Redefining the treponemal history through pre-Columbian genomes from Brazil.

The origins of treponemal diseases have long remained unknown, especially considering the sudden onset of the first syphilis epidemic in the late 15th century in Europe and its hypothesized arrival from the Americas with Columbus' expeditions1,2. Recently, ancient DNA evidence has revealed various treponemal infections circulating in early modern Europe and colonial-era Mexico3-6. However, there has been to our knowledge no genomic evidence of treponematosis recovered from either the Americas or the Old World that can be reliably dated to the time before the first trans-Atlantic contacts. Here, we present treponemal genomes from nearly 2,000-year-old human remains from Brazil. We reconstruct four ancient genomes of a prehistoric treponemal pathogen, most closely related to the bejel-causing agent Treponema pallidum endemicum. Contradicting the modern day geographical niche of bejel in the arid regions of the world, the results call into question the previous palaeopathological characterization of treponeme subspecies and showcase their adaptive potential. A high-coverage genome is used to improve molecular clock date estimations, placing the divergence of modern T. pallidum subspecies firmly in pre-Columbian times. Overall, our study demonstrates the opportunities within archaeogenetics to uncover key events in pathogen evolution and emergence, paving the way to new hypotheses on the origin and spread of treponematoses.

Child development, physiological stress and survival expectancy in prehistoric fisher-hunter-gatherers from the Jabuticabeira II shell mound, South Coast of Brazil.

In this study, we shed light on the interdependency of child growth, morbidity and life expectancy in the fisher-hunter-gatherers of the Jabuticabeira II shell mound (1214-830 cal B.C.E. - 118-413 cal C.E.) located at the South Coast of Brazil. We test the underlying causes of heterogeneity in frailty and selective mortality in a population that inhabits a plentiful environment in sedentary settlements. We reconstruct osteobiographies of 41 individuals (23 adults and 18 subadults) using 8 variables, including age-at-death, stature, non-specific stress markers (cribra orbitalia, porotic hyperostosis, periosteal reactions, periapical lesions and linear enamel hypoplasia), as well as weaning patterns based on stable isotope data to examine how stress factors module growth and survival. Our results show that shorter adult statures were linked to higher morbidity around weaning age and higher chances of dying earlier (before 35 years) than taller adult statures. In addition, short juvenile stature was related to physiological stressors and mortality. The adult "survivors" experienced recurrent periods of morbidity during childhood and adulthood, possibly associated with the high parasite load of the ecosystem and dense settlement rather than to malnourishment. An association between early-stress exposure and premature death was not demonstrated in our sample. To explain our data, we propose a new model called "intermittent stress of low lethality". According to this model, individuals are exposed to recurrent stress during the juvenile and adult stages of life, and, nevertheless survive until reproductive age or later with relative success.