There is a certain kind of individual who dreams of retiring and opening a farm. The idea of escaping to the country, buying a small cottage and raising sheep and pigs. Oddly enough, many of these people appear to have been raised in the city, and have very little experience of mucking out a pig pen.
But the rural dream can turn into a nightmare. Especially in the case that we are about to discuss.
A 28 year old man was working with pigs. During the course of his work, he had to catch a piglet (ungreased). Pigs can actually run deceptively fast, reaching a top speed of 11 miles per hour.
So this task is difficult enough. But then we have to take into consideration that this was a baby pig, and that pig mothers can be very protective. Not only would one have to run fast enough to catch the piglet, but fast enough to escape the enraged sow that will no doubt be in hot pursuit.
Such was the fate of the subject of this paper. In the process of trying to capture a piglet, it's mother wrought the worst kin of vengeance. It clamped its jaws around his crotch.
Now I should clarify that it did not bite his penis off. Instead, it inflicted an injury known as a "Degloving ". If I were to draw you a picture, it would probably be one with an adorable snake wearing an equally adorable custom made jumper pulled off of it. Except the jumper being removed is actually human skin, and the snake is actually a writhing collection of bloody viscera.
The surgeons cleaned out the wound and realised that most of the "degloved" skin had already died. They replaced it with a skin graft from the patients thigh. The paper tells us that the patient could resume his sexual life 1 month after the operation.
We may never truly know the full story of the pig. Perhaps it broke it's bonds, and roams free in the countryside exacting traumatic revenge on nervous male adolescents. Perhaps it prowls the corridors of parliament, adding fears of literal emasculation as well as metaphorical emasculation to liberal democrats. As you read this, you may notice the quiet sensation, a warm wet breath across your nether regions, and you realise that it is standing under your desk, just waiting for you to look down so it can see your expression when it strikes.
Georgiou P., Liakopoulos P., Gamatsi E. & Komninakis E. (2001). Degloving Injury of The Penis from Pig Bite, Plastic and Reconstructive Surgery, 108 (3) 807. DOI: 10.1097/00006534-200109010-00052
Field of Science
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From Valley Forge to the Lab: Parallels between Washington's Maneuvers and Drug Development4 weeks ago in The Curious Wavefunction
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Political pollsters are pretending they know what's happening. They don't.4 weeks ago in Genomics, Medicine, and Pseudoscience
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Course Corrections5 months ago in Angry by Choice
TMI Friday: Oh, How long has that been there ?
I remember searching through an old jacket, and finding a torchlight within it. It had been in that jacket so long that I forgot that I had even lost it. I'm sure we've all been in that situation of finding something long after it had been lost, that combination of surprise and relief when it is found.
Ahmad M. Intravaginal vibrator of long duration., European journal of emergency medicine : official journal of the European Society for Emergency Medicine, PMID: 11989500
So let us put ourselves in the shoes of the 62 year old widow who wondered into an Accident and Emergency unit in Stockport. She had been experiencing horrible smelling bloody discharge from her "Intimate area". But after a bit of questioning, it turned out that there were some complications. It was a long term issue, and she had been too embarrassed to seek medical help.
It was her new boyfriend who had convinced her to go to hospital and finally see a Doctor about it.
Three years before, she was using a vibrator when the device got lodged up her vagina. She was completely unable to extract it.
I was told of a similar situation, of a gentleman who had come into A & E with a similar problem. The gentleman was in intense pain, and after the surgeons had worked out the cause, they tired removing it. They soon realised that this would be impossible. Because the Vibrator he had inserted into his body was still fully activated. It was too far inside the man for anyone to reach the switch and turn it off. So they had to keep this gentleman waiting in the emergency room until the damned things batteries ran out.
So this ladies decision to wait may not have been a completely silly decision. However, leaving a vibrator marinating in her vagina for three years before seeking medical attention was a little bit extreme.
In fact, it was incredibly dangerous. It had worked its way through the vaginal wall and into the rectum, causing a horrible condition known as a rectal fistula. The damage the vibrator had caused to her digestive system was so severe that she had to undergo a colostomy. This is usually done when a large part of the intestine is no longer able function, and a new opening needs to be made to allow faeces to leave the digestive system. Although drastic, this was enough to stop her condition get any worse.
And so ends Girls month. I hope you've enjoyed reading about all of the embarrassing things that the "fairer" sex get up to. Next week we'll be returning to the embarrassing world of men. But make no mistake, if I hear an embarrassing story involving a woman, I will not wait to have another girls month to tell you about it.
And so ends Girls month. I hope you've enjoyed reading about all of the embarrassing things that the "fairer" sex get up to. Next week we'll be returning to the embarrassing world of men. But make no mistake, if I hear an embarrassing story involving a woman, I will not wait to have another girls month to tell you about it.
#MicroTwJC: Bacteria in SPAAAAACE !!
In 2011, Stephen Hawking declared that humanity may not survive to see the next millenium "without escaping beyond our fragile planet." That may seem like an overly dramatic statement, but there is some truth to it. As long as we confine ourselves to earth, we tie our fate to the fate of this world. It is a big uncaring universe containing unstoppable threats that can any time blast us from the surface of this world.
If we want to ensure that our species survives, we need to colonise space. This is a challenge that no other life form (as far as we know) has achieved. There are no environments on earth that can possibly prepare us for the fatigues of space. We evolved without having to worry about radiation, within the constant grasp of gravity. If we are to make space our home, we need to figure out how to adapt our physiology to make it hospitable.
The paper being reviewed in this weeks Microbiology Twitter Journal Club aims to investigate how our bacteria will be affected when we go into space. Our gut encompasses an entire bacterial ecosystem that is essential to our health, and that we still barely understand. We know that when bacteria adhere to the surfaces within the body, they aggregate together into convoluted structures known as biofilms. These colonies allow the bacteria to communicate with each other, and survive within the harsh environments of the body. A biofilms are critical to bacterial survival within the body, and by proxy, could be crucial to our survival. But what happens to these films when they are grown in space ?
How do we even find out ?
It's simple. We go there.
TMI Friday: I'll never look at carrots the same way again
Carrots are a brilliant and versatile vegetable.You can grate them into salads, you can roast them and you can even try frying them. We humans have such great degrees of ingenuity that we are forever finding new uses for this vegetable.
However, today we'll be talking about one freak incident in which one person found a novel use for a carrot, with unfortunate consequences.
It begins with a corpse and a mystery. The woman was discovered in bed, dead. There were signs of trauma on the body. So what killed this woman ?
An autopsy revealed air bubbles in the woman's heart, as well as air bubbles within the surviving blood vessels. This woman had been killed by an air embolism. An air embolism occurs when air enters the circulatory system, and blocks up the passage of blood into the heart. It's similar to air locks that happen in plumbing systems. Only this can be deadly. Because you need blood to flow through your body to live.
But what caused this air embolism ? Perhaps the carrot that was found nestled between the dead woman's thighs may be a clue. They tested the surface of the carrot using a PAP staining kit, and found that vaginal cells were on its surface. This carrot had been inserted into the woman's vagina at some point prior to death.
But did it play a role in her death ?
It is important to note that this woman had an intrauterine device as well. This woman's death may have been an unfortunate freak accident that occurred when she masturbated with the carrot. The theory is that the intrauterine device damaged the surface of the vaginal walls, exposing blood vessels. The carrot acted like a piston, pushing air into the vagina, and into the exposed blood, causing air bubbles to enter the blood stream.
This freak set of events turned an innocent tryst with a carrot into an event with fatal consequences.
Marc B., Chadly A. & Durigon M. (1990). Fatal air embolism during female autoerotic practice, International Journal of Legal Medicine, 104 (1) 59-61. DOI: 10.1007/BF01816487
Antibiotics & Agriculture part 5: Stokstad's Genie
When Robert Stokstad discovered antibiotic growth promoters, he was operating in industrial farming's nascent era. In the 1920's, farmers realised that with the right levels of vitamin supplements, they could raise chickens indoors safely cocooned from the outside environment. But this innovation came with some costs, as chicks born in this environment had poor survival, and didn't grow as fast as they did in the wild.
Stokstad's discovery of growth promoters was like a wish come true. Just by adding a low dose antibiotics, we could help more chicks survive into adulthood, and allow them to grow to full size whilst saving money feeding them. But, just like in any morality tale, wishes can come with consequences.
It turns out that the wholesale saturation of the industrial farming environment with antibiotics provided the perfect incubator for antibiotic resistance.
There have been a number of dangerous outbreaks of antibiotic resistant pathogens which can be traced directly to their usage in the agricultural industry. Salmonella, E.coli and even some strains of Staphylococcus aureus have acquired resistance to antibiotics from farms.
Even more disturbing is that agricultural antibiotic usage has increased the numbers of resistance genes in the overall environment. These genes have been proven to transfer between different bacterial species. Even if the bacteria they reside in are themselves not a threat to human health, these genes can be transferred to pathogens that are threats.
The mounting evidence of this threat prompted some countries to act.
In 1984, after hearing reports that consumer confidence in meat safety was dropping, due to the antibiotic resistance threat, Swedish farmers requested a ban on all growth promoters. They were the first country to implement a ban, but they were not the last.
If you wanted to show the pitfalls of banning agricultural growth promoters, you can find no better example than that of the Netherlands. In these cases, the ban came into force before the farmers could improve infection control practices. As a result, they were beset by outbreaks of bacterial disease that required the use of more therapeutic antibiotics. In the Netherlands, this meant that there was no net change in the amount of antibiotics sold to the agricultural industry.
Sweden was not immune to this effect. Whilst the initial results of the ban showed promising reductions in antibiotic use, it was also characterised by increases in disease outbreaks on farms. The appetite for therapeutic antibiotics increased in direct response to these outbreaks, until it eventually rose to pre-ban levels.
When Denmark embarked on a similar plan to ban antibiotic growth promoters, they did so with an eye on the experiences of previous nations. With this system, they managed to reduce antibiotic use by around 90%. Somehow their ban managed to reduce infections without changing the welfare of their animals, and still managed to keep the Danish pig industry competitively priced.
So why did the Danish experience differ so much from the experiences of other nations ?
When they implemented the ban, they also ensured there was a comprehensive monitoring system in place to send out the alarm if new antibiotic resistant bacteria were produced, and a way of regulating the doses of therapeutic antibiotics given by veterinarians. They didn't ban all of their growth promoters at once. They first rolled back the use of avoparcin in 1995, then followed it with a ban on virginiamycin in 1998, and then finally a ban on all growth promoters in 2000. This gave the farmers the time to change the way they did farming to compensate for the loss of these growth promoters.
In preparation for the ban, Danish farms implemented basic infection controls. The routine disinfection of workers clothes, the workers themselves and their vehicles is now standard in many countries, to prevent the transfer of diseases between farms. Veterinary vigilance became watch words, with herds regularly inspected to ensure that outbreaks were caught and dealt with as early as possible.
The authorities also madee sure that every part of their system was committed to the reduction of antibiotic use. Veterinarians were prevented from directly selling antibiotics to farmers, they could only issue prescriptions, removing a potential conflict of interest. The numbers of antibiotic prescriptions given to specific herds was carefully monitored. Farms that were consuming high levels antibiotics could be spotted more easily under this system, and given the appropriate support.
Denmark also brought in new laws which changed the way that their pigs were raised and weaned. They recognised that a lot of their infection problems could be traced to their piglets being weaned too early and forced into an infection riddled world without the protective antibodies in their mother's milk, and immune systems not fully able to deal with the infection riddled world into which they were being exposed.
When Denmark put its ban in place, it did so with the knowledge that a massive full spectrum ban on antibiotic growth promoters could potentially harm its precious pork industry. When they drew up plans to ban antibiotic growth promoters, they paid attention to the science. They thought carefully about the consequences of the ban, and how they could best compensate for these effects using the best science available. Then they brought in the ban slowly, allowing farmers and veterinarians time to adapt to the new system, and ensured that the incentives presented by this new system were geared to limiting further usage of antibiotics.
In 2006, a broad ban on all antibiotic growth promoters was implemented across the European Union in response to mounting public pressure. Countries across the EU are now for better or for worse have to adapt their farming strategies to compensate for the loss of antibiotic growth promoters.
There are signs that the ban is working. The numbers of antibiotic resistance genes in the environment are decreasing.
But let's not pop the champagne corks just yet. There are a few problems with these bans that require further inspection.
In the initial stages of all the bans, outbreaks of bacterial disease often occur more frequently. In some scenarios, Veterinarians can be reticent in prescribing more antibiotics to treat these diseases, leaving the animals to suffer longer, and exposing them to greater risk of death. Improvements to infection control and animal husbandry only go so far in preventing outbreaks of disease. The situation in some countries is so bad that banning agricultural antibiotics actually increases the numbers of therapeutic antibiotics being used. The levels of antibiotics in some cases reaches the levels seen before the ban.
Every time an antibiotic is used, be it in animals, or in humans, has a chance of increase the numbers of resistant strains in the population. Taking this viewpoint, you may say that some of these bans have no effect at all. But you would be ignoring a crucial detail.
In his Nobel prize speech, Fleming himself gave a warning about how mass underdosing could trigger the creation of antibiotic resistant strains, yet within ten years underdosing became standard practice within the agricultural industry.
It is crucial that we make sure that antibiotics are always used responsibly. The key reason why banning antibiotic growth promoters was that it was one demonstrable case in which antibiotics were used irresponsibly.
The other key problem with these bans is that no one knows the extent to which it will affect human health. It should prevent new strains of antibiotic resistant bacteria evolving on farms, such as livestock associated MRSA, or antibiotic resistant Enterococci.
However, expecting these bans to eliminate all antibiotic resistance is to unfairly place all of the blame on farming and agriculture for our current situation. The primary environment in which antibiotic resistant bacteria most commonly evolve, and where they are at their most dangerous, is found in hospitals. Any antibiotic resistance genes which have already made the jump into this environment are here to stay. Regulating antibiotic use in hospitals is difficult, because that is where we, as humans, need them the most. As much as we may worry about how the price of meat may be affected, if we cannot accept that relatively minor sacrifice, we will not be able to accept the changes and the costs needed to eradicate antibiotic resistance from our healthcare systems.
The genie of antibiotic resistance is out of the bottle, but it wasn't just Robert Stokstad who had a hand in releasing it. We may sneer at growth promoters because they are the worst example of how we have squandered antibiotics. We may lament at how some faceless evil within the agri-business made the calculation that our future is worth trading for cheaper meat today. But we all had a hand in shaking the genie out of its bottle. We still have a hand in determining our own future. Even those of us who currently live in Europe may soon be inundated with american meat raised antibiotic growth promoters if certain trade agreements are successful. They will once again be faced with the same choice facing everyone else in the world, the choice between a full stomach today or better health tomorrow.
References
The WHO's internal evaluation on the termination of antimicrobial growth promoters in Denmark
http://www.who.int/gfn/en/Expertsreportgrowthpromoterdenmark.pdf
Danish Pig production in a European Context
http://www.lf.dk/~/media/lf/Aktuelt/Publikationer/Svinekod/LFEUBenchUK110318.ashx
Cogliani C., Goossens H. & Greko C. (2011). Restricting Antimicrobial Use in Food Animals: Lessons from Europe, Microbe, 6 (6) 274-279. DOI:
Stokstad's discovery of growth promoters was like a wish come true. Just by adding a low dose antibiotics, we could help more chicks survive into adulthood, and allow them to grow to full size whilst saving money feeding them. But, just like in any morality tale, wishes can come with consequences.
It turns out that the wholesale saturation of the industrial farming environment with antibiotics provided the perfect incubator for antibiotic resistance.
There have been a number of dangerous outbreaks of antibiotic resistant pathogens which can be traced directly to their usage in the agricultural industry. Salmonella, E.coli and even some strains of Staphylococcus aureus have acquired resistance to antibiotics from farms.
Even more disturbing is that agricultural antibiotic usage has increased the numbers of resistance genes in the overall environment. These genes have been proven to transfer between different bacterial species. Even if the bacteria they reside in are themselves not a threat to human health, these genes can be transferred to pathogens that are threats.
The mounting evidence of this threat prompted some countries to act.
In 1984, after hearing reports that consumer confidence in meat safety was dropping, due to the antibiotic resistance threat, Swedish farmers requested a ban on all growth promoters. They were the first country to implement a ban, but they were not the last.
If you wanted to show the pitfalls of banning agricultural growth promoters, you can find no better example than that of the Netherlands. In these cases, the ban came into force before the farmers could improve infection control practices. As a result, they were beset by outbreaks of bacterial disease that required the use of more therapeutic antibiotics. In the Netherlands, this meant that there was no net change in the amount of antibiotics sold to the agricultural industry.
Sweden was not immune to this effect. Whilst the initial results of the ban showed promising reductions in antibiotic use, it was also characterised by increases in disease outbreaks on farms. The appetite for therapeutic antibiotics increased in direct response to these outbreaks, until it eventually rose to pre-ban levels.
When Denmark embarked on a similar plan to ban antibiotic growth promoters, they did so with an eye on the experiences of previous nations. With this system, they managed to reduce antibiotic use by around 90%. Somehow their ban managed to reduce infections without changing the welfare of their animals, and still managed to keep the Danish pig industry competitively priced.
So why did the Danish experience differ so much from the experiences of other nations ?
When they implemented the ban, they also ensured there was a comprehensive monitoring system in place to send out the alarm if new antibiotic resistant bacteria were produced, and a way of regulating the doses of therapeutic antibiotics given by veterinarians. They didn't ban all of their growth promoters at once. They first rolled back the use of avoparcin in 1995, then followed it with a ban on virginiamycin in 1998, and then finally a ban on all growth promoters in 2000. This gave the farmers the time to change the way they did farming to compensate for the loss of these growth promoters.
In preparation for the ban, Danish farms implemented basic infection controls. The routine disinfection of workers clothes, the workers themselves and their vehicles is now standard in many countries, to prevent the transfer of diseases between farms. Veterinary vigilance became watch words, with herds regularly inspected to ensure that outbreaks were caught and dealt with as early as possible.
The authorities also madee sure that every part of their system was committed to the reduction of antibiotic use. Veterinarians were prevented from directly selling antibiotics to farmers, they could only issue prescriptions, removing a potential conflict of interest. The numbers of antibiotic prescriptions given to specific herds was carefully monitored. Farms that were consuming high levels antibiotics could be spotted more easily under this system, and given the appropriate support.
Denmark also brought in new laws which changed the way that their pigs were raised and weaned. They recognised that a lot of their infection problems could be traced to their piglets being weaned too early and forced into an infection riddled world without the protective antibodies in their mother's milk, and immune systems not fully able to deal with the infection riddled world into which they were being exposed.
When Denmark put its ban in place, it did so with the knowledge that a massive full spectrum ban on antibiotic growth promoters could potentially harm its precious pork industry. When they drew up plans to ban antibiotic growth promoters, they paid attention to the science. They thought carefully about the consequences of the ban, and how they could best compensate for these effects using the best science available. Then they brought in the ban slowly, allowing farmers and veterinarians time to adapt to the new system, and ensured that the incentives presented by this new system were geared to limiting further usage of antibiotics.
In 2006, a broad ban on all antibiotic growth promoters was implemented across the European Union in response to mounting public pressure. Countries across the EU are now for better or for worse have to adapt their farming strategies to compensate for the loss of antibiotic growth promoters.
There are signs that the ban is working. The numbers of antibiotic resistance genes in the environment are decreasing.
But let's not pop the champagne corks just yet. There are a few problems with these bans that require further inspection.
In the initial stages of all the bans, outbreaks of bacterial disease often occur more frequently. In some scenarios, Veterinarians can be reticent in prescribing more antibiotics to treat these diseases, leaving the animals to suffer longer, and exposing them to greater risk of death. Improvements to infection control and animal husbandry only go so far in preventing outbreaks of disease. The situation in some countries is so bad that banning agricultural antibiotics actually increases the numbers of therapeutic antibiotics being used. The levels of antibiotics in some cases reaches the levels seen before the ban.
Every time an antibiotic is used, be it in animals, or in humans, has a chance of increase the numbers of resistant strains in the population. Taking this viewpoint, you may say that some of these bans have no effect at all. But you would be ignoring a crucial detail.
In his Nobel prize speech, Fleming himself gave a warning about how mass underdosing could trigger the creation of antibiotic resistant strains, yet within ten years underdosing became standard practice within the agricultural industry.
It is crucial that we make sure that antibiotics are always used responsibly. The key reason why banning antibiotic growth promoters was that it was one demonstrable case in which antibiotics were used irresponsibly.
The other key problem with these bans is that no one knows the extent to which it will affect human health. It should prevent new strains of antibiotic resistant bacteria evolving on farms, such as livestock associated MRSA, or antibiotic resistant Enterococci.
However, expecting these bans to eliminate all antibiotic resistance is to unfairly place all of the blame on farming and agriculture for our current situation. The primary environment in which antibiotic resistant bacteria most commonly evolve, and where they are at their most dangerous, is found in hospitals. Any antibiotic resistance genes which have already made the jump into this environment are here to stay. Regulating antibiotic use in hospitals is difficult, because that is where we, as humans, need them the most. As much as we may worry about how the price of meat may be affected, if we cannot accept that relatively minor sacrifice, we will not be able to accept the changes and the costs needed to eradicate antibiotic resistance from our healthcare systems.
The genie of antibiotic resistance is out of the bottle, but it wasn't just Robert Stokstad who had a hand in releasing it. We may sneer at growth promoters because they are the worst example of how we have squandered antibiotics. We may lament at how some faceless evil within the agri-business made the calculation that our future is worth trading for cheaper meat today. But we all had a hand in shaking the genie out of its bottle. We still have a hand in determining our own future. Even those of us who currently live in Europe may soon be inundated with american meat raised antibiotic growth promoters if certain trade agreements are successful. They will once again be faced with the same choice facing everyone else in the world, the choice between a full stomach today or better health tomorrow.
References
The WHO's internal evaluation on the termination of antimicrobial growth promoters in Denmark
http://www.who.int/gfn/en/Expertsreportgrowthpromoterdenmark.pdf
Danish Pig production in a European Context
http://www.lf.dk/~/media/lf/Aktuelt/Publikationer/Svinekod/LFEUBenchUK110318.ashx
Cogliani C., Goossens H. & Greko C. (2011). Restricting Antimicrobial Use in Food Animals: Lessons from Europe, Microbe, 6 (6) 274-279. DOI:
Antibiotics & Agriculture Part 4: The Transfer of Antibiotic Resistance
The patient was in dire condition. A forty year old woman from Michigan, she had suffered badly from diabetes, kidney failure and a number of complications related to those diseases. Two years after she had started dialysis, disaster struck. She developed painful foot ulcers, and an infection in her leg that was so severe that the whole leg had to be amputated. What was worse was that immediately after the operation, her amputation wound became infected, with Staphylococcus aureus. In her only stroke of luck that day, the Staphylococcus aureus was susceptible to antibiotics. But the next year, the foot ulcers were back, and she required even more amputations, as well as treatments to prevent the bacterial infections causing these ulcers from becoming fatal.
The catheter that linked her blood to the hospital's dialysis machine, the replacement for her riven kidneys, provided Methicillin-Resistant Staphylococcus aureus with easy entry into her blood. There was only one antibiotic that could stop this MRSA infection. Vancomycin was given to the patient while the physicians removed the infected catheter. In its place, the physicians used a number of temporary catheters, to ensure that the patient could still use the dialysis machine.
But a number of these catheters also became infected. When the physicians examined these catheters, they realised that against all odds, things had taken a turn for the worse. They discovered that the Staphylococcus aureus on this catheter had been joined by Vancomycin resistant Enterococci. Now the Staphylococcus aureus were resistant to Vancomycin too. They searched all of the possible options that could have lead to this situation, and it was the DNA evidence that revealed what had happened. The Vancomycin resistant Enterococci, commonly found in the community but rarely infectious, had given its resistance genes to MRSA.
This was the first of a series of outbreaks of VRSA that occurred in Michigan, and all of them had a similar theme. A person with an MRSA infection would spontaneously develop full blown resistance to vancomycin out of nowhere. The only commonality in all of these cases was the presence of vancomycin resistant Enterococci both before and during these cases. So how did vancomycin resistant Enterococci pass along their resistance to MRSA ?
The answer lies with DNA molecules known as plasmids.
These are rings of DNA which can carry genes between different bacteria. The exchange of plasmids between bacteria is a key driver of bacterial evolution, as it allows species to share genes between eachother. They enable bacteria to acquire new traits from other bacteria in the vicinity, which can allow them to adapt to their environment in new ways. In this case, the vancomycin resistance "trait" was carried on a plasmid in Enterococci, and this plasmid could be very easily transferred to Staphylococcus aureus. The high abundance of Enterococci with vancomycin resistance increased the probability of this occurring.
This constant transfer of plasmids between bacteria plays a key role in their evolution. It allows a bacterium entering a new environment to steal some useful genes from the bacteria that are already there, helping it adapt to that niche. This is what happened in the cases discussed above, and is one of the more insidious methods through which antibiotic resistance can spread.
As we've seen in the previous posts, the unregulated use (and in some cases regulated use) of antibiotics in agriculture leads to the evolution of new resistant strains of bacteria. These strains can exchange this resistance using plasmids. The transfer of these plasmids to human pathogens is a major threat to human health.
Making things worse is that some plasmids can carry multiple resistance genes, rendering a variety of different antibiotics useless. The problem with using antibiotics in agriculture comes primarily from increasing the net amount of these non-pathogenic bacteria with resistance genes.
In the above case study, we have seen that Enterococci can exchange its resistance with Staphylococcus aureus. But we only know about Enterococci because on rare occasions, they can cause disease in humans. We don;t keep a track of all of the bacteria that don't cause disease. These are the bacteria that live in our bodies, that help us digest food and maintain an immune system. we are constantly exchanging these bacteria with our environmental surroundings.
They live under the radar, and nobody notices when they develop antibiotic resistance. Since they never cause disease in humans, we never need to prescribe antibiotics against them. The only time they would encounter sustained levels of antibiotics is on a farm, where they are constantly infused into the feeds of their animal hosts. Here they can evolve new resistances, and when they get transferred to humans, can exchange their antibiotic resistances with the bacteria they find in their new niche.
It is difficult for us to tell what kind of resistances an invading pathogen could potentially pick up from these bacteria.
To use an analogy, these silent bacteria may act as weapons merchants, hoarding resistances until the can share them with one of our potential enemies.
One way for researchers to investigate this is to simply take a snapshot of bacteria within an area, and just test for the resistance genes. Instead of looking for the weapons merchants, they are focussing on checking for the weapons.
With this technique, the scientists directly checked for the presence of resistance genes in an environment. This is known as the “resistome”.
Recently a group of researchers took it upon themselves to catalogue the “resistome” of three different countries. They compared the types of resistances they found in different countries to the way antibiotics were used in each of them.
The types of antibiotics that bacteria were resistant to were slightly different in each of the three countries they investigated (USA, Spain and Denmark). The antibiotics to which bacteria were most commonly resistant were the ones that were approved for use in animals. Antibiotic resistances were lowest in the places that had the ban in place for the longest time.
This all indicates that the agricultural use of antibiotics has contributed to the creation of a number of antibiotic resistant bacteria, but increased the number of resistance genes in our environment available for other pathogens to become resistant.
The mountain of evidence is indisputable. There is no doubt that new strains of antibiotic resistant bacteria owe their genesis to the reckless use of the drugs on farms. But is it fair for farms to take on the full brunt of the blame for the fall of antibiotics ? Would we not have antibiotic resistant bacteria in our hospitals even if the farms had banned them ?
I'll be dealing with this question in the conclusion of this series next time.
To be continued.....
References
Chang S., Sievert D.M., Hageman J.C., Boulton M.L., Tenover F.C., Downes F.P., Shah S., Rudrik J.T., Pupp G.R. & Brown W.J. & Infection with vancomycin-resistant Staphylococcus aureus containing the vanA resistance gene., The New England journal of medicine, PMID: 12672861
Zhu W., Murray P.R., Huskins W.C., Jernigan J.A., McDonald L.C., Clark N.C., Anderson K.F., McDougal L.K., Hageman J.C. & Olsen-Rasmussen M. & (2010). Dissemination of an Enterococcus Inc18-Like vanA Plasmid Associated with Vancomycin-Resistant Staphylococcus aureus, Antimicrobial Agents and Chemotherapy, 54 (10) 4314-4320. DOI: 10.1128/AAC.00185-10
Forslund K., Sunagawa S., Kultima J.R., Mende D., Arumugam M., Typas A. & Bork P. (2013). Country-specific antibiotic use practices impact the human gut resistome., Genome research, PMID: 23568836
The catheter that linked her blood to the hospital's dialysis machine, the replacement for her riven kidneys, provided Methicillin-Resistant Staphylococcus aureus with easy entry into her blood. There was only one antibiotic that could stop this MRSA infection. Vancomycin was given to the patient while the physicians removed the infected catheter. In its place, the physicians used a number of temporary catheters, to ensure that the patient could still use the dialysis machine.
But a number of these catheters also became infected. When the physicians examined these catheters, they realised that against all odds, things had taken a turn for the worse. They discovered that the Staphylococcus aureus on this catheter had been joined by Vancomycin resistant Enterococci. Now the Staphylococcus aureus were resistant to Vancomycin too. They searched all of the possible options that could have lead to this situation, and it was the DNA evidence that revealed what had happened. The Vancomycin resistant Enterococci, commonly found in the community but rarely infectious, had given its resistance genes to MRSA.
This was the first of a series of outbreaks of VRSA that occurred in Michigan, and all of them had a similar theme. A person with an MRSA infection would spontaneously develop full blown resistance to vancomycin out of nowhere. The only commonality in all of these cases was the presence of vancomycin resistant Enterococci both before and during these cases. So how did vancomycin resistant Enterococci pass along their resistance to MRSA ?
The answer lies with DNA molecules known as plasmids.
These are rings of DNA which can carry genes between different bacteria. The exchange of plasmids between bacteria is a key driver of bacterial evolution, as it allows species to share genes between eachother. They enable bacteria to acquire new traits from other bacteria in the vicinity, which can allow them to adapt to their environment in new ways. In this case, the vancomycin resistance "trait" was carried on a plasmid in Enterococci, and this plasmid could be very easily transferred to Staphylococcus aureus. The high abundance of Enterococci with vancomycin resistance increased the probability of this occurring.
This constant transfer of plasmids between bacteria plays a key role in their evolution. It allows a bacterium entering a new environment to steal some useful genes from the bacteria that are already there, helping it adapt to that niche. This is what happened in the cases discussed above, and is one of the more insidious methods through which antibiotic resistance can spread.
As we've seen in the previous posts, the unregulated use (and in some cases regulated use) of antibiotics in agriculture leads to the evolution of new resistant strains of bacteria. These strains can exchange this resistance using plasmids. The transfer of these plasmids to human pathogens is a major threat to human health.
Making things worse is that some plasmids can carry multiple resistance genes, rendering a variety of different antibiotics useless. The problem with using antibiotics in agriculture comes primarily from increasing the net amount of these non-pathogenic bacteria with resistance genes.
In the above case study, we have seen that Enterococci can exchange its resistance with Staphylococcus aureus. But we only know about Enterococci because on rare occasions, they can cause disease in humans. We don;t keep a track of all of the bacteria that don't cause disease. These are the bacteria that live in our bodies, that help us digest food and maintain an immune system. we are constantly exchanging these bacteria with our environmental surroundings.
They live under the radar, and nobody notices when they develop antibiotic resistance. Since they never cause disease in humans, we never need to prescribe antibiotics against them. The only time they would encounter sustained levels of antibiotics is on a farm, where they are constantly infused into the feeds of their animal hosts. Here they can evolve new resistances, and when they get transferred to humans, can exchange their antibiotic resistances with the bacteria they find in their new niche.
It is difficult for us to tell what kind of resistances an invading pathogen could potentially pick up from these bacteria.
To use an analogy, these silent bacteria may act as weapons merchants, hoarding resistances until the can share them with one of our potential enemies.
One way for researchers to investigate this is to simply take a snapshot of bacteria within an area, and just test for the resistance genes. Instead of looking for the weapons merchants, they are focussing on checking for the weapons.
With this technique, the scientists directly checked for the presence of resistance genes in an environment. This is known as the “resistome”.
Recently a group of researchers took it upon themselves to catalogue the “resistome” of three different countries. They compared the types of resistances they found in different countries to the way antibiotics were used in each of them.
The types of antibiotics that bacteria were resistant to were slightly different in each of the three countries they investigated (USA, Spain and Denmark). The antibiotics to which bacteria were most commonly resistant were the ones that were approved for use in animals. Antibiotic resistances were lowest in the places that had the ban in place for the longest time.
This all indicates that the agricultural use of antibiotics has contributed to the creation of a number of antibiotic resistant bacteria, but increased the number of resistance genes in our environment available for other pathogens to become resistant.
The mountain of evidence is indisputable. There is no doubt that new strains of antibiotic resistant bacteria owe their genesis to the reckless use of the drugs on farms. But is it fair for farms to take on the full brunt of the blame for the fall of antibiotics ? Would we not have antibiotic resistant bacteria in our hospitals even if the farms had banned them ?
I'll be dealing with this question in the conclusion of this series next time.
To be continued.....
References
Chang S., Sievert D.M., Hageman J.C., Boulton M.L., Tenover F.C., Downes F.P., Shah S., Rudrik J.T., Pupp G.R. & Brown W.J. & Infection with vancomycin-resistant Staphylococcus aureus containing the vanA resistance gene., The New England journal of medicine, PMID: 12672861
Zhu W., Murray P.R., Huskins W.C., Jernigan J.A., McDonald L.C., Clark N.C., Anderson K.F., McDougal L.K., Hageman J.C. & Olsen-Rasmussen M. & (2010). Dissemination of an Enterococcus Inc18-Like vanA Plasmid Associated with Vancomycin-Resistant Staphylococcus aureus, Antimicrobial Agents and Chemotherapy, 54 (10) 4314-4320. DOI: 10.1128/AAC.00185-10
Forslund K., Sunagawa S., Kultima J.R., Mende D., Arumugam M., Typas A. & Bork P. (2013). Country-specific antibiotic use practices impact the human gut resistome., Genome research, PMID: 23568836
TMI Friday: Perfume, is there anything it can't do ?
We've all been there (I assume). You've caught the eye of someone at a party, or some other social gathering, and you've felt that instant attraction. And before you know it you've both drank yourselves stupid, and blurrily stumble towards some form of sexual activity. You'll both probably regret it tomorrow, but there'll be a lot of things you'll regret tomorrow, such as those evil drinks with the umbrellas in them. As you lock together in a clumsy lustful fumble, you realise that the emergency condom you'd kept in your wallet for the past decade had finally crumbled to dust. What do you do ?
Chapman G.W. An unusual intravaginal foreign body., Journal of the National Medical Association, PMID: 6471118
The year is 1984, Orwell's dystopia failed to materialise, but Prince was riding high in the charts and Ghostbusters was ruling the Box Office. A 20 year old woman arrived at the outpatient clinic the day after the night of passion. She and her partner had been faced with the conundrum I described above. with no condoms available, what could they do to satiate their mutual lust ?
Luckily , one of them had a perfume bottle, which they used for *ahem* stimulation. Unluckily, during the course of this stimulation, the perfume cap came loose from the rest of the perfume bottle, and became lodged in the woman's vagina. It was for this reason that the woman had to go to hospital. After taking an X-ray of the object, the physicians gave the patient some local anaesthesia, and pulled the offending object out with a speculum. Fortunately it turned out okay for the patient.
Can we just decide right now that bottles and genitalia don't go together ?
Antibiotics & Agriculture Part 3: The Spread of Resistant Bacteria
The application of antibiotics to livestock has provided a boon to the agricultural industry. Unfortunately an outbreak of Salmonella showed that this application could have some untoward side effects. The farmers and veterinarians not only failed to contain this outbreak of Salmonella, but botched the antibiotic treatment so thoroughly that a multi-drug resistant strain of this pathogen emerged and spread to humans.
Such was the outcry in response to this outbreak that the government set up the Swann report, which attempted to promote more responsible usage of antibiotics. Even though the 1964 outbreak was primarily a result of improper medication for farm animals, the use of antibiotic growth promoters emerged as a specific concern. One of the sole achievements of this report was to separate the antibiotics used in humans to those used in animals, with specific restrictions on the use of antibiotic growth promoters.
Other countries experienced similar issues. An investigation in the US found that between 1971-1983, the majority of outbreaks of Multi-drug resistant Salmonella stemmed from contact with either farms or animal products. These antibiotic resistant Salmonella proved to be more lethal than their antibiotic sensitive counterparts. In 1977 the FDA decided that it was no longer safe to use certain antibiotics as growth promoters. They tried to stop front-line antibiotics such as penicillin and tetracycline being used as agricultural growth promoters. But for reasons that are unknown, they never followed up on their declarations. It is likely that the FDA simply didn't have the resources or the public support to pass such a law.
In contrast, Northern Europe had begun to implement restrictions on the usage of antibiotics in livestock. Often these restrictions consisted of allowing only one set of antibiotics for the agricultural industry and one for the medical community. But this soon encountered a major setback.
Clinicians began to encounter Vancomycin resistant strains of Enterococci. Vancomycin is often the drug of last resort, and was supposedly tightly regulated so as to prevent resistance developing. These outbreaks often occurred in hospitals, but not always. When doctors examined patients to find out where this bacterium was coming from, they found something surprising. The source of these Vancomycin resistant Enterococci infections originated from the community. The doctors redoubled their efforts to work out the source of this infection. They checked farm animals, food from shops, sewage outflows, and any other possible place where Enterococci could hide. What they found surprised them. They found this bacterium in farm animals and food sources and the sewage outflow. They found that not only were these hospital outbreaks traceable to these community sources, but there was a veritable reservoir of vancomycin strains out there that had not yet reached the hospital. But this presented a puzzle.
Vancomycin was only available to hospitals. In accordance with laws, the farms in the area were using different antibiotics. So why were these bacteria in the community, who should never have even seen Vancomycin, suddenly becoming resistant to it ?
The truth is that the bacteria had not specifically developed a resistance to Vancomycin. They had developed a resistance to a drug named Avoparcin. The vancomycin resistance was just a lucky side effect of this. You may not have heard of Avoparcin. This is because it was never meant to be used in humans. It was one of the few antibiotics allowed to be used as a growth promoter. What no-one had foreseen was that it's structure was so similar to vancomycin that it would breed resistance to it. And as a result, one of the key antibiotics to stop hospital outbreaks was rendered useless against the Enterococci.
But why should we worry about these bacteria. Enterococci aren't much of a threat outside of the hospital, and even then they tend not to have multiple drug resistances. Whilst we can worry about Salmonella, we should remember that the best ways of treating Salmonella don't require antibiotics at all. So why should the spread of these antibiotic resistant bacteria be a worry for us ?
To Be Continued.....
References
Holmberg S., Wells J. & Cohen M. (1984). Animal-to-man transmission of antimicrobial-resistant Salmonella: investigations of U.S. outbreaks, 1971-1983, Science, 225 (4664) 833-835. DOI: 10.1126/science.6382605
Bates J., Jordens J.Z. & Griffiths D.T. (1994). Farm animals as a putative reservoir for vancomycin-resistant enterococcal infection in man, Journal of Antimicrobial Chemotherapy, 34 (4) 507-514. DOI: 10.1093/jac/34.4.507
O'Brien T. (2002). Emergence, Spread, and Environmental Effect of Antimicrobial Resistance: How Use of an Antimicrobial Anywhere Can Increase Resistance to Any Antimicrobial Anywhere Else, Clinical Infectious Diseases, 34 (s3) S78-S84. DOI: 10.1086/340244
http://docs.nrdc.org/health/files/hea_12032301a.pdf
Such was the outcry in response to this outbreak that the government set up the Swann report, which attempted to promote more responsible usage of antibiotics. Even though the 1964 outbreak was primarily a result of improper medication for farm animals, the use of antibiotic growth promoters emerged as a specific concern. One of the sole achievements of this report was to separate the antibiotics used in humans to those used in animals, with specific restrictions on the use of antibiotic growth promoters.
Other countries experienced similar issues. An investigation in the US found that between 1971-1983, the majority of outbreaks of Multi-drug resistant Salmonella stemmed from contact with either farms or animal products. These antibiotic resistant Salmonella proved to be more lethal than their antibiotic sensitive counterparts. In 1977 the FDA decided that it was no longer safe to use certain antibiotics as growth promoters. They tried to stop front-line antibiotics such as penicillin and tetracycline being used as agricultural growth promoters. But for reasons that are unknown, they never followed up on their declarations. It is likely that the FDA simply didn't have the resources or the public support to pass such a law.
In contrast, Northern Europe had begun to implement restrictions on the usage of antibiotics in livestock. Often these restrictions consisted of allowing only one set of antibiotics for the agricultural industry and one for the medical community. But this soon encountered a major setback.
Clinicians began to encounter Vancomycin resistant strains of Enterococci. Vancomycin is often the drug of last resort, and was supposedly tightly regulated so as to prevent resistance developing. These outbreaks often occurred in hospitals, but not always. When doctors examined patients to find out where this bacterium was coming from, they found something surprising. The source of these Vancomycin resistant Enterococci infections originated from the community. The doctors redoubled their efforts to work out the source of this infection. They checked farm animals, food from shops, sewage outflows, and any other possible place where Enterococci could hide. What they found surprised them. They found this bacterium in farm animals and food sources and the sewage outflow. They found that not only were these hospital outbreaks traceable to these community sources, but there was a veritable reservoir of vancomycin strains out there that had not yet reached the hospital. But this presented a puzzle.
Vancomycin was only available to hospitals. In accordance with laws, the farms in the area were using different antibiotics. So why were these bacteria in the community, who should never have even seen Vancomycin, suddenly becoming resistant to it ?
The truth is that the bacteria had not specifically developed a resistance to Vancomycin. They had developed a resistance to a drug named Avoparcin. The vancomycin resistance was just a lucky side effect of this. You may not have heard of Avoparcin. This is because it was never meant to be used in humans. It was one of the few antibiotics allowed to be used as a growth promoter. What no-one had foreseen was that it's structure was so similar to vancomycin that it would breed resistance to it. And as a result, one of the key antibiotics to stop hospital outbreaks was rendered useless against the Enterococci.
But why should we worry about these bacteria. Enterococci aren't much of a threat outside of the hospital, and even then they tend not to have multiple drug resistances. Whilst we can worry about Salmonella, we should remember that the best ways of treating Salmonella don't require antibiotics at all. So why should the spread of these antibiotic resistant bacteria be a worry for us ?
To Be Continued.....
References
Holmberg S., Wells J. & Cohen M. (1984). Animal-to-man transmission of antimicrobial-resistant Salmonella: investigations of U.S. outbreaks, 1971-1983, Science, 225 (4664) 833-835. DOI: 10.1126/science.6382605
Bates J., Jordens J.Z. & Griffiths D.T. (1994). Farm animals as a putative reservoir for vancomycin-resistant enterococcal infection in man, Journal of Antimicrobial Chemotherapy, 34 (4) 507-514. DOI: 10.1093/jac/34.4.507
O'Brien T. (2002). Emergence, Spread, and Environmental Effect of Antimicrobial Resistance: How Use of an Antimicrobial Anywhere Can Increase Resistance to Any Antimicrobial Anywhere Else, Clinical Infectious Diseases, 34 (s3) S78-S84. DOI: 10.1086/340244
http://docs.nrdc.org/health/files/hea_12032301a.pdf
#MicroTwJC : The Creation of a Superbug
The year was 2004. The patient was a 6 month old baby girl. She was about to enter thoracic surgery, when the doctors found that she was harbouring methicillin resistant Staphylococcus aureus. Now, in most western hospitals, the origin of this bacterium would not be a mystery. But this was a hospital based in the Netherlands. The Dutch have a "search and destroy" mentality when it comes to dealing with superbugs, and have been very successful at keeping their hospitals free of MRSA. They wanted it to stay that way. They had to find the source of this MRSA, and put a stop to it. The hospital equipment was scrutinised for any traces of the bacterium. None could be found.
They eliminated the MRSA from the baby, and then sent her home with her parents. But when they followed up, the baby was once again colonised with MRSA. They went through the same process again and again, until they realised that the baby was continuously being re-infected with the bacterium from an unknown source. The doctors found that the babies parents were also carriers of MRSA. but where did they get the disease from ? If it wasn't coming from the hospital, then where was it coming from ?
It turned out that the family lived on a farm raising pigs. The pigs were tested. They were the source of the MRSA.
Other pigs on different farms in that area also carried this strain of MRSA. A number of other cases of farmers and vets catching MRSA off their pigs. They concluded that farmers were 760x more likely to get an MRSA infection than any other Dutch people. Further research revealed that 39% of pigs entering a slaughterhouse carried MRSA. Hospitals in close proximity to pig farms tended to see more patients with MRSA than hospitals that were far from pig farms. This MRSA appears to be different from the hospital associated MRSA's we are more familiar with. It is primarily carried by pigs, and was a leading cause of MRSA infection in the Netherlands.
So now we know that pigs can carry MRSA, it is time to ask an important question. How did they get MRSA ? How did this particular strain evolve ? These are the questions that this weeks #MicroTwJC paper aims to answer.
They eliminated the MRSA from the baby, and then sent her home with her parents. But when they followed up, the baby was once again colonised with MRSA. They went through the same process again and again, until they realised that the baby was continuously being re-infected with the bacterium from an unknown source. The doctors found that the babies parents were also carriers of MRSA. but where did they get the disease from ? If it wasn't coming from the hospital, then where was it coming from ?
It turned out that the family lived on a farm raising pigs. The pigs were tested. They were the source of the MRSA.
Other pigs on different farms in that area also carried this strain of MRSA. A number of other cases of farmers and vets catching MRSA off their pigs. They concluded that farmers were 760x more likely to get an MRSA infection than any other Dutch people. Further research revealed that 39% of pigs entering a slaughterhouse carried MRSA. Hospitals in close proximity to pig farms tended to see more patients with MRSA than hospitals that were far from pig farms. This MRSA appears to be different from the hospital associated MRSA's we are more familiar with. It is primarily carried by pigs, and was a leading cause of MRSA infection in the Netherlands.
So now we know that pigs can carry MRSA, it is time to ask an important question. How did they get MRSA ? How did this particular strain evolve ? These are the questions that this weeks #MicroTwJC paper aims to answer.
TMI Friday: I'll tell you where you can stick that Bratz doll !
I missed the whole "Bratz" craze, on account of not being a pre-teen girl at the time it happened. But I am aware that it existed, and that there were some out there who disapproved of it. I heard that there was something of a "Bratz" controversy, because the toys were "oversexualized" and presented an unrealistic body image, as opposed to Barbie dolls. Because Barbie doesn't present an unrealistic body image or is overly sexual, obviously.
One four year old child, who showed up to an emergency room with trouble in her genital area. After questioning the child, and her mother, the surgeons could not figure out what happened. So they took an X-ray, which showed a pair of legs, curiously without feet. This clued the physicians into the brand of doll in question. Bratz Dolls have interchangeable feet, to allow different shoe designs to be used with each doll and so girls can re-enact the final scene of Saw, minus Cary Elwes performance.
It turned out that this girl had stuck a Bratz Doll up her vagina for reasons that may never become clear. I still have no idea why I ate toilet paper when I was four, and probably never will. I hadn't even learned to spell "Logic" at that age, let alone know how to apply it. The theory was that she was mimicking her mother, whom she had seen inserting a tampon. Which is probably the most damning criticism of a Bratz doll as I've seen anywhere.
I mean if the accident occurred during the course of play, it would almost be understandable. It's like getting a Boba Fett action figure lodged in your partners rectum whilst re-enacting the Sarlacc scene from Return of the Jedi, as opposed to it being the closest available object scratch their haemarrhoids. One of those reasons implies that the toy was still fulfilling its function, the other indicates that it was just a convenient piece of plastic.
Someshwar J., Lutfi R. & Nield L.S. (2007). The Missing "Bratz" Doll, Pediatric Emergency Care, 23 (12) 897-898. DOI: 10.1097/pec.0b013e31815c9dd2
One four year old child, who showed up to an emergency room with trouble in her genital area. After questioning the child, and her mother, the surgeons could not figure out what happened. So they took an X-ray, which showed a pair of legs, curiously without feet. This clued the physicians into the brand of doll in question. Bratz Dolls have interchangeable feet, to allow different shoe designs to be used with each doll and so girls can re-enact the final scene of Saw, minus Cary Elwes performance.
It turned out that this girl had stuck a Bratz Doll up her vagina for reasons that may never become clear. I still have no idea why I ate toilet paper when I was four, and probably never will. I hadn't even learned to spell "Logic" at that age, let alone know how to apply it. The theory was that she was mimicking her mother, whom she had seen inserting a tampon. Which is probably the most damning criticism of a Bratz doll as I've seen anywhere.
I mean if the accident occurred during the course of play, it would almost be understandable. It's like getting a Boba Fett action figure lodged in your partners rectum whilst re-enacting the Sarlacc scene from Return of the Jedi, as opposed to it being the closest available object scratch their haemarrhoids. One of those reasons implies that the toy was still fulfilling its function, the other indicates that it was just a convenient piece of plastic.
Someshwar J., Lutfi R. & Nield L.S. (2007). The Missing "Bratz" Doll, Pediatric Emergency Care, 23 (12) 897-898. DOI: 10.1097/pec.0b013e31815c9dd2
Antibiotics & Animals Part 2: The First Warnings
In the previous post, we were wowed by the miraculous discovery that antibiotics could improve the growth and well being of farmed animals, such as pigs and baby chicks. The use of these growth promoters enabled farmers to save money on animal feed and improve the health of their animals. Soon, nearly 50% of all antibiotic sales went to the agricultural industry. Whilst there were some concerns over this unregulated use triggering the development of antibiotic resistant bacteria, without evidence these fell on deaf ears. This would soon change.
We begin this chapter of the story at the Enteric Reference laboratory. The job of this reference laboratory was to receive and catalogue samples of bacteria obtained from intestinal infections occurring around the country. It was during the 1960's that they began to receive samples from concerned farmers.
The environments on intensive farms of this era could best be described as overcrowded factories for disease. The farmers had noticed that calves were particularly prone to getting diarrhoeal infections. The bacteria causing these infections was Salmonella typhimurium, the bacterium responsible for human typhoid disease. This was not only a threat to the health of the herd, and those who interacted with them. Calves were dying. The Salmonella outbreaks needed to be brought under control. This is where it all started to go wrong.
There were two methods that were used to put a stop to Salmonella on these farms. The first method was to use high doses antibiotics to treat visibly sick cattle. The second method was to give lower doses of antibiotics to the rest of the visibly healthy herd, to prevent them getting ill. I say "visibly" because cows can carry Salmonella without showing any symptoms, so it is likely that plenty of the cows with Salmonella received the lower doses of antibiotic.
Unbeknownst to the veterinarians, they were creating the perfect environment for bacteria to develop resistance.
Antibiotic resistant strains began to make their first appearance in the beginning of 1963, when a strain developed resistance to sulfonamides and streptomycin. A year later these bacteria had become resistant to six more antibiotics.
Soon, this multi-resistant strain of Salmonella began to spread to humans. The Enteric reference laboratory received over 500 samples of this same bacterial strain, obtained from human infections. The antibiotics that would normally used in these situations turned out to be useless. This outbreak provided dramatic evidence of the hazards of utilising antibiotics in agriculture. The UK government was forced into action
In 1969, the Swann committee convened to change the way we used antibiotics, so that this kind of outbreak would never be repeated. They recommended that a quasi-non governmental organisation (Quango) be created, which would act to oversee the use of antibiotics for both humans and animals. It was there to increase transparency, to make sure that people knew what antibiotics were being used for, and how much they were used. It would bring together the usage of both veterinary and medical antibiotics under one authority. This co-ordination would enable scientists to better understand the threat of resistance in all of its facets.
Whilst the committee’s job was to regulate the use of antibiotics in both humans and animals, it ran into a number of problems. But the various different interest groups involved in antibiotics had no compulsion to co-operate. The committee had no real power to control the use of antibiotics, nor did it have any resources to investigate the impact of antibiotic overuse. Eventually it died a quiet death, having never quite lived up to the promise of its birth.
To be Continued NextTuesday... Thursday...
Anderson E.S. (1968). Drug Resistance in Salmonella Typhimurium and its Implications, BMJ, 3 (5614) 333-339. DOI: 10.1136/bmj.3.5614.333
(1981). Death of a quango., BMJ, 282 (6274) 1413-1414. DOI: 10.1136/bmj.282.6274.1413-a
http://www.guardian.co.uk/society/2006/mar/22/health.science
We begin this chapter of the story at the Enteric Reference laboratory. The job of this reference laboratory was to receive and catalogue samples of bacteria obtained from intestinal infections occurring around the country. It was during the 1960's that they began to receive samples from concerned farmers.
The environments on intensive farms of this era could best be described as overcrowded factories for disease. The farmers had noticed that calves were particularly prone to getting diarrhoeal infections. The bacteria causing these infections was Salmonella typhimurium, the bacterium responsible for human typhoid disease. This was not only a threat to the health of the herd, and those who interacted with them. Calves were dying. The Salmonella outbreaks needed to be brought under control. This is where it all started to go wrong.
There were two methods that were used to put a stop to Salmonella on these farms. The first method was to use high doses antibiotics to treat visibly sick cattle. The second method was to give lower doses of antibiotics to the rest of the visibly healthy herd, to prevent them getting ill. I say "visibly" because cows can carry Salmonella without showing any symptoms, so it is likely that plenty of the cows with Salmonella received the lower doses of antibiotic.
Unbeknownst to the veterinarians, they were creating the perfect environment for bacteria to develop resistance.
Antibiotic resistant strains began to make their first appearance in the beginning of 1963, when a strain developed resistance to sulfonamides and streptomycin. A year later these bacteria had become resistant to six more antibiotics.
Soon, this multi-resistant strain of Salmonella began to spread to humans. The Enteric reference laboratory received over 500 samples of this same bacterial strain, obtained from human infections. The antibiotics that would normally used in these situations turned out to be useless. This outbreak provided dramatic evidence of the hazards of utilising antibiotics in agriculture. The UK government was forced into action
In 1969, the Swann committee convened to change the way we used antibiotics, so that this kind of outbreak would never be repeated. They recommended that a quasi-non governmental organisation (Quango) be created, which would act to oversee the use of antibiotics for both humans and animals. It was there to increase transparency, to make sure that people knew what antibiotics were being used for, and how much they were used. It would bring together the usage of both veterinary and medical antibiotics under one authority. This co-ordination would enable scientists to better understand the threat of resistance in all of its facets.
Whilst the committee’s job was to regulate the use of antibiotics in both humans and animals, it ran into a number of problems. But the various different interest groups involved in antibiotics had no compulsion to co-operate. The committee had no real power to control the use of antibiotics, nor did it have any resources to investigate the impact of antibiotic overuse. Eventually it died a quiet death, having never quite lived up to the promise of its birth.
To be Continued Next
Anderson E.S. (1968). Drug Resistance in Salmonella Typhimurium and its Implications, BMJ, 3 (5614) 333-339. DOI: 10.1136/bmj.3.5614.333
(1981). Death of a quango., BMJ, 282 (6274) 1413-1414. DOI: 10.1136/bmj.282.6274.1413-a
http://www.guardian.co.uk/society/2006/mar/22/health.science
Antibiotics & Agriculture Part 1: The Discovery of Growth Promoters
This story begins with Robert Stokstad, an agricultural scientist brought up on a Californian poultry farm . He had started his career fighting against malnutrition in chicks. He had found that a haemorraghic disease in chicks was in fact caused by malnutrition. He had followed this up by examining the diet of baby chicks, to work out which parts of the diet are the most essential, and which of those, if neglected could lead to disease. He was one of the first to discover that folic acid is an important component of nutrition in chicks, before people realised it’s importance for humans.
It was at Lederle pharmaceuticals, whilst working with Thomas Juke, that he made another significant discovery about the right things to feed baby chicks. He had found during his work that feeding chicks a diet of vegetables alone was not enough. In fact, many chicks would end up dying on this diet. If they were to survive, then some degree of animal protein was needed. Other people working in his field had found that adding a small amount of “sardine meal” to the mix helped this. But then in a later paper, those same researchers, Hammond and Titus, found that mixing in cow manure produced a similar effect. Yes, you read that right, there were people feeding chicks cow manure, and found that it was more healthy than feeding them a diet of just vegetables.
It was known at the time that vitamin B12 was a key factor needed for chicks to grow, and that often the vegetable diets given to these chicks did not have enough of it. So Stokstad and Juke fed the chicks different mixtures of foods, and looked at how well they grew afterwards. One of the foods they included was a bacterium, Streptomyces aureofaciens, which they grew up and dried out and added to the feeds of the chicks. This was to work out why the cow manure turned out to be such a great dietary supplement. Stokstad knew that manure is full of bacteria, and that bacteria could produce B12. So the reason that cow manure was good for chicks was that it was a source of B12.
But Stokstad was not the sort to rule anything out. He decided to compare the potency of Streptomyces aureofaciens against B12 purified from liver extract. He found that the purified liver extract improved the growth of the chicks, nearly doubling their final weight. But when he fed the chicks Streptomyces aureofaciens , he discovered that they grew far faster and bigger than the ones fed with just the liver extract. This growth spurt was about more than vitamin B12. Streptomyces aureofaciens was producing something else that was boosting the growth of these chicks. So what was this mysterious factor which made these chicks grow up so well ?
It was a compound known then as aureomycin, and it was amongst the first tetracycline antibiotics ever discovered. It was also one of the first antibiotic growth promoters. Other researchers were also beginning to discover the benefits of antibiotics in promoting the growth of animals. The use of antibiotics as feed additives caught on like wildfire.
One of the first to express their concerns over the growth of this industry was Robert Wrigglesworth, who in 1952 wrote a letter to the British Medical Journal
To Be Continued.....
References
STOKSTAD E.L.R. & JUKES T.H. (1949). The multiple nature of the animal protein factor., The Journal of biological chemistry, PMID: 18135798
Shane B. & Carpenter K. (1997). E. L. Robert Stokstad, Journal of Nutrition, (127) 199-201. DOI:
Wigglesworth R. (1952). Value of Organic Manures, BMJ, 1 (4772) 1357-1358. DOI: 10.1136/bmj.1.4772.1357-c
It was at Lederle pharmaceuticals, whilst working with Thomas Juke, that he made another significant discovery about the right things to feed baby chicks. He had found during his work that feeding chicks a diet of vegetables alone was not enough. In fact, many chicks would end up dying on this diet. If they were to survive, then some degree of animal protein was needed. Other people working in his field had found that adding a small amount of “sardine meal” to the mix helped this. But then in a later paper, those same researchers, Hammond and Titus, found that mixing in cow manure produced a similar effect. Yes, you read that right, there were people feeding chicks cow manure, and found that it was more healthy than feeding them a diet of just vegetables.
It was known at the time that vitamin B12 was a key factor needed for chicks to grow, and that often the vegetable diets given to these chicks did not have enough of it. So Stokstad and Juke fed the chicks different mixtures of foods, and looked at how well they grew afterwards. One of the foods they included was a bacterium, Streptomyces aureofaciens, which they grew up and dried out and added to the feeds of the chicks. This was to work out why the cow manure turned out to be such a great dietary supplement. Stokstad knew that manure is full of bacteria, and that bacteria could produce B12. So the reason that cow manure was good for chicks was that it was a source of B12.
But Stokstad was not the sort to rule anything out. He decided to compare the potency of Streptomyces aureofaciens against B12 purified from liver extract. He found that the purified liver extract improved the growth of the chicks, nearly doubling their final weight. But when he fed the chicks Streptomyces aureofaciens , he discovered that they grew far faster and bigger than the ones fed with just the liver extract. This growth spurt was about more than vitamin B12. Streptomyces aureofaciens was producing something else that was boosting the growth of these chicks. So what was this mysterious factor which made these chicks grow up so well ?
It was a compound known then as aureomycin, and it was amongst the first tetracycline antibiotics ever discovered. It was also one of the first antibiotic growth promoters. Other researchers were also beginning to discover the benefits of antibiotics in promoting the growth of animals. The use of antibiotics as feed additives caught on like wildfire.
One of the first to express their concerns over the growth of this industry was Robert Wrigglesworth, who in 1952 wrote a letter to the British Medical Journal
We have the prospect of more antibiotics being sold in the USA, as growth promoters for food in farm animals than are used for clinical medicine.But at the time, these kinds of concerns were brushed aside, with some justification. So what if the bacteria that infect livestock become slightly resistant to antibiotics ? The bacteria that live within pigs and chicken don’t pose a problem to the health of people, because the only time that those aforementioned bacteria could possibly come into contact with us is after being thoroughly cooked. Right ?
To Be Continued.....
References
STOKSTAD E.L.R. & JUKES T.H. (1949). The multiple nature of the animal protein factor., The Journal of biological chemistry, PMID: 18135798
Shane B. & Carpenter K. (1997). E. L. Robert Stokstad, Journal of Nutrition, (127) 199-201. DOI:
Wigglesworth R. (1952). Value of Organic Manures, BMJ, 1 (4772) 1357-1358. DOI: 10.1136/bmj.1.4772.1357-c
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