Trade Agreement between Bacteria, Viruses and Human Skin — A fly in the ointment 细菌、病毒与人皮的经贸协定 — 美中不足的共生
Staphylococcus is a group of Gram-positive cocci. It is named because it appears spherical (cocci) and form in grape-like clusters [1-4] under the microscope. Staphylococci live all over us, and seem to have adapted to conditions in our skin that are uncongenial to most other bacteria [1,4-6]. Considering that its numbers exceed us by multiple times, it is remarkable how little trouble we have with the relation. Only a few of us are plagued by boils, and we can blame a large part of the destruction of tissues on the zeal of our own leukocytes. We live with them for long periods without any awareness of their existence; then cyclically, for reasons not understood but probably related to immunologic reactions on our part, we sense them, and the reaction of sensing is the clinical disease, eg. suppurative inflammation of various tissues and organs, food poisoning, staphylococcal scalded skin syndrome (SSSS), toxic shock syndrome (TSS), etc.
Some bacteria are only harmful to us when they make exotoxins or endotoxins, and they only do this when they are, in a sense, diseased themselves. The toxins of staphylococcus, diphtheria bacilli and streptococci are produced when the organisms have been infected by bacteriophage which is a kind of virus; it is the virus that provides the code for toxin. Uninfected bacteria are uninformed. When we catch impetigo it is a virus infection, but not of us. Virus (bacteriophage) infects Staphylococcus, then staphylococci release toxins and enzymes to fight the bacteriophage (virus). When we sense toxins and enzymes released by staphylococci, we are likely to turn on every defense at our disposal; we will decapitate, bomb, defoliate, blockade, seal off, and destroy all the tissues in the area. Our soldier cells (leukocytes) become more actively phagocytic, release lysosomal enzymes, turn sticky, and aggregate together in dense masses, occluding capillaries and shutting off the bleed supply. Complement is switched on at the right point in its sequence to release chemotactic signals, calling in leukocytes from everywhere. Vessels become hyperreactive to epinephrine so that physiologic concentrations suddenly possess necrotizing properties. Pyrogen is released from leukocytes, adding fever to hemorrhage, necrosis, and shock. We are completely out of order.
Our involvement is not that of an adversary to bacteria or virus in a straightforward game, but more like blundering into someone else’s accident, it seems that the two creatures of China and the United States that were originally friendly and symbiotic on the host earth’s biosphere suddenly turned their heads and erupt into violent warfare. In real life, however, even in our worst circumstances we have always been a relatively minor interest of the vast microbial world. Pathogenicity is not the rule. Indeed, it occurs so infrequently and involves such a relatively small number of species, considering the huge population of bacteria on the earth, that it has a freakish aspect. Disease usually results from inconclusive negotiations for symbiosis, an overstepping of the line by one side or the other, a biologic misinterpretation of borders .
- Guoqing Xia and Christiane Wolz. Phages of Staphylococcus aureus and their impact on host evolution. Infection, Genetics and Evolution. Volume 21, January 2014, Pages 593-601
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- A. Belley, M. Callejo, F. Arhin, M. Dehbi, I. Fadhil, J. Liu, G. McKay, R.Srikumar, P. Bauda, D. Bergeron, N. Ha, M. Dubow, P. Gros, J. Pelletier, G. Moeck. Competition of bacteriophage polypeptides with native replicase proteins for binding to the DNA sliding clamp reveals a novel mechanism for DNA replication arrest in Staphylococcus aureus. Mol. Microbiol., 62 (2006), pp. 1132-1143
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- Lewis Thomas. The lives of a Cell: Notes of a Biology Watcher.Publisher, Penguin Books, 1978. P55