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Biomedical subjects

Paul W Ewald

Publications and source records attributed to Paul W Ewald.

5 recordsLinked to original sources

Evolution of virulence.

At the close of the 19th century, the germ theory had generated a new understanding of the causes of acute infectious diseases and revealed new directions for study. This understanding contributed to the greatest improvements in health in the history of medicine. At the end of the 20th century, the second stage of this disciplinary development is occurring. The old germ theory is being expanded into a new germ theory, which, by integrated the full spectrum of biologic disciplines. This new germ theory is emphasizing how environments and human activities influence the characteristics of infectious agents and the broader role of infection as a cause of chronic diseases.

Animals↗

Pathogen survival in the external environment and the evolution of virulence.

Recent studies have provided evolutionary explanations for much of the variation in mortality among human infectious diseases. One gap in this knowledge concerns respiratory tract pathogens transmitted from person to person by direct contact or through environmental contamination. The sit-and-wait hypothesis predicts that virulence should be positively correlated with durability in the external environment because high durability reduces the dependence of transmission on host mobility. Reviewing the epidemiological and medical literature, we confirm this prediction for respiratory tract pathogens of humans. Our results clearly distinguish a high-virulence high-survival group of variola (smallpox) virus, Mycobacterium tuberculosis, Cornynebacterium diphtheriae, Bordetella pertussis, Streptococcus pneumoniae, and influenza virus (where all pathogens have a mean percent mortality > or = 0.01% and mean survival time >10 days) from a low-virulence low-survival group containing ten other pathogens. The correlation between virulence and durability explains three to four times of magnitude of difference in mean percent mortality and mean survival time, using both across-species and phylogenetically controlled analyses. Our findings bear on several areas of active research and public health policy: (1) many pathogens used in the biological control of insects are potential sit-and-wait pathogens as they combine three attributes that are advantageous for pest control: high virulence, long durability after application, and host specificity; (2) emerging pathogens such as the 'hospital superbug' methicillin-resistant Staphylococcus aureus (MRSA) and potential bioweapons pathogens such as smallpox virus and anthrax that are particularly dangerous can be discerned by quantifying their durability; (3) hospital settings and the AIDS pandemic may provide footholds for emerging sit-and-wait pathogens; and (4) studies on food-borne and insect pathogens point to future research considering the potential evolutionary trade-offs and genetic linkages between virulence and durability.

Animals↗

Genes, germs, and schizophrenia: an evolutionary perspective.

Literature on schizophrenia and other mental illnesses has emphasized the compatibility of evidence with genetic causation without adequately considering alternative hypotheses of disease causation. Although some studies from the mid-20th century reported associations between certain pathogens and schizophrenia, only recently has the possibility of infectious causation of schizophrenia again become an active focus of research. Infectious causation of schizophrenia is still, however, generally regarded as less well demonstrated than genetic causation. This article evaluates the evidence that has been used to support genetic and infectious causation. Our consideration of infectious causation focuses on the protozoan Toxoplasma gondii but also assesses other pathogens that may contribute to the development of some of the illnesses currently categorized as schizophrenia. Although evidence generally accepted as demonstrating genetic causation can be readily explained by hypotheses of infectious causation, some of the evidence implicating infectious causation cannot be similarly explained by genetic causation. This asymmetry indicates that a scientific approach to the causation of schizophrenia needs to put a greater emphasis on tests that distinguish hypotheses of genetic causation from those of infectious causation.

Animals↗

Timing of transmission and the evolution of virulence of an insect virus.

We used the nuclear polyhedrosis virus of the gypsy moth, Lymantria dispar, to investigate whether the timing of transmission influences the evolution of virulence. In theory, early transmission should favour rapid replication and increase virulence, while late transmission should favour slower replication and reduce virulence. We tested this prediction by subjecting one set of 10 virus lineages to early transmission (Early viruses) and another set to late transmission (Late viruses). Each lineage of virus underwent nine cycles of transmission. Virulence assays on these lineages indicated that viruses transmitted early were significantly more lethal than those transmitted late. Increased exploitation of the host appears to come at a cost, however. While Early viruses initially produced more progeny, Late viruses were ultimately more productive over the entire duration of the infection. These results illustrate fitness trade-offs associated with the evolution of virulence and indicate that milder viruses can obtain a numerical advantage when mild and harmful strains tend to infect separate hosts.

Analysis of Variance↗

Evolutionary health promotion.

Health promotion's promise is enormous, but its potential is, as yet, unmatched by accomplishment. Life expectancy increases track more closely with economic prosperity and sanitary engineering than with strictly medical advances. Notable achievements in the past century--the decreased incidences of epidemic infections, dental caries, and stomach cancer--are owed to virologists, dentists, and (probably) refrigeration more than to physicians. Prevention speaks against tobacco abuse with a single voice, but in many other areas contradictory research findings have generated skepticism and even indifference among the general public for whom recommendations are targeted. Health promotion's shortcomings may reflect lack of an overall conceptual framework, a deficiency that might be corrected by adopting evolutionary premises: (1) The human genome was selected in past environments far different from those of the present. (2) Cultural evolution now proceeds too rapidly for genetic accommodation--resulting in dissociation between our genes and our lives. (3) This mismatch between biology and lifestyle fosters development of degenerative diseases. These principles could inform a research agenda and, ultimately, public policy: (1) Better characterize differences between ancient and modern life patterns. (2) Identify which of these affect the development of disease. (3) Integrate epidemiological, mechanistic, and genetic data with evolutionary principles to create an overarching formulation upon which to base persuasive, consistent, and effective recommendations.

Biological Evolution↗