D. Ann Herring

A draft genome of Yersinia pestis from victims of the Black Death

Technological advances in DNA recovery and sequencing have drastically expanded the scope of genetic analyses of ancient specimens to the extent that full genomic investigations are now feasible and are quickly becoming standard. This trend has important implications for infectious disease research because genomic data from ancient microbes may help to elucidate mechanisms of pathogen evolution and adaptation for emerging and re-emerging infections. Here we report a reconstructed ancient genome of Yersinia pestis at 30-fold average coverage from Black Death victims securely dated to episodes of pestilence-associated mortality in London, England, 1348–1350. Genetic architecture and phylogenetic analysis indicate that the ancient organism is ancestral to most extant strains and sits very close to the ancestral node of all Y. pestis commonly associated with human infection. Temporal estimates suggest that the Black Death of 1347–1351 was the main historical event responsible for the introduction and widespread dissemination of the ancestor to all currently circulating Y. pestis strains pathogenic to humans, and further indicates that contemporary Y. pestis epidemics have their origins in the medieval era. Comparisons against modern genomes reveal no unique derived positions in the medieval organism, indicating that the perceived increased virulence of the disease during the Black Death may not have been due to bacterial phenotype. These findings support the notion that factors other than microbial genetics, such as environment, vector dynamics and host susceptibility, should be at the forefront of epidemiological discussions regarding emerging Y. pestis infections.

Weaning and infant mortality : Evaluating the skeletal evidence

Studies of prehistoric patterns of health and disease focus on interpretations of the evidence from hard tissue remains of past peoples. These interpretations are based on observations of living peoples and the sources of stress which may be expected to leave a record in their bones and teeth. One presumed source of stress that has received wide attention in the recent literature is weaning. The process of weaning is often associated with elevated risks of infant mortality and morbidity because infants no longer receive passive immunity from their mothers, and they are exposed to new sources of infection through the weaning diet. The process of weaning has also been tied to the duration of the contraceptive effects of nursing and the return of fecundity, which in turn provides information about birth spacing and population growth. Recently some of the basic assumptions about nursing and weaning, and their effects on morbidity, mortality and population growth, have been challenged, based on new technical and cross-cultural information. It is clear from the demographic literature that some studies based on skeletal samples tend to be too simplistic in terms of the causes of infant morbidity and mortality. This paper reviews current research which relates weaning and infant mortality to health and reproduction in past populations and evaluates studies of enamel hypoplasia and bone chemistry for reconstructing infant feeding practices in the past.

Explaining Biased Sex Ratios in Human Populations: A Critique of Recent Studies [and Comments and Reply]

DANIELA F. SIEFF is a graduate student in human ecology at the University of California, Davis (Davis, Calif. 956I6, U.S.A.). Born in I965, she received a B.A. from Oxford University in I987 and an M.A. in anthropology and psychology from the University of Michigan in I989. Her research interests are parental-investment strategies and the costs of children in traditional societies. She is currently engaged in a study of the interaction of womens work, polygyny, fertility, and child care among the Dotoga pastoralists of northern Tanzania. The present paper was submitted in final form 30 vi 89.

Age-specific mortality during the 1918 influenza pandemic: unravelling the mystery of high young adult mortality.

The worldwide spread of a novel influenza A (H1N1) virus in 2009 showed that influenza remains a significant health threat, even for individuals in the prime of life. This paper focuses on the unusually high young adult mortality observed during the Spanish flu pandemic of 1918. Using historical records from Canada and the U.S., we report a peak of mortality at the exact age of 28 during the pandemic and argue that this increased mortality resulted from an early life exposure to influenza during the previous Russian flu pandemic of 1889–90. We posit that in specific instances, development of immunological memory to an influenza virus strain in early life may lead to a dysregulated immune response to antigenically novel strains encountered in later life, thereby increasing the risk of death. Exposure during critical periods of development could also create holes in the T cell repertoire and impair fetal maturation in general, thereby increasing mortality from infectious diseases later in life. Knowledge of the age-pattern of susceptibility to mortality from influenza could improve crisis management during future influenza pandemics.

Modeling the influence of settlement structure on the spread of influenza among communities

Several factors play critical roles in the geographic spread of infectious diseases, including the movement of people between communities and the social and economic structure of groups of communities. A mathematical model has been developed to examine the individual and shared impact of these factors. This model was applied to the spread of the 1918–1919 influenza epidemic in three Aboriginal communities in central Canada. Previously published results from simulations of the model used parameter estimates for mobility patterns that were derived from historical documents from the study communities, especially Hudsons Bay Company post journals. We have termed this model the Frontier pattern. In this paper we extend that work to consider the consequences of three additional travel scenarios, which represent idealized trade and travel relationships between different communities. The three patterns include (a) the Central Marketplace scenario, an idealization of relations between a central community and its satellites in which a single central community satisfies all needs of the satellite communities; (b) the Sister Towns scenario, which allows travel among all communities and overemphasizes communication between satellites so that the ramifications of small town interactions are easier to observe; and (c) the Circuit scenario, which represents a hypothetical trade network that is a series of unidirectional dyad relationships linking all communities within a region. Results from simulations of the four mobility patterns are compared to assess the potential impact different social and economic relationships among communities may have had on the geographic spread of the 1918 influenza epidemic in central Canada and in other regions. These results reinforce conclusions that show that variation in patterns of mobility significantly influences the timing of epidemic peaks but only minimally alters the number of cases within a community. In addition, comparisons of the different models indicate that a central location in the social and political hierarchy of a region may be more important in influencing patterns of epidemic spread than just a central location with regard to travel patterns. Furthermore, who was actually travelling and where they were travelling had important consequences for epidemic spread. Am. J. Hum. Biol. 12:736–748, 2000.

Plasmodium falciparum malaria in 1st–2nd century CE southern Italy

The historical record attests to the devastation malaria exacted on ancient civilizations, particularly the Roman Empire [1]. However, evidence for the presence of malaria during the Imperial period in Italy (1st-5th century CE) is based on indirect sources, such as historical, epigraphic, or skeletal evidence. Although these sources are crucial for revealing the context of this disease, they cannot establish the causative species of Plasmodium. Importantly, definitive evidence for the presence of malaria is now possible through the implementation of ancient DNA technology. As malaria is presumed to have been at its zenith during the Imperial period [1], we selected first or second molars from 58 adults from three cemeteries from this time: Isola Sacra (associated with Portus Romae, 1st-3rd century CE), Velia (1st-2nd century CE), and Vagnari (1st-4th century CE). We performed hybridization capture using baits designed from the mitochondrial (mtDNA) genomes of Plasmodium spp. on a prioritized subset of 11 adults (informed by metagenomic sequencing). The mtDNA sequences generated provided compelling phylogenetic evidence for the presence of P. falciparum in two individuals. This is the first genomic data directly implicating P. falciparum in Imperial period southern Italy in adults.

Pandemic Paradox: Early Life H2N2 Pandemic Influenza Infection Enhanced Susceptibility to Death during the 2009 H1N1 Pandemic

ABSTRACT Recent outbreaks of H5, H7, and H9 influenza A viruses in humans have served as a vivid reminder of the potentially devastating effects that a novel pandemic could exert on the modern world. Those who have survived infections with influenza viruses in the past have been protected from subsequent antigenically similar pandemics through adaptive immunity. For example, during the 2009 H1N1 “swine flu” pandemic, those exposed to H1N1 viruses that circulated between 1918 and the 1940s were at a decreased risk for mortality as a result of their previous immunity. It is also generally thought that past exposures to antigenically dissimilar strains of influenza virus may also be beneficial due to cross-reactive cellular immunity. However, cohorts born during prior heterosubtypic pandemics have previously experienced elevated risk of death relative to surrounding cohorts of the same population. Indeed, individuals born during the 1890 H3Nx pandemic experienced the highest levels of excess mortality during the 1918 “Spanish flu.” Applying Serfling models to monthly mortality and influenza circulation data between October 1997 and July 2014 in the United States and Mexico, we show corresponding peaks in excess mortality during the 2009 H1N1 “swine flu” pandemic and during the resurgent 2013–2014 H1N1 outbreak for those born at the time of the 1957 H2N2 “Asian flu” pandemic. We suggest that the phenomenon observed in 1918 is not unique and points to exposure to pandemic influenza early in life as a risk factor for mortality during subsequent heterosubtypic pandemics. IMPORTANCE The relatively low mortality experienced by older individuals during the 2009 H1N1 influenza virus pandemic has been well documented. However, reported situations in which previous influenza virus exposures have enhanced susceptibility are rare and poorly understood. One such instance occurred in 1918—when those born during the heterosubtypic 1890 H3Nx influenza virus pandemic experienced the highest levels of excess mortality. Here, we demonstrate that this phenomenon was not unique to the 1918 H1N1 pandemic but that it also occurred during the contemporary 2009 H1N1 pandemic and 2013–2014 H1N1-dominated season for those born during the heterosubtypic 1957 H2N2 “Asian flu” pandemic. These data highlight the heretofore underappreciated phenomenon that, in certain instances, prior exposure to pandemic influenza virus strains can enhance susceptibility during subsequent pandemics. These results have important implications for pandemic risk assessment and should inform laboratory studies aimed at uncovering the mechanism responsible for this effect. IMPORTANCE The relatively low mortality experienced by older individuals during the 2009 H1N1 influenza virus pandemic has been well documented. However, reported situations in which previous influenza virus exposures have enhanced susceptibility are rare and poorly understood. One such instance occurred in 1918—when those born during the heterosubtypic 1890 H3Nx influenza virus pandemic experienced the highest levels of excess mortality. Here, we demonstrate that this phenomenon was not unique to the 1918 H1N1 pandemic but that it also occurred during the contemporary 2009 H1N1 pandemic and 2013–2014 H1N1-dominated season for those born during the heterosubtypic 1957 H2N2 “Asian flu” pandemic. These data highlight the heretofore underappreciated phenomenon that, in certain instances, prior exposure to pandemic influenza virus strains can enhance susceptibility during subsequent pandemics. These results have important implications for pandemic risk assessment and should inform laboratory studies aimed at uncovering the mechanism responsible for this effect.

The first wave of the 1918 influenza pandemic among soldiers of the Canadian expeditionary force

This article evaluates the evidence for the presence of the first, mild wave of the 1918 influenza pandemic among soldiers in the Canadian Expeditionary Force (CEF).

Collecting, Collections, and Practice in the Anthropologies of Health and Disease

Anthropologists studying health and disease collect data ranging from human remains to peoples’ lived experiences. Each of the books reviewed here reveals the social processes that shape how disease phenomena are observed, assessed, classified, and interpreted, both by the individuals who experience them and the researchers who study them. The classic anthropological themes of collection, exchange, circulation, social relations, and reciprocity resonate throughout. Theoretical and methodological differences aside, anthropologists remain united by a commitment to holistic and integrative approaches and the shared goal of providing historically and socially contextualized, nuanced understandings of the human condition.