Category Archives: Plague

The Promiscuous Human Flea

Female Pulex irritans, the human flea, from the Katja ZSM collection (CC3.0)
Female Pulex irritans, the human flea, from the Katja ZSM collection (CC3.0)

by Michelle Ziegler

The human flea seems like a misnomer today. We are not its current primary host, but that doesn’t mean that it once wasn’t our primary flea.  Pulex irritans  was first described by Carl Linnaeus as the “house flea” in 1758 (Krasnov 2012:4) and it is still found in homes in many parts of the world.

For the most part, the human flea is a nuisance, an irritant as its name implies. Except when it isn’t, when it occasionally transmits Yersinia pestis, the plague, to people. Pulex irritans has been  in homes with human plague cases from Arizona to Madagascar (Archibald & Kunitz, 1971; Ratovonjato et al, 2014). In 2006, Drancourt, Houhamdi, and Raoult argued that either the human flea or louse played a major role in human plague epidemics.

Human fleas have been found in the homes in several areas where plague occurs. P. irritans infected with Y. pestis were found on a dog in a home of a plague victim on Navajo land in Arizona in 1968. They also report knowledge  Y. pestis being isolated from  P. irritans fleas on dogs in the home of an infected child in Kayneta in 1968 (Archibald & Kunitz, 1971).   A recent survey of plague regions in Tanzania found 50% of the fleas in homes were P. irritans (Haule et al, 2013). A recent survey of fleas in Madagascar found that 98% of the fleas found inside control homes  in the control region of the study were Pulex irritans (Miarinjara et al, 2016). The fact that they did not find them in the homes within the area of the plague outbreak a month earlier may be due to extensive spraying of insecticide to end the epidemic. Human fleas are suspected of being the vectors for a variety of zoonotic diseases in Iran today (Rahbari, Nabian, & Nourolahi, 2008).

The human flea, Pulex irritans, has had a very interesting and convoluted history. All of the Pulex fleas are thought to have evolved in South America, perhaps on guinea pigs or piccary . P. irritans is the only member of its genus  that has left the Americas.  It made it to Eurasia long before the “Columbian Exchange”.  So it crossed a land bridge at some point to begin spreading in Eurasia, and it need not have crossed on a human.  Ötzi the 5000 year old ice mummy from the Italian Alps yielded two human fleas from his  artifacts (Schedl, 2000). P. irritans has also been found Egypt from 3500 BC  (Bain 2004) and 1350-1323 BC (Panagiotakopulu, 2001) showing that it does well in warm, dry climates also. So not only where they present for the entire known period of plague but they have been specifically found in warm and cold regions. Pulex irritans has been found in floor debris of uncovered sites from Roman Britain (Kenward, 1998). They were common inhabitants of early medieval Irish homes (O’Sullivan, 2008).  They are fairly common finds in Norse Greenland settlements. Unfortunately flea surveys have not been done on most continental archaeological sites (or at least I haven’t found them).

So why is P. irritans called a promiscuous flea? It has nothing to do with sex! In this case promiscuous means that it will feed off of a wide variety of host species. It has a truly impressive host range beyond humans including pigs, dogs, cats, goats and sheep, cattle, chickens, porcupines, multiple species of foxes, wolves, coyotes,  golden jackel of Iran,  badgers, prairie dogs,  rabbits, wild cats,  and mice. There are undoubtably more species that could be added. It seems to be very common on foxes in North America and Europe. These are, of course, primarily predators of rodents.  Given its wide range of hosts, its distribution and frequency among hosts has probably fluctuated wildly due to environmental and biodiversity changes over the last millennia.

Such a wide host range also makes it a potential bridging vector, one that can move disease between a wild reservoir to a domestic space transmitting it to domestic rodents, pets, and humans. Importantly, bridging vectors work in both directions, meaning that it could be instrumental in developing a wildlife reservoir after a human epidemic in a new region.

General flea life cycle (CDC). Adults are only 5% of flea biomass.

flea-pyramid-1P. irritans has a life cycle that is well suited to thriving in buildings like houses, barns, sheds, and animal nests or dens. Most of their biomass is in the egg stage. Small white eggs are often laid on the host but almost always fall off on to the floor. They do particularly well on the floor of stables and animal sheds where fermenting manure and debris keeps the eggs warm and moist.  They also do well in human homes where it is usually warmer and more humid than outdoors. They breed all year around. The eggs will hatch into larvae that resemble maggots within 4-6 days. The very active larvae will feed on organic debris including feces of the adult flea and other animals. After three molts it will develop a cocooned pupae where it will undergo a metamorphosis to the adult flea. It can remain in the pupa for several months if necessary until the conditions are suitable. So although human fleas are usually not present in stables or sheds during the coldest months the pupa can easily span the winter to emerge as adults in the early spring. This may explain why they are often the most abundant in the spring when all of the pupae from the late fall and winter emerge. It is unclear if the lifecycle pauses inside a heated human home. A well fed adult can live up to 513 days and even starved can last 135 days (Krasnov, 2012: 54). It is unclear how long they live after being infected by Yersinia pestis (or other pathogens). Fleas only feed on blood as adults so this is their only phase that can be infected by Yersinia pestis.

Modern infestations of P. irritans in Greece and Iran can give a few insights into its disease ecology. Sheep and goats are consistently the most heavily infested animals with P. irritans in modern Iran and Greece. In parts of Iran, P. irritans is the most common flea captured from humans or domestic livestock: goats, sheep, cattle and chickens (Moemenbellah-Fard et al, 2014; Rahbari,  Nabian, & Nourolahi, 2008;  Rafinejad et al, 2013). In some modern surveys, P. irritans is over 90% of the fleas collected in rural areas, found on sheep, goats, cattle, humans and chickens — “wherever the animal infestation was high the fleas easily transmitted to humans” (Rahbari et al, 2008:44). In Greece, Christodoulopoulos et al. (2006) made a very important observation:

“fleas accumulated in the goat environment with each successive generation leading to an increase in their number. This conclusion could be corroborated by the observation that the most successful flea control measure was the change of barn location with movement of the goats to another far away new-constructed barn.” (p. 142-143)

So even with modern insecticides, sheep dips, and building techniques available, the infestation of the building could not be controlled. This has implications for human housing. Observations of flea ecology in Iran back this up, albeit without addressing methods of eliminating infestations.

The Iranian reports discuss human flea bites more. Noting that men who worked with animals had a higher bite rate. Bites are primarily around the ankles and lower legs, often multiple bites in a row.  In Iran they noted that human reactions to the flea bites varied from highly allergic to no sensitivity at all (Rahbari, Nabian, & Nourolahi, 2008). This is a difference in human immunology to the fleas and sensitivity is likely to alter the immune response to not only the bite but also bacteria in the bite. There is also likely to be heterogeneity in which humans and animals are bitten.

As we begin to take Pulex irritans more seriously as a plague vector, there is a lot of basic biology that needs to be done yet. How long can they survive infected? How does it effect their feeding behavior? Some studies showed that a small percentage of P. irritans can block, so what effect does that have on transmission in that small percent of fleas?


Archibald, W. S., & Kunitz, S. J. (1971). Detection of plague by testing serums of dogs on the Navajo Reservation. HSMHA Health Reports, 86(4), 377–380.

Bain, A. (2004). Irritating intimates: the archaeoentomology of lice, fleas, and bedbugs. Northeast Historical Archaeology, 33(1), 81–90.

Barnes, Jefferey. (22 April 2014)  Human flea, Arthropod Museum Notes, Number 108. University of Arkansas.

Buckland, P. C., & Sadler, J. P. (1989). A biogeography of the human flea, Pulex irritans L.(Siphonaptera: Pulicidae). Journal of Biogeography (UK).

Christodoulopoulos, G., Theodoropoulos, G., Kominakis, A., & Theis, J. H. (2006). Biological, seasonal and environmental factors associated with Pulex irritans infestation of dairy goats in Greece. Veterinary Parasitology, 137(1-2), 137–143.

Dobler, G., & Pfeffer, M. (2011). Fleas as parasites of the family Canidae. Parasites & Vectors, 4, 139–139.

Drancourt, M., Houhamdi, L., & Raoult, D. (2006). Yersinia pestis as a telluric, human ectoparasite-borne organism. The Lancet Infectious Diseases, 6(4), 234–241.

Eisen, Rebecca J., David T. Dennis, and Kenneth L. Gage. “The Role of Early-Phase Transmission in the Spread of Yersinia pestis.” Journal of medical entomology 52.6 (2015): 1183-1192.

Haule, M., Lyamuya, E. E., Kilonzo, B. S., Matee, M. I., & Hangombe, B. M. (2013). Investigation of fleas as vectors in the transmission of plague during a quiescent period in North-Eastern, Tanzania. Journal of Entomology and Nematology, 5(7).

Hufthammer, Anne Karin, and Lars Walløe. “Rats cannot have been intermediate hosts for Yersinia pestis during medieval plague epidemics in Northern Europe.” Journal of Archaeological Science 40.4 (2013): 1752-1759.

Kenward, H. (1999). Insect remains as indicators of zonation of land use and activity in Roman Carlisle, England. Reports from the Environmental Archaeology Unit (Vol. 99, pp. 1–30).

Kotti, B. K. (2015). Fleas (Siphonaptera) of mammals and birds in the Great Caucasus. Entomological Review, 95(6), 728–738.

Krasnov, Boris (2012) Functional and Ecological Ecology of Fleas: A Model for Ecological Parasitology. Cambridge University Press.

Laudisoit, A., Leirs, H., Makundi, R. H., Van Dongen, S., Davis, S., Neerinckx, S., et al. (2007). Plague and the human flea, Tanzania. Emerging Infectious Diseases, 13(5), 687–693.

Miarinjara A, Rogier C, Harimalala M, Ramihangihajason TR, Boyer S. Xenopsylla brasiliensis fleas in plague focus areas, Madagascar. Emerg Infect Dis. 2016 Dec [3 Sept 2016].

Moemenbellah-Fard, M. D., Shahriari, B., Azizi, K., Fakoorziba, M. R., Mohammadi, J., & Amin, M. (2014). Faunal distribution of fleas and their blood-feeding preferences using enzyme-linked immunosorbent assays from farm animals and human shelters in a new rural region of southern Iran. Journal of Parasitic Diseases, 40(1), 169–175.

O’Sullivan, A. (2008). Early medieval houses in Ireland: social identity and dwelling spaces. Peritia, 20, 225–256.

Panagiotakopulu, E. (2001). Fleas from pharaonic Amarna. Antiquity, 75, 499–500.

Pulex irritans, Animal Diversity Web, accessed 18 June 2016.

Rahbari, S., Nabian, S., & Nourolahi, F. (2008). Flea infestation in farm animals and its health implication. Iranian Journal of Parasitology, 3(2), 43–47.

Rafinejad, J., Piazak, N., Dehghan, A., Shemshad, K., & Basseri, H. R. (2013). Affect of some environmental parameters on fleas density in human and animal shelters. American Journal of Research Communication.

Ratovonjato, J., Rajerison, M., Rahelinirina, S., & Boyer, S. (2014). Yersinia pestis in Pulex irritans Fleas during Plague Outbreak, Madagascar. Emerging Infectious Disease, 20(8), 1414–1415.

Reilly, E. (2003). The contribution of insect remains to an understanding of the environment of Viking-age and medieval Dublin.  pp. 40-61 In: Medieval Dublin IV. Four Courts Press.

Schedl, W. (2000). “Contribution to insect remains from the accompanying equipment of the Iceman”. pp. 151-155 In S. Bortenschlager & K. Oeggl (Eds.), The Iceman and his Natural Environment. Springer.

Yakhchali, M., & Bahramnejad, K. (2015). A survey of Pulex irritans (Linnaeus 1758, Siphonaptera: Pulicidae) infestation in sheep and residential areas in Kurdistan Province, Iran. The Iranian Journal of Veterinary Science and Technology, 7(1), 40–47.


Plague in 6th century Aschheim and Altenerding, Bavaria

Since I last wrote about Bavaria, the aDNA centers have been busy. With the accepted manuscript of the second new paper available this past week, its time for an update. The fourth paper on Aschheim not only confirmed the first three, but it also produced the first full genome of Yersinia pestis for the Plague of Justinian (Wagner et al, 2014). This paper also confirmed the Bavarian strain’s placement in the phylogeny of Y. pestis. The availability of the first full genome will primarily be important for comparison to newly discovered samples from elsewhere. Using newer technology, the newest paper refined some of the Aschheim sequence and produced a full genome of Y. pestis from a woman buried at Altenerding, about 20 km from Aschheim (Feldman et al, 2016). Radiocarbon dating from both sites places the epidemic in the mid-sixth century; it can not differentiate which specific epidemic ‘wave’.  The Altenerding epidemic was from the same Y. pestis lineage as Aschheim proving that this was a regional epidemic, possibly the same epidemic event. The phylogeny for the first pandemic is still based on a single epidemic from one geographic region, so the time is not yet ripe to use the phylogeny to tell inform us on the transmission or route of the pandemic.

6th cent Bavaria
Map of Roman Bavaria showing the Roman roads with Aschheim and Altenerding marked. The half circle/mound mark designates Roman villas. (modified from the Pelagios project)

It is, however,  time to start thinking a little more about the environment of these sites. They are both located on the Munich gravel plain, foreland (foothills) north of the Alps. Aschheim is located closer to the Alps at an elevation of 500 meters with Altenerding 20 km further north at a lower elevation in small valley formed by a tributary of the River Isar. The Roman road running horizontally across the map runs west to Augsburg, the capital of the Roman province of Raetia Secunda and east to the city of Batavia, a colony in the province of Noricum. The road running by Altenerding would take traffic eventually north toward Regensburg (Casta Regina).

Large water feature is Speichersee lake with a man-made 20th century reservoir used to power hydroelectric plants and serve some of the water needs of the Munich region. As far as I can tell, none of this would have been present in the Late Antique period. The River Isar is the green line to the west of both sites. Munich will later be founded where the road crosses the river from monastic land in about 1158. There was nothing special at the river crossing in the sixth century. Although the road crosses the river, there is no indication of a Roman bridge on the map.

Both Aschheim and Altenerding are located in what would have been the province of Raetia II. While they are along Roman roads, this would have been a rural area. Both Aschheim and Altenerding were sites of Roman villas and Dornach near Aschheim was a small settlement. How much of this would have been occupied and further developed (or not) after the Roman army left is unclear. The cemetery at Altenerding is triple the size of Aschheim. Yet, there is reason to think that Aschheim was hit harder by the plague and based on the carbon dates of graves with some molecular plague signal, probably more than once. Michael McCormick (2015:83) suggests that the Aschheim cemetery gathered graves from a dispersed settlement that probably had fewer than 70 people at any one time.

A living history museum in Munich area at Kirchheim has reconstructed typical buildings from the early medieval Merovingian period. Although this area was nominally under Merovingian Frankish hegemony there is little specifically Frankish about the archaeology. They were all wooden construction. Below is a picture of a sunken pit building, an ‘out building’ and a long house.

Reconstruction of 6th-7th century Bavarian buildings at Kirchheim in the Munich district close to Aschheim. (Photo by Leporollo, Wikipedia CC3.0)

Continue to think of the Plague of Justinian in Constantinople and Pelusium, it was surely there. Just remember that most of its geographic spread may have looked more like this picture.


Feldman, M., Harbeck, M., Keller, M., Spyrou, M. A., Rott, A., Trautmann, B., et al. (2016). A high-coverage Yersinia pestis Genome from a 6th-century Justinianic Plague Victim. Molecular Biology and Evolution, 1–31. [Accepted manuscript]

McCormick, M. (2015). Tracking mass death during the fall of Rome’s empire (I). Journal of Roman Archaeology, 28, 325–357.

Wagner, D. M., Klunk, J., Harbeck, M., Devault, A., Waglechner, N., Sahl, J. W., et al. (2014). Yersinia pestis and the Plague of Justinian 541–543 AD: a genomic analysis. The Lancet Infectious Diseases, 14(4), 1–8.


Plague Dialogues: Monica Green and Boris Schmid on Plague Phylogeny (II)

Monica H. Green (,@MonicaMedHist) is a historian of medieval medicine. An elected Fellow of the Medieval Academy of America, she teaches both global history and the global history of health. She was the editor in 2014 of Pandemic Disease in the Medieval World: Rethinking the Black Death, the inaugural issue of a new journal, The Medieval Globe.

Boris Schmid (@BorisVSchmid) is a theoretical biologist at the University of Oslo, Norway, and specializes in disease ecology and epidemiology. He recently described a link between climate fluctuations in medieval Central Asia and what looks like repeated introductions of plague into Europe’s harbors, a hypothesis that can be tested by the analysis of ancient DNA samples of Y. pestis. He works in a multidisciplinary team of theoreticians, archeologists, microbiologists and historians, led by Nils Chr. Stenseth.


In our previous blog post, Monica and I discussed how different lineages of plague – Yersinia pestis – collected their own genetic signature (SNP profile) as they diversified from a common ancestor. Monica also summarized in broad terms what ancient DNA samples of Y. pestis (extracted from plague victims) are now available from the initial Black Death outbreak and how they are related, using the latest plague studies of Haensch, Bos and Spyrou.

In this blog post Monica will delve into the nitty gritty details of these aDNA plague studies, and give an example of how to transform those details into a new understanding of the past rodent reservoirs and global mobility of plague, one of the deadliest diseases of our collective past. And I close the post by reflecting on the potential of aDNA to connect the fields of history and biology.


Thanks, Boris. It might be important to remind readers that we don’t have any aDNA evidence from past rodent populations yet. All the samples to date have been retrieved from human victims. But the SNP study that Seifert et al. published earlier this year from samples in Brandenburg, an inhumation from the time of the 30 Years War (1618-1648); the whole genome study that Bos and Herbig et al. also published this year, reporting on the samples from 18th-century Marseille; and the sample from Ellwangen included in the new study by Spyrou et al., all document that Branch 1A (see tree in our previous post) “focalized,” that is, it set up shop in some rodent population(s) and happily continued to proliferate for another 400 years. But all that happened, it is clear, separately from what was going on with Branch 1B, what I have taken to call the pestis secunda.

In their most recent study, the Tübingen/Jena team headed by Krause give us further insight into the early stages of Branch 1B. The beginning of Branch 1B was first documented in the 2011 London study, though it was only earlier this year that I realized that London sample 6330 likely dates from the 1360s and does not come from the initial Black Death outbreak. (It comes from a different burial ground, St Mary Graces.) In Bos and Herbig et al. 2016, it was reported that sample 6330 differed from the 1348-50 London Y. pestis genome by two SNPs. In the present study, interestingly, Spyrou et al. report something slightly different. Sample 6330 does indeed differ from the London Black Death genome by two SNPs (p3 and p4), but a third SNP in sample 6330 they are reporting here for the first time (p5) seems to be unique, a ‘G’ to ‘T’ switch at position 4,301,295 not found in any other historic genome or in the reference strain, CO92. (Spyrou et al. did not include London 6330 on their Table 1, so we offer a modified version of it here in fig. 3.)

CORRECTED fig03 for Contagions blog, (a) Spyrou et al 2016 fig02B Y pestis phylogenetic tree (detail of origins of Branches 1A and 1B), (b) Table 1 with 6330 SNPs added (06272016)
Fig. 3: (a) Detail of Spyrou et al. 2016, fig 2B: Yersinia pestis phylogeny – SNPs distinguishing Branches 1A and 1B; (b) Spyrou et al. 2016, Table 1, modified with data on London sample 6330 drawn from Spyrou et al. 2016, Table S4, SNP table. The SNPs unique to London 6330 and Bolgar City are highlighted in yellow.


First of all, we might say that those three SNPs are significant for the time gap they suggest between the Black Death and the 2nd wave of plague to hit London in 1361-63; for the sake of argument, we’ll say “21 years,” to use your formula (3 x 7 years), Boris. But think about the implications of that: plague arrives in London at the end of 1348 as a new disease, and a new strain (with 3 new SNPs) is causing a major new outbreak in 1361-63, which is when this burial seems to date from. 21 years have not passed since the previous outbreak. So what gives? Obviously, the “time-to-SNP” calculus we’re using is an average, not an absolute. But it does make us stop and wonder: did all this really happen so fast? And did it really happen in western Europe?

Which brings us to the Bolgar City sample. It, clearly, is a “descendant” of the same strain as London 6330: it has the two new SNPs, p3 and p4. (It doesn’t have that unique p5 SNP of London 6330, but that may have arisen as little as three days before this person died. We cannot attach any evolutionary significance to it until we see it documented somewhere else.) But note this: the Bolgar City strain has evolved further. It now has the p6 SNP that will define all the rest of Branch 1B and it has its own unique SNP, p7. And again, we have a problem of time compression: the Bolgar City sample (if we can trust the dating of the coins which were said to have been found with the body) may date as early as the late 1360s.

Remember what we need to have an outbreak in humans from a new lineage of Y. pestis: not simply does that new lineage have to arise from a single change in a single cell of Y. pestis, but that new SNP needs to proliferate enough in a reservoir rodent population to cause a new epidemic in humans. So looking over all these SNPs, p1-p7, we can see that they cluster into two “founder effect” phenomena: one that creates the initial Black Death lineage (Branch 1A) and one that creates the pestis secunda lineage (Branch 1B).

Where did those two lineage foundations happen? Let’s go back to Caffa, the “hurling bodies over the walls” scenario. Clearly, if we can believe that story (and remember, we have only one account of it, and that from a non-eye-witness), it tells of an already proliferating plague outbreak. By October 1346, Y. pestis was multiplying by the millions in rats and mice and rodents of whatever kind that lived in and around Caffa.

One, and only one, of those gazillions of Caffese offspring gave rise to Branch 1B. It, too, needed to find a place to set up shop and proliferate to make gazillions of (nearly) identical copies. And where was that place? Was it (as Krause seemed to imply in his April lecture) in London? Maybe it was in or near Bergen op Zoom (NL), where we find a sample with the same SNP profile as the London 6330 sample (Haensch et al. 2010)? Or was it near the same place where Branch 1A had already established its original home, before it reached the Black Sea? Haensch et al. had already proposed in 2010 a “northern” route for the introduction of the pestis secunda strain that reached the Netherlands. I’ll admit, I was skeptical for the longest time. But now I see that this possibility might bear more analysis. At the very least, the question shifts our focus away from western Europe and back to the areas around the Black and Caspian Seas. And that’s exactly where our Bolgar City sample is from, the one that is already showing two SNPs of further evolution beyond London 6330 but might not be a whole lot younger than it. As we said, jetting out of Heathrow wasn’t yet an option in the 14th century. But there was plenty of activity in these central Eurasian areas dominated by the Mongol Golden Horde to connect lots of rodent reservoirs to a bacterium looking for a new place to call home.


Thanks Monica! The amount of information that follows from a few different nucleotides between aDNA samples is quite amazing, and learning how to interpret this data historically is rightly one of the transformative processes now happening in Biology (and if I say so, in Medical History as well).

Monica’s interpretation of plague’s past mobility is based on the same genetic data as the one sketched out in Spyrou 2016, and highlights the challenge of interpreting ancient DNA, given that the ancient DNA sequences of plague are still so sparsely sampled across time and space. One thing that strikes me as especially important is how much the argument of “favor the most simple, parsimonious explanation” changes based on whether you think of plague largely in terms of a human epidemic (which Wagner 2014, and by extension Spyrou 2016 appear to do), or as a disease that spread through human and wildlife both, as Monica and I do. If you include the possibility of new wildlife reservoirs of plague (and plague has created numerous new wildlife reservoirs in time), say near Bolgar City, the logic of how plague moved across Eurasia changes.

As more aDNA data becomes available, it will be very interesting to see the geographic range that a lineage of plague bacteria can spread without collecting changes in its SNP profile. Once we have a good idea of that, and a more complete view of the SNP profiles that existed during the past pandemics, SNP profiles might be used to shed light on the actual source of a historic plague outbreak, and thus offer an independent way of checking the reliability of historic sources that blame particular smugglers, ships, refugees or clothing as the source of a plague outbreak.

Wow, thanks, Monica, for this great discussion. This is an example on how history and biology can intertwine, and while we are all waiting for more revelations from aDNA and historic sources, it seems prudent to start more interactions between historians and biologists. There is an inherent bias to doubt your own data too much, and trust another fields’ data too blindly, leading to mistakes at both sides: we blindly pick some historic report as authoritative, or put too much faith in a report on the (in-) efficiency of plague transmission by different flea species, whilst a single mutation that causes the loss of a gene can have drastic effects on how well the disease transmits (Hinnebusch, 2016). The only practical way to avoid falling into such pitfalls is by investing in cross-talk between scholars of the humanities and natural sciences!


Thank you, Boris. This was great. And very special thanks to Michelle Ziegler, for hosting our discussion on her super blog, Contagions.


Bos, K. I., Herbig, A., Sahl, J., Waglechner, N., Fourment, M., Forrest, S. A., et al. (2016). Eighteenth century Yersinia pestis genomes reveal the long-term persistence of an historical plague focus. eLife, 5, 17837.

Cui, Y., Yu, C., Yan, Y., Li, D., Li, Y., Jombart, T., et al. (2012). Historical variations in mutation rate in an epidemic pathogen, Yersinia pestis. Proceedings of the National Academy of Sciences, 110(2), 577-582.

Haensch, S., Bianucci, R., Signoli, M., Rajerison, M., Schultz, M., Kacki, S., et al. (2010). Distinct Clones of Yersinia pestis Caused the Black Death. PLoS Pathogens, 6(10), e1001134.

Hinnebusch, B. J., Chouikha, I., & Sun, Y.-C. (2016). Ecological Opportunity, Evolution, and the Emergence of Flea-borne Plague. Infection and Immunity, IAI.00188–16–31.

Krause, Johannes (4-12-2016)  Oral Presentation #S577:  Ancient pathogen genomics: what we learn from historic pandemics. European Congress  of Clinical Microbiology and Infectious Diseases

Seifert, L., Wiechmann, I., Harbeck, M., Thomas, A., Grupe, G., Projahn, M., et al. (2016). Genotyping Yersinia pestis in Historical Plague: Evidence for Long-Term Persistence of Y. pestis in Europe from the 14th to the 17th Century. PLoS ONE, 11(1), e0145194-8.

Spyrou, M. A., Tukhbatova, R. I., Feldman, M., Drath, J., Kacki, S., de Heredia, J. B., et al. (2016). Historical Y. pestisGenomes Reveal the European Black Death as the Source of Ancient and Modern Plague Pandemics. Cell Host and Microbe, 19(6), 874–881.

Wagner, D. M., Klunk, J., Harbeck, M., Devault, A., Waglechner, N., Sahl, J. W., et al. (2014). Yersinia pestis and the Plague of Justinian 541–543 AD: a genomic analysis. The Lancet Infectious Diseases, 14(4), 1–8.