Drug-Resistant Bacteria Are Big Fans of E-Cigs
You, as a healthy or at least relatively healthy human (the rest of us will have to imagine), are not free of harmful pathogens. There's a massive universe of potentially bad creatures that we live with every day, that are simply kept at bay by our immune systems as a matter of course.
An example is the common fungus Candida albicans, which is found in about 80 percent of humans and for the vast majority, causes no problems. It's typically kept in check by the body's immune system and via competition with other microorganisms, like its bacteria housemates. If something happens, however, like the disappearance or weakening of one of those two limiting factors, either via immune system damage or bacterial colony damage, C. albicans is not just free to multiply, but also to change. It becomes virulent, pathogenic: instead of living with your body, it tries to take it over.
There are a lot of things like that, particularly different varieties of bacteria and fungi. But even viruses can behave as such, just living with you in relative peace for as long as it suits them. The herpes simplex virus, for example, goes to sleep for very long periods of latency and a human might never be aware they've been infected with it; it's been estimated that some 90 percent of all humans are hosts. To activate the virus' "bad side" it might just take some psychological stress or immune system damage. Even just sunlight exposure can do the trick.
And then there's methicillin-resistant Staphylococcus aureus (MRSA), the archvillain and progeny of the antibiotic resistance crisis. In a very large percentage of humans, it just hangs out too, living in relative peace, usually in the nasal cavity, while waiting for a good reason for an outbreak to become virulent and very bad. And according to research being presented this week at the 2014 American Thoracic Society International Conference, e-cigarettes might be one factor in not just setting MRSA off, but in making it even more resistant to antibiotic treatment.
The reason for the winding path to today's big research headline (besides it just being interesting) is to make the point that these would-be pathogens, like MRSA or Candida, are just all around you and, well, inside of you. Waiting. That they keep waiting is dependent on complex balancing acts; it's how an antibiotic drug can set off a fungal infection. One rich site of microorganism party times is your nasopharynx region, e.g. the place where your nasal passage connects to your throat, where all of the junk outside your body meets its first mucous membrane. This is ground zero for collisions between the inhaled outside world and the warm, wet insides of the body. So, when you take a drag of an e-cigarette, cigarette, or anything else at all, the nasopharynx takes all of it head-on.
The nasopharynx then is a gathering place for all sorts of infections, like the bacteria responsible for meningitis, the virus behind mononucleosis, and, yes, good old methicillin-resistant Staphylococcus aureus (MRSA). The researchers, led by the University of California at San Diego's Laura E. Crotty Alexander, looked at both normal cigarettes and e-cigarettes and their relative impacts on five key factors in the development of an otherwise peaceful MRSA colony to a full-blown, life-threatening infection: growth rate, susceptibility to damaging reactive oxygen species, surface charge, biofilm formation, and hydrophobicity, which influences how well bacteria can adhere to things.
Of those five, the most significant impacts the researchers found were to biofilm formation and surface charge. The change is surface charge means that immune cells lose their ability to attach their antimicrobal death proteins to the surfaces of the MRSA, while the increase in biofilm production both makes the bacteria more sticky—such that they can attach to your healthy tissues—and more protected from immune system defenses. In addition, the team found that the e-cig vapor "induces MRSA to produce acids as a defense mechanism within the first three hours of exposure, which raises similarities to their mechanism against nitric oxide, one of the components of innate immune responses to infection."
The going hypothesis for why this happens is that inhalation of e-cig vapor dramatically increases the pH of the nasopharynx environment, sending it from 7.4 to 8.4. That's high for both bacteria and for humans, and the result is new stress put upon the MRSA cells, which then go into danger mode. Danger mode for a bacterium looks an awful lot like attack mode from the perspective of a host human. Note that this is a shift in the opposite direction relative to regular cigarettes, which induce a slight drop in pH, to around 7.1.
Here's the caveat, or would-be caveat: E-cigs aren't quite at the level of plain cigarette smoke. With regular smoky cigs, you get a 10-fold increase in the surface charge changes seen in e-cigs. In mouse models of pneumonia, regular cigarette smoke-exposed MRSA had a four-fold increase in survival rates in the lungs, while e-cig vapor resulted in a three-fold increase.
The weight of this will likely depend on which e-cig argument you subscribe to. There's the Jenny McCarthy obliviousness—which might be interpreted as the "totally safe" pole—and there's the reasonably rational harm-reduction angle, in which e-cigs are touted not as a thing you smoke in the club to look cool, but as a thing you smoke because it's less harmful than the alternative of full-on combustion-based cigs.
However skeptical I am of the e-cig movement and its boosters, I do see the harm-reduction side and would be leery of anything that pushes people back to cigarettes. However, I'm also cognizant of the reality that harm-reduction is being used as a red herring by many boosters who just want to sell as many vaping devices as possible, which means not limiting to cessation. Never doubt that the industry wants new customers, not just its old customers switching to a new product.
Standing somewhere off to the side in the whole vaping discussion are doctors, who just want to give an honest answer to their patients. "As health care professionals, we are always being asked by patients, 'Would this be better for me?'" Crotty Alexander said in a press release. "In the case of smoking e-cigarettes, I hated not having an answer. While the answer isn't black and white, our study suggests a response: even if e-cigarettes may not be as bad as tobacco, they still have measurable detrimental effects on health."
An interesting thing about e-cigarettes is that, as far as nicotine delivery systems go, it's possible to regulate the chemistry of the product fairly closely. That means that it might be relatively easy to make them safer, if it's just a matter of manipulating their effect on the pH of your inner-nose. In an email, Crotty Alexander added, "I hope that by finding out how the e-cigarette vapor causes these changes, we can figure out how to change the e-cig juice to help make a safer product
An example is the common fungus Candida albicans, which is found in about 80 percent of humans and for the vast majority, causes no problems. It's typically kept in check by the body's immune system and via competition with other microorganisms, like its bacteria housemates. If something happens, however, like the disappearance or weakening of one of those two limiting factors, either via immune system damage or bacterial colony damage, C. albicans is not just free to multiply, but also to change. It becomes virulent, pathogenic: instead of living with your body, it tries to take it over.
There are a lot of things like that, particularly different varieties of bacteria and fungi. But even viruses can behave as such, just living with you in relative peace for as long as it suits them. The herpes simplex virus, for example, goes to sleep for very long periods of latency and a human might never be aware they've been infected with it; it's been estimated that some 90 percent of all humans are hosts. To activate the virus' "bad side" it might just take some psychological stress or immune system damage. Even just sunlight exposure can do the trick.
And then there's methicillin-resistant Staphylococcus aureus (MRSA), the archvillain and progeny of the antibiotic resistance crisis. In a very large percentage of humans, it just hangs out too, living in relative peace, usually in the nasal cavity, while waiting for a good reason for an outbreak to become virulent and very bad. And according to research being presented this week at the 2014 American Thoracic Society International Conference, e-cigarettes might be one factor in not just setting MRSA off, but in making it even more resistant to antibiotic treatment.
The reason for the winding path to today's big research headline (besides it just being interesting) is to make the point that these would-be pathogens, like MRSA or Candida, are just all around you and, well, inside of you. Waiting. That they keep waiting is dependent on complex balancing acts; it's how an antibiotic drug can set off a fungal infection. One rich site of microorganism party times is your nasopharynx region, e.g. the place where your nasal passage connects to your throat, where all of the junk outside your body meets its first mucous membrane. This is ground zero for collisions between the inhaled outside world and the warm, wet insides of the body. So, when you take a drag of an e-cigarette, cigarette, or anything else at all, the nasopharynx takes all of it head-on.
The nasopharynx then is a gathering place for all sorts of infections, like the bacteria responsible for meningitis, the virus behind mononucleosis, and, yes, good old methicillin-resistant Staphylococcus aureus (MRSA). The researchers, led by the University of California at San Diego's Laura E. Crotty Alexander, looked at both normal cigarettes and e-cigarettes and their relative impacts on five key factors in the development of an otherwise peaceful MRSA colony to a full-blown, life-threatening infection: growth rate, susceptibility to damaging reactive oxygen species, surface charge, biofilm formation, and hydrophobicity, which influences how well bacteria can adhere to things.
Of those five, the most significant impacts the researchers found were to biofilm formation and surface charge. The change is surface charge means that immune cells lose their ability to attach their antimicrobal death proteins to the surfaces of the MRSA, while the increase in biofilm production both makes the bacteria more sticky—such that they can attach to your healthy tissues—and more protected from immune system defenses. In addition, the team found that the e-cig vapor "induces MRSA to produce acids as a defense mechanism within the first three hours of exposure, which raises similarities to their mechanism against nitric oxide, one of the components of innate immune responses to infection."
The going hypothesis for why this happens is that inhalation of e-cig vapor dramatically increases the pH of the nasopharynx environment, sending it from 7.4 to 8.4. That's high for both bacteria and for humans, and the result is new stress put upon the MRSA cells, which then go into danger mode. Danger mode for a bacterium looks an awful lot like attack mode from the perspective of a host human. Note that this is a shift in the opposite direction relative to regular cigarettes, which induce a slight drop in pH, to around 7.1.
Here's the caveat, or would-be caveat: E-cigs aren't quite at the level of plain cigarette smoke. With regular smoky cigs, you get a 10-fold increase in the surface charge changes seen in e-cigs. In mouse models of pneumonia, regular cigarette smoke-exposed MRSA had a four-fold increase in survival rates in the lungs, while e-cig vapor resulted in a three-fold increase.
The weight of this will likely depend on which e-cig argument you subscribe to. There's the Jenny McCarthy obliviousness—which might be interpreted as the "totally safe" pole—and there's the reasonably rational harm-reduction angle, in which e-cigs are touted not as a thing you smoke in the club to look cool, but as a thing you smoke because it's less harmful than the alternative of full-on combustion-based cigs.
However skeptical I am of the e-cig movement and its boosters, I do see the harm-reduction side and would be leery of anything that pushes people back to cigarettes. However, I'm also cognizant of the reality that harm-reduction is being used as a red herring by many boosters who just want to sell as many vaping devices as possible, which means not limiting to cessation. Never doubt that the industry wants new customers, not just its old customers switching to a new product.
Standing somewhere off to the side in the whole vaping discussion are doctors, who just want to give an honest answer to their patients. "As health care professionals, we are always being asked by patients, 'Would this be better for me?'" Crotty Alexander said in a press release. "In the case of smoking e-cigarettes, I hated not having an answer. While the answer isn't black and white, our study suggests a response: even if e-cigarettes may not be as bad as tobacco, they still have measurable detrimental effects on health."
An interesting thing about e-cigarettes is that, as far as nicotine delivery systems go, it's possible to regulate the chemistry of the product fairly closely. That means that it might be relatively easy to make them safer, if it's just a matter of manipulating their effect on the pH of your inner-nose. In an email, Crotty Alexander added, "I hope that by finding out how the e-cigarette vapor causes these changes, we can figure out how to change the e-cig juice to help make a safer product
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