Comments:The Road to Microbial Endocrinology

Thank you for your question. The answer is a very definite "yes". In 2003, I and my colleagues published in Lancet (see Lancet 361(9352):130-5, 2003)that the catecholamine inotropes, such as norepinephrine and dobutamine (analog of dopamine) which are used in critically ill patients for the maintenance of cardiac and renal function, are also responsible for stimulating the growth of Staphylococcus epidermidis leading to biofilm formation and contamination of indwelling medical devices such as catheter lines in the patient. Subsequent to the publication of that article (as well as other preceding articles), their have been calls in a number of journal for the re-design of clinical agents such as the inotropes so that they selectively perform their stated function (such as cardiac and renal maintenance) and not at the same time stimulate bacterial growth.

I also have a story that goes along with that. The second time I presented these ideas way back in the mid-1990's was at a surgical infectious disease meeting attended mainly by surgical chiefs and medical residents. After I presented my talk there was complete silence until the session chair asked the question if I (as a non-M.D.) knew what the name of norepinephrine on the clinical floors was. I didn't and he then said it is "levophed". I said "ok" and didn't get it. He then said (with everyone in the audience staring at us) that the nickname for levophed is "leave-em-dead". He continued to say that it was well know that the administration of levophed to septic patients often resulted in a worsening condition and a quicker death. The chair said that they always blamed such deaths on residents giving the wrong dosage of norepinephrine. But, he asked, was I saying that it wasn't their fault after all and it was the concept that giving norepinephrine just made things worse through stimulation of additional bacterial growth? My answer was "yes" and after that I was mobbed by clinicians in the hallways going over their cases. It is a great example of how bench-top results can have real clinical impact.

Dr. Lyte do you feel that your research has implications in the use of norepinephrine for blood pressure support in septic patients?

good discussion.Thank you Prof Lyte, I always feel that mouse get stress in the share mouse housing cage because of the hierarchy within the group, and that the stress will effect the host immune response and and hence the result.

Here is a good discussion of how stress promotes iron availability, and the roles of norepinephrine and epinephrine as quorum sensing molecules:
http://mpkb.org/home/social/stress

Thank you Prof Lyte, I always feel that mouse get stress in the share mouse housing cage because of the hierarchy within the group, and that the stress will effect the host immune response and and hence the result. I think I can use some of your papers as a reference in my discussion in my thesis.


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