Plague Time: How Stealth Infections Cause Cancer, Heart Disease, and Other Deadly Ailments - Hardcover

Ewald, Paul W.

Hardcover

ISBN 10: 0684869004 ISBN 13: 9780684869001

Publisher: Free Press, 2000

Synopsis

A noted biologist defends his controversial thesis that most of our worst killers--including heart disease, cancer, and diabetes--are in fact caused by infectious diseases.

About this title

About the Author

Paul W. Ewald, professor of biology at Amherst College, was the first recipient of the George R. Burch Fellowship in Theoretic Medicine and Affiliated Sciences. The publication of his Evolution of Infectious Disease is widely acknowledged by doctors and scientists as a watershed in the emergence of the new discipline of evolutionary medicine. He has been featured in The Atlantic, Newsweek, Discover, and Forbes. He lives in Amherst, Massachusetts.

Reviews

Plague Time is about the likelihood that infections cause atherosclerosis, some cancers, and other chronic diseases. This is certainly a current theory, and the book could be useful to readers who have not followed the literature in support of this thesis. Among the conclusions presented are that most of our diseases are caused by unrecognized infections and that more money should be spent on research on infectious diseases.

I laud these conclusions, yet I cannot applaud the book. Ewald is guilty of overkill. A constantly recurring theme in the book is that the medical establishment has been too slow to recognize new ideas and to effect change. An example is that successful antibiotic treatment of peptic ulcers was first tried in 1955, and the fact that it took 40 years for the medical establishment to accept the notion that peptic ulcers are a treatable infectious disease has caused many to suffer and die. Another is that of cervical cancer and the "high-risk" subtypes of human papillomavirus. Ewald argues that thousands have probably died from cervical cancer because it was treated as bad luck rather than as a preventable sexually transmitted disease.

Ewald believes that there is a bias against attributing diseases to infectious causes. The credo he recommends to modern-day microbe hunters is to investigate the chronic diseases that most experts do not think are caused by infection and figure out how to control them. Ewald believes that the emphasis of modern genetics is misplaced and that the Human Genome Project is a case in point. The important genes, he believes, will turn out to be those of infectious agents and those that control the human response to infection.

Ewald argues that we set the standard for the acceptance of such theories too high and that we should lower our thresholds. He wants anecdotal information, screened by some good method, to be used more effectively. But we already live in a world in which everything gets published somewhere. If you believe something, you can certainly find some report, somewhere, to support it.

A number of conditions are discussed extensively, including atherosclerosis, which, notes Ewald, may be caused by Chlamydia pneumoniae, a very common infection. This issue is currently the subject of intense international research activity, but researchers have yet to prove a causal relation.

The bottom line is that the contentions here are carried too far. Ewald seems to believe that any deviation from the norm could be caused by an infection -- even, he suggests, artistic creativity. I find this way of thinking frightening.

Ewald also stresses that the supposition that the infectious agent and its host will, over time, put selective pressures on each other toward the persistence of both and the least damage to either is not necessarily true. The evidence against this principle comes from situations in which the rapid transmission of an organism occurs, with selection for increased virulence -- for instance, in locations where there is a high degree of crowding, mobility, and sexual contact as well as poor sanitary conditions. Ewald discusses such short-term success of highly virulent organisms as a revelation of "evolutionary biology." However, Sir Macfarlane Burnet, one of the leading proponents of the theory that successful host-parasite relationships adapt in the direction of benignity, actually discussed it about 50 years ago: "If the microorganism causing an epidemic is susceptible to variations in the direction of higher virulence, then opportunities for rapid spread in susceptible persons will cause an apparent increase in virulence by selection of the fittest, i.e. most virulent, bacteria" (The Natural History of Infectious Disease. Cambridge, United Kingdom: Cambridge University Press, 1953).

This book has a somewhat self-congratulatory tone -- the author likes to assert that he made predictions and then to congratulate himself for having been right, as in the case of an accurate prediction that the Spanish influenza strain would not reappear during the 1990s. That a population becomes susceptible to the epidemic spread of an infection because acquired immunity has waned does not necessarily mean that the pathogen is still sitting there, waiting to reinfect people.

There are also some errors and misinterpretations in this book. For example, Ewald asserts that the transmission of genital herpesvirus infections is caused by stress, which induces the replication of the virus, the formation of blisters, and the subsequent transmission of the virus from lesions. The current understanding, however, is that inapparent infection and the asymptomatic shedding of virus are probably responsible for transmission in most cases. In trachoma, blindness is not caused by "puffiness" of the conjunctiva but is, rather, secondary to the scarring of the conjunctiva. Genital chlamydial infections (with secretions, Ewald supposes, contaminating the garments of persons in areas where trachoma is endemic) are not considered to have a role in the transmission of trachoma. The model Ewald presents of the replication of human papillomavirus in his discussion of cervical cancer probably has little relevance for the actual transmission of that virus. Young, sexually active women have very high rates of inapparent infection, and long-lasting dysplasia reflects a persistence of infection. That women with multiple sexual partners have a higher prevalence of infection with the "high-risk" types of human papillomavirus need not reflect increased virulence (there is no evidence of changes in the virulence of specific types of the virus); it can, instead, be easily explained by increased exposure and the more persistent nature of the infection caused by these types of the virus. The bottom line: an important subject, a disappointing book.

Julius Schachter, Ph.D.
Copyright © 2001 Massachusetts Medical Society. All rights reserved. The New England Journal of Medicine is a registered trademark of the MMS.

Ewald's thesis is that the medical profession has been and remains slow to recognize that many chronic diseases have an infectious causation. "Thousands suffered and died because antibiotic treatment of peptic ulcers was generally recognized in 1995 instead of 1955. Thousands more probably suffered and died over a similar period because cervical cancer was treated as bad luck rather than a preventable sexually transmitted disease." Ewald, professor of biology at Amherst College, says the situation results from medicine's poor understanding of microbial evolution. "Throughout the twentieth century, leading authorities in the health sciences believed that coevolution of pathogens with their hosts would inevitably lead to benign coexistence." But "a more careful application of evolutionary principles leads to the conclusion that some pathogens will evolve toward benignity and some will not." Ewald presents his view of that process and lists several chronic diseases (among them atherosclerosis, Alzheimer's, impotence and some cancers) that probably will be proved to have an infectious causation.

EDITORS OF SCIENTIFIC AMERICAN

Could breast cancer be caused, not by genes, but by a pathogen passed to humans from mice? Very possibly, according to Amherst College biology professor Ewald (Evolution of Infectious Disease) in this controversial page-turner that's certain to garner attention. In a cogent defense of our evolutionarily selected genes, Ewald proposes that the true culprits behind chronic ailments and even mental disorders are pathogens. He propels his argument by noting the "biases of human thought" that inhibited scientific growth in the 19th century (when the notion of microbes was first rejected) and those that are, he believes, stifling the research of infectious diseases today. For example, the infectious origin of peptic ulcers wasn't recognized until the mid-1980s, more than 30 years after physicians demonstrated the effectiveness of antibacterial agents in ulcer patients. The reason for this "scientific paralysis" lies in the prevalent misconception that most infectious diseases are like the common cold, acute yet ephemeral rather than chronic. Challenging this popular mindset, Ewald thoroughly examines the calculated attack strategies of a number of chronic, sexually transmitted diseases (such as herpes, syphilis and AIDS). In contrast to the complex task of determining disease origins, however, Ewald's solutions are surprisingly simple: clean water, safe sex, home care when you're ill, awareness of pathogen evolution and more funding. The world of infectious diseases, Ewald makes clear, continues to thriveAand anyone involved in the study or practice of medicine and any scientifically literate reader curious about the origins of disease will want to read this challenging work. Author tour. (Nov. 14)
Copyright 2000 Reed Business Information, Inc.

For many years stomach ulcers were thought to be the product of stress, acid, and spicy foods; now we know they are caused by bacteria. Amherst biology professor Ewald (Evolution of Infectious Diseases) suggests that many other chronic diseasesDincluding clogged arteries, diabetes, cancer, and schizophreniaDare at least partially caused by infectious agents, and here he presents research that bolsters his claims. Beyond this, he argues that studying how infectious agents evolve can lead to techniques for more effective control of killer diseases such as malaria and AIDS through decreasing their virulence. He also discusses some ethical issues related to treating diseases. An example is whether it is best to treat an individual with antibiotics when this may cause problems for a whole population if antibiotic resistance in bacteria is a result. Ewald's ideas are controversial but intriguing and have far-reaching implications. His clear, entertaining, and well-documented style makes the book appealing to a wide variety of readers. Highly recommended for all types of libraries.DMarit MacArthur Taylor, Auraria Lib., Denver
Copyright 2000 Reed Business Information, Inc.

Although it is at times tough getting through this book, the payoff is great. For biology professor Ewald confers on attentive readers a broad understanding of the medical advances that probably will be made during the next few decades. He believes that infectious diseases play major roles in many chronic conditions, and he backs his belief with sound documentation and exemplification. In practice, this means leading readers from such concrete examples as the bacterial causation of peptic ulcers and the viral causation of cervical cancer to hypotheses that seem well worth pursuing. Tweaking the immune system, he argues, will probably be more productive in the long run than improving antimicrobials and vaccines, and increased funding of basic biological research, along with improving medical education to produce graduates with open, prepared minds, should speed progress. Ewald pertinently cites medical history and creative literature, too, to help make his points in this well thought out, clearly written, provocative book. William Beatty
Copyright © American Library Association. All rights reserved

Edition details

• Publisher: Free Press
• Publication date: 2000
• Language: English
• ISBN 10: 0684869004
• ISBN 13: 9780684869001
• Binding: Hardcover
• Edition number: 1
• Number of pages: 288