I see once again the “superbug” is in the news, with poor old North Shore Hospital attempting to control an outbreak by splitting up their wards. Having worked in such an environment, I know exactly how frustrating that can be for nursing staff. Reverse barrier nursing (gloves, gowns, caps and overshoes to protect the nurse rather than the patient) makes everything take twice as long. Doctors and hospital administrators also become frustrated because they often can’t admit patients to empty beds because the patient is “clean” and the room is “contaminated”. Or vice versa.
Extended Spectrum Beta Lactamase (ESBL) resistant bugs (superbugs) have really only been in the country for less than a decade but are already a real nuisance in hospitals. A contaminated patient is not normally at risk unless they are very sick or to be operated on. The ESBL bug is only a problem if it enters your bloodstream. Septicaemia (blood-borne infection) is fatal unless treated with an antibiotic, but ESBL is resistant to most, making it very hard to treat. Most people with ESBL, however, are merely carriers and are in no danger.
Microbiologists tend to blame the development of superbugs on the over-use of antibiotics. While this is true, I am not convinced that it is the overuse of antibiotics by GPs in the community that produces this sort of resistance, but rather the blind use of very broad spectrum antibiotics in hospital situations. Community organisms seem to maintain a certain level of resistance to an antibiotic and that level does not seem to rise or fall much. Despite the increase in MRSA and ESBL superbugs, most Staphylococcal infections of the skin seem to clear up with Augmentin, despite it’s being in use for 40 years, to use but one example. The levels of resistance and antibiotic recommendations for community diseases have barely changed over the last 20 years. In addition, people rarely seem to become ESBL positive in the community, even when they live with an ESBL family member. It seems to be a bug you almost entirely acquire in hospital
These two things suggest to me that it is not GPs handing out antibiotics for viral infections that causes the development of these resistant bacteria. Use of very-broad-spectum antibiotics in hospital increases every year. This is because one cannot wait for a microbiologist to tell you which type of bug and which type of antibiotic to use, if the patient is seriously ill. Bacterial cultures take days to get a result. Therefore one tends to simply hit the infection with everything you’ve got. The common practice is then to switch to the more specific antibiotic when the culture results return. I suspect that some bacteria manage to survive this massive onslaught for a couple of days and go on to be the ESBL of the future when the powerful antibiotics are stopped. I suspect that, if one carried the very-broad-spectrum regime on for a week to 10 days, this kind of resistance bug would not survive to form resistant colonies.
I firmly expect stroppy comments from microbiologists and pharmacists. Don’t disappoint me.
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Oct 25 09 1:03 pm
Even better-
Man-made antibiotics vs MRSA – Fail (except Augmentin?)
Bee vomit vs MRSA – kachingg
http://bio.waikato.ac.nz/honey/potential.shtml
On a personal note some UMF16+ manuka honey has completely wacked my stomach upsets that I’ve had for about 5 years right out of the park- wouldn’t go anywhere without it now.
Yeah. You don’t ever see a bear with diarrhoea, now, do you?
Oct 25 09 1:13 pm
I’d be running too fast to find out- if it caught me, what a way to go!
Oct 25 09 8:18 pm
I would advose against being blase about community organisms.
Have a look at how the emergence of the “community associated methicillin resistant Staphylococcus aureus” (CA-MRSA) has changed first line treatment for community skin and soft tissue infections in North America and Europe in the last three years. (a Medline search on CA-MRSA or USA-300 will throw up lots of papers). Not only is this a strain of Staph aureus which is resistant to all the penicillins (including Augmentin), but it has both an increased ability to spread from person to person and to cause serious, including life threatening infections in previously healthy people.
The USA-300 strain of CA-MRSA is in New Zealand, but so far fairly rare. In the USA, it is the commonest strain of Staph. aureus.
Oct 25 09 8:49 pm
All the more reason to promote the use of something completely natural and effective against most if not all super-bugs. Waikato researchers commented that they haven’t yet found a bug that was resistant to manuka honey with active UMF factor, and yet the use of it is not widespread except in some specialist burn units. Maybe someone should let the drug companies know- snort.
Oct 25 09 9:47 pm
I would challenge you to produce one good clinical study which shows that manuka honey is better than any other honey, or indeed any other hyperosmolar dressing in promoting wound healing. It works, but so do thers, and the mechanism is mainly the osmotic sucking out of tissue fluids (oedema).
The antimicrobial activity is, in my opinion, a red herring. Manuka, like every other plant, produces antibacterial and antifungal substances (Evolution – any plant which doesn’t will rot where it stands). Tens of thousands of antimicrobial substances from plants have been investigated for possible medical use, but the vast majority fail because at the concentration needed to have a useful effect, they are toxic to the host tissues.
The proponents of manuka honey are correct that honey (per se, not specifically manuka) promotes wound healing. They are also correct that manuka honey is more inhibitory to microbes in the petri dish than other honey. What they have not shown is that this greater antimicrobial activity matters in wound healing, nor, very importantly, have they shown that manuka honey is safe.
A rule that I have never seen fail is that if something kills all known germs, it also kills human tissue. (Similarly, for any medicine or supposed medicine: if it has pharmacological activity, it has side effects!)
My guess is that the toxic substance in manuka honey is not present in an adequate concentration in wounds either to cause harm or to have any beneficial effect.
Oct 25 09 10:20 pm
That’s a bit premature though, isn’t it. I mean the reason manuka honey is being used in burn units is because you get badly burnt patients who would otherwise die who are getting better from this stuff.
It also is being used to allow the healing of gangrenous wounds that normally would have resulted in amputations,and has successfully been used for the care of open wounds after cosmetic and facial surgery. The applications appear to be exciting (not put some stem cells in my knee and have my cartilage grow back exciting, but pretty good)
Have a hunt around the work of Dr PC Molan at the waikato university honey unit and other info- I think you will be surprised.
From the site:
“There is much anecdotal evidence to support its use, and randomised controlled clinical trials that have shown that honey is more effective than silver sulfadiazine and a polyurethane film dressing (OpSite®) for the treatment of burns.”
Oct 25 09 11:06 pm
Sorry, doesn’t answer my skepticism. I agree that there is evidence that honey (and such other hyperosmolar sugar solutions as treacle and molasses) is a good wound dressing. What I have not seen is anything that shows manuka honey to be superior to supermarket clover honey.
As for other dressings: silver sulfadiazine is pretty obsolete. I would be far more interested in a comparison with calcium alginate or hydrocolloid dressings.
To my cynical mind it is a great marketing story, but not a great medical one. Manuka honey used to be considered so vile tasting that apiarists would throw it away. A market has now been created for it, and at a price premium relative to other honey! I just don’t see the science to justify that premium.
I have looked. I prefer to base my opinion on peer-reviewed papers by researchers not dependent on funding from the makers of the products they are researching.
Oct 25 09 11:35 pm
Good luck finding one of those mythical ‘peer-reviewed papers from researchers not dependent on funding from the makers of the products they are researching’ for products in a doctor’s practice or hospital. You haven’t commented on whether there is any objective merit to anything said from Waikato University on the issue of active manuka honey vs ordinary honey.
You’re missing the point that the cost of research is so high that if pharma money doesn’t support it- it often doesn’t get done. Dr Molan was probably doing his research long before there was even a nickel to be made from it- who gives a crap about something we put on our toast anyway, and something that a bunch of house-wives think fixes a few scabs? The answer- now it’s our fastest growing industry.
I suggest to avoid the hype and the scam artists that you only bother buying that honey that the research unit used for their research- summerglow apiaries (tastes good too but still has that manuka tang). Only one producing pharmaceutical grade stuff apparently, and their prices are much better than anything you’ll see in the supermarket (or airport!). Next time the stomach gives you grief, it’s a great, cheap fix.
Oct 26 09 7:43 am
Here is a direct quote hidden near the bottom of a page on the Waikato research unit website:
“None of the results being obtained clinically should be considered evidence that Active Manuka Honey is more effective than other honey – a comparative clinical trial will be needed to establish that. Nevertheless, there are good theoretical reasons for choosing to use Active Manuka Honey with a good level of the non-peroxide antibacterial activity for management of wound infections.”
You can make a theoretical case for just about anything, and I don’t buy their theory.
Oct 26 09 2:22 pm
gp’s have a relatively limited number of antibiotics they can use.
i would be interested to know if the widespread use of advanced antibiotics in the veterinary industry has anything to do with the emergence of resistant organisms.
a microbiologist told me a couple of years ago he went to a vet conference where they were advertising 3rd generation cephalosporins for use in animals. the poor old gp’s in nz are still on the 1st generation!
Oct 26 09 2:47 pm
Wally, which generation a cephalosporin, or any other antibiotic, belongs to doesn’t determine its value. Few of the infections a GP will likely see in his practice should be treated with a third-generation cephalosporin – but many of them could be treated with a first-generation. For some infections good old penicillin G from 1942 is still the best drug.
I’d like to know for what indications the manufacturer was encouraging the vets to use a 3rd generation cephalosporin, though. That does ring alarm bells.
You have a point about the overuse of antibiotics in animal husbandry (not particularly in veterinary practice, but rather as feed supplements). I understand that the poultry industry in North America some years back was dosing birds with enrofloxacin (closely related to human drugs Noroxin, Ciproxin and others), which might have been part of the reason that that class of drugs are becoming less useful in practice. Richard, any comment?
Oct 26 09 6:26 pm
The giving of low doses of antimicrobials to animals over a prolonged period is the ideal experimental setup if one wants deliberately to generalt resistance. Whereever people have looked at it, animals from farms, or indeed countries in which it is usual to use antimicrobials as growth promoters carry higher proportions of resistant organisms in their bowels. Meat from the slaughterhouse is inevitably contaminated by faecal matter, so if you culture thouse plastic wrapped tasty chunks of meat at the supermarket, they will carry faecal bacteria.
If absoluttely scrupulous food hygiene is not practiced (and where is it?), bacteria will be transferred from raw meat to ready to eat food, and may colonise the eater’s bowel.
Even if the transferred bacterium is not a pathogen (that is, it doesn’t cause disease, and the vast majority of bacteria are not pathogens) the genes for resistance to antimicrobials are often on “transposable elements”, bits of DNA that can go from one bacterium to another, often only remotely related bacterium.
How often this happens, and how important it is for human disease are very difficult to say. Most bacteria are very fussy in terms of the hosts in whcih they can live, and the overwhelming majority of the bacteria in a load of animal faeces consumed with your salad will not be able to survive in the human bowel. Some, though, may do a bit of swapping of DNA before they die.
A few bacteria, however, do infect both humans and animals. The best studied of these is Campylobacter. Almost all cases of ciprofloxacin resistant campylobacteriosis diagnosed in Denmark (the country in which use of antibiotics as growth promoters has longest been banned) are in people who have eaten chicken imported into Denmark, not locally raised. Other studies, also in Europe, show that, while one is more likely to pick up a Campylobacter from organic free-range chicken, that Campylobacter is much less likely to be antibiotic resistant. There is similar evidence around antibiotic resistant Salmonella.
For some other intestinal organisms, such as the strains of Escherichia coli that cause urinary tract infection, there is somewhat weaker evidence linking resistance to animal husbandry practices.
For non-enteric organisms (for example Staphylococcus aureus), there is little or no evidence that animal husbandry practices affect resitance rates in humans.
Whatever happens on the farm, the biggest risks are in the intensive care units of hospitals (everyone on antibiotics, tubes in every orifice, lots of care procedures done by staff too busy to disinfect their hands before and after every patient contact, even though they know they should).
The spread of antimicrobial resistance requires not only the antimicrobial selective pressure which comes from the use and abuse of antibiotics, but also circumstances which allow for spread from one host to another, whether through poor food hygiene, poor household hygiene or lapses in hospital infection control. Only addressing both selective pressure AND spread do we have any hope of slowing the rise of resistance.
A bit off topic, but the third generation cephalosporin most used by New Zealand GPs will almost certainly be ceftriaxone, given as a single intramuscular injection for treatment of gonorrhoea. Only around three years ago, the first line drug would have been a single tablet of ciprofloxacin. When the gonococcus becomes resistant to third generation cephalosporins, there is no easy next option. A few such horribly resistant strains have been reported from Japan. They have still been susceptible enough to be treated with a higher dose of ceftriaxone – given by intravenous infusion – but for how much longer?