Justinianic Plague Research Articles

New World, New Germs: The Role of European Expansion in the Development of Germ Theory

Whenever cultures meet, exchange is inevitable. There will be exchanges of goods, of languages, of cultures, and of disease. The epidemics and pandemics sparked by European expansion in the fifteenth and sixteenth centuries were devastating but ultimately encouraged scholars to think critically about disease and its origins. By examining the language and ideas of first-hand accounts of plague, scurvy, syphilis, and smallpox, the evolution of European theories of disease can be traced from the Justinian Plague of 560 AD to the London Plague of 1625 AD. Examining the impact that the European voyages of discovery had on theories of disease shows that expansionism served to catalyze the development of our modern germ theory.

INVESTIGATING A MURDER THE CASE OF THE JUSTINIANIC PLAGUE IN SCYTHIA MINOR

The study beforehand applies a logical scheme of analysis over a possible presence of the Justinianic plague in the province of Scythia Minor. Following a logic borrowed from the criminalistics, we tried to apply this scheme in order to see if the theory of presence of the epidemic is viable in the given region. Although we have not come with decisive pieces of evidence, a great deal of research is still necessary in order to confirm or infirm this theory. We therefore aim to open a discussion, considering the problem plausible, for the disease had the means and opportunity to affect the province. As previously stated this study is merely a plan of study that shall be developed in a forthcoming work.

Pandemics and passages to late antiquity: rethinking the plague of c.249–270 described by Cyprian

Pandemic events are surpassingly rare in human history. Yet the period we call late antiquity could be considered the age of pandemic disease. It began and ended with the Antonine plague that erupted in the mid-160s A.D. and the Justinianic plague of the mid-6th c. Modern interest in these pandemics has waxed and waned. It was long taken for granted that these events played a major rôle in the fate of the Roman empire. In the mid-20th c., however, attention subsided. Historical demography struggled to make inroads into the discipline of ancient history. In the case of the Antonine plague, a critical article of J. F. Gilliam turned focus away from the disease for a generation. Only in the last 20 years, with the rise of historical demography in ancient studies, and a broader interest in environmental history, have the Antonine and Justinianic plagues received their proper due. Attention has focused on the epidemiology and impact of these events. The Antonine plague is most plausibly identified as smallpox, based on the presentation of the disease described by the contemporary physician Galen, and should qualify as the first pandemic in all of human history. It struck the empire at the apex of its power and prosperity. Its severe demographic effects now seem widely accepted, although there is lively debate about its long-term geopolitical and social consequences. For the Justinianic plague neither its demographic scope nor the long-range consequences are in doubt. Securely identified by both clinical description and paleomolecular evidence, Yersinia pestis arrived in 541 and struck recurrently for over two centuries; like the Black Death in the 14th c., the first bubonic plague fundamentally reshaped the trajectory of European populations.

Pulling teeth from history: DNA from ancient teeth can help to yield information about our ancestors' health, diet and diseases.

Molecular biology has made considerable contributions to the study of human history from the earliest days of our species, when our ancestors began to walk on the savannah, to the dawn of civilization and the more recent history of mankind. The analysis of contemporary mitochondrial DNA, for example, has told us that Homo sapiens first appeared in Africa; the sequencing of the Neanderthal genome has revealed that Homo sapiens and Homo neanderthalensis lived along each other and interbred before the latter disappeared; last year, the analysis of DNA extracted from a skeleton found under a parking lot in Leicester, UK, showed that it was the remains of King Richard III. Although the advent of next‐generation sequencing and advances in bioinformatics have boosted research using ancient DNA, a major hurdle has always been the quantity and quality of the DNA itself: DNA molecules quickly degrade over time into smaller fragments, and microbial contamination makes it challenging to identify human fragments within a sample. Intriguingly, teeth have proven to be an excellent source of high‐quality ancient DNA, yielding insights into the evolution of the human diet, disease and immunity since the onset of agriculture some 10,000 years ago. Dental calculus has been the most complete source of historical sequence data, especially for probing oral microbiome populations. At the same time, dental pulp—the connective tissue at the centre of teeth—has been an important source of information about ancient diseases. Archaeologist Keith Dobney, from the University of Aberdeen in the UK, and his colleagues first identified the potential of dental calculus as a source of information about past diets and microbial populations long before the advent of ancient DNA studies [1]. Now, almost 30 years later, Dobney is among those at the forefront of the revolution in ancient DNA analysis. “It appears that dental …

Summaries of Doctoral Dissertations

This study establishes long-term trends in the purchasing power of the wages of unskilled workers and develops estimates for GDP per capita for medieval Egypt and Iraq. Wages were heavily influenced by two long-lasting demographic shocks, the Justinian Plague and the Black Death and the slow population recovery that followed. As a result, they remained above the subsistence minimum for most of the medieval era. We also argue that the environment of high wages that emerged after the Justinian Plague contributed to the Golden Age of Islam by creating demand for higher income goods.

Plagues, Wages, and Economic Change in the Islamic Middle East, 700–1500

This study establishes long-term trends in the purchasing power of the wages of unskilled workers and develops estimates for GDP per capita for medieval Egypt and Iraq. Wages were heavily influenced by two long-lasting demographic shocks, the Justinian Plague and the Black Death and the slow population recovery that followed. As a result, they remained above the subsistence minimum for most of the medieval era. We also argue that the environment of high wages that emerged after the Justinian Plague contributed to the Golden Age of Islam by creating demand for higher income goods.

Yersinia pestis and the Plague of Justinian 541–543 AD: a genomic analysis

Yersinia pestis has caused at least three human plague pandemics. The second (Black Death, 14-17th centuries) and third (19-20th centuries) have been genetically characterised, but there is only a limited understanding of the first pandemic, the Plague of Justinian (6-8th centuries). To address this gap, we sequenced and analysed draft genomes of Y pestis obtained from two individuals who died in the first pandemic. Teeth were removed from two individuals (known as A120 and A76) from the early medieval Aschheim-Bajuwarenring cemetery (Aschheim, Bavaria, Germany). We isolated DNA from the teeth using a modified phenol-chloroform method. We screened DNA extracts for the presence of the Y pestis-specific pla gene on the pPCP1 plasmid using primers and standards from an established assay, enriched the DNA, and then sequenced it. We reconstructed draft genomes of the infectious Y pestis strains, compared them with a database of genomes from 131 Y pestis strains from the second and third pandemics, and constructed a maximum likelihood phylogenetic tree. Radiocarbon dating of both individuals (A120 to 533 AD [plus or minus 98 years]; A76 to 504 AD [plus or minus 61 years]) places them in the timeframe of the first pandemic. Our phylogeny contains a novel branch (100% bootstrap at all relevant nodes) leading to the two Justinian samples. This branch has no known contemporary representatives, and thus is either extinct or unsampled in wild rodent reservoirs. The Justinian branch is interleaved between two extant groups, 0.ANT1 and 0.ANT2, and is distant from strains associated with the second and third pandemics. We conclude that the Y pestis lineages that caused the Plague of Justinian and the Black Death 800 years later were independent emergences from rodents into human beings. These results show that rodent species worldwide represent important reservoirs for the repeated emergence of diverse lineages of Y pestis into human populations. McMaster University, Northern Arizona University, Social Sciences and Humanities Research Council of Canada, Canada Research Chairs Program, US Department of Homeland Security, US National Institutes of Health, Australian National Health and Medical Research Council.

The Justinianic plague: evidence from the dated Greek epitaphs of Byzantine Palestine and Arabia

The Justinianic plague, the first historically attested pandemic of bubonic plague, has recently made headlines with the publication of the genomic analysis of the bacterium responsible for its outbreak.1 Though its primary contribution is to the field of epidemiology, this study is a welcome addition to the growing body of research on the first plague pandemic, for which the literary evidence is still the main source of information.2 A number of attempts have been made to find non-literary evidence for this plague in order to substantiate the literary evidence and gain insight into areas for which the literary sources are insufficient, and the present study joins those by analyzing the corpus of dated Greek epitaphs of the 4th through 7th c. A.D. from the Byzantine provinces of Palaestina Prima, Palaestina Secunda, Palaestina Tertia (or Salutaris),3 and Arabia. The findings appear to confirm the traditional dating of the outbreak of plague to 541, and may even suggest that this first wave was particularly virulent; they are less informative about the succession of later waves.

Pestis (<i>Yersinia pestis</i>) - As Biological Weapons

Yersinia pestis (formerly Pasteurella pestis) is a type of bacterium. It is believed to have been responsible for plagues of the early 1300s. More accurately, it is a Gram-negative rod-shaped coccobacillus. It is a facultative anaerobe that can infect humans and other animals. Human Y. pestis infection takes three main forms: pneumonic, septicemic, and bubonic plagues. All three forms are widely believed to have been responsible for a number of high-mortality epidemics throughout human history, including the Justinianic Plague of the sixth century and the Black Death that accounted for the death of at least one-third of the European population between 1347 and 1353. It has now been shown conclusively that these plagues originated in rodent populations in China. More recently, Y. pestis has gained attention as a possible biological warfare agent and the CDC has classified it as a category A pathogen requiring preparation for a possible terrorist attack. Every year, thousands of cases of plague are still reported to the World Health Organization, although, with proper treatment, the prognosis for victims is now much better. A five- to six-fold increase in cases occurred in Asia during the time of the Vietnam war, possibly due to the disruption of ecosystems and closer proximity between people and animals. Plague also has a detrimental effect on non-human mammals. In the United States of America, animals such as the black-tailed prairie dog and the endangered black-footed ferret are under threat from the disease.

The End of Antiquity

Pathogens The Justinian Plague, which resurfaced regularly between the 6th and 8th centuries, is thought to have assisted the decline of the Roman Empire, but it has, until now, only been speculatively diagnosed as bubonic plague caused by the bacterium Yersinia pestis. Using stringent ancient DNA anticontamination protocols, Harbeck et al. have genotyped new material from the early medieval graveyard at Aschheim, Bavaria, dating from the 6th century. This graveyard contained 438 individuals, often in multiple burials—a sign of crisis. The amount of bacterial material available was scant, but Y. pestis was identified from one individual using five key single-nucleotide polymorphisms identified in recent phylogenies. Genotyping confirmed this isolate as basal to isolates from the 14th-century Black Death and the modern (19th-century) third pandemic and that, like the other pandemics, it originated in China or Mongolia. ![Figure][1] CREDIT: JAMES LE PLAMER/WIKIMEDIA COMMONS PLoS Pathogens 9 , 10.1371/journal.ppat.1003349 (2013). [1]: pending:yes

Yersinia pestis DNA from Skeletal Remains from the 6th Century AD Reveals Insights into Justinianic Plague

Yersinia pestis, the etiologic agent of the disease plague, has been implicated in three historical pandemics. These include the third pandemic of the 19th and 20th centuries, during which plague was spread around the world, and the second pandemic of the 14th–17th centuries, which included the infamous epidemic known as the Black Death. Previous studies have confirmed that Y. pestis caused these two more recent pandemics. However, a highly spirited debate still continues as to whether Y. pestis caused the so-called Justinianic Plague of the 6th–8th centuries AD. By analyzing ancient DNA in two independent ancient DNA laboratories, we confirmed unambiguously the presence of Y. pestis DNA in human skeletal remains from an Early Medieval cemetery. In addition, we narrowed the phylogenetic position of the responsible strain down to major branch 0 on the Y. pestis phylogeny, specifically between nodes N03 and N05. Our findings confirm that Y. pestis was responsible for the Justinianic Plague, which should end the controversy regarding the etiology of this pandemic. The first genotype of a Y. pestis strain that caused the Late Antique plague provides important information about the history of the plague bacillus and suggests that the first pandemic also originated in Asia, similar to the other two plague pandemics.

Crystallization of the acyl-CoA thioesterase TesB from Yersinia pestis.

Yersinia pestis is a highly virulent human pathogen and is the causative agent of bubonic plague. Spread through the bite of infected fleas, plague epidemics have marked important events in history, including the Justinian plague (6th century), the Black Death (14th century) which decimated nearly one quarter of the European population, and more recently the Orientalis plague (1894). To date, deaths are still being reported and, without treatment, the disease kills most people within 4 days. One of the thioesterases from Y. pestis, TesB, is a broad-range acyl-CoA thioesterase and is highly conserved within prokaryotes and throughout evolution, sharing sequence similarity with the HIV Nef binding protein ACOT8. Here the expression, purification, crystallization and diffraction of TesB are reported. TesB has been recombinantly expressed and crystallized using the vapour-diffusion hanging-drop technique at pH 7.0 and 290 K. After optimization, crystals diffracted to 2.0 Å resolution at the Australian Synchrotron and belong to the space group P12(1)1 (a = 73.55, b = 170.82, c = 101.98 Å), with eight molecules likely to be present in the asymmetric unit.

Yersinia pestis: New Evidence for an Old Infection

The successful reconstruction of an ancient bacterial genome from archaeological material presents an important methodological advancement for infectious disease research. The reliability of evolutionary histories inferred by the incorporation of ancient data, however, are highly contingent upon the level of genetic diversity represented in modern genomic sequences that are publicly accessible, and the paucity of available complete genomes restricts the level of phylogenetic resolution that can be obtained. Here we add to our original analysis of the Yersinia pestis strain implicated in the Black Death by consolidating our dataset for 18 modern genomes with single nucleotide polymorphism (SNP) data for an additional 289 strains at over 600 positions. The inclusion of this additional data reveals a cluster of Y. pestis strains that diverge at a time significantly in advance of the Black Death, with divergence dates roughly coincident with the Plague of Justinian (6th to 8th century AD). In addition, the analysis reveals further clues regarding potential radiation events that occurred immediately preceding the Black Death, and the legacy it may have left in modern Y. pestis populations. This work reiterates the need for more publicly available complete genomes, both modern and ancient, to achieve an accurate understanding of the history of this bacterium.

Climate change and the Justinianic Plague: an intercomparison of high-resolution lake sediment and documentary records

Climate change and the Justinianic Plague: an intercomparison of high-resolution lake sediment and documentary records

Plague: History and contemporary analysis

Plague has caused ravaging outbreaks, including the Justinian plague and the "black death" in the Middle Ages. The causative agents of these outbreaks have been confirmed using modern molecular tests. The vector of plague during pandemics remains the subject of controversy. Nowadays, plague must be suspected in all areas where plague is endemic in rodents when patients present with adenitis or with pneumonia with a bloody expectorate. Diagnosis is more difficult in the situation of the reemergence of plague, as in Algeria for example, told by the first physician involved in that outbreak (NM). When in doubt, it is preferable to prescribe treatment with doxycycline while waiting for the test results because of the risk of fatality in individuals with plague. The typical bubo is a type of adenitis that is painful, red and nonfluctuating. The diagnosis is simple when microbiological analysis is conducted. Plague is a likely diagnosis when one sees gram-negative bacilli in lymph node aspirate or biopsy samples. Yersinia pestis grows very easily in blood cultures and is easy to identify by biochemical tests and MALDI-TOF mass spectrometry. Pneumonic plague and septicemic plague without adenitis are difficult to diagnose, and these diagnoses are often made by chance or retrospectively when cases are not part of an epidemic or related to another specific epidemiologic context. The treatment of plague must be based on gentamicin or doxycycline. Treatment with one of these antibiotics must be started as soon as plague is suspected. Analysis of past plague epidemics by using modern laboratory tools illustrated the value of epidemic buboes for the clinical diagnosis of plague; and brought new concepts regarding its transmission by human ectoparasites.

What Disease was Plague? On the Controversy over the Microbiological Identity of Plague Epidemics of the Past, by Ole J. Benedictow

Beware of the Black Death! Students of plague are no strangers to controversy: the subject remains highly popular among varied constituencies including universities, the press, television producers and audiences. There are myriad debates and fiercely-held opinions. Was the Black Death of 1346–53, and subsequent plagues, the precursor of enclosure and of Reformation? Or was the plague which recurred from the 1340s to the 1720s the second of three ‘pandemics’—the first being the one known as the plague of Justinian, and the third that which began in the Far East c.1890 and petered out in Felixstowe, Glasgow, and Liverpool? Among historians of demography (Benedictow is one of these), economy, and mentalité, debates continue about the scale of mortality and why populations continued to decline after 1350, when recovery might have been predicted. Ole Benedictow’s important new book of 746 pages of close argument refutes a generation of critics of the theory with which historians of a certain age grew up—namely that the Black Death in particular, and plague in general, was spread by rats and fleas. In seeking to refute revisionism, Benedictow takes readers back to basics: observations by those who , amidst that Far Eastern epidemic, identified the plague bacillus in the 1890s—the Japanese Kitasato and the Swiss student of Pasteur, Yersin. Such first-hand information, whether from more recent scholars who solved the mystery of the nature of historic plague, or medieval witness-accounts, form the core of this book. However, many of those who unravelled the mysteries of plague more than a century ago and set in place the bubonic view of plague, are now dead. Benedictow’s book is ‘not a work of intellectual love, but of scholarly duty’ to uphold ‘the life work of a large number of fine and dedicated medical and historical scholars, many of whom cannot rise from their graves to defend themselves’—an ‘ethical duty’ embarked on ‘very reluctantly’ (p. xv). Why?

Dendroarchaeology of the mid-first millennium AD in Constantinople

The 1st millennium AD was a time of great transition in Europe and the Mediterranean. At the heart of the Byzantine Empire, Constantinople (modern day Istanbul) was a pivotal trade hub for the Aegean region. Establishing a precise and accurate dating framework for the development of this remarkable city and a chronological reference for this critical time period for the Mediterranean region is of great importance to a wide range of scholars. Here we present a new 213 year tree-ring record from 89 oak samples placed in time by dendrochronology and supported by radiocarbon analysis and historical documentation. It represents the middle of the first millennium AD in Constantinople. The tree-ring series are derived from pilings recovered from the extraordinary excavations of the so-called “Theodosian harbor” at Yenikapı, Istanbul, along with timbers from other sites and buildings around the city, including one of the most famous sites on the Istanbul sky-line—Hagia Sophia. They provide potential for new insight into a time period in which earthquakes, the Justinianic plague, and even a possible tsunami struck the city, and during which dramatic changes in climate have been recorded in other paleoenvironmental proxies. The chronology is the first published tree-ring series from the Aegean region to cover the ‘event’ years of AD 536–7 and 542 which are characterized by anomalous growth in other tree-ring series from around the world, but interestingly these event years are not evident in this tree-ring sequence.

Finally, plague is plague

eval plague was not caused by a Medievalis biotype strain, and that Justinian plague was not caused by an Antiqua biotype strain [13,14]. This point warrants further analysis: knowing which Y. pestis biotype(s) has the capacity to promote huge, deadly epidemics matters in the current situation of several thousands of new plague cases reported every year to the WHO. Somewhat disappointing was the observation that the medieval Y. pestis complete genome lacked any unique virulence trait that might have explained the unique epidemiological features of the Black Death, an epidemic that reportedly killed one-third of the European medieval population, that extended to the north of Europe, and occurred in the absence of the known rat reservoir [15]. Therefore, the coauthors of the twin papers advocate several environmental factors that may have contributed to these unique epidemiological traits. In fact, it was proposed that Black Death did not result from any specific virulence trait in the medieval Y. pestis strain, but rather from the adaptation of this Y. pestis strain to an additional vector, most likely the human louse [16]. Detailed investigation of its genome sequence may reveal specific genetic traits that are related to such adaptation. Finally, these twin papers close a period of confusion based on a single flawed paper regarding the aetiology of Black Death; 13 years later, it has been finally proven that medieval plague was plague.

Yersinia pestisDNA Sequences in Late Medieval Skeletal Finds, Bavaria

To the Editor: Yersinia pestis, the causative agent of plague, is held responsible for 3 human pandemics: the Justinian plague (5th–7th century), the Black Death (13th–15th century), and modern plague (1870s to present). In 1894, Alexandre Yersin identified Y. pestis during an epidemic of plague in Hong Kong (1). However, whether Y. pestis was indeed responsible for the medieval epidemic is still controversial. Y. pestis­­ specific DNA has been detected in medieval skeletal finds (2,3), although some investigators have failed to do so (4), leading to the suggestion that a viral hemorrhagic fever was the agent of these medieval pandemics (5). Against this background, we investigated a mass burial site that was discovered under the sacristy of the St. Leonhard Catholic church in Manching-Pichl, near Ingolstadt in Bavaria, Germany. In 1984, during the renovation of this church, 75 human skeletons and several scattered skeletal elements were discovered under the sacristy. The skeletons lay densely packed in 4 layers. Apparently, no grave pit had been dug at all, but the bodies were obviously deposited side by side and covered with dirt layer by layer. An approximation of the time of burial was possible only by means of accompanying building structures, which were dated to the Gothic period (1250–1500 ce). In the course of research preceding this study, our research group found Y. pestis DNA in 10 of 33 examined individual skeletal remains from the mass grave beneath the sacristy (6) by using the primer pair YP12D/YP11R (3). In the current study, the remains of 6 persons from the mass burial site that had positive Y. pestis DNA results before were further investigated. DNA from additional tooth samples of these persons was extracted, and more markers mapped on the Y. pestis high copy number plasmid pPCP1 were included. In addition to the primer systems YP12D/YP11R and YP11D/YP10R (3), the following primer systems were used. The primer pair YP14F (5′-TCCGGGTCAGGTAATATGGA-3′)/YP13R (5′-ACCAGCCTTTCACATTGAGG-3′) amplifies another sequence section (positions 6953–7082, reference: Y. pestis strain CO92 plasmid pPCP1 sequence {type:entrez-nucleotide,attrs:{text:AL109969.1,term_id:5763810,term_text:AL109969.1}}AL109969.1) on the Y. pestis pla gene (encoding plasminogen activator). The plasminogen activator belongs to the virulence factors of Y. pestis. The primer pair pst-F (5′-GGTAAATCGCTGAACCGAAG-3′)/pst-R (5′-AACAGCACCTCTGACGCTTT-3′) amplifies a 129-bp sequence section (positions 5026–5154, GenBank accession no. {type:entrez-nucleotide,attrs:{text:AL109969.1,term_id:5763810,term_text:AL109969.1}}AL109969.1) on the pst gene (encoding pesticin activity protein). Pesticin is a bacteriocin that is active against only a few closely related microorganisms. The primer pair PCP-F (5′-CATCCACATGCTCAACCCTA-3′)/PCP-R (5′-CTGAACGCATTTCAGTGGTG-3′) can amplify a 128–130-bp sequence section (positions 8428–8555, GenBank accession no. {type:entrez-nucleotide,attrs:{text:AF053945.1,term_id:2996216,term_text:AF053945.1}}AF053945.1; positions 8428–8557, GenBank accession no. {type:entrez-nucleotide,attrs:{text:AL109969.1,term_id:5763810,term_text:AL109969.1}}AL109969.1) on plasmid pPCP1. These 3 new primer sets, designed with the aid of the software component Primer3 (7), were applied by using a suicide PCR method (3,8); i.e., new primer pairs targeting sequences not previously amplified in the laboratory were used. At no time during all examinations was any modern Y. pestis DNA included. The sample preparation, DNA extraction, PCR setup, electrophoretic separation, and sequencing of amplicons are described elsewhere (6,9); however, we used 0.20 µmol/L of each primer, an annealing temperature of 54°C, and 45 amplification cycles. PCR blanks containing all reagents except for DNA and extraction blanks were included in every PCR set. Results of the amplification reactions are listed in the Table. All accompanied extraction and PCR controls remained free of amplification products. All amplicons resulting from suicide PCRs were sequenced. Amplicons resulting from the use of primer pairs YP14F/YP13R and pst-F/pst-R matched the reference sequence to 100% (GenBank accession no. {type:entrez-nucleotide,attrs:{text:AL109969.1,term_id:5763810,term_text:AL109969.1}}AL109969.1). Amplicons resulting from the use of primer pair PCP-F/PCP-R matched this reference sequence to only 97.78%. This deviation is because of a 2-bp insertion (2 Ts, positions 8531 and 8532, GenBank accession no. {type:entrez-nucleotide,attrs:{text:AL109969.1,term_id:5763810,term_text:AL109969.1}}AL109969.1) at Y. pestis strain CO92 plasmid pPCP1. The sequences obtained from 3 persons’ remains showed in the pPCP1 sequence section between nucleotide positions 8528–8532 only 3 Ts instead of 5 Ts described for Y. pestis strain CO92 plasmid pPCP1 (GenBank accession no. {type:entrez-nucleotide,attrs:{text:AL109969.1,term_id:5763810,term_text:AL109969.1}}AL109969.1). The sequences found in this study were deposited in GenBank under accession nos. {type:entrez-nucleotide-range,attrs:{text:HQ290521-HQ290523,start_term:HQ290521,end_term:HQ290523,start_term_id:310756648,end_term_id:310756652}}HQ290521-HQ290523. Table Amplification results obtained from the skeletal remains of 6 persons excavated at the St. Leonhard Catholic church, Manching-Pichl, Bavaria, Germany* To conclude, the successful recovery of several Y. pestis plasmid pPCP1 DNA sequences in skeletal finds from the mass burial site excavated in Manching-Pichl suggests that these persons died of plague. Moreover, our findings constitute a molecularly supported confirmation for the presence of Y. pestis, the etiologic agent of plague, in late medieval (1250–1500 ce) southern Germany. In future studies, we will attempt to recover chromosomal Y. pestis DNA from the mass grave skeletal remains to obtain clues as to the specific Y. pestis strain and the microbiology of past plague in Europe.

Population Dynamics in Italy in the Middle Ages: New Insights from Archaeological Findings

Studies of settlements in Italy indicate that during the Early Middle Ages (6th–9th centuries) the Italian population was stagnant, whereas a slow but persistent growth followed during the High Middle Ages (10th–13th). However, the components of the dynamics of the Italian population in the long period between the Justinian Plague (around 565 in Italy) and the Black Death (1348) are largely unknown. In this article, data from anthropometric analysis of the skeletons in 154 Italian cemeteries that date between the 1st century BCE and the 13th century are used to gain new insights on mortality of adults and nutrition. Adult mortality was higher during the Early Middle Ages than during the Roman Empire and the High Middle Ages, suggesting that the stagnation of population was determined by higher mortality. During the Early Middle Ages, however, nutritional levels were higher, as suggested by taller statures, more widespread meat consumption, and longer periods of breastfeeding. We discuss some possible research lines to resolve this apparent contradiction.