Staphylococcus aureus (S. aureus) is a Gram positive (thick wall) bacterium that is believed to be carried by about one third of the general population and is responsible for common and serious diseases. A growing amount of medical literature suggest that Staphylococcus aureus enterotoxins (intestinal toxins)could affect airway disease including Asthma.
To further the WAF misson to improve our understanding of what drives Severe Asthma, the World Asthma Foundation reached out to Rodney Dietert, PhD for his thoughts on the topic of Asthma and Staphylococcus aureus.
Rodney Dietert, PhD is a Cornell University Professor Emeritus, Health Scientist Head of Translational Science + Education for SEED and the Author of the Human Super-Organism How the Microbiome is Revolutionizing the Pursuit of a Healthy Life
This is the first interview of three on the topic of Staphylococcus aureus with Rodney Dietert, Phd. We learn about:
* Connection between Asthma and Staph A
* Skin, nose and gut Microbiome
* Asthma and the immune system
World Asthma Foundation: Dr. Dietert, can you connect Staphylococcus Aureus or Staph A and Chronic Disease including Asthma for us?
Rodney Dietert, PhD: Yes, well, it’s very interesting because there’s a lot of research starting to come out on infectious agents and chronic diseases. We used to think that never the two shall meet but in fact, they do in many cases, either by inducing chronic diseases or by exacerbating those conditions.
Staph A, that is gram-positive bacterium, it is serious in terms of potential infections. We have it most often on the skin and in the nose. It can be either carried there or it can be a transient exposure. It also contributes to food poisoning. It’s one of the agents that, if contaminated, food can produce serious GI problems. It has a number of products that it makes including what are called enterotoxins or exotoxins. These can punch holes in cells. They can damage epithelial layers in the gut or in the airways.
They also are very interesting, in the case of Staph A or Staphylococcus aureus because some of these toxins can serve as allergens. They are actually sensitizing agents and that is the unknown, until recently, discovery, that when you’re looking for allergens that may contribute to asthma, you’d better include integral elements of that particular bacterium because that may be your allergen, that you may or may not have tested for.
World Asthma Foundation: Can you explain the interaction between the Microbiome, Staph A and Asthma?
Rodney Dietert, PhD: Well, as with any potential opportunistic pathogen, the status of our microbiome in the body sites that carry it, and that would be where we’re exposed to the environment, so the airways, respiratory system, the skin, the gut, the urogenital tract, the status of that microbiome is incredibly important in terms of whether those pathogens can gain a foothold and then produce an infection. That is absolutely the case with Staph A.
Breaking the skin may give it (an opportunity to infect) , or surgery (as well). You have Staph A, and particularly drug-resistant Staph A, (as) a potential risk with surgeries but, (also) I mentioned food poisoning, breaking the skin. Also, dysbiosis, we call it, or a problem with the microbiome in the nose really can result in (Staph A problems), not just chronic sinusitis or reoccurring infections, but asthma. (The bacterium) can be inducing the condition, (and/or) it can be exacerbating already existing asthma.
Rodney Dietert, PhD: (Staph A) has been identified as one of the major culprits that is in the nose and where it can gain a foothold, (it) can produce some real problems.
World Asthma Foundation: What’s the distinction between infection and colonization in the context of Staph A and Asthma?
Rodney Dietert, PhD: Well, colonization is really where it’s able to attach to the proximity of the epithelium, or maybe directly to the surface. It can then produce its toxins and damage the epithelium and also have a nutrient source and spread. The thing to keep in mind is your friendly bacteria, your microbiota, that are mutualistic bacteria, or commensals they’re also called, the ones that we take as probiotics. Those actually have something like double-digit processes they can use to block pathogens like Staph A. Their being in place and metabolizing, in this case in the nose, is really important.
There is a recent really beautiful study that was published looking at early life and looking at colonization by bacteria in the nose and the prognosis for those children to develop asthma or not and some of the parameters related to that. That is where you can really see that starting to think about Staph A and asthma is critical immediately at birth and in the early few months. That’s where some of these distinctions are made and where, unfortunately, you can set up the immune system for inflammation in the lung.
World Asthma Foundation: You have a background in Immmunotoxicology. Can you define this role?
Rodney Dietert, PhD: Immunotoxicity is basically any environmental or external directed alteration to the immune system, in a negative way, damage to the immune system. That damage can take all kinds of different forms. Now, I have to say in my earlier years as a professor in the era of AIDS, HIV and AIDS, everybody thought, well, it’s all immunosuppression. My mantra has been, I contend that there are very few things that produce (only) pure immunosuppression. Something goes down and usually something else goes up (within the immune system) quite frankly. That part of what goes up is (often) allergy, autoimmunity, and inflammatory disease.
We used to measure, in the earlier days of immunology, we’ll measure things and say, “Wow, the antibody levels are reduced,” or something like that. We weren’t measuring more complex indicators for auto-immunity allergic diseases like asthma and psoriasis, inflammatory conditions. Had we been doing that (measuring the more complex indicators of immune-inflicted chronic diseases), we would see that some things we thought that were either immunosuppressive or not (and deemed safe), were not actually where the excitement (most significant risk) was for damage to the immune system.
The damage (connected to improper immune enhancement/balance) can (lead to) self-inflicted disease produced largely by immune cells (that are) out of control and misregulated. When you’re talking about asthma, that’s where you are. (It) is (that) you have cells and mediators in the lung doing things out of balance that they shouldn’t be doing.
World Asthma Foundation: You advocate and have written extensively about Sustainable Healthcare. In fact, you write about the cost of chronic disease. Can you summarize the findings of the World Economics Council and Harvard study predicting that Chronic Disease will consume 48% of Global GDP by 2030?
Rodney Dietert, PhD: That’s worldwide net worth, and we can’t afford it. If you’re thinking about healthcare being sustainable and being available for people in the future, for our children, for our grandchildren, then we’ve got to do things differently. We should do a better job of preventing chronic diseases like asthma and we certainly should do a better job of managing these (chronic diseases) with the life course in mind.
When a child presents with asthma, the pediatrician quite frankly, in my opinion, should be asking, “What can I do for that child today? What can I do to prevent comorbid diseases 10, 20, 30, 40 years from now?” I think the second part of that we have not yet fully embraced and dealt with.
World Asthma Foundation: What would you like researchers to know about the relationship between Staph A and chronic disease?
Rodney Dietert, PhD: I think they need to realize again that the starting point, birth and the first few months, is the time to do something. (In early life) it is easier (to make the most significant changes) and (those actions taken during early development are) likely to be more permanent (as the infant ages). (Also, there is an opportunity to insulate that child from even some problems, maybe diet or otherwise, later in life that (otherwise) could be a risk factor.
That’s the time to do something. Where you get bigger bang for the buck, is early (in life). Researchers simply need to know to look for infectious agents that are involved with conditions like asthma and to start to realize that their management needs to start and stop with the microbes that are protecting the individual, the friendly microbes or microbiota, and to ensure that that is in balance.
If you’re hoping to nudge the immune system in a more useful way, you’re hoping to control inflammation, it’s my contention that if you don’t correct the microbiome, you’re going to be back in the same boat, on the leakyboat, (the) sinking boat, shortly, with your treatments.
There’s sort of a fingerprint of (the) respiratory microbiome, and particularly in the nose, that reflects asthma existing. There’s the chicken or egg question, which comes first, and what’s a result of (what)? Nevertheless, if you don’t actually address that (the respiratory microbiome which affects both risk of Staph A infection and lung immune status) in any meaningful way, then you’ve got to know that the tendency is there that (it is) going to snap back at some point. It’s going to bite you (with an elevated risk of and/or exacerbation of asthma) .