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.
Although Brown et. al’s conclusion makes sense to me, I have still found some unexplained concepts in the article. The authors devote a whole section to defining the terms “pathogen” and “virulence.” Although their definitions seem sound, the authors mention that they cannot use Koch’s postulates in categorizing whether or not a species is pathogenic. However, the article neither mentions what Koch’s postulates are, nor does it give me a citation for reference. Most importantly, the article recommends that public health officials examine the evolution of virulence in pathogens but never really gives a concrete example that shows the usefulness of doing so. In order to investigate these areas of interest myself, I have come across other sources that give more information about Koch’s postulates and the evolution of virulence in pathogens. My findings describe that the ideas found in Brown et al’s article—that virulence impacts the force of a pathogen—can be applied to vaccinations and disease prevention in the sense that certain vaccines can increase or decrease virulence.
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“Crossing the Line: Selection and Evolution of Virulence Traits” defines pathogen as “an organism capable of colonizing a host organism where the interaction results in a disease.” 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.
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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 me: “Vaccines rarely provide full protection from disease.” Captivated by the first sentence, I read further and discovered that vaccines that reduce pathogen growth rate and toxicity actually lead to higher virulence and greater harm for unvaccinated individuals. In contrast, anti-infection and anti-transmission vaccines result in the opposite. Such a result occurs in anti-growth rate and anti-toxin vaccines because the host becomes resistant to a pathogen, and the force of evolution causes the pathogen to increase in virulence. Anti-infection and anti-transmission vaccines, however, cause pathogens to evolve at lower levels if superinfection (the efficiency with which a pathogen invades an already affected host relative to invading an uninfected host) occurs.
Gandon et al.’s article’s relates to Brown et al.’s idea of examining the evolution of virulence for the sake of public health. This connection is underscored as the theoretical findings about vaccines are applied to producing a potential malaria vaccine. Anti-disease, anti-toxin and anti-growth rate, vaccines have the best individual short-term effect but may, in fact, increase the risk for non-immunized individuals. In contrast, anti-infection and anti-transmission vaccines reduce the force of infection and malarial prevalence. Gandon et al.’s article furthermore mentions that vaccines can generate different outcomes when administered to individuals in clinical trials versus when administered to a population as a whole.
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This final conclusion seems to be the most important because it links to Brown et al.’s article and shows the importance of examining virulence in implementing a public health strategy. Gandon et al. provide a concrete example in which public health concerns can be addressed through studying evolutionary biology. Moreover, the final conclusion shows how much society misconstrues the overall benefit of a vaccine just based on clinical trials. Vaccines that are successful in such trials may be detrimental toward virulence, and the overall effects of a vaccine and pathogen need to be examined to determine whether or not a vaccine is viable. I would consider Gandon et al.’s article essential to understanding what Brown et al. are advocating, but the article’s findings intrinsically are worthy of further study. The difference between types of vaccinations is important to researching more vaccines, and researchers should, for the sake of less pathogen resistance, consider these findings as they design vaccines.
Brown et al. in their article “Crossing the Line: Selection and Evolution of Virulence Traits” underline the importance of accounting for the evolution of virulence when implementing public health policy. Though I agree with Brown et al.’s public health concerns, I do not agree with their terminology, namely the way they defined “pathogen” and then dismissed Koch’s postulates without a citation or much explanation. Through an article in Nature, I found out that Koch’s postulates are not impossible to test and are actually more specific than the definition of pathogen that Brown et al. offer. Also, I thought it was somewhat contradictory for Brown et al. to emphasize host-pathogen interaction but dismiss Koch’s postulates, which also stress exactly that. My second area of interest was Brown et al.’s concern toward public health policy. The authors express the notion that investigating the evolution of virulence is important in shaping public health policy. Although their concern is valid, they do not suggest an example in which doing so would result in better public health. In an effort to find such an example, I stumbled upon an article from Nature that explained how certain types of vaccinations—seemingly beneficial devices to disease prevention—can actually backfire and result in increased virulence. Besides highlighting how examining virulence can lead to better public health decisions, the article’s findings proved worthy of further study because a vaccine’s success in a clinical trial does not guarantee that the vaccine will reduce virulence. Researchers need to look beyond clinical trials in examining vaccines and use the evolution of virulence to evaluate their findings.
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