roche has written to the British medical journal the Lancet.

READER: As the manufacturer of Avoparcin, a product which improves an animal's digestion by controlling the growth of undesirable intestinal bacteria, we agree that the increase in Vancomycin resistance is a potentially serious issue. However, to say that this increased resistance results from the use of Avoparcin is an over-simplification. A more useful exercise would be to investigate the role that human antibiotics, including Vancomycin, have had in the development of antibiotic resistance in man.

GORDON TAYLOR: And yes, Roche's note did prompt a response from the medical profession, also as a letter to the Lancet.

READER: Experience in both the UK and Germany strongly suggests that the resistance determinant, the Van A gene, can be selected by Avoparcin when the product is used as a feed additive, that it can enter the human food chain and be incorporated into the bowel flora of patients. There's now much public concern about additives fed to animals that are destined for human consumption. There needs to be full debate on how and when we use antimicrobials in animals and man. Commercial considerations of food production have to be balanced against potential adverse affects on man. Do I hear an echo of the mad cow debate?

GORDON TAYLOR: It was only after a close examination of the VRE cases in Australia that a startling scenario emerged. It's all a bit complex, but basically there are three distinct strains of VRE. Research by the Europeans suggests that one type, known as Van A, comes from the use of Avoparcin in animals and is transferred to humans. To the surprise of doctors here, the VRE in the three cases at Newcastle's John Hunter Hospital and the original case at Austin Hospital in Melbourne, all were of this Van A type - that is, all of the type that originates in animals.

Professor John Turnidge.

JOHN TURNIDGE: At the moment we don't know for sure where these particular strains from the John Hunter of the Austin Hospital have come from. But based on the European experience, we've got a strong suspicion that it may be the type that comes from animals, and the use of Avoparcin in pigs and poultry in particular.

GORDON TAYLOR: So the three Newcastle cases look like they came from animals. The New South Wales Health Department has started testing the faeces of farm animals to find the bug's origin. Two hundred cows, pigs and chickens on 40 farms across the lower Hunter Valley are being tested as concern mounts about the origin of VRE. The chicken producers say there is nothing to fear. Dr Jeff Fairbrother again.

JEFF FAIRBROTHER: I don't believe that that resistance can be transferred. Certainly, there is no reason whatsoever to ban Avoparcin, and I'll give you a couple of reasons why I say that: first of all, Avoparcin has been used for about 24 years and there has never been a suggestion until this one paper by the Danes suggested there could have been a problem with it. This is the transfer resistance to Vancomycin. In the United States, Avoparcin has never been used, and the most serious problem in the world with VRE occurs in the United States. And just on that evidence alone, it would indicate that there's not a problem with Avoparcin.

Avoparcin is one of the safest products, as far as I'm concerned, that's on the market, and I can see absolutely no reason for a ban. Now, surely, it's true that the Danes did ban it, and the Germans followed suit on a voluntary, temporary sort of ban, and that's what prompted the EU to have a really detailed look at the product, and, as I say, the results of their really detailed look is that there is no reason why the product should be banned.

GORDON TAYLOR: But we've had three cases of VRE in the John Hunter Hospital in Newcastle. Some of the medical authorities in this country are suggesting that maybe that VRE did come from animals. How do you react to that?

JEFF FAIRBROTHER: Well, I still don't believe that it's necessarily any relationship, and in fact what's going to happen out of the John Hunter experience is that there will be a limited survey in the field, looking at droppings from poultry, from beef cattle and from pigs, to see if they can isolate any Avoparcin-resistant organisms from the faeces of these animals. As far as John Hunter Hospital specifically is concerned, I believe that the biggest problem we have with antibiotic resistance in this country is the overuse of antibiotics generally over the years by the medical profession. And it was suggested to me that: why would we suddenly find three problems in the John Hunter Hospital? Well, as far as I know, this was all to do with the intensive care unit - this is where you find the sickest people - and if you're going to have a problem, that's the most likely place it would be. If you had one isolated case, people may say, 'Well, by chance.' I say that, if you have three, the first could be by chance, and the second could be a problem within the hospital.

GORDON TAYLOR: But Dr Stuart Levy in Boston disagrees and sees a clear link between antibiotic use in animals and antibiotic resistance in humans.

STUART LEVY: Well, I have been a longstanding opponent of the use of human therapeutics as animal supplements for growth. I have no problem with their use for therapy, although I would like some of our major human therapeutics that we rely on to be avoided. For instance, I wouldn't like Vancomycin to be used in animals unless it was absolutely essential, and some of the third generation cephalosporins and even our quinolines, because resistance will emerge.

GORDON TAYLOR: We have a situation where we have an analog virtually almost of Vancomycin being used in agriculture - not in the United States, but in Australia and Europe - and that's Avoparcin, also Glycopeptide, very similar to Vancomycin, and there's some suggestion by the Danes that Vancomycin resistance can basically be transferred from the animal to the human world. How much credence do you put on that?

STUART LEVY: I'd put a lot of credence on that. Unfortunately, some other societies and decision-makers don't see that as a problem. I do. I think that the many years of use of Avoparcin has created an environment of hundreds and hundreds of millions and millions of Vancomycin Resistant Enterococci in the intestinal tracts of these animals. We eat these animals; the organisms have been found in the retail shops on the meat, and on the poultry. So can we really believe that there is no introduction of them from animal to man? I don't think how we can, especially when they've done the typing and the studies of these enterococci, and they are shared, they're the same kind.

My last understanding of the European Union is that, despite the action of the Danes and despite the recent action of the German Government to ban Avoparcin as of mid-January of next year, there is not an agreement in the European Union to avoid and to eliminate this as a supplement - not as a therapy, as a supplement.

GORDON TAYLOR: So you would think it was almost inevitable that that transfer from animals to humans of Vancomycin resistance would occur?

STUART LEVY: That's correct. Now, there's a kind of irony here, that when we're up against the wall with no drug to use for the treatment of staph aureus, and now even the pneumococcus, we're grabbing at the only drug left on our shelf, which is Vancomycin, which was not used to any great extent until the present five or six years, and it's been used in animals for many years because there was no problem - we were not using anything that looked like Avoparcin until now. It's almost as if we've gone to an animal drug to now treat a human disease. I mean, that's not really true, but in a sense when Avoparcin was introduced, Vancomycin was a tiny, tiny percent of any pharmacy's sales in the hospitals - less than .01 per cent.

GORDON TAYLOR:Should we stop the use of Avoparcin?

STUART LEVY: I think we should stop the use of Avoparcin, and I think we should curtail the use and the misuse of Vancomycin in people.

GORDON TAYLOR:VRE is a killer in weakened, and immuno-suppressed hospital patients, a deadly bug that Australia's hospitals could well have done without. But its importance goes much further than that. The danger is that VRE transfers its Vancomycin resistance to the well-established and distinctly nasty Golden Staph bacteria.

Director of Microbiology at Adelaide's Womens' and Children's Hospital, Professor John Turnidge.

JOHN TURNIDGE: Vancomycin is still our gold standard treatment for the seriously-ill patient with resistant Golden Staph. We never want to lose that activity against that because, at the moment, there is really nothing significant in the pipeline to replace it.

GORDON TAYLOR:How serious would it be if we lost Vancomycin, if the bugs were resistant to that - how serious would it be?

JOHN TURNIDGE: Well, it would be back to the bad old days before antibiotics, like more than 50 years ago when people just got over infection or died.

GORDON TAYLOR: There is a nightmare scenario: if the untreatable Vancomycin Resistant Enterococcus transfers the secret of total antibiotic resistance to the more virulent staphylococcus, then there would be no treatment for Golden Staph. That transfer has already happened in a laboratory in London. The deadly bacteria are in a test tube under lock and key in a freezer at St Thomas' Hospital in London. The experiment was done by Professor William Noble. But could it escape, or could nature learn the same trick?

Professor Noble.

WILLIAM NOBLE: I think the chance that the resistance will transfer is fairly high. I think it's probable that it will happen. I can't give you any time; it might be next week and it might be the year 2050. But I think the probably is that it will occur.

GORDON TAYLOR:Professor Noble says it will come next week or next year. Melbourne's Dr Harvey believes that, when it does arrive, it will be devastating.

KEN HARVEY: Well, it would be absolutely disastrous because staph aureus is a much more significant pathogen, it's much more likely to cause serious infections, and septicaemias, wound infections, and other things. And if we were left with nothing to treat staphylococcal infections, we would be in a very serious situation indeed.

GORDON TAYLOR: Where would we be? What would we be, back to the days before antibiotics?

KEN HARVEY: Well, essentially, we would be, and all the people can probably remember our means of dealing with infections in those days were basically draining pus and excising dead tissue, and we wouldn't like to go back to that.

GORDON TAYLOR: A Vancomycin resistant Golden Staph is so dangerous that Dr Levy has been very critical of Professor Noble's experiments. His fear is that these very dangerous bacteria could escape. Whether they escape, or it happens in nature, Dr Levy is alarmed.

STUART LEVY: It is clearly the nightmare scenario of the present-day, 1996, and this century, because many believe that the Vancomycin resistant staph aureus will appear somewheres in the world, if it hasn't already, in this decade. And the real question is: How will we contain it?

GORDON TAYLOR: So you think it's inevitable that it will appear?

STUART LEVY: That is correct.

GORDON TAYLOR:How terrible would such an organism be?

STUART LEVY: Well, if you realise in the United States that maybe two million people are getting infections in hospitals, of which 30 per cent could be staph aureus, that we're trying to treat 600,000 people with an effective antibiotic. Now, all of them, we think, at the beginning will be susceptible to Vancomycin. But as we get more and more percentage of resistance, we have nothing to treat them. So we're going to lose patients, we're going to have people dying because we can't treat staph aureus.

PETER COLLIGNON: We are particularly concerned with implications for more aggressive germs rather than the enterococcus. It's aggressive enough, and if you're unlucky enough to get that infection, obviously it's a problem. But in comparison to germs like Golden Staph, it's not in the same league, and if the resistance can develop in enterococcus, which we would have thought of before as not likely to occur, or hopefully would not occur, the worry is that resistance might develop in Golden Staph or that resistance from the enterococcus may transfer to Golden Staph, and that would be a major disaster. If we had an aggressive germ like Golden Staph with resistance to the available agents, obviously we're back where we were in the 1920s and 1930s before we really had any antibiotics.

GORDON TAYLOR: Dr Peter Collignon. Entrenched in our hospitals for years, Golden Staph is greatly feared, but still treatable. We don't know the full number of cases across the country, nor where they are happening. Hospitals try to keep such infections quiet, so the public won't become alarmed. Golden Staph infection is not a notifiable disease.

Dr Peter Collignon, an infectious diseases physician at Canberra's Woden Valley Hospital, estimates a thousand or more Australians die from Golden Staph infections each year.

PETER COLLIGNON: It is widely spread. On studies that have been done around Australia, most hospitals or major hospitals in Australia do have this germ and it often is entrenched in the hospital and gets spread from patient to patient. Small hospitals are not exempt either. There are many smaller hospitals in the country, and countryside, where they also have large numbers or large percentages of these germs.

GORDON TAYLOR: Is it simply a nuisance that's in all of our hospitals, or is it a real problem? Does it kill people, does it maim people, how bad is it?

PETER COLLIGNON: Well, it's all of those things. I mean, with any of these germs, many people come in contact with it, and luckily the majority of people don't get infection. But a percentage of people do get infected, and the severity of what happens to them depends on what actually happens. Probably the worst case you can have is for these germs to get into your bloodstream and cause what we call bacteraemia or blood poisoning, and that's associated with a high, both death and complication rate, because this germ is very good at getting into bones, getting on heart valves and many other tissues in the body, and if it does that, it causes a lot of destruction. And obviously, if it's on your heart valve, or bones, or whatever, and causes a lot of damage, that causes a lot of problem actually at the time, but may give you long-term residual complications if you do survive the illness, so that you have problems for many years into the future.

GORDON TAYLOR: What sort of ballpark figures are we talking about? Are we talking about hundreds, thousands?

PETER COLLIGNON: Oh, I think we're talking about thousands of people in Australia per year who acquire significant infection with Golden Staph in hospitals per year. Quite a number of those people will die as a result of that, and many more will have serious, long-term complications because of it.

GORDON TAYLOR: There are many stories of the horrors of Golden Staph. Meg Colquhoun's experience in one of Adelaide's top private hospitals, the Memorial, is one. She became infected with Golden Staph while in hospital for surgery on her spine. She had to stay in hospital for more than three months as the doctors threw all they could at the infection. The operation involved placing stainless steel rods along Meg's spine, which have provided the ideal breeding ground for the staph. Her husband, Des, thought that she would die, as the infection took hold. Meg was eventually able to return home, but still with a suppurating wound on her back. In their house in the Adelaide suburb of Dulwich, Meg remains too ill to talk. Her husband Des is still shocked at what happened.

DES COLQUHOUN: Yes, there was a neurosurgeon and an orthopaedic surgeon; they tied her backbone to a rod through to there, which was supposed to fix the problem. And it seemed at first to be a brilliant success. The operation was very good, apparently, and the surgeons were excited and we were excited and it all looked pretty good.

GORDON TAYLOR: And so then what happened?

DES COLQUHOUN: Then it was determined that Meg had the dreaded MRSA.

GORDON TAYLOR: Golden Staph that is, resistant Golden Staph.

DES COLQUHOUN: That's right, Golden Staph, yes. And the scene changed. Instead of coming home in 10 to 14 days. She was in there for 14 weeks, and went through absolute hell in the meantime; a great lot of pain, a lot of misery, a lot of treatment; and she's now come home, still with a wound in her back which just won't heal, and still having dressings by the district nurse. It was ghastly, she had a wound right down her back from the operation and the lower half of it would just not heal. It had opened up into a great suppurating wound a man could put his fist in, and it's taken 14 weeks to get down to the size of a matchbox.

GORDON TAYLOR: Stories like Meg Colquhoun's are surprisingly common. Harold Stevens was also unlucky: he entered Sydney's Prince Henry Hospital for a routine operation to fit an artificial valve on his urethra.

HAROLD STEVENS: The operation was done on the Monday morning and I was discharged on the Friday. Everything appeared to be okay; temperature was up a bit during the week but that sort of came down to the normal acceptable levels. I had no complaints, except, say, I came home, and then five days later, I started to feel .. on the Monday, that was a Friday - on the Monday, I started to feel rather sick and by the Tuesday night, that's 24 hours-odd, that's right, I was basically in pain. I could not move, I couldn't pass urine, so my doctor, I rang my doctor, or my wife rang my doctor, and he came down and said 'Go straight to hospital.'

GORDON TAYLOR: Now, you ended up staying in hospital that second time around because of the infection, for how long?

HAROLD STEVENS: Approximately a month.

GORDON TAYLOR:And it took that long to clear up the infection?

HAROLD STEVENS: It took three-odd weeks to clear it up before they decided that they would remove the implant. The reason they removed it was because I had a perforated urethra. The infection had eaten away the urethra and all the urine was by-passing it into my stomach. So they removed it the next day; I had the X-ray, and the next day they removed it, and I had another week in hospital after that before getting myself in a condition to come home, by getting better.

GORDON TAYLOR: And did they ever tell you what was wrong with you, what the infection was? Was there any acknowledgment from the hospital about the infection?

HAROLD STEVENS: No. No communication in relationship to what the infection was. I don't even know what the antibiotics were. They were pumping the antibiotics into my chest because they say if they went into my arm they would collapse the veins. So I don't know what the infection was or what the antibiotics were.

GORDON TAYLOR: Did they tell your doctor?

HAROLD STEVENS: No, the specialist notified my specialist that I had an infection about a week and a half after I came out of hospital. But when I spoke to him within a few days of coming home, he did not know anything had happened.

GORDON TAYLOR:Harold Stevens had a serious bacterial infection known as pseudomonas. Like Golden Staph, it is now resistant to many antibiotics, and is proving difficult to treat. Good hygiene reduces the risk of Golden Staph and other infections taking hold. Doctors and nurses must wash their hands constantly. What was the level of cleanliness at Prince Henry Hospital?

HAROLD STEVENS: Very, very bad. Again, what they class as sterile to me is just not the case. The room was dirty, dust was on the floor, dust was on the venetian blinds, they had containers with pads in the bathroom which remained there for three days. They didn't change the bed for three days after the operation. I lay there, I had not had a wash, I had not had my teeth cleaned, I had not had a shave, or anything, from the Monday until the Wednesday. So I think this is something that should be looked at.

GORDON TAYLOR: Prince Henry Hospital says that Harold Stevens was in a newly refurbished ward, where the hospital is very pleased with the level of hygiene. Prince Henry says there was no breakdown of hygiene during Harold Stevens' stay in the hospital.

Hospitals are often unwilling to admit that they have serious infections like Golden Staph and VRE. It's very difficult to get information on infections, much less admission that there have been lax standards.

Dr Peter Collignon.

PETER COLLIGNON: It's always a two-edged sword because you don't want to engender needless panic about this also. But I basically think we are not as open about this as what is desirable. The problem is, this is always bad news and I guess we never like giving out bad news. But I think because we don't let the facts - or we often, I might say, don't have the figures because they're not really collected in any meaningful way and in any national sort of way, but because we don't have those figures, or when they exist there is a lack of desire to widely publish them, I think the general community, including the medical and nursing staff, often don't appreciate how big the problem is.

When you actually tell people, or you show people what a large percentage of hospital admissions get infections, they're often quite surprised. In Australia, there's over four million hospital admissions per year, and a number of studies have suggested that anywhere between 6 per cent and 10 per cent of these patients acquire infections from whatever the medical or hospital procedure was. Now, 10 per cent of four million is about 400,000 people a year, which is obviously big numbers. Now luckily, the majority of those people, or the infections they get, are minor and they get over them without any problems. But a sub-set of these patients can have life-threatening or major infections, including bloodstream poisoning, and this obviously causes many thousands of people to be involved and deaths in many hundreds, if not thousands. And that sort of magnitude I don't think is appreciated by either the general community or the medical and nursing profession. And the problem is if we don't appreciate the magnitude, then it's less likely that something will be done.

GORDON TAYLOR:It may already be too late. In an internal report, the World Health Organisation says that the time for complacency is over, that medical science internationally must urgently address the issue of antibiotic resistance. Before the use of penicillin in the 1940s, even small infections could run out of control, and a simple wound could only be dealt with by surgery or amputation.

Before World War II, many bacteria, like Golden Staph and tuberculosis would mean a death sentence. But ironically, the original discovery of penicillin that has made it all possible has become a parable for the antibiotic age.

Dr Ken Harvey.

KEN HARVEY: Penicillin, as some people probably recall, was discovered initially in a laboratory by a Scottish microbiologist called Fleming, back in the '30s. He was unable to actually purify and synthesise it, and wrote it up as an interesting phenomenon that killed particularly the Golden Staph on culture plates. It was in the Second World War where Florey, an Australian at Oxford, was responsible for the war effort of looking into research for treating war wounds. And he read back over Fleming's original work, realised that this was potentially an important compound. He had a very clever chemist called Chan (?), Ernst Chan, and they succeeded in isolating the active ingredient of this mould that was killing Golden Staph, and it was penicillin, but in those days they could only get it in very small amounts, and not very pure.

The first patient that they tried it on was a policeman who'd nicked himself shaving, had got a nasty cellulitis, an infection of the skin which had rapidly spread and was life-threatening, and he was dying when they administered the first small doses, and his recovery was absolutely dramatic. For the first couple of days, he was brought back from death's door. But then, regrettably, they ran out of their small supplies of penicillin and he died; having almost recovered, he died. And yes, that is hopefully not an accurate parable of the antibiotic era, but it certainly reminds us of where we might end up if the germs become resistant and we run out of antibiotics.

GORDON TAYLOR: The antibiotic blanket that has protected every generation since the Second World War is weakening. Dr Collignon.

PETER COLLIGNON: We've had new drugs, but they've basically been variations in the same class of antibiotics. If you like, they've often been 'Me Too' drugs that have got some slight improvement that are not a quantum shift. To actually get drugs in a complete new class, which is what you need, I think that will be difficult. I mean, there are still occasional breakthroughs but that only occurs once every 10 years and it seems to be occurring less often now than in the past. And that is one of the problems: we have to have other approaches other than relying on just new drugs becoming available to do something about this. We've got to do as much as we can to slow the rate of resistance, as well as relying on pharmaceutical companies or other research interests to come up with, if you like, magic bullets, because those magic bullets are becoming fewer and fewer between us.

GORDON TAYLOR: Well, what can be done? Do we have to think laterally maybe? Do we have to find innovative ways of dealing with these diseases?

PETER COLLIGNON: Well, I think we do have to look at multiple ways of decreasing both the amount of resistance that's developing, but if it does, decreasing the rate that it's going to increase in the future, and that's everything from sensible antibiotic prescribing to restricting what drugs are available and who can use them - you know, can you use them in animal products as well as human products, for instance? What do you do about other approaches to improving the immune system or decreasing the chance that a patient will become susceptible to the infection?

GORDON TAYLOR: But do we have to go back to basics as well? Many people have said simply improving hand washing in hospitals would make a big difference, for instance, to Golden Staph.

PETER COLLIGNON:Well, I think we do have to go back to basics, including even simple things like hand washing. There are innumerable surveys that show that people often think it's a good idea but just don't get around to doing it, and by that I mean staff, doctors, nurses, medical staff in general. And in some ways, we're almost transfixed by many of the wonders of medical modern science, you know the modern machines, the modern interventions, the terrific things that can be done to help people.

But basic things like making sure we decrease as much as possible the number of bacteria on our hands, and particularly those that are more likely to cause disease, we forget that something simple like soap and water can make a lot of difference. And we need to change people's behaviour so that they do those things more often, and not only in hand washing but everything we do with patients and in the hospital environment. We use often commonsense approaches, but make sure it happens, to make sure the chance that anything will occur and there will be cross-infection, is minimised. We'll never get rid of the risk altogether because, obviously, whenever we do anything to anybody, there is a risk that's involved, but that's not to say we can't decrease the risk by putting in different procedures, different behaviour.

GORDON TAYLOR: Dr Stuart Levy is a leading international expert on the hazards of antibiotic misuse. Based at Boston's Tuft's University, he places much of the responsibility on us as patients.

STUART LEVY: I think we have lost a number of battles, and I .... that in terms of each patient and each community and each hospital. We've lost them, clearly we've lost them. If we didn't and if we were still ahead we wouldn't have this outcry worldwide, with even the World Health Organisation making it one of the major issues, public health issues of the century. It is clearly an issue for today and it is clearly at a time when we have not the upper ground. But what do we do? We have to look at how we've been using antibiotics and, when we've done that, and many of us have done it for many years, but more are looking at it now, we see how we have mishandled, misused and overused these drugs. Even people in their homes have misused these drugs, both by demanding them of their physicians, and better yet, getting them and then not using them totally, but storing them so that they don't have to go to see a physician, they just take it out of the medicine chest or out of their refrigerator and give it to any member of their family.

Just think of the numbers of bacteria out there that are affected by this misuse. I believe that 50 per cent of the problem in the developed world, and more so in the developing world, is consumer misuse of the antibiotic.

GORDON TAYLOR:So can we solve that problem? It suggests that we need a better relationship between doctor and patient.

STUART LEVY:You're absolutely right. We need a better relationship between doctor and patient; we need to the patient not to demand but rather to ask, 'Do I need the antibiotic? Do I have a bacterial infection?' We need to educate the patient that antibiotics are not the cure-all, that viruses and flus and colds are not antibiotic-treatable; we have to deal with them ourselves.

GORDON TAYLOR: Coordinating Producer is Linda McGinness; Technical Producers were Jeremy Moore and Mark Don. Research by Suzan Campbell. Background Briefing's Executive Producer is Kirsten Garrett. I'm Gordon Taylor.