In my chapter on syphilis and smallpox, both major issues with the European discovery of America, I explained the various theories of the origin of syphilis. The New York Times today has an article on further developments in this story. Genetic studies have confirmed that syphilis, a non-venereal disease in the New World, became a terrible scourge when it arrived in Europe with Columbus’ fleet. There was some evidence for an African origin as Yaws, a related disease of children, was present in Africa. The question was whether it was there before Columbus voyage. That is still not settled.
The story of smallpox has been distorted for political reasons but it was not an attempt at genocide but rather the consequences of the introduction of a new disease into a susceptible population. Syphilis devastated Europe just as smallpox devastated the Americas. The story was repeated in the 19th century when measles wiped out thousands of Polynesians when carried to the Pacific Islands by explorers.
Dr. K. wasn’t syphilis a swift killer when it first arrived in Europe? Now it takes a long time to kill. But then….
It fits Paul Ewald’s theories about the evolution of virulence, actually.
Hey, I remember being told that the British called syphilis “the French disease,” while the French called it “the British disease.”
Descriptions of syphilis in the 16th century were horrendous. Faces eaten away, etc. A classic case of virulence shift in a new host.
Dear Dr. K.
This business of the evolution virulence fascinates me. We don’t think of the “pathogenic perspective” when it comes to disease, just about how to recognize or treat it—but understanding that “perspective” can be helpful in treatment. Evolution, as always, is involved.
Paul Ewald has done some great work on this.
http://en.wikipedia.org/wiki/Paul_W._Ewald
I think you might be interested in Ewald’s work.
His last book is pretty sensationalistic, but interesting (curious what you would think of it—if you are interested, I would be happy to send you a copy, since I have an extra one):
Plague Time: The New Germ Theory of Disease, Anchor, 2002, ISBN 0-385-72184-6
This older book made his reputation:
Evolution of Infectious Disease, Oxford University Press, 1993, ISBN 0-19-506058-X.
That one is WELL worth your time.
And I thought this review was interesting:
Infect Dis Clin North Am. 2004 Mar;18(1):1-15. Links
Evolution of virulence.
Ewald PW.
Department of Biology, University of Louisville, Louisville, KY 40292, USA.
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.
Anyway, I would be interested in your thoughts about Ewald’s thesis. In your copious free time, of course!
I’ll look at it. No one knows why plague went away in the last century. It is unexplained. Smallpox had episodes of waxing and waning of virulence over the centuries that are unexplained.
Dr. K., on the subject of Paul Ewald, I thought you might be interested in these three abstracts—the last one in particular!
1: Perspect Biol Med. 2007 Spring;50(2):181-202.
Premenstrual syndrome: an evolutionary perspective on its causes and treatment.
Doyle C, Ewald HA, Ewald PW.
Department of Biology, University of Louisville, KY 40292, USA.
Premenstrual syndrome is a collection of heterogeneous symptoms that are attributed to hormonal fluctuations and that vary among individuals for unknown reasons. We propose that much of what is labeled “premenstrual syndrome” is part of a broader set of infectious illnesses that are exacerbated by cyclic changes in immunosuppression, which are induced by cyclic changes in estrogen and progesterone. This cyclic defense paradigm accords with the literature on cyclic exacerbations of persistent infectious diseases and chronic diseases of uncertain cause. Similar exacerbations attributable to hormonal contraception implicate hormonal alterations as a cause of these changes. The precise timing of these cyclic exacerbations depends on the mechanisms of pathogenesis and immunological control of particular infectious agents. Insight into these mechanisms can be obtained by a comparison of timing of menstrual exacerbations with the timing of exacerbations associated with pregnancy.
2: Perspect Biol Med. 2003 Summer;46(3):317-48.
Genes, germs, and schizophrenia: an evolutionary perspective.
Ledgerwood LG, Ewald PW, Cochran GM.
Department of Biology, Amherst College, MA 01002, USA.
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.
3: J Infect Dis. 2000 Jun;181 Suppl 3:S394-401.
Chlamydia pneumoniae and cardiovascular disease: an evolutionary perspective on infectious causation and antibiotic treatment.
Ewald PW, Cochran GM.
Department of Biology, Amherst College, Amherst, MA 01002-5000, USA. pwewald@amherst.edu
Evolutionary considerations implicate infectious causation of atherosclerosis and help to resolve different risk factors as parts of an overall process of disease causation. An evolutionary approach also provides insight for the timing of research efforts to provide better control of pathogen evolution. In particular, evolutionary considerations emphasize the need to understand the transmissibility of Chlamydia pneumoniae from systemic infections in order to control the evolution of antibiotic resistance.
Before you chuckle at this, remember the ulcer versus Helicobacter pylori story. From what I heard, physicians in the 1950s knew that antibiotics could treat peptic ulcers…but in the 60s and 70s the stress model became the dominant paradigm (also, the 50s findings were not backed up with a model). Who knows what else we think of as non-bacterial is actually due to infectious disease?
Something to think about, anyway.
Helicobacter is a cautionary tale for everyone looking at these diseases. I doubt that schizophrenia is infectious in origin. I lean to the developmental school. I tend to this theory.
I love the Helicobacter story. I love the fact that Barry Marshall actually drank a culture of the organism and gave himself ulcers to “prove” his hypothesis. I guess a Nobel Prize was warranted to his very personal devotion to his research!
http://en.wikipedia.org/wiki/Barry_Marshall
Speech, language, and brain functioning fascinate me, but are far removed from my own speciality. Still, genetics is genetics.
The whole foxP2 gene story is fascinating. Here is a good review:
J Neurosci. 2006 Oct 11;26(41):10376-9.
“Singing mice, songbirds, and more: models for FOXP2 function and dysfunction in human speech and language.”
White SA, Fisher SE, Geschwind DH, Scharff C, Holy TE.
Department of Physiological Science, University of California, Los Angeles, California 90095, USA. sawhite@ucla.edu
In 2001, a point mutation in the forkhead box P2 (FOXP2) coding sequence was identified as the basis of an inherited speech and language disorder suffered by members of the family known as “KE.” This mini-symposium review focuses on recent findings and research-in-progress, primarily from five laboratories. Each aims at capitalizing on the FOXP2 discovery to build a neurobiological bridge between molecule and phenotype. Below, we describe genetic through behavioral techniques used currently to investigate FoxP2 in birds, rodents, and humans for discovery of the neural bases of vocal learning and language.
But the one that continues to freak me out is the whole “doogie mice” business.
http://www.sciam.com/article.cfm?articleID=00075ED9-33D5-1C75-9B81809EC588EF21
Hard to believe that the NR2B gene, encoding the NMDA receptor, can be tweaked to give this kind of effect. The work hasn’t gone much further than mice.
Wouldn’t it be interesting to make transgenic monkeys (which we can now do) with a human foxP2 gene and enhanced NR2B genes? Would we get much smarter monkeys with language ability?
As for schizophrenia, I keep thinking about the effect that parasites have on the behavior of their hosts.
http://www.livescience.com/technology/060210_technovelgy.html
Who says that the ideas in science fiction are farfetched? The material in the link above is far weirder than most SF, and is also true!
The story about Toxoplasma being affected by haloperidol is interesting because there are studies going on in which high risk teenagers, with some early behavior typical of schizophrenia, are being treated with anti-psychotic drugs to “prevent” the development of psychosis. That would fit the Toxoplasma model.