By Paul W. Ewald
Findings from the sphere of evolutionary biology are yielding dramatic insights for well-being scientists, in particular these fascinated with the struggle opposed to infectious ailments. This ebook is the 1st in-depth presentation of those insights. In detailing why the pathogens that reason malaria, smallpox, tuberculosis, and AIDS have their exact sorts of deadliness, the ebook indicates how efforts to regulate nearly all ailments would get advantages from a extra thorough software of evolutionary rules. while seen from a Darwinian point of view, a pathogen isn't easily a disease-causing agent, it's a self-replicating organism pushed via evolutionary pressures to go on as many copies of itself as attainable. during this context, so-called "cultural vectors"--those features of human habit and the human atmosphere that let unfold of illness from immobilized people--become extra very important than ever. Interventions to regulate ailments do not easily prevent their unfold yet could cause pathogens and the ailments they engender to adapt into extra benign varieties. actually, the union of future health technological know-how with evolutionary biology bargains a completely new size to coverage making, because the danger of making a choice on the long run process many ailments turns into a fact. via proposing the 1st unique rationalization of an evolutionary viewpoint on infectious disorder, the writer has completed a real milestone within the synthesis of health and wellbeing technological know-how, epidemiology, and evolutionary biology. Written in a transparent, obtainable variety, it truly is meant for a large readership between execs in those fields and basic readers attracted to technological know-how and well-being.
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Additional resources for Evolution of Infectious Disease
The difficult decisions about treatment would have to weigh the expected harm to the patient due to treatment against the expected benefits to others who might otherwise contract the disease. When infected people are less capable of practicing hygienic measures, the tradeoff shifts toward symptomatic treatment. When infected people are isolated from others, the tradeoff shifts toward withholding of treatment. These decisions also must consider the degree to which the diseases can be controlled by measures other than symptomatic treatment.
When the symptom aids both parasite and infected host, these pressures diminish. The losers are those who become infected as a result of the diarrhea. But their loss does not influence the evolutionary game played by the parasite and the host from which they were infected (unless the recipients are relatives of the infected people). Their loss however, is relevant to policymaking. When a symptom benefits both host and parasite, symptomatic treatment may be a difficult and sensitive social issue.
But treatment with acetaminophen is not associated with Reye's syndrome (Hall et al. 1988). We can therefore rule out the hypothesis that Reye's syndrome results from a simple sabotaging of a defensive fever or defensive pain. But unlike aspirin, acetaminophen does not reduce inflammation. The inflammatory response may defend against viruses in two ways: (1) by mobilizing immunological defenses at the site of infection, and (2) by slowing the flow of blood and hence virus from sites of infection.
Evolution of Infectious Disease by Paul W. Ewald