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Health interventions can change systemic and cultural determinants of STI/HIV transmission

30 Mar, 17 | by Leslie Goode, Blogmaster

The causal pathway linking intimate partner violence (IPV) and health may be two-way.  We are used to thinking of IPV as a determinant of STI; but sexual health also has an impact on IPV.  This, at any rate, is the conclusion of a recently issued working-paper from the US National Bureau of Economic Research uniting a highly interdisciplinary team of researchers from a range of US universities and medical institutions.  The researchers seek to demonstrate that health is kind of human capital, and that a technological advance in medicine can affect ‘some of the most frustratingly persistent social problems’.  This finding will be particularly interesting to readers of this journal.  Health, in the context of this study, happens to be sexual health, and the technological advance is the introduction of HAART in 1996.

Papageorge & Pollack (P&P) base their work on data from the Women’s Intra-Agency HIV Study (WIHS), and compare a cohort of HIV+ women who were, in 1996, just beginning to experience immune system deterioration, with two control cohorts, using a ‘difference in difference’ approach.  One control consisted in HIV+ women not experiencing such effects, another in HIV- women included in the same WIHS data.  Much of the researchers’ task consists in establishing the relative dependence/independence of causal pathways linking IPV with drug use, perceived mental and physical health, and employment.  Their headline finding is a c.10% reduction in IPV a c.15% reduction in IDU attributable to HAART introduction.

The idea that the causative link could flow from STIs to IPV, as well as from IPV to STIs, may not be new to our readers.  Indeed, an ongoing concern for sexual health interventions has been that STI/HIV disclosure (a potentially important element of risk reduction) could result in domestic violence (Partner delivered STI self-testing (STI/blogs)).  This has not prevented other studies from pointing to a potentially positive role for sexual health clinics in relation to IPV (Lockart & McNulty (STIs); Decker and Silverman I (STIs); Decker & Silverman II (STIs)).  The nature of IPV itself is not always well understood, and probably varies with social and cultural context.  For example, it is not restricted to short-term or casual relationships (Silverman & Raj (STIs)), and may be reciprocal (Norris & Hindin (STIs)) as well as man-on-woman.  The nature of the causal link with HIV/STI might be expected to vary with the nature of the IPV itself.

So there is nothing new about the idea that a change in respect to sexual health could influence IPV.  What P&P contribute to the debate is genuinely encouraging, for all that.  Recent characterizations of the global efforts to curb the HIV epidemic (e.g. UNAIDS: On the Fast Track) make a two-fold classification of interventions into, on the one hand, biomedical interventions such as PrEP or cART, and, on the other, vaguer, and longer-term non-biomedical interventions such as legislative or attitudinal change.  The latter correspond to systemic or cultural determinants of sexual health that can seem to mark the ultimate limits on sexual health interventions rather than realistic targets for those interventions.  However, P&P point in this report to the case of a biomedical intervention that would, for once, seem to have achieved something more than an immediate biomedical impact.  HAART introduction, on P&P’s interpretation, effectively provided an additional ‘source of human value’ – an enhancement of women’s social ‘capital’.  Thereby, it would seem to have impacted the fundamental social and cultural determinants of sexual health – those ‘frustratingly persistent social problems’ that constitute the constraints within which sexual health is normally compelled to operate.

Location of HIV-2 emergence determined by distribution of indigenous cultural practices of male circumcision

16 Jan, 17 | by Leslie Goode, Blogmaster

Sousa & Vandamme demonstrate a robust correlation between HIV-2 prevalence at the time of the 1980s surveys and the absence of indigenous practices of male circumcision earlier in the century.  This is a complex and interdisciplinary study, involving some of the earliest large-scale, West African serological surveys of HIV-2 (1980s) and extensive ethnography of the region throughout the twentieth century.

HIV-2 seems to have crossed the species barrier into humans from a primate called the ‘sooty mangabey’.  The two epicentres of the 1980s HIV-2 epidemic – south-west Côte I’Ivoire and Guinea Bissau – correspond to the two points along the band of sooty mangabey territory where ethnic groups were to be found who did not practice circumcision (Côte I’Ivoire), or performed it only late in life or very intermittently (Guinea Bissau).  The complexity of this study arises from the fact that, thanks to waves of islamicization, male circumcision has been widely adopted across the region even in areas where it was traditionally prohibited.  Hence investigation of the correlation with HIV-2 emergence, probably in the 1940s, required the authors to go back to ethnographic accounts preceding islamicization.

Of course, the certainty of a causal link cannot be established.  But Sousa & Vandamme discover a strong negative correlation between male circumcision and HIV-2 (Spearman rho = -0.546).  Their results are supported by studies that establish the same negative relationship with HIV-1, both in sub-Saharan Africa (Moses and Plummer) and, more recently in Papua New Guinea (MacLaren & Vallely/STIs).  A likely causative mechanism might be the prevalence of ulcerative sexually transmitted infections (Weiss & Hayes/STIs).

So Sousa & Vandamme offer an additional ‘ecological’ reinforcement of the public health rationale for encouraging voluntary male medical circumcision (VMMC).  Yet what is also interesting, from a public health perspective, is the importance their study attributes to culture in the adoption of a practice like male circumcision.  In the present case, for once, the impact would appear to have been very positive from the medical point of view. The authors speak, for example, of islamicization, along with ethnic intermarriage in the cities, as having given rise to ‘social pressure to be circumcised in order to be accepted by women’, and the ‘abandonment of traditional prohibitions of male circumcision’. Of course, the impact of indigenous culture may often be less benign from a medical point of view – as the source of conservative attitudes that tend to hold back and limit the uptake of VMMC.  As, for example, where males have seen male circumcision as the practice of potentially hostile neighbouring groups (Cultural constraints on uptake of circumcision/STI/blogs), or as a practice uniquely suited to those younger age groups on whom it was traditionally performed (Mbabazi/STIs).  But, either way, it is noteworthy that the influence of local culture would often seem to be so decisive.  So there may be an argument, for electing to promote infant circumcision, as an evidently medical practice that runs less risk of falling foul of prevailing cultural attitudes that restrict ‘demand’ (Gray & Kigozi/STIs; Feasibility of infant circumcision/STIs/blogs).

 

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Global patterns in ante-natal syphilis prevalence: Why is sub-Saharan Africa different?

18 Jul, 16 | by Leslie Goode, Blogmaster

‘Can a meaningful pattern be discerned in the large variations in syphilis rates over the last century?’ This is the question addressed by a recent systematic review – Kenyon & Tsoumanis (K&T) – based on published data on ante-natal syphilis prevalence (ASP) from those countries for which that data is available since at least 1951.   This cutoff reduces the number of countries that qualify for inclusion, but allows more recent trends in the late twentieth, and early twenty-first, centuries, to be set against the background of the impact of the introduction of penicillin in the 1950s. A pattern emerges from the data, which K&T then to seek to explain by investigating its association with various potential variables through multivariate analysis: per capita GDP; circumcision practice; health expenditure; efficacy of diagnosis/treatment; geographical region.

The pattern itself is: in most parts of the world, a more or less steep decline following the introduction of penicillin – ultimately, by the 1990s, to below 1%, and by the 2000s, to below (massively below, in many cases) 0.5%; in sub-Saharan Africa alone, a decline plateauing out at around 6% up until the end of the twentieth century, when there is a further decline to just above 1.5%.  A limitation of the study is its concentration on eleven countries for which ASP data is available from before the days of penicillin, with only two of those countries being in sub-Saharan Africa (South Africa and Zimbabwe).  So far as concerns more recent evidence for ASP prevalence, the kind of rates that the authors give for SA and Zimbabwe seem, broadly, to be replicated in other countries of sub-Saharan Africa (Otieno-Nyunya & Kaiser/STIs (Kenya); Makasa & Sandoy/STIs (Zambia); Kirakoya-Samadoulougou & Nagot/STIs (Burkina-Faso);  Ardu-Sarkodie & Peeling/STIs (Ghana), and their rates for the other regions to be replicated in other non-sub-Saharan African settings (Cheng & Cai/STIs (China); Galdava & Domeika/STIs (Georgia) Thirumoorthy & Lim/STIs (Singapore)).

As for the explanation of this pattern, the authors find no association on multivariate analysis with any of their potential variables, save with residence in sub-Saharan Africa.  This is itself an interesting negative finding, and prompts the authors to consider other population-level correlations also included in the evidence reviewed – notably, with prevalence of HIV and HSV-2; ‘the populations that in the 1990s had high prevalences of syphilis and HSV-2 went on to have high HIV prevalences’.  The correlation with prevalence of HSV-2 is of particular interest because it is unlikely that the prevalence of the one infection could have influenced that of the other (see also: Hochberg & Dandona/STIs).  To K&T, it suggests the likely importance of ‘more connected sexual networks’ and ‘greater partner concurrency’ in explaining traditionally – and currently – high relative ASP levels in sub-Saharan Africa.  However, they refer to studies that contest this hypothesis, and emphasize the need for further research to elucidate the factors underpinning difference in syphilis rates – especially given the possibility that the successful use of ART in those countries may be accompanied by the re-establishment of former sexual networks.

Tracking the origin, early spread, and ignition of pandemic #HIV-1 through new approaches to phylogenetic analysis

17 Nov, 14 | by Leslie Goode, Blogmaster

“Distribution of HIV-1 subtypes in a population”, state Mumtaz & Raddad (STI) in a study of the HIV pandemic in the Middle East, “tracks the spread and evolution of the epidemic”.  Various studies covered in our previous blogs have attempted to read the history of the progress of the HIV epidemic through the evidence of the distribution of HIV genetic sub-types: Tatem & Salemi (STI/blogs) have investigated its spread throughout Africa; Zhao & Roca (STI/blogs) pass beyond the human epidemic to consider the genetic evidence for repeated transmission from chimpanzees to humans.

Now Faria & Lemey (F&L), in a paper recently appearing in Science, offer an account of the critical early phase of limited spread within Central Africa and the ignition of pandemic HIV-1 around 1960, bringing statistical approaches to bear to HIV-1 sequence data.  F&L produce a time-scaled phylogenetic “tree” of HIV-1 group M lineages, matching these up in each case with the geographical location of their earliest manifestation.

This approach points to the very strong likelihood (PP = 0.99) of an origin of the HIV1 epidemic in Kinshasa around 1920. Study of lineage migration shows comparatively early spread from Kinshasa to Brazzaville (Republic of Congo (RC)), and Mbuji-Mayi and Lubumbashi (southern Democratic Republic of Congo (DRC)) along the railway network, and its arrival around a decade later in Bwamanda and Kisangani (northern DRC).  The crucial period around 1960 (1952-1968) sees, for group M HIV-1, an exponential growth in levels of M-group transmission, while growth in group O transmission remains at previous levels.

But the most interesting aspect of the study relates to conditions around the sudden surge in group M HIV-1 transmission, as indicated by the accelerated ramification of viral lineages during the crucial period.  The authors consider the hypothesis that associates this ramification with the geographic dispersal of the epidemic, with the lineages emerging in the more widely distributed populations now being infected.  They reject this hypothesis, however, on the grounds that, when the epidemic history of lineages maintaining ancestry within Kinshasa is constructed, these turn out to exhibit phylo-genetic characteristics that are comparable to those of lineages in central Africa.

They conclude that the crucial explosion of pandemic HIV-1 transmission probably occurred in Kinshasa as a result of a historic contingency affecting a particular population subgroup.  Prime contenders are iatrogenic transmission as a result of the administration of unsterilized injections at STI clinics, and/or post-independence changes in sexual behaviour e.g. among commercial sex-workers.  The authors find support for the iatrogenic hypothesis in a study of the hepatitis C virus in the DRC which shows that it exhibits an age cohort effect, and in reports of an epidemic of hepatitis B in Kinshasa around 1951-2.

Was the “sexual revolution” triggered by the decline of syphilis?

26 Mar, 13 | by Leslie Goode, Blogmaster

The year 1939 saw total US syphilis deaths at 15 per 100,000 and syphilis deaths of black males at 72.5 per 100,000: this is a death rate comparable to that for HIV/AIDS at the height of the epidemic in 1995 when total deaths and deaths of black males stood, respectively, at 16.2 and 80.2 per 100,000.  Subsequently, in the late 40s and early 50s, incidence and mortality from syphilis were to fall precipitously – thanks to penicillin.  A recent paper in the Archives for Sexual Behavior by an economist, Andrew Francis, argues for the importance of this collapse in the “cost” of syphilis in spurring the sexual revolution (http://link.springer.com/article/10.1007%2Fs10508-012-0018-4). His exploration of this hypothesis prompts general reflection on the link between the “cost” of disease (which he equates with absence of an effective treatment) and sexual behaviour.

The paper correlates data across US states on syphilis incidence and mortality with measures of “risky non-traditional sex” – which, in the context of the poverty of relevant data for the period, is evaluated on the basis of gonorrhoea rate, illegitimate birth ratio and teen birth share.  Coefficients are given from regressions of measures of sexual behaviour on indicators for the number of years since syphilis collapse (which varies by state).  As regards illegitimate birth ratio and teen birth share, a positive correlation emerges which goes back as early as three years or less from syphilis collapse; gonorrhoea, however, continues to decline from its WW2 peak, as we might expect.

Ultimately, however, Francis’s argument rests also on the claim that his own explanation of sexual revolution fits the facts better than the alternative explanations, of which the most familiar is that “anti-conception technology”, especially the pill, played a decisive role.  Francis admits that, from the late sixties, conception technologies and measures of risky behaviour increase simultaneously.  Yet measures of risky sexual behaviour, he claims, had already been rising sharply for a decade before anti-conception technology began to make its impact.  His own data show that the two changes do not coincide.   Nor do measures of permissive values or religious observance show any discontinuous change that would coincide with the increase in risky behaviour.  So if Francis’ hypothesis is wrong, then the precise timing of the sexually revolution remains mysterious.  Francis gestures vaguely towards the possibility of the change in sexual behaviour being triggered by still less definable “economic, social and cultural changes”.

The obvious recent parallel to the syphilis collapse in our own times would be impact of the introduction of HAART on HIV/AIDS mortality.  The concern that an effective therapy might lead to disinhibition has been widely discussed in STI journal and elsewhere.  An increase in risk-taking behaviour among MSM during the late 1990s has been established:  http://sti.bmj.com/content/77/3/184.abstract?sid=5d909365-4627-4232-8ef4-a93445f5baed (Stolte & Coutinho: Amsterdam);  http://sti.bmj.com/content/80/6/451.abstract?sid=5d909365-4627-4232-8ef4-a93445f5baed (Elford & Hart: London); http://sti.bmj.com/content/80/6/518.abstract?sid=5d909365-4627-4232-8ef4-a93445f5baed(Cox & Allard: Montreal); http://sti.bmj.com/content/79/1/7.abstract?sid=5d909365-4627-4232-8ef4-a93445f5baed (Stephensen & Williams: London).  But opinions on the contribution of HAART to changing sexual behaviour seem divided, with Stolte & Coutinho supporting the hypothesis, and the others inclined to attribute it to other factors.  The probable future emergence of multi-resistant gonorrhoea (http://sti.bmj.com/content/87/Suppl_2/ii39) represents the inverse case (loss of a therapy leading to potential inhibition).  If the diminished “cost” of an STI (syphilis) can spur an increase in risky sexual behaviour, should we not expect an increased cost to have the opposite result?  Time will tell.

Tracking the history of HIV back to chimpanzees: is the evidence in the West African genome?

7 Feb, 13 | by Leslie Goode, Blogmaster

Papers explored in earlier STI blogs have traced the distribution through the world of the different HIV subtypes (http://blogs.bmj.com/sti/2013/01/04/reading-the-history-of-the-progress-of-the-hiv-epidemic-through-the-evidence-of-hiv-subtype-distribution/?q=w_sti_blog_sidetabhttp://sti.bmj.com/content/87/2/101.full?sid=2b7658a8-4f84-4d8a-b2bc-d5104c523180), and have used this information to track the origins of HIV-AIDS in central/western Africa probably at the beginning of the last century (http://journals.lww.com/aidsonline/pages/results.aspx?k=Tatem%20AND%20Salemi&Scope=AllIssues&txtKeywords=Tatem%20AND%20Salemi).  Now a research article published in Evolutionary Biology – Zhao, Roca et al. – has attempted to take back the story a further stage to the crossing of the species barrier and before (http://www.biomedcentral.com/1471-2148/12/237/abstract). Certainty in these matters is impossible; but Zhao, Roca et al. develop an interesting hypothesis based on genetic evidence – which is as follows.

Their point of departure is that transmission of the virus from the common chimpanzee to humans must have taken place at least four times, since the four principal HIV-1 strains present in humans (M, N, O, P) are closer in genetic sequence to strains of SIV, the chimpanzee form of HIV, than they are to the various HIV-1 sub-groups (A,B,C etc.) that derive from  strain M. On this basis, the authors hypothesize that, given the existence of SIV strains for 20,000 years, if the virus crossed the species barrier four times (between 1884 and 1924), in all probability it crossed it repeatedly over the centuries, but failed to generate persistent outbreaks in humans before the appearance of large cities.  If this hypothesis is correct, then genomic “signatures” in the chromosomes of the descendants of the affected populations ought to reflect the generation of selection pressure in these populations for resistance to SIV/HIV.

Among the diverse populations intensively genotyped as part of the human genome diversity panel are the Biaka Western Pygmies of the Central African Republic who have always resided within range of the SIV infected common chimpanzee.  The researchers seek genetic evidence for selection among the Biaka, by running pairwise genomic comparisons between the Biaka and four other central African peoples (including the Mbuti Eastern Pygmies, who are genetically close to the Biaka, but have always lived out of range of SIV infected chimpanzees).  They look for regions of the genome that: 1. signal strong selection pressure, and 2. have been associated with HIV-1 by various kinds of studies.

What they find is that of the ten possible pairwise comparisons between the five peoples, five comparisons detect regions with strong selection associated with HIV.  These involved CUL5, TRIM5, PARD3B and TSG101 which are detected as under strong selection eight times across the pairwise comparisons.  Seven out of the eight involve the Biaka.  The probability that randomly drawn genes would overlap seven or more signals of selection in a single population is reckoned by the authors at 0.05.  For the purposes of this analysis the researchers exclude from consideration host-genes associated with HIV that are below a genome-wise significance p<5×108.  Where this restriction is lifted a total of eight genomic regions are specified as showing protective variants.

On the basis of this evidence the authors consider their hypothesis that SIV/HIV has shaped the genomes of some west central African populations as worthy of further investigation.

Impact on sexual behaviour of “Don’t Ask, Don’t Tell” policy in US navy

6 Nov, 12 | by Leslie Goode, Blogmaster

Epidemiological research has sometimes addressed the impact on men who have sex with men (MSM) sexual behaviour of being “non-gay identifying” (NGI) (Yun, Wang et al. (http://sti.bmj.com/content/87/7/563.full?sid=a367a77d-f830-46ee-b761-eec8d9e22da2 ); Mercer & Cassell (http://ijsa.rsmjournals.com/content/20/2/87.full) or of belonging to a culture in which openness about sexuality by MSM is sometimes difficult and personally costly (Lane, Kegeles et al. (http://sti.bmj.com/content/84/6/430.full?sid=ab090fad-0769-479b-a7d5-e6ba10da5609).

The position of MSM in the US military under the recently abolished “Don’t Ask, Don’t Tell” (DADT) policy was an extreme case – possibly a limit-case – of this situation:  up until September 2011, an admission of sexual orientation by MSM, or evidence such as hand-holding, could result in ejection from the military.

How does this kind of situation influence patterns of HIV transmission among MSM, and what is the impact on the sexual behaviour of those MSM who engage in relationships with men regardless?  Would we expect the repressive effects of DADT to result in a relatively lower proportion of total HIV infection due to MSM sexual contact than in the general population – or the reverse?

Results of a recent online survey of the sexual behaviour prior to forced HIV testing of  US Navy and Marine Corps personnel who sero-converted under DADT intriguingly lifts the lid on this formerly closed epidemiological world – and perhaps, to some degree, on other similarly closed worlds.  Of course, the survey itself has major limitations: most importantly its restriction to a minority (64 (524): 26%), and an apparently not very representative minority, who responded to the survey; also the often considerable lapse of time since the behaviours reported.  Despite all these limitations the forced imposition of an HIV test on the whole group allows the survey to capture HIV prevalence at a moment in time.

Among the men who became HIV-infected  84% had had sex with men in the 3-year period prior to diagnosis: 55% reporting sex with just men, and 30% reporting sex with both men and women.  DADT would not then appear to have had much impact on reducing the burden of MSM infection as a proportion of total burden.  This higher figure relative to earlier surveys of the US military (84% as opposed to 59% reporting sex with men) probably reflects the liberalizing effects of DADT repeal.  The frequency of inconsistent condom use with anal sex was 65%, and more than three quarters expressed surprise at their HIV diagnosis.

The story these figures tell mirrors other “repressive” settings such as those with which we began our blog.  On the whole, a culture of repression drives the unwelcome sexual behaviour underground rather than eliminating it, while, at the same time, discouraging responsible behaviour and the adoption of risk-reduction strategies.  As the authors note,  “Several opportunities for primary prevention messaging now possible after DADT repeal are evident”.

Managing gonorrhoea in a world without antibiotics

25 Jun, 12 | by Leslie Goode, Blogmaster

On 6th June the World Health Organization (WHO) put out an alert regarding drug-resistant gonorrhoea (http://www.who.int/mediacentre/news/notes/2012/gonorrhoea_20120606/en/ ) simultaneously with the publication of a Global Action Plan (http://whqlibdoc.who.int/publications/2012/9789241503501_eng.pdf).  The last year or so has seen the emergence of strains of the infection that are resistant to cephalosporins, the antibiotics of last resort.  The plan includes: increased awareness of correct use of antibiotics; systematic monitoring and reporting of treatment failure; improved surveillance; research into new treatment regimens.  But the brute fact remains that with no new drugs even on the horizon, we face a future in which there will increasingly be no effective treatment for Neisseria gonorrhoea.

This may raise in some minds the questions of how we ever coped in the days before antibiotics.

If you have ever wondered what the venereological world was like before the 1940s, the STI journal archive contains a wealth of material.  Contrasted assessments of the various treatment regimes for gonorrhoea current in the 1920s and their drawbacks can be found in papers by Prof.  Jadassohn, 1926 (http://sti.bmj.com/content/2/6/152.full.pdf+html?sid=cb748843-f7a4-40c9-99aa-b50a4d6faeea) and F.W.F. Purcell, 1931 (http://sti.bmj.com/content/7/3/187.full.pdf+html?sid=cb748843-f7a4-40c9-99aa-b50a4d6faeea).  I would particularly recommend a paper by L.W. Harrison in commemoration of venereologist Albert Neisser (http://sti.bmj.com/content/31/2/65.full.pdf+html?sid=8635f797-ed0e-4f71-a264-72f060bf8461).  Harrison profits from the occasion to reminisce at length on his own venereological career going back to experiences in charge of a clinic during World War I; he offers frank opinions of the treatments used at different periods by himself and others, and what he felt these owed to Neisser.

Use of injections of silver nitrate via urinary meatus go back to the nineteenth century and continue until the 1940s. The late C19th also saw the employment of an eye-watering range of injected “astringents” from potassium permanganate to hot water and sulphurous acid (Harrison).  These treatment regimens partly give way in the early C20th to the use of silver nitrate and a range of organic silver compounds (protargol, ichthargan, albargin etc.) – a change that Harrison attributes to the influence of Neisser.  A wide range of treatments, however, continue to be described in the literature (see above).  Occasional doubts are voiced as to the effectiveness of organic silver compounds, as compared with silver nitrate (http://sti.bmj.com/content/1/4/245.full.pdf+html?sid=cb748843-f7a4-40c9-99aa-b50a4d6faeea).

 

Did syphilis really originate in the New World? An old theory reconsidered.

31 Jan, 12 | by Leslie Goode, Blogmaster

Outside Naples, 1495, an unknown epidemic struck the mercenary army of the French King Charles VIII, subsequently considered to be the first recorded outbreak of syphilis in the Old World.  As early as the sixteenth century, the sudden emergence of the disease was popularly attributed to Columbus’ recent voyage to the New World.  Yet doubts have frequently been raised.  Did syphilis really originate in the Americas?  Or had it always existed in the Old World, and just by coincidence emerged with exceptional virulence shortly after Columbus’ return?

Twenty years ago, a comprehensive review of evidence for treponemal disease in the New and Old Worlds (Baker & Armalagos 1988) lent support to the popular theory of Columbian origin.  Since then, however, a growing number of cases of treponemal disease have been reported in the pre-Columbian Old World.  A paper published last month (Harper & Armelagos) returns to the old question in the light of the new evidence, and provides a comprehensive assessment of the evidence to date.

The evidence is hard to assess – for two reasons.  The first is the difficulty of the identification of dry bone lesions that are specific to treponemal disease – let alone syphilis.  The second relates to the dating of the evidence; this is rendered more complex by the so-called “marine reservoir effect”, as a result of which ante-mortem consumption of marine foods can generate dates that are too early by a factor of hundreds of years.

On the first issue Harper et al. argue that it is impossible with certainty to distinguish syphilis from other treponemal disease in the fossil record, but concur with Hackett (1976) that there are two macroscopic features that may be considered diagnostic of treponemal disease.  These features do occur in the fossil record.  Ultimately, it is the second issue, that of dating, which poses the greater obstacle to any conclusive argument on the origin of syphilis.  Of the 54 papers reviewed 12 include information on radiocarbon dating, and of these only 4 discuss the effect of marine reservoir.  None of the cases considered can with certainty be assigned to the pre-Columbian period.  Ultimately, therefore, the evaluation of Harper et al. concludes that there is not a single published case from the Old World that can be confidently diagnosed as treponemal, and that has a radiocarbon date that places it firmly in the pre-Columbian period.  Yet there is overwhelming evidence for its prevalence in the New World before this date, and for its occurrence in the Old World thereafter.

Thus, 20 years after Baker & Armelagos’ comprehensive review, the evidence still suggests that syphilis or its progenitor arose in the New World.

Kristin N. Harper, George J. Armelagos et al., “The Origin and Antiquity of Syphilis Revisited: An Appraisal of Old World Pre-Columbian Evidence for Treponemal Infection”, Yearbook of Physical Anthropology 54: 99-133, 2011.

http://onlinelibrary.wiley.com.libproxy.ucl.ac.uk/doi/10.1002/ajpa.21613/full

Baker B. & Armelagos G., “The origin and antiquity of syphilis: paleopathological diagnosis and interpretation”, Current  Anthropol ogy, 29:703–738, 1988.

Hackett C.,  Diagnostic criteria of syphilis, yaws and treponarid (treponematoses) and of some other diseases in dry bones (for use in osteo-archaeology), Berlin: Springer-Verlag, 1976.

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