Del writes: (re: episode 77)
I was looking forward to this discussion, after hearing you hint about it in a previous podcast. As a practicing ID doc, I have been fascinated by the difference in pain induced by cellulitis from presumed or proven Staph or Strep infections. I see some patients whose pain resolves in a day or so after antibiotics, and some fewer patients who have a much more protracted course of pain, with tenderness to minimal touch or change in position. I have suspected that different isolates produce different toxins to explain these clinical differences, as my clinical judgement and experience argues that patient personality differences or 'pain thresholds' are simply not enough explanation for the variation I see. It also seems to "be there, or not be there," more distinctly than a simple continuum would explain. I am grateful for the basic science work being done in the field at present, and for your discussion.
Thanks to you all for the work you put into this podcast. I am learning every week, and finding connections in areas I would have never before considered.
All the best,
Del DeHart MD FACP
Associate Professor of Medicine
Michigan State University
I realize that this is a bit behind the times but I have two questions related to beta-lactamase (hope I got that right) form episode 6 - "Antibacterial Therapy with Bacteriophage".
1) We all know that the proliferation of bacterial resistance to antibiotics has a direct influence on infection recovery in humans and animals. What I'm pretty sure most people forget is that most antibiotics began their "careers" as part of microbial defense systems. Are you folks aware of any studies looking at the effects of increasing antibiotic resistance in environmental microbiomes? I would think that this human-induced change has got to be skewing microbial populations and interactions. Indeed, I'm having trouble even imagining what the impacts on the microbial and, therefore macrobial world might be.
2) During your discussion of beta-lactamase gene development in the environment, I thought of a possible counter that might help us continue to use beta-lactam antibiotics a little longer. Are you aware of any groups who are researching anti-beta-lactamase drugs that could be added to antibiotics allowing the beta-lactams to retain some effectiveness against resistant microbes? If someone developed a low-toxicity drug that had a significantly higher and, one would like, non-reversible affinity for beta-lactamase than beta-lactam. then one could, presumably, administer it along with beta-lactam and it would inactivate the beta-lactamase while leaving the beta-lactam free to do it's work. Such a system probably wouldn't be effective within a microbe but it should be effective for running interference at cell membranes.
Thanks for the interesting shows,
Dr. Schmidt's viral illness would be quite serious if there was consolidation as was asserted.
Consolidation refers to the gross characteristics of the lung when it turns from fluffy and pliant into solid as the air spaces become filled with cellular and proteinaceous exudates in pneumonias. Bad enough with bacteria and the antibiotic resistance problem; if it is a viral pneumonia, the treatment modalities are mostly supportive care.
It's been found that nasal carriage of Staphylococcus aureus is associated with increased risk of infection due to dispersal of SA from the nose while breathing and by nose-picking and not washing your hands. Some individuals are colonized with SA and are more prone to infection. Now there's a lot of research on how best to decolonize the nose of SA, because it survives antibiotics and quickly recolonizes the body. Mupirocin is typically used, but results are not good and resistance is likely. Seems to me that the aim of decolonization is stupid, since it is impossible to kill every last cell in and on the body, and even if you could there's plenty more in an individual's environment (which can survive for months on surfaces) to recolonize them anyway. Surely a better aim is to find out why some people do not become colonized and reproduce whatever they have in colonized people. Presumably, there's something about uncolonized peoples' immune systems and/or microbiomes which makes it hard for SA to become a problem. Maybe it's like the problems some people have with gut bacteria, where gut bacteria (shit) transplants have been shown to be effective. Maybe similar transplants of bacteria from the skin and/or nose of uncolonized individuals would be as effective for SA depopulation? It's a revolting idea, but no more disgusting than a poo-transplant!
Didn't recognize "Speak friend and enter!" and "NIN" ?!? What kind of barbarians do you invite on this show?!
Just kidding. TWIM # 73 was another amazing and wonderful podcast. I am only a geologist, so I can sometimes only vaguely hum along with yours, Michele's, and Michael's biochemistry arias. Nonetheless, TWIM is one of my favorite podcasts. When I listen on my walking commute from my home to my office in Seattle, I arrive smarter!. And grateful. I am always grateful after listening. Thank you!