From extending lifespan to bolstering the immune system, the drug’s effects are only just beginning to be understood.
Researchers are zeroing in on the origin of syphilis and related diseases, which continue to plague the human population some 500 years after the first documented case.
February 1, 2014|
© SCIENCE SOURCE/COLORIZATION BY JESSICA WILSON
By the close of the 15th century, chaos reigned in Naples, Italy. At the invitation of Pope Innocent VIII, the French King Charles VIII invaded the city with 25,000 troops. Soon after, a terrible new disease appeared among the soldiers and the prostitutes who accompanied them. Boils as big as acorns that burst and left scabs, terrible joint pain, rotting flesh, and a revolting odor tortured the infected. By the dawn of the 20th century, it was estimated that as many as 10 percent of London residents, 15 percent of Parisians, and 20 percent of US army recruits had the disease—dubbed syphilis after the hero of a 16th-century poem who is afflicted with the infection as a punishment for insulting the god Apollo.
The pale, corkscrew-shaped bacterium responsible for the outbreak, Treponema pallidum, was identified in 1905, and the prevalence of the infection plummeted in the developed world after the discovery of antibiotics. Still, roughly 12 million people are diagnosed with syphilis each year, and it remains an important public health problem in low-income countries.
There continues to be disagreement about where syphilis originated. Much evidence seems to point the finger at Christopher Columbus and his crew, who may have picked up the pathogen on their legendary first visit to the New World. Some have claimed that the disease existed in Europe before Columbus’s time, however, with environmental or social changes during the Renaissance causing it to erupt with a vengeance. Historians have long questioned whether or not vague passages in famous texts describe syphilis, and arguments over the dates of pertinent historical documents are common.
Recently, many researchers, our group included, have taken a new approach to the study of the origin and evolution of syphilis and its cousins, and the breadth of these diseases’ reach today. Leveraging techniques from genetics, biological anthropology, and wildlife disease ecology, syphilis researchers are now beginning to answer questions that have been pondered for hundreds of years. The skeletal, genetic, and ecological information scientists are now uncovering could inform our understanding of how T. pallidum has evolved and how we can best control it today.
© BIOPHOTO ASSOCIATES/SCIENCE SOURCE; © BIOPHOTO ASSOCIATES/SCIENCE SOURCEOTIS HISTORICAL ARCHIVES NAT'L MUSEUM OF HEALTH & MEDICINE/WIKIMEDIA COMMONSAfter rulers from across Italy banded together to expel King Charles VIII from Naples, the French soldiers returned home, taking syphilis with them. Medical historians have used historical documents to trace the rapid spread of the infection across Eurasia. Going backward in time, however, to uncover where syphilis originated, has proven more difficult.
The timing of the first epidemic led contemporary scholars to postulate that syphilis originated in the New World and was transmitted to the Old World by Columbus and his crew, who returned to Europe just before King Charles VIII’s invasion of Naples. Known as the Columbian hypothesis, this explanation dominated for hundreds of years. Then, in the 20th century, researchers proposed the pre-Columbian hypothesis, suggesting that syphilis may have existed in the Old World long before the Neapolitan outbreak without being recognized as a distinct disease until the Renaissance. Perhaps prior to 1495 it was conflated with other infections, such as leprosy, scholars posited.
Another theory, known as the unitarian hypothesis, also emerged. It suggests that syphilis, as well as the related diseases yaws and bejel, are caused by identical types of T. pallidum. Like syphilis, yaws and bejel are chronic, debilitating diseases. Unlike syphilis, they are not sexually transmitted and are usually contracted in childhood. Yaws is found in tropical regions of the world and spreads via skin-to-skin contact, while bejel is found in arid regions, such as the Middle East, and appears to spread via contaminated utensils and drinking vessels. According to the unitarian hypothesis, T. pallidum manifests in different ways depending on environmental conditions and other factors, such as the age at which a person becomes infected. If this hypothesis is correct, then the Renaissance epidemic of syphilis could simply reflect the response of the pathogen to changes in the social and sexual environment of the time, such as improved hygiene and lax urban sexual mores.
To address these possibilities, researchers have turned to skeletal remains. Syphilis, yaws, and bejel—collectively known as the treponemal diseases—sometimes leave a telltale signature upon the skeleton: bone lesions that develop as a result of infection. Although most skeletal lesions do not provide conclusive evidence of treponemal disease, a few lesions are diagnostic. A suite of crater-like areas on the exterior of the skull called caries sicca, for example, can be confidently attributed to treponemal disease, as can shinbones that are both swollen with new growth and pitted with shallow cavities. By searching for these diagnostic lesions among skeletons from ancient populations, biological anthropologists can learn more about where treponemal disease was—and wasn’t—over the course of human history.
Much evidence seems to point the finger at Christopher Columbus and his crew, who may have picked up the pathogen
on their first visit to the New World.
In 2005, paleopathologists Mary Lucas Powell, professor emeritus at the University of Kentucky, and Della Collins Cook of Indiana University found indisputable cases of treponemal infection throughout the Americas, some dating back to the pre-Columbian New World. Based on the ages of the affected skeletons, many of which were juvenile, most researchers believe that the disease was not transmitted sexually, as syphilis is known to be. It’s possible that this New World treponemal pathogen was transported by Columbus’s crew across the Atlantic, evolving into a sexually transmitted form because the clothing worn by 15th-century Europeans would have limited the potential for skin-to-skin transmission.
But the skeletal evidence for infection in the Old World is more ambiguous, making it difficult to pinpoint the appearance and spread of the pathogen on the eastern side of the Atlantic Ocean. In 1988, one of us (G.J.A.) reviewed available research on this subject and found no compelling evidence that treponemal disease was present in pre-Columbian Europe.1 Since then, however, a steady trickle of reports describing Old World skeletons with lesions that predate Columbus’s New World voyages, sometimes by thousands of years, has appeared in the literature.
In light of the new evidence, we performed another comprehensive review in 2011.2 After establishing rigorous, evidence-based criteria for dating and diagnosis, we found a number of Old World cases with a strong treponemal diagnosis and a number with solid pre-Columbian dates. Strikingly, however, we did not find a single case that had both a compelling diagnosis and a reliable date, leading us to question whether the pathogen did indeed appear in Europe before Columbus sailed the ocean blue. Of course, some areas of the Old World, like sub-Saharan Africa and Asia, have received much less attention from archaeologists and paleopathologists, and ancient skeletons with diagnostic treponemal lesions may be waiting there to be discovered.
With the enormous advances in genomics made in the past two decades, it was only a matter of time before genetics answered the basic question that had plagued researchers for years: are the pathogens that cause syphilis, yaws, and bejel genetically distinct? In 1998, researchers sequenced the genome of a common lab strain of syphilis, originally isolated from a patient in the Washington, DC, area some 86 years earlier. This sequence, along with data from other treponemal strains, validated the current convention of dividing the bacterium into three different subspecies: T. pallidum subsp. pallidum (syphilis), T. pallidum subsp. pertenue (yaws), and T. pallidum subsp. endemicum (bejel).3 Within each of these subspecies exist various strains.
Genetics also affords researchers the ability to track the evolution of syphilis. To this end, we collected T. pallidum strains from around the world and used them to construct a phylogenetic tree.4 Our analysis suggested that the closest genetic relatives of syphilis strains are non-sexually transmitted, yaws-causing strains of T. pallidum found in the South American country of Guyana. These strains were collected by Mike Silverman of the University of Toronto and colleagues from children in remote, indigenous communities who had developed unusual lesions. The sores were found in areas of the body, such as the shins, that were consistent with yaws; however, they were more similar in appearance to the smooth chancres of syphilis. Thus, in terms of both genetics and clinical manifestations, these South American strains appear to occupy a space midway between yaws and syphilis. This supports the idea that modern syphilis-causing strains descended from a non-sexually transmitted pathogen in the Americas. However, this study also yielded evidence that some kinds of treponemal disease may have been present in the pre-Columbian Old World.
Unfortunately, with only a small number of T. pallidum strains available to study, a rigorous phylogeographic analysis is difficult. We currently have only five laboratory strains of T. pallidum subsp. pertenue and two strains of T. pallidum subsp. endemicum; even the number of T. pallidum subsp. pallidum strains is relatively limited, with most coming from North America. And because this bacterium can’t be grown in a petri dish, gathering new strains is not easy, typically involving the infection of a suitable rodent with bacteria from a human lesion. In the unlikely event that the strain takes hold, researchers must passage the bacteria through a series of animals in hopes that they will someday grow at a reasonable rate. This is a lengthy, expensive, and laborious process, and due to the scant quantities and poor quality of T. pallidum DNA in infectious lesions, obtaining whole genome sequences from swabs and biopsies has proven difficult. Moreover, yaws is often found in remote, isolated communities, and bejel is exceedingly rare. Although one bejel case was reported from Iran last year, the last reported case before that occurred in Turkey nearly 20 years ago.
Another significant research challenge is the high degree of genetic similarity between T. pallidum strains. Phylogenetic trees based on so few genetic polymorphisms lack resolution, hindering the ability to draw conclusions about the relationships among and within the various subspecies. Moreover, most T. pallidum polymorphisms fall within a single family of rapidly recombining genes, which makes them unsuitable for phylogenetic analysis. Luckily, thanks to recent advances in whole-genome sequencing, a group led by David Šmajs of Masaryk University in the Czech Republic has been steadily turning out the genomes of syphilis- and yaws-causing laboratory strains.5,6 Perhaps one day it will be possible to obtain whole-genome sequences from bejel-causing strains and clinical samples as well.
Another source of new genomes is the T. pallidum strains that infect various wild primate populations in Africa. For decades, positive serological tests have demonstrated that some populations of monkeys and apes suffer from treponemal disease. In West African monkeys, the manifestations are mild and appear to be limited to small sores around the muzzle and near the armpits, if they are present at all; in East African monkeys, the disease is more vicious.
In the late 1980s, researchers at Tanzania’s Gombe Stream National Park reported a gruesome disease that affected the genitals of resident baboons. By the mid-1990s, this disease had been detected at other national parks in the country. At Lake Manyara, New Scientist quoted a wildlife activist saying that “the genitals kind of rot away, then they just drop off,”7 and wardens confirmed that some males had died from the infection.
Working with our colleagues at the Tanzania Wildlife Research Institute (TAWIRI) and Sascha Knauf of the German Primate Center, we subsequently demonstrated that T. pallidum was responsible for these cases.8 Sequencing revealed that two strains collected at different sites in Tanzania exhibited genetic variability, but both were closely related to human yaws-causing strains. In fact, one of the strains was indistinguishable from a group of human yaws strains.9
Yaws is a chronic, debilitating disease that most commonly affects children. In the mid-20th century, the World Health Organization (WHO) launched a yaws eradication campaign that was tremendously effective, treating hundreds of millions of people worldwide with injections of penicillin and eliminating the disease entirely from many countries. Since then, however, yaws has returned. Cases have popped up in Ghana and the Republic of the Congo, as well as in remote areas in other parts of the world with little health infrastructure. These emerging cases—and a 2012 report in The Lancet, which showed that a single oral dose of azithromycin is as effective as a standard penicillin shot—led the WHO to launch a second counteroffensive in March 2012, more than 50 years after the conclusion of the first campaign. The number of active yaws cases today is unknown, but in 1995 the WHO estimated that 2.5 million individuals suffered from yaws or bejel and 460,000 of them were infectious.
Understanding animal-infecting strains of these pathogens is of particular importance to the eradication effort. One of the hallmarks of an eradicable disease is that it occurs only in humans. Otherwise, animals can serve as continuous reservoirs of infection, foiling attempts at eradication. Smallpox, the only human infectious disease eradicated to date, had no known animal reservoir. The two other diseases that are the subject of active eradication campaigns right now, polio and dracunculiasis (i.e., guinea worm disease), also have no known animal reservoirs.
As we learn more about the presence of yaws in wild, nonhuman primates, there is more and more reason to doubt the feasibility of eradication.
As we learn more about the presence of yaws in wild, nonhuman primates, there is more and more reason to doubt the feasibility of eradication. In one ethically questionable experiment described in the early 1970s, researchers demonstrated that a simian strain collected from a baboon in Guinea could indeed cause sustained infection in inoculated human volunteers.10 The entire genome sequence of this baboon strain was recently published, and it is sufficiently similar to the other T. pallidum subsp. pertenue strains sequenced thus far to be considered part of the same subspecies.11 Additionally, areas of Africa with a high prevalence of nonhuman primate infections are the same places in which yaws was once endemic in humans,12 further suggesting that strains may be circulating between humans and nonhuman primates. (See map below.)
Future studies should help clarify the relationship between human yaws-causing strains and nonhuman primate strains, and the risk of the bacterium making the jump from animals to people (or vice versa). In addition, the unique manifestations of the T. pallidum strains in East African baboons may provide a rare opportunity to identify genetic changes associated with genital infection. Is it possible that sexual transmissibility has evolved twice in T. pallidum, once in humans and once in baboons? If so, can we identify parallel genetic changes between the genomes of sexually transmitted strains in the two species? We hope that obtaining whole genome sequences from simian samples will allow us to answer some of these intriguing questions, and we are attempting to isolate new, simian laboratory strains for additional in-depth studies as well.
At the same time, skeletal investigations of ancient treponemal disease continue to forge ahead. As our knowledge of T. pallidum in both past and present populations grows, fostered by molecular techniques that yield novel data, it is possible that a combination of paleopathology, genetics, and wildlife disease ecology will yield a compelling solution to the mystery of syphilis’s origins, and a strategy to slow its spread, once and for all.
Kristin N. Harper is a health researcher at MetaMed, which offers personalized medical research services. She is interested in using population genetics to learn more about our shared past with pathogens. Molly K. Zuckerman is an assistant professor in the Department of Anthropology and Middle Eastern Cultures at Mississippi State University. George J. Armelagos is Goodrich C. White Professor of Anthropology at Emory University, Atlanta, Georgia.
1492: L. PRANG & CO., BOSTON/WIKIMEDIA COMMONS; 1905: PD-LAYOUT; PD-USGOV-HHS-CDC/WIKIMEDIA COMMONS; MID-20TH CENTURY IMPERIAL WAR MUSEUM/WIKIMEDIA COMMONS; LATE 1980s: CHARLES J. SHARP/WIKIMEDIA COMMONS; 2005: CDC/DR. LYLE CONRAD; 2008: © HENDRIKDB/ISTOCKPHOTO.COM; TODAY: JOURNAL OF EMERGING INFECTIOUS DISEASES/WIKIMEDIA COMMONS
Correction (February 3, 2014): This map in this story has been updated from its original version to correctly reflect that the data on nonhuman primates come from research over the last several decades, not just the 1990s. The Scientist regrets the error.
February 5, 2014
Sypilis is a sexually transmitted disease, but we fail to show that it is the practice of bestiality, homosexuality and heterosexuality that combine in the spreading of this disease.
A lot of people have problems with certain theology and its teaching on sexuality, but it is biology that dictates if certain lifestyles are health inhancing.
Toxoplasma is driving AIDS patients mad.
The Laws of Nature MUST be respected, otherwise they will destroy us!
February 5, 2014
No mention of Paul Erlich, and his early 20th century discovery of arsphenamine to cure syphilis?
February 5, 2014
In the "Historia General y Natural de las Indias " written in 1537, by Gonzalo Fernandez de Oviedo,
Governor of the West Indies, is reported the origin American of disease, transmitted to the sailors of
Columbus by indigenous women. De Oviedo, who lives, more than a decade in Hispaniola,
as an spanish administrator, writes: "We can take for sure that this disease comes from India and it is was brought to Europe from the New World. "
The disease, endemic and particularly benign in the island, already called by the Spanish, Bubas, term introduced by Lopez de Villalobos, was called by natives of the place, guayanaras, hipas, taybas, isas. Moreover some authors who would see the syphilitic disease already present in the Babylonian Code of Hammurabi (2200 B.C.), where a disease with characteristics similar to syphilis, called Benu, is cause of withholding of contract, in case of sale of a sick slave. Other cases are described in the Babylonian poem "Gilgamesh", the character of the Mesopotamian myths, mythical king of Sumer, the oldest human settlement in Persia, today's Iraq, near the Persian Gulf. Also reported other cases of presumed syphilis in the Egyptian papyrus Ebers (1550 BC).
In Latin verse "De Gonorrea violenta" Massimo d'Ascoli Pacific (1400?-1500?), speaking of syphilis and its origin, wrote :
"India me genuit, peperit me Gallia mater, me alit Parthenopes: dic mihi quae Patria? ".
February 5, 2014
Is there any change in the bacterial genome as the disease progresses through the primary, secondary, and tertiary forms?
February 5, 2014
Biological basis for syphylis (2006, Clinical Microbiol. Rev.)
Maybe forms have variable morphology (found in many Chlamydiae). T. pallidum is very likely an endosymbiont of amoeba (fits the ecology of both organisms). That suggests that the disease may have indeed been acquired in the New World and carried back to the Old World.
The other key is the structure of new cities as cultural centers - a result of a sudden jump in population arising from boreal forest clearing and the expansion of agriculture between 1000-1500 (Medieval Warm period):
For reference, the estimated global population in the year 1AD was 200 million.
Agreed that warfare during the period helped spread this disease, but it was also likely the arduous trans-Atlantic voyage home in small, cramped ships with poor hygiene, and likely contamination of food stuffs brought home by Columbus, that may have spread the disease rapidly within European cities.
There are several other factors that aided rapid dispersal and intensification of the advanced stages in human hosts that are complex and beyond the confines of a letter reply to your insightful question.
S Churchill PhD
Microbial Ecology and Civil/Environmental Engineering
February 6, 2014
Thank you for this article which contains the breadth and depth to give a really good insight into the problem and the difficulties of giving a clear answer to what may have seemed initially either a simple or to others an insoluble question. It shows how scientists have approached and are still addressing this ancient plague and its related pathogens. It also shows how important it is to get an answer; eradicating the treponemal diseases depends on such investigations. Keep up the good work, and more such excellent articles in The Scientist!
PS: the notes from readers with zany comments on moral codes, religion and historic references without accurate description of the diseases discussed are rather pathetic by comparison.
February 6, 2014
Yes mentioning important people and breakthroughs, in this case one who set a new paradigm in medical treatment and diagnosis is important, if it doesn't detract from the main theme. Not mentioning names of innovative scientists and groups is a general deficit in scientific journalism, especially enhanced by a long term egocentric trend in the USA which seems to want to imply to the reader that nothing outside is worth referencing. This often has a political background, e.g. in the Pasteur Museum in Dole, France, some 10 years ago, Pasteur's student Alexandre Yersin who cultivated and identified the pathogen causing the bubonic plague outbreak in Hongkong was barely mentioned. Yersin codeveloped a bubonic-plague vacine, built up a modern public health program in Vietnam, and introduced quinine-producing trees from South America to combat malaria. His tomb in this communist country bears an inscription 'Benefactor and humanist, venerated by the Vietnamese people'.
February 13, 2014
The recent article by Harper, Zuckerman and Armelagos (1) provides an intriguing perspective of disease. They now recognize tibial periosteal reaction as a sign attributable to treponemal disease, although their citation of Cook and Powell is curious. Cook originally claimed such pathology was caused by trauma (2), a speculative notion that was disproved by Rothschild (3,4). Harper, Zuckerman and Armelagos’ limited comments (1) exemplify the risk of “selective” citation that permeates the approach to paleopathology and identification of disease origins that has so compromised anthropology (5). It was Rothschild and colleagues that first identified treponemal disease as responsible for the high frequency of tibial periosteal reaction in what is now the United States prior to 1400 (6), an evidentiary perspective that Harper, Zuckerman and Armelagos wrongly attributed to Cook and Powell (1). Harper, Zuckerman and Armelagos (1) repeat the oft-rebuffed (7) speculation that the current location of the various treponematoses defines their previous distribution. Our team actually studied the skeletons of individuals with the various treponemal diseases (8) and identified characteristics specific to yaws, the disease actually present (7). Harper, Zuckerman and Armelagos are incorrect as to their comments on absence of pre-Columbian treponemal disease in Europe (1). That comment is valid for continental Europe, but treponemal disease has been clearly demonstrated in Medieval England, apparently from importation of slaves from endemic areas (9).
If a character is identified as critical or at least pertinent to diagnosis of a disease, any investigator must have demonstrated ability to recognize that character. That must be questioned in the case of the authors of Syphilis: Then and now (1), given previous involvement in a paper reporting observation that phenomenon (periostitis) in the Bahamian Blue Hole site (10). The tibia of skeletons from that site were pristine – without a hint of periosteal reaction (11). Such bizarre reporting (10) unfortunately appears representative of historical anthropologic misadventures, given Powell’s (12) reported on Irene Mound. The latter was an oft-studied archeological site in which the frequency of tibial periosteal reaction was variously reported as zero or 100% by senior anthropologists (12). Obviously both cannot be correct and, actually, both were in error (13). Rothschild (13) speculated that periosteal reaction would alter the physical properties of the affected bone and used the second law of thermodynamics to test that theory. Indeed, areas with periosteal reaction had a different heat loss “signature” than that of normal bone or of bone surfaces altered by abrasion (taphonomy). It was suggested that those desiring to recognize periosteal reaction have their perspectives validated by use of such a standard.
Caries sicca is another phenomenon which has specificity for treponemal disease (14), but only when there is adherence to its original definition as depression(s) with star-like cracks radiating from the edges (14). Unfortunately, the definition by Harper, Zuckerman and Armelagos of caries sicca (1) and its application in the anthropologic literature has been more “liberal” with unfortunate loss of the desired diagnostic specificity (14,15).
Review articles on the origins of syphilis and other treponemal diseases must be interpreted in light of the authors’ expertise and adherence to scientific standards of methodology and attribution (19,20). Claude Bernard and Will Rogers have stated that “it is not so much what we don’t know that gets us into trouble, as what we know, that ain’t so” (21). Speculation is a starting point, not a result. It is important to assure information is actually scientifically-documented and that promulgation of results, no matter how “inconvenient” is not compromised by “selective” citation.
1. K.N. Harper, M.K. Zuckerman, G.J. Armelagos, ”Syphilis: Then and now.” The Scientist 2014(2):44-50, 2014.
2. D.C. Cook, “Subsistence and health in the lower Illinois valley: Osteological evidence.” In: Paleopathology at the Origins of Agriculture, M.N. Cohen, G.J. Armelagos, Eds. pp. 235-269. Orlando: Academic Press, 1984.
3. B.M. Rothschild, C. Rothschild, “Analysis of treponemal disease in North Africa: The case for Bejel in the Sudan, but absence in West North Africa.” Hum Evol 11:11-15, 1996.
4. B.M. Rothschild, F.J. Ruhli, C. Rothschild, V. Naples, I. Hershkovitz , J. Sebes, M. Billard, “Virgin Europe: Periosteal reaction prior to the 15th century and the potential influence of slavery.” Paleobios 13:26-31, 2004.
5. B.M. Rothschild, “Extirpolation of the mythology that porotic hyperostosis is caused by iron
deficiency secondary to dietary shift to maize.” Adv Anthropol 2:157-160,
6. B.M. Rothschild, C. Rothschild, “Treponemal disease in the New World: A tale of two seeds.” Curr Anthropol 37:555-561, 1996.
7. B.M. Rothschild, L.D. Martin.” Skeletal Impact of Disease. New Mexico Museum of Natural History, 2006.
8. B.M. Rothschild, C. Rothschild, “Treponemal disease revisited: Skeletal discriminators for Yaws, Bejel, and venereal syphilis.” Clin Infect Dis 20:1402-1408, 1995.
9. B.M. Rothschild, C. Rothschild, “From Poundbury to Spitalfields: 1400 year transition from null state to syphilis.” Amer J Phys Anthropol Suppl 22:204-205, 1996.
10. M.E. Mack, G.J. Armelagos, “Skeletal analysis of the Sanctuary Blue Hole Remains: The Lucayan Taino. Report submitted to the Bahamian Department of Archives, Nassau, The Bahamas, 1992.
11. B. Rothschild, “Preconceived notions and hypothesis testing: Holes in the Blue Hole.”
Chungara, Rev Antropol Chil 32:141-146, 2000.
12. M.L. Powell, L.E. Eisenberg, "Syphilis in Mound Builders' bones": Treponematosis in the prehistoric Southwest. Amer J Phys Anthropol Suppl 26:180, 1998.
13. B.M. Rothschild, C. Rothschild, “Thermodynamic resolution of periosteal reaction and taphonomic change.” Reumatismo 55:195-201, 2003.
14. R. Virchow, “Beitrag zur Geschichte der Lues.” Dermatologische Z 3:1-9, 1895.
15. J.L. Turk, “Syphilitic caries of the skull – the changing face of medicine.” J Roy Soc Med 888:146-148, 1995.
18. M.K. Zuckerman, K.N. Harper, G.J. Armelagos, “Response to Cole and Waldron’s ‘Letter to
19. B.M. Rothschild, “Scientific integrity, conflict of interest and mythology related to analysis of treponematoses: the importance of being ernest.” Chungara, Rev Antropol 37:265-267, 2005.
20. B.M. Rothschild, C. Rothschild, ”Pseudoscience and treponemal disease in the Western Pacific.“ Curr Anthropol 40:69-71, 1998.
21. D. H. . H.Spodick, “On experts and expertise. The effect of variability in observer performance.” Amer J Cardiol 36:592-596, 1975.
February 21, 2014
I believe several sets of skeletal remains of young females were found among the remains of victims found in a cellar in Pompeii, which skeletons were determined to have the evidence characteristic of syphilis. If so, that would definitely put syphilis in the Old World in 79 A.D.
February 28, 2014
Syphilis and yaws are very similar strains of treponeme and probably don't deserve the title of separate subspecies, and they change over time too. Clinically they can be misdiagnosed, e.g. a Haitian boy diagnosed with yaws was shown on further tests to have syphilis. Severe yaws is worse than mild syphilis. The DNA evidence suggests that syphilis is derived from an endemic American strain (causing pinta), but my understanding is that no really good American isolate is available for genome sequencing, and African yaws taken over by slaves has largely replaced the endemic strain, except perhaps in very isolated tribes. See this article in Plos:
March 3, 2014
Researchers have found that certain genes evolve rapidly as disease progresses, as the bacterium tries to evade the host's immune system. In particular, there is a family of genes called the tpr genes, and at least one of them shows all sorts of variation within a single host. You might be interested in checking out the work that the Lukehart lab at University of Washington has done on the tprK gene.
In the future, it would be neat to compare whole genome sequences from samples taken from different organs, to see which genes might be involved in adaptation to different host niches. Luckily for patients (but not so great for researchers working on a project like this), advanced cases of sypilis, where the infection has time to advance, have become pretty rare in high income nations like the US. Still, it might be possible to take a look at this!
March 3, 2014
Hi Steve C,
To the best of my knowledge, the skeletons from Pompeii with putative signs of congenital syphilis still haven't been presented in the peer-reviewed literature, so it's difficult to know whether they actually represent Pre-Columbian syphilis in the Old World. So far, we've looked at dozens of reports of Pre-Columbian syphilis in Europe, and each case has been problematic either because the diagnosis isn't solid or the Pre-Columbian date isn't reliable. The fact that research on the skeletons from Pompeii hasn't been published yet might indicate that there is a problem with the diagnosis. It's pretty tricky work!