Ancient Treponema in Colombia and the peopling of America

Apaper published two days ago, on Jan 22, 2026, reported that the authors had detected and dated the genome of a bacteria belonging to the Treponema genus, which causes syphilis, yaws, bejel, and pinta. The pathogen that was found in human remains that are 5,500 years old, in Bogotá, Colombia.

The paper published in Science is the following: Davide Bozzi et al.(2026). A 5500-year-old Treponema pallidum genome from Sabana de Bogotá, Colombia. Science 391, eadw3020. DOI:10.1126/science.adw3020

The microbe is a Treponema pallidum subspecies, but it is closer to the base of the tree, an older relative of the other branches, that carry subspecies that cause syphilis, yaws, pinta, and bejel.

The paper then tried to date how old this variant, named TE1-3, is. They estimated it split around 13,700 years ago from its sister lineatges: 6768 to 20,592 cal yr B.P. The authors noted that "This suggests that the divergence between TE1-3 and the modern, genomically characterized T. pallidum subspecies occurred during the Late Pleistocene to Early Holocene, closely following the peopling of the Americas, whereas the diversification of the known subspecies themselves took place more recently, within the Holocene ~6000 cal yr B.P. (3622 to 9452 cal yr B.P. 95% HPD)."

As mentioned in previous posts, I wonder if the date fit was "eased" into a recent window that coincides with the currently accepted date for the peopling of America. What would a date of 40,000 y BP have meant?. The Methods don't specify how this date was calculated. The methods describes the process:

"Given TE1-3 is several thousand years older than all ancient T. pallidum sequenced to date, it is an ideal tip calibration for molecular clock analyses. To assess temporal signal, we performed a root-to-tip regression using radiocarbon-dated ancient genomes and collection dates for modern genomes (table S9). This analysis confirmed a strong temporal structure (R2 = 0.67; fig. S17).
We then applied tip-dated Bayesian inference in BEAST2 (49), which yielded a mean substitution rate of 8.86 × 10−8 substitutions per site per year [95% Highest Posterior Density (HPD): 6.5 to 11.2 × 10−8]. The divergence of TE1-3 from the other T. pallidum lineages is estimated at 13,746 cal yr B.P. (95% HPD: 6768 to 20,592 cal yr B.P. )"

However, the root-to-tip regression used a lot of recent data points from the late 1900s, and 2010s a few from the 1700s, and 1500s, and then a few older ones from 1371 AD, 1329 AD, 3438 BP. These are given in their Table S9 (Supplementary table S9. Tip dates used in assessment of temporal signal and root-to-tip regression).

"Regression" is a statistical tool that helps see the trend in a series of scattared data points, assign a function to explain the data and use that function to calculate other data points. For instance, the black dots in the image below are data points and the red line is the best fitting curve (in this case it is a linear regression of the y= a + bx type, the equation for a line. Once the line is known, we can extrapolate the value of y for a given x value.

The fitting isn'd done manually, there is a mathematical-statistical tool to do so. The so called "correlation coefficient" or R squared (R2 mentioned above) its value ranges from 0 to 1, where 0 is no correlation and 1 is a 100% correlation. In this case they state the value is 0.67. But in my engineer point of view, it is heavily skewed by the data points in their Figure S17 shown below, where all the data points (upper left) are lined in vertical strips, and one solitary data point dated 3438 BP in the lower left is used to align the function.

Furthermore, in their Fig. 17, they report two lower values for R2, of 0.294 and 0.127!

Fig. S17 in this paper. Supplementry Figures

The authors caption for Fig. S17. "Root-to-tip regression. Inspection of the temporal signal of the dataset... the root-to-tip regression displaying the temporal signal of the dataset (black line) and of specific clades: TPA in dark green and TPE/TEN in light green. For the global clock rate we observe a rate of 1.336 x 10^-7 with an R2 of 0.667, while a weaker temporal signal (lower R2) but similar evolutionary rates were observed within the other two clades: 1.202 x 10^-7 for TPA (R2 = 0.127) and 1.190 x 10^-7 for TPE/TEN (R2 = 0.294). Plot generated with clockor2 (112)".

The authors also state that " We see that using the even more divergent Cuniculi A genome as a reference pushes the date back in time. Consequently, our estimate when using the Nichols reference genome is best viewed as a lower bound for divergence of TE1-3." It seems that the split between Old World human variants and the Amerindian one would have been older if they used the Treponema paraluisleporidarum Cuniculi A genes as a basal reference! The paper mentions how the "trimmed" genes to adapt it to their needs.

Comments

The paper is relevant because it gives an American origin, and an old date of over 13 ky, to a bacteria with high virulence: "All previously identified virulence factors common to Treponema pallidum are present in TE1-3, including immune evasion and tissue tropism tpr paralogs, suggesting that it possesses the same virulence potential as T. pallidum."

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Patagonian Monsters - Cryptozoology, Myths & legends in Patagonia Copyright 2009-2026 by Austin Whittall © 

2025 Update, Syphillis and the peopling of America

In 2014 I posted on syphillis and the peopling of America. Since then, research and genetic analysis has advanced and new information is available. A paper published in Dec. 2024 in Nature (Ancient genomes reveal a deep history of Treponema pallidum in the Americas) sheds new light on the subject.

Now we know, thanks to genetic studies, that yaws is much younger than previously thought. This paper summarizes its findings as follows:

"This study confirms the presence in the Americas of deeply derived lineages for all three known T. pallidum subspecies prior to the first Columbian expedition in 1492. Consideration of these broad data in two different molecular dating approaches has yielded an upper bound of around 9000 bp for emergence of the most recent ancestor common to all T. pallidum. This post-dates both current genetic estimates for the initial divergence of Indigenous American populations from East Asians43 and archaeological estimates for human arrival in the Americas44. Our data thus support a scenario in which all genomically typed ancient and modern T. pallidum stem from an origin in the Americas during the middle Holocene epoch, possibly as a zoonotic infection from an unidentified host."

In my posts, I mentioned the genetic clock used to time the clades, and the mutation rate. This paper uses (6.7 × 10_-8 and 8.4 × 10_-8 substitutions per site per year) similar to the rate used in the studies commented in my previous posts. So my comments still stand.

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Patagonian Monsters - Cryptozoology, Myths & legends in Patagonia Copyright 2009-2025 by Austin Whittall © 

Syphilis and the Early Peopling of America - Conclusion

Yesterday's post on Treponemal diseases among humans (Treponema pallidum is a bacteria whose subspecies provoke yaws, bejel, pinta and venereal syphilis) suggested that the dates mentioned in academic papers are underestimates. I disputed the dates because they are based on the assumption that humans entered America only 16.5 kya and also because the manifestations of Treponemal disease in Homo erectus was rejected because the calculated mutation rates for the T. pallidum bacteria was considered too slow.

I believe a bit of proof for my position is required, and that is what today's post will look into.

The phylogenetic tree of Treponemal subspecies

In my previous post, I mentioned a paper (Harper et al., 2008) [1], which presented a phylogenetic tree rooted on a non primate species (rabbits, which are affected with venereal syphilis, caused by the Treponema paraluiscuniculi strain). The tree included the human subspecies which cause yaws T. pallidum subsp. pertenue, endemic syphilis or bejel T. pallidum subspecies endemicum and the agent of venereal syphilis, T. pallidum subsp. pallidum is the cause of venereal syphilis.

Additionally it showed a strain of T. pallidum that infected baboons (Papio cynocephalus) in Guinea.

The tree is shown below (from Harper et al., 2008) [1]:

The distance between the rabbit syphilis strains (T. paraluiscuniculi) and the human - baboon strains of T. pallidum (T.p.) is clear, but not so remarkable. What is striking is the very little variation between all human subspecies and the very close proximity of the Baboon Strain from Guinea (1962) to the human pertenue subspecies.

Actually, the simian strain is so similar to the human ones that the paper [1] pointed out that it "could not be distinguished from subsp. pertenue strains using the polymorphic data in this study" [1].

The authors noticed this similarity and genetic closeness, and since the ancestors of Humans and baboons split some 25.7 to 62.5 Mya [2], which is quite a long period of time, they suggest an "early emergence of these strains in human history" [1]. Early indeed, I would say very ancient, rooted in our distant ancestors (H. erectus? H. habilis?).

Another explanation for these very similar strains could be a shared disease that affects both humans and primates, in which there are recent cross-species infections between both parties. This means that baboons may in fact be a reservoir of the disease in the wild or, alternatively that they became infected due to human contact. The authors [1] noted that the wild baboons are infected with yaws in West Africa but could not establish any links to humans. [1]

This alternative was further investigated in another paper by Harper et al., 2012, [3]: During the four years that separated both studies, the Guinean baboon strain collected in 1962 was typed as belonging to the Fribourg-Blanc strain which is "more closely related to T.p. subsp. pertenue laboratory strains than to subsp. pallidum or endemicum strains" [3], in other words it is closer to the yaws vector than to the bejel and venereal syphilis strains. And this is exactly what the tree above shows.

More recently, Zobaníková M et al, (2013), [5] studied the genetic sequence of the T.p. Fribourg-Blanc strain and suggested renaming it as Treponema pallidum ssp. pertenue strain Fribourg-Blanc. They also confirmed that it "clustered with other TPE strains (especially with the TPE CDC-2 strain)", that is, with the human yaws causing T.p. subsp. pertenue of Western Africa and Indonesia. The Tree published in that paper (Fig 1. in [5]) portrays this proximity in a very clear manner.

Harper et al.'s new paper [3] also has a phylogenetic tree, basically the same as the one shown above, from their previouspaper, but now including two new baboon T. p. samples, from olive baboons (Papio hamadryas anubis) taken at two separate sites in the African bush: [3]

The tree shows that the baboon strains from Serengeti National Park (SNP) and Guinea were thee first (oldest) to split from the tree leading to all human strains and to the Lake Manyara National Park (LMNP) baboon strain. This LMNP strain falls within the yaws provoking subspecies in humans (T.p. subsp. pertenue). Below is a Wikipedia photograph of an olive baboon:

So we have two wild varieties found in baboons from two separate locations very distant from each other (Guinea on the West coast of Africa and SNP in Tanzania, on the Eastern side of Africa) and despite belonging to non-humans, they are genetically very close to humans.

But despite the similarity between the human T.p. pertenue strain and the baboon strains, the authors were unable to find which was "the closest relative to the baboon strains among the human subspecies". [3]

As the presence of yaws among baboons was noticed only recently, this fact suggests that it may be a new ailment caused by a novel T.p. subspecies among baboons, however the paper [3] finds evidence to the contrary: these strains are indeed very old and the reasons are the following:

• Humans and LMNP baboons share two synonymous substitutions which could only have arisen from a common ancient origin for the strains shared by both species. The probability of a convergent evolution which replicated the same mutation in different strains affecting different species is virtualy zero. So they were inherited by baboons and humans from a common ancestor.
• The national parks where the baboon strains were collected (SNP and LMNP) are not far from each other (only some 170 km - 105 mi.) yet, the tree shows that the strains are genetically different: four mutations found in four different genes. This diversity implies that the LMNP strain split from the SNP strain a long time ago.

The paper concludes that: [3]

"If baboons are an important source of human infection, one might have expected human subsp. pertenue strains from West Africa to resemble the Fribourg-Blanc baboon strain collected in Guinea rather than other human subsp. pertenue strains from distant locations such as Samoa and Indonesia. Instead, all human T. pallidum strains appear to share a common origin. If further evidence demonstrates that the LMNP strain, like the other baboon strains, diverged prior to all human strains, and that the baboon strains form a paraphyletic group from which human strains are excluded, this will provide further support for the hypothesis that the T. pallidum strains that infect baboons have inhabited their hosts for a long period of time, are genetically diverse, and are distinct from human strains. Further, if T. pallidum strain phylogenies are congruent with host phylogenies, the evidence will indicate that this pathogen has evolved with its primate hosts, including humans, over millions of years." [3]

The non-orthodox comments

Those conclusions are obvious: how could South East Asian and Melanesian human strains resemble African baboon strains unless they shared a common origin. And may I add, that at least is older than the Out of Africa migration of mankind (orthodox science places this event some 70 kya) and maybe older if we accept a Homo erectus migration as the carrier of T.p. out of Africa around 1.6 Mya.

So it is now evident that baboons and humans share a similar strain of this bacteria. It has been with baboons for millions of years (we split form baboons over 25 Mya)[2] and it has mutated very little over this long span of time. The human strains should, by analogy be very ancient too, and looking at the trees depicted above, the distance between human and baboon strains is very small: the branches are all very short. The only exception, the only one with relatively "longer" branches is the venereal syphilis agent, T.p. subspecies palidum (in blue in both trees). This is of course the most recent mutation, which took place in America.

The fact that it is "recent" and appeared in America among humans immediately boxes it into the mental mindset of orthodox scientists as being not older than 15-20 ky. So they will focus their studies and seek support in data that validates this date (being biologists and not anthropologists, they assume the date is correct, so they use it in their calculations).

But in my mental framework, recent means that it is younger than the other subspecies, which may be 1.5 My old, so then this strain is younger than one and half million years old. Just how young depends on the calculations and the assumptions used.

The T.p. bacteria mutates very slowly. This is evident by the lack of diversity found between all strains even though millions of years have elapsed.

The slower the mutation rate the older the most recent common ancestor will be, yet the paper by de Melo et al., [4] dismissed the possible appearance of tremponematosis among H. erectus because they calculated a mean mutation rate of 6.35×10^-10 substitutions⁄site⁄year. Which was, according to them, far too slow compared to other bacteria: E. coli: 4.5–5.0×10^-9, Buchnera 8.2×10^-9 subs⁄site⁄year).

It is worthwhile pointing out that the mutation rates in bacteria are variable, see for instance Helicobacter pylori with rates between 6.2×10^-7 and 9.2×10^-7 [4] which compared to E. coli and Buchnera give a difference of more than two orders of magnitude: 75 to 200 times!

As expected, de Melo et al.'s paper settled for the option which gave them a mutation rate for T.p., which is intermediate between both extremes (of 4.09x10^-8 subs⁄site⁄year). A Salomonic decision which fitted neatly with their calculations for an American origin for T.p. subsp. pallidum between 16.5 and 5 kya.

But this time frame differs with the conclusions of Harper et al.: "...this pathogen has evolved with its primate hosts, including humans, over millions of years." [3]

I decided to check their calculations, and the values I obtained are shown below:

De Melo et al., use the expression TMRCA = K ⁄ 2 x Rate. In their paper they indicate that K= 2,96 x 10^-4 subs⁄base pair. Which arises from dividing the 327 substitutions detected by the 1.1 Million base pairs found in T. pallidum.

The "Rate" is the "substitution rate" or mutation rate of the bacteria being studied.

I used the "rates" that they obtained in their paper for each of the hypothesis that they tested; I also used their average mutation rate for T. pallidum, and for each of them I used the above formula to calculated the TMRCA. I was quite surprised to see that my values differed from those calculated in the paper[4] by between 3 and 20 times! I mentioned yesterday that I could not understand their calculations (I am an engineer by the way so I am very used to cracking numbers and equations), and today I ratify my comment. I am baffled.

The TMRCA calculated using their expression are far to "young" and in fact are smaller than the ages calculated by de Melo et al.

Closing comment

In my opinion the reason for this discrepancy and the recent age obtained for TMRCA using the expression above is due to the "Rate" used in the formula.

The value for the mutation rate for T. pallidum is much lower than estimated by de Melo [4]. Using a smaller "rate" in the expression above will give a higher -older- value for TMRCA. And, as Harper et al., proved [1], T.p.'s mutation rate is indeed extremely low, and that is why there is so little difference between the baboon strain and human strains after such a long period of time since the divergence of both our species.

The fact that other bacteria mutate quicker is irrelevant, each microbe adapts to its host and if doing so implies less mutations, it should be recognized and accepted.

The closing comment is therefore: the human versions of T. pallidum are much older than the dates proposed by de Melo et al., [4], the youngest of all subspecies, the venereal disease agent, T.p. subsp. pallidum very likely originated in America as thjey suggest, but did so long ago, well before the 16.5 ky indicated by them [4]. The H. erectus origin of our T.p. subspecies can not be dismissed in this context:

The similar geographic ranges of the oldest subspecies of T.p., (yaws causing agent pertenue) in Southeast Asia and Africa matches that of Homo erectus in Asia and its homeland in Africa. This may not be a coincidence, but a casual relationship: T.p. reached Asia inside its host, H. erectus.

The other mutations of T.p. (such as bejel) match the regions occupied by Eastern Neanderthal and Denisovans... could there be a relationship between them and the bacterial strain?

Yesterday's paper showed that there were two possible mutational routes from the African yaws strain or the Eurasian bejel strain to the Amerindian yaws (and venereal syphilis) strains. The yet non-sequenced pinta strain in America may hold the key to understanding which of those routes is the most probable one:

• If it is the African yaws strain, maybe it shows the Modern Human emergence and migration OoA carrying the variant that eventually reached America.
• If it is the Eurasian Neanderthal strain, then it was them who reached the New World, originating pinta there and later Amerindian yaws.

Further research is needed to clarify the issue.

Sources

[1] Harper KN, Ocampo PS, Steiner BM, George RW, Silverman MS, et al. (2008). On the Origin of the Treponematoses: A Phylogenetic Approach. PLoS Negl Trop Dis 2(1): e148. doi:10.1371/journal.pntd.0000148
[2] Galina V. Glazko and Masatoshi Nei, (2003). Estimation of Divergence Times for Major Lineages of Primate Species. Mol. Biol. Evol. 20(3):424–434. 2003 doi: 10.1093/molbev/msg050
[3] Harper KN, Fyumagwa RD, Hoare R, Wambura PN, Coppenhaver DH, et al., (2012). Treponema pallidum Infection in the Wild Baboons of East Africa: Distribution and Genetic Characterization of the Strains Responsible. PLoS ONE 7(12): e50882. doi:10.1371/journal.pone.0050882
[4] de Melo FL, de Mello JCM, Fraga AM, Nunes K, Eggers S., (2010). Syphilis at the Crossroad of Phylogenetics and Paleopathology. PLoS Negl Trop Dis 4(1): e575. doi:10.1371/journal.pntd.0000575
[5] Zobaníková M. et al., (2013). Whole genome sequence of the Treponema Fribourg-Blanc: unspecified simian isolate is highly similar to the yaws subspecies.. PLoS Negl Trop Dis. 2013 Apr 18;7(4):e2172. doi: 10.1371/journal.pntd.0002172. Print 2013.

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Patagonian Monsters - Cryptozoology, Myths & legends in Patagonia Copyright 2009-2014 by Austin Whittall © 

Syphillis and the Early Peopling of America

A A spring-shaped bacteria belonging to the genus Treponema causes several diseases in humans, one of them is well known for the devastating effects it produced in humans until the advent of antibiotics: syphilis. It is also the only venereal treponemal disease, because the other three (yaws, bejel and pinta) are transmitted via oral and⁄or skin contact.

Today's post will look into the treponemal diseases to see if it can help us gauge when America was peopled and if any of our more distant ancestors made it to the New World before Homo sapiens did.

Treponemal disease

There are four different varieties of the spirochete Treponema bacteria, and each one causes a different disease: T. carateum provokes pinta, T. pallidum subsp. endemicum causes bejel, also known as endemic or non-venereal syphilis, T. pallidum subsp. pertenue leads to yaws and T. pallidum subsp. pallidum is the cause of venereal syphilis (it is pictured above).

The interesting part is that they are morphologically and serologically identical and the genetic variability between them is very small (0.2% between yaws and syphillis) so this makes it very hard to distinguish between them (there are no specific serological tests to pinpoint the type of infection affecting individuals) [3].

The genetic sequencing of all the subspecies of T pallidum (except one, the vector of Pinta, T. carateum -more on this below) shows that ther are five genogroups which do not identify "discrete organisms for each treponemal disease [instead] there may in fact be a genetic continuum of the pathogenic Treponema, individual components of which affect pathogenesis in an individual host in concert with social or environmental factors that influence routes of transmission and disease manifestations." [3].

In other words, they are virtually identical but are assumed to be different "subspecies" because they appear in different geographical areas around the world and produce manifest themselves in different manners and virulence.

The range of each "subspecies" is the following: Pinta is quite rare and was found in Central and South America. Yaws appears across Central and Western Africa, Southeast Asia, New Guinea, Northern Australia, Indonesia and the coastal regions of tropical Central and South America. Endemic Syphilis is found in the Middle East, the Balkans, South Central Asia, North Africa and central Australia. Venereal Syphilis, is global.

A genetic analysis

The controversy over the origin of these diseases continues: Is venereal syphillis an American disease or did it originate in the Old World?, how are the different subspecies related? The modern tools of genetics will be able to settle these issues once more information is obtained and analysed. However initial studies by Harper et al, 2008 [5](which regrettably do not include the analysis of Pinta) have reached some interesting conclusions:

• A maximum likelihood tree placed all of the T. pallidum subspecies (strains) within a single clade showing their very close relationship in comparison to other Treponemes which infect primates.
• Two of the subspecies subsp. pallidum (venereal syphillis) and subsp. endemicum (endemic or non-venereal syphillis) grouped seprately from the subsp. pertenue (yaws).
• The different strains within subsp. pertenue are closer to the root of the tree, meaning that it is the "oldest" lineage in the family, the ancestral population to all other subspecies.
• pertenue (yaws) and endemicum (non-venereal syphillis or bejel) are genetically closer to each other than to the venereal strain subsp. pallidum. The paper [5] obviously interprets this as meaning that venereal syphillis is caused by the youngest strain (the one that "diverged most recently" [5])

The geographic distribution of the diseases is used together with the Treponemal gdp gene sequences for each subspecies to try to elucidate the realtionship and origin of each strain. The following map which I have adapted from figure 4 in [5] shows the reasonable proposal of Harper et al., (2008) [5]:

Global distribution of Treponemal diseases and their origin. Adapted from [5]

The map is based on the assumption that the Old World yaws is the ancestral form, and that the gdp gene's GATG sequence is the basal one. As the map above shows (red shaded regions are those with different varieties of yaws), this ancestral form is found in Southeast Asia and Africa. I added the Pinta strain, in pink, in America, absent in the original map because it is relevant as we will see below.

This strain mutates into another variety of yaws, only found in Africa, with the GATA sequence (in other word the final "G" mutates to "A").

It also mutates by switching the second "A" for a "G", becoming GGTG in Eurasia and North Africa, becoming the vector for Endemic Syphillis (shaded green on the map).

This ties in with the close genetic distance between the endemicum and pertenue subspecies mentioned further up.

The interesting part is that the American variety of yaws has a very distinct sequence, removed by three mutations from the Eurasian GGTG or the African GATA, the Amerindian yaws sequence is: AGGA which is also the same sequence found in the pallidum subspecies!, the one that causes venereal syphillis. In other words it seems to prove that this disease appeared in America as a more virulent strain of yaws.

It is a pity that the agent causing Pinta was not sequenced, it probably lies somewhere in between the Eurasian strain (for endemic syphillis) and the Amerindian yaws strain.

The paper proposes that this three mutation gap between New World yaws (and venereal syphillis sequence) and the Old World sequences is split into two steps: they place a hypothetical intermediate strain one mutation away from either the African or the Eurasian strains (GGTA) and this strain with two mutations becomes the AGGA Amerindian one:

"The pattern of substitutions suggest that a hypothetical intermediate strain, arising from either the group II subsp. pertenue strains [African yaws] or endemicum strains [Eurasian endemic syphillis], once existed and was a progenitor to both New World subsp. pertenue[yaws] and to all subsp. pallidum [venereal syphillis] strains. This data also suggests that the New World subsp. pertenue strains belong to a group distinct from the Old World subsp. pertenue strains, occupying a phylogenetic position somewhere between Old World non-venereal strains and modern subsp. pallidum strains." [5]

The authors conclude that " a T. pallidum strain from the Americas was introduced back into the Old World, probably as a result of the European exploration of the Americas, becoming the progenitor of modern syphilis-causing strains. Third, modern subsp. pallidum [venereal syphillis causing] strains disseminated from Europe to the rest of the world." [5].

I do believe that the tree is coherent and the sequence propsed is also adequate, I also agree that the venereal syphillis is the most recent strain to appear, my doubts are, as always, on the issue of the dates assigned to these events. The paper does not make any conjectures regarding dates it merely indicates that the Amerindian strains "diverged most recently, indicating that they emerged relatively recently in human history" [5], which if in line with mainstream science means any time between the discovery of America in 1492 AD and 16,000 ya -the date that Asians are supposed to have entered America from Beringia.

These findings are supported by another paper (Melo et al., 2010) [1] which statistically tests three scenarios and concluded:

1. A recent emergence of venereal syphilis. This rececent (500 years ago) origin is found "utterly unlikely, be it in the New or the Old World". [1] This time span was chosen because the first reports of the epidemic of syphilis which quickly spanned Europe, are from 1495. By the way, this epidemic reached India in Portuguese ships (1498) and Japan (1510), killing thousands. The disease seemed to mutate to a more benign and slower-killing strain.
2. An Homo erectus origin. Treponematoses have been plaguing our ancestors at least since the days of H. erectus. But it is not likely that the strain that caused it is one of the contemporary ones. It is probably due to "ancestral forms still unknown". [1] I differ, but we will go into that later.
3. If it emerged in the Americas between 16,500 and 5,000 years ago. They find it the most likely alternative. We will discuss it below.

The dates. As usual the paper is based on the orthodox dates for the "time of the first colonization of the Americas", which is set at 16,500 years. The other date of 5 kya is based on "the oldest probable evidence of venereal syphilis in the world." [1].

What would they have concluded if instead of 16.5 kya they had used 75 kya or 100 kya? Later we will try to work it out.

Melo et al., using this 16.5 - 5 ky time range conclude that they could not reject the hypothesis based on the mutation rates of treponemes, which is "compatible with those observed in other bacteria" (see my comments below). They are cautious however because there are "claims of precolumbian venereal syphilis outside the Americas [to be] taken into account", so they conclude that "the place of origin remains unsolved." [1].

In other words, it could have originated in Asia and moved from there into America and also remained in Asia or, originated in Asia and only moved into America or, finally, appeared exclusively in the New World and reached the Old World after the voyages of Columbus in 1492.

What do ancient remains tell us?

Since Pinta leaves no skeletal marks, we cannot say much about its prevalence in the past. The other forms of treponemal diseases do leave very distinct marks on the bones and can be identified (though as usual, there is always some disagreement between experts).

The paelopahtological studies. Amerindian remains dating back to 7,000 years ago [5] show that treponemal disease afflicted the natives. There are some disputed and isolated cases of pre-Columbian treponemal disease in the Old World [5].

Melo et al., 2010 [1] review these studies and finds that "treponemal diseases in general were well established in pre-Columbian times all over the world. The oldest dates we are aware of refer to bejel in Sudan 15,000 yBP, yaws in Florida some 7,900 yBP, and treponematosis in Peru more than 8,000 yBP" as well as those from Indian Knoll in the U.S. (5,300 yBP) and Colombia (5,000 yBP) with osseous evidences of venereal syphilis in the whole World, and in my opinion support an Amerindian origin of this disease. [1]

Checking the calculations

Melo et al., [1] assumed that the venereal syphillis subspecies split from the others, in America between 16.5 and 5 kya, and then calculated that the most recent common ancestor for the human treponeme group lived 77.4 kya (this is their 95%HPD), which means that H. erectus did not have a "modern" human kind of treponeme. This time frame allows for Old World dispersal of yaws and endemic syphillis as well as an American or Asian origin of venereal syphillis.

Which is very neat and tidy. But why did they dismiss the appearance of treponematosis in H. erectus? Well, I have gone over their Table 2 several times and believe that there is a mistake in the table: the other two tables give the MRCA for venereal syphilis as younger than the whole group, but this table has syphilis as older than the yaws - bejel subspecies, which contradicts the conclusions of Harper et al., [5] mentioned above, where yaws mutated into venereal syphilis. The text itself mentions 175,000 years as the MRCA for one of the subspecies but the table says 1.75 My... it is confusing! What is clear is that the age of these bacteria would be similar to that of H. erectus and the authors conclude that the microbial mutation rate would be too slow, so this hypothesis is discarded.

I am inclined to believe that the date may be in fact older than 16 kya. Looking at Table 4, the oldest date of 77.4 ky for all human treponemes is linked to a 12.5 ky date for the subsp. pallidum. Roughly 6.2 times greater than the MRCA for venereal syphilis.

If we assume that human treponematosis appeared 300 kya, the venereal strain would have appeared: 300/6.2 = 48 kya in America, which is in line with some of the oldest (not accepted by orthodoxy) sites in the Americas. This would imply a Neanderthal origin for these diseases. Extrapolating further, if it appeared 1.6 Mya among Homoe erectus, then syphilis would have appeared 258 kya, also, among Neanderthals. Or maybe among East Asian H. erectus.

Looking at the map and the temporal sequence suggested by Harper et al. the following scenario seems plausible and maybe even probable:

• Since the oldest genetic sequence is found in Africa and Southeast Asia, we can assume an African origin and an out of Africa Migration of this oldest sequnce, with the first OoA migrants: H. erectus.
  The coastal route along the Indian Ocean towards Indonesia is actually where this subspecies prevails and it is identical to the territories once occupied by Homo erectus. It also coincides with the Y chromosome haplogroup C range, which I have suggested mirrors the OoA migration of H. erectus.
• Those who remained in Africa mutated into a second clade of yaws, and it is still found there, and only there.
• The Asian variant carried by H. erectus mutated into the bejel or endemic syphilis kind, found only in Eurasia and North Africa (maybe due to a back-migration). When did this take place? Was it among H. erectus? Denisovans? Neanderthals? Surprisingly this green area is very similar to the range occupied by Neanderthals. The Australian patch may reflect a Denisovan admixture.
• Then these people moved into America, where the mutations leading to the American pinta (whose sequence is not known, but I bet will be found to be intermediate between the Eurasian bejel and the Amerindian yaws) arose. Very likely the Neanderthals took it into America and there it mutated again, into the Amerindian yaws - venereal syphilis kind.
• Perhaps it was quite lethal in America, maybe Neanderthal carried the benign kind. Absent in the Old World, when Columbus' crew took it back to Europe, it spawned a colossal epidemic.

See Second part and conclusion of this post.

Pinta

Pinta which is said to be caused by Treponema carateum is quite unique among all the Treponemal diseases because it is the least aggressive one and only causes changes in the color of the skin of those afflicted with it. [5]

It is also unique because it is an exclusively American disease. But it has become rare: at one time it was endemic in the Caribbean, Central America and Northern South America, now it is hard to find. [5]

I included it in the map above (pink shaded region), because it is quite interesting in its distribution: it is in the region where haplogroup C (Y chromosome) is found in America, Colombia, Ecuador, Mexico.

Paleopathological studies of Pinta are not possible because it leaves no visible lesions on the bones (like the other treponemal diseases do), so it is quite elusive!

The problem is that there is no pinta available for study: "no strains of this organism are available" [3], so it could not be sequenced. Additionally, "Treponema carateum is the etiological agent of pinta, although no isolates of this organism are known to exist" [4], the actual bacteria has not been collected and stored in any lab!

It was "Once found in Central and South America, this mild disease is characterized solely by alterations in skin color.[...] no strains or samples of T. carateum survive. Furthermore, it is uncertain whether the disease pinta still exists. No cases have been reported to the World Health Organization from the former endemic countries Mexico or Colombia since 1979." [5].

The issue of mutation rates is controversial: allow me to quote "Our data suggest that the T. pallidum genome is evolving in a largely clonal manner amenable to phylogenetic analysis" [5]. This is interesting because clonal evolution stabilizes favorable multilocus associations, "restrained recombination on an evolutionary scale, with genetic exchange scarce enough to not break the prevalent pattern of clonal population structure" [2]

Actually scholars recognize that "A limitation on comparative studies has been the small amount of variation present in the T. pallidum genome [...] the level of polymorphism found between T. pallidum strains is quite low [...] for this reason, the level of resolution in the phylogenetic tree is relatively poor."[5]

The authors of one paper conclude that "it is unlikely that these SNPs have accumulated in a clockwork manner." [5].

I have expressed my reservations regarding "clocks", and in the case of T. pallidum, with a small genome, clonal evolution and limited variation between the different subspecies, it is in my opinion difficult to consider if a mutation rate is slow, fast or correct (as Melo et al. do). Perhaps it is a slow evolving bacteria, 10 or even 100 times slower than other bacteria. The dates calculated on bacterial mutation rates may be well off mark.

Sources

[1] de Melo FL, de Mello JCM, Fraga AM, Nunes K, Eggers S, (2010). Syphilis at the Crossroad of Phylogenetics and Paleopathology. PLoS Negl Trop Dis 4(1): e575. doi:10.1371/journal.pntd.0000575
[2] Michel Tibayrenc and Francisco J. Ayala, (2012 Reproductive clonality of pathogens: A perspective on pathogenic viruses, bacteria, fungi, and parasitic protozoa. PNAS (2012) www.pnas.org/cgi/doi/10.1073/pnas.1212452109
[3] Arturo Centurion-Lara et al., (2013). Fine Analysis of Genetic Diversity of the tpr Gene Family among Treponemal Species, Subspecies and Strains. PLoS Negl Trop Dis. May 2013; 7(5): e2222. Published online May 16, 2013. doi: 10.1371/journal.pntd.0002222
[4] RR Gray et al., (2006). Molecular Evolution of the tprC, D, I, K, G, and J Genes in the Pathogenic Genus Treponema. Mol Biol Evol (2006) 23 (11): 2220-2233. doi: 10.1093/molbev/msl092. First published online: August 22, 2006
[5] Harper KN, Ocampo PS, Steiner BM, George RW, Silverman MS, et al., (2008). On the Origin of the Treponematoses: A Phylogenetic Approach. PLoS Negl Trop Dis 2(1): e148. doi:10.1371/journal.pntd.0000148

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