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Examining Vaccines In Light Of The Evolution Of Virulence

1452 words - 6 pages

Making policies about infection-control not only requires information about pathogen transmission but also information about pathogen evolution. According to Nat F. Brown et al. in their article “Crossing the Line: Selection and Evolution of Virulence Traits,” pathogens and hosts have a paradoxical relationship—pathogens damage the same host that they depend on for survival. However, Brown et al. argue that pathogens are still evolutionarily flourishing species because different strains and variations of pathogens exist. In order to successfully combat infections, public health officials, according to the authors, should see how each of these strains evolves and acquires virulence.
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” The article then mentions Koch’s postulates but quickly dismisses them because testing these postulates is a challenge for experimenters. This immediately intrigued my attention, and in order to investigate Koch’s postulates further, I found an article from Nature entitled “Molecular Koch’s Postulates Applied to Bacterial Pathogenicity—A Personal Recollection 15 Years Later.” The author, Stanley Falkow, advocates using Koch’s postulates because they are strong guidelines to collecting evidence of pathogenicity. He also argues that Koch’s postulates are as good as the technology used to apply them and that Koch’s postulates have been modified to include slow viruses and other newly discovered pathogens. Additionally, Koch’s postulates—after the advent of molecular methods of study—have been modified to “proposed molecular postulates” so that they include new terminology.
Falkow’s article is relevant to the assigned reading because of the second revised Koch’s postulate. The first part of the second postulate states that inactivation of the gene(s) associated with the suspected virulence trait should lead to a measurable loss in pathogenicity or virulence. Falkow’s application of this postulate in his article contradicts Brown et al.’s earlier assertion that selecting an appropriate host to test the virulence of a pathogen that affects other hosts is challenging. Although Falkow admits that the genome of a host has an important role in host-pathogen dynamics, he also states that that role can be understood by mapping genes. He uses this approach with Salmonella enterica and gene-knockout animals, animals which lack proteins or enzymes necessary for causing disease. Falkow injected mice with Salmonella pathogenicity island 1 (SPI1) and explained that SipB, an encoded effector protein, induces host cell death while interacting with Caspase-1, a proinflammatory enzyme. In knockout mice (mice that lack Caspase-1), three hours after injection, Salmonella is not visible microscopically, whereas in normal mice, the cells have responded with the traditional acute inflammatory response. With this process, Falkow not only validates Koch’s second molecular postulate but also proves that Brown et al. are wrong in saying that testing the virulence of a host is challenging. Certainly, after my findings, Koch’s molecular (revised) postulates are both worthy of further study and inclusion into Brown et al.’s definition of pathogen. Not doing so will fail to give a set of guidelines that helps in determining pathogenicity and will fail to elucidate host-pathogen interactions, an idea that Brown et al. strive to explain in their article.
My second area of interest was a concrete example in which the evolution of virulence could impact public health. In order to find one, I came across an article, published in Nature, entitled “Imperfect Vaccines and the Evolution of Pathogen Virulence” by Gandon et al. Immediately, the first sentence of the article shocked...

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