Mapping Malaria in Anglo-Saxon England

Guthlac at Croyland in the marshes of the Wash.

England once looked very different. Much of southern Britain was marshland for most of the island’s occupied history. These bogs, fens, and marshes ensured that areas of virtual wilderness persisted  from before Roman Britain through the Norman period and beyond. Despite the difficulties of using fenlands, these areas were not only occupied throughout the Anglo-Saxon period, but important centers like Croyland, Bardney, and Ely eventually developed in the marsh.

The largest fenland region was known as ‘the Wash’.  This low-lying region drained four rivers into  a square bay of the North Sea that forms the corner between Lincolnshire and Norfolk. In Anglo-Saxon times, this tidal marsh and bog was a vast border region between the region of Lindsey and East Anglia.  Places like Croyland and Ely were islands in the wetlands.  The eighth century Life of Guthlac describes the environment of Croyland when Guthlac arrived:

There is in the Midland district of Britain a most dismal fen of immense size, which begins at the banks of the river Granta not far from the camp which is called Gronte (Cambridge) and stretches from the south as far north as the sea. It a very long tract, now consisting of marshes, now of bogs, sometimes with black waters overhung by fog, sometimes studded with woodland islands and traversed by the windings of tortuous streams. (Hill, 1981:11 cited in Gowland & Western, 2011).

These marshes are ideal for malaria, but evidence of malaria in Anglo-Saxon England has been lacking. It is supposed that malaria would have been brought to Britain with the Romans (1). Unfortunately, there is no evidence that I know of that malaria became endemic in Roman Britain much less lasted into the early medieval (Anglo-Saxon) period. It has also been speculated that ‘spring fever’ (lecten adl) found in Anglo-Saxon leechbooks is the spring manifestation of tertian malaria (1) caused by Plasmodium vivax. This would fit the pattern of malaria in cool or cold climates like that found in Finland discussed in a recent post. Indoor transmission in Anglo-Saxon earthen floored, open structured wooden homes with thatched roofs would be an ideal way to concentrate malaria in a thinly populated marsh.  (Without chimneys homes had to open enough to allow smoke to escape from a central hearth.)

Incidence of Malaria in England, 1840-1910 (2)

It has long been known that Britain can environmentally support endemic malaria. Malaria was fairly wide-spread in 19th century Britain when it was first mapped (figure to left) (2). The upper black area on the map includes much of ‘the Wash’. However, proof of malaria is more tenuous for the medieval period.  Together with the unhealthy reputation of the brackish marshlands there is at least enough evidence to suggest that endemic malaria reached back into the late medieval period.

Malaria went by a variety of local names before the early modern period. Malaria-like fevers are mentioned in literature from Geoffrey Chaucer to William Shakespeare (2, 3). Terminology for malaria was not settled upon the Italian ‘malaria’ until the early modern period. Before then, it went by a variety of terms the most universal being ‘ague’, meaning the shakes, and sometimes  ‘fever and ague’ referring to the cyclic breaking of a fever.

Gowland and Western (2011) took a new approach to finding evidence of malaria in Anglo-Saxon England (400-1100 AD) (4). Malaria caused by Plasmodium vivax causes chronic hemolytic anemia that may result in cribra orbitalia due to expansion of the bone marrow in the cranium. Gowland and Western correlated the presence of cribra orbitalia in Anglo-Saxon skeletal remains with the presence of the malarial vector Anopheles atroparavus and reports of ‘ague’ in 19th century England.

The Anglo-Saxon cemeteries used in their study are mapped in the figure below on the left. Note that not many cemeteries are located near the modern coastline of ‘the Wash’. This area would have likely been too wet for settlement.

Anglo-Saxon cemeteries (4)

Map of A. atroparvus with 19th century "ague" records. (4)

Gowland and Western  determined areas capable of sustaining malaria by mapping the presence of A. atroparvus from a 1900 AD British Museum survey (shown above on the right) (4).  The darker the shading the more reports of mosquitoes. This survey was reported to not have been systematic, so they augmented it with 19th century ‘ague’ reports (triangles).  There are some notable areas with high levels of mosquitoes that lack ague reports. This map was use to determine malarial regions for correlation with either cribra orbitalia or the poor nutrition control enamel hypoplasia. It also roughly correlates with the 1840-1910 malaria incidence in the color map above by Kuhn et al (2).

An inverse distance map showing A. atroparus incidence vs. hot and cold spots for cribra orbitalia. (4)

In this last map, malarial areas are plotted with hot and cold spots for cribra orbitalia.  Purple and blue areas on the map indicate the highest areas of A. atroparvus in 1900, while red and orange circles indicate the cribra orbitalia ‘hot’ spots. Areas of cribra orbitalia correlate very well with malarial areas around the Wash.  Cribra orbitalia ‘cold’ spots (blue circles) correlate with areas of low A. atroparvus. They found no correlation between enamel hypoplasia with either ‘malarial’ or ‘non-malarial’ areas (4).

If this cribra orbitalia is due to malaria, it is likely an underestimate of the amount of malaria in the English wetlands. Cribra orbitalia forms in children so it will not indicate adults who contract malaria. Communities like Ely, Croyland and Peterborough were large monasteries who probably drew many into the marsh as adults.

Confirmation of malaria in Anglo-Saxon England will have to wait for molecular evidence, but this skeletal evidence strengthens the hypothesis that it was endemic in early medieval Britain. It also should be informative for the areas to concentrate efforts to find molecular evidence.

References:

(1) Cameron, M.L. (1993, repr. 2006) Anglo-Saxon Medicine. Cambridge University Press.

(2) Kuhn, K., Campbell-Lendrum, D., Armstrong, B., & Davies, C. (2003). Malaria in Britain: Past, present, and future Proceedings of the National Academy of Sciences, 100 (17), 9997-10001 DOI: 10.1073/pnas.1233687100

(3) Reiter P (2000). From Shakespeare to Defoe: malaria in England in the Little Ice Age. Emerging infectious diseases, 6 (1), 1-11 PMID: 10653562

(4) Gowland RL, & Western AG (2011). Morbidity in the marshes: Using spatial epidemiology to investigate skeletal evidence for malaria in Anglo-Saxon England (AD 410-1050). American journal of physical anthropology PMID: 22183814

Mapping Smallpox, Malaria, and Leprosy

Contagion by Haisam Hussein of Lapham's Quarterly (Click the map to enlarge)

I love looking at infection maps. Hat-tip to Michael Walsh at Germscape for finding this map. There is a lot of information on this map and unfortunately any text that might have come with it at Lapham’s Quarterly is not readily available. So we have the map to figure out without any explanation. The red arteries represent the origin of Leprosy in central Africa and the blue veins represent the origin of smallpox in northern Africa and its spread. Transmission lines for malaria are not shown; the yellow areas seem to represent modern endemic malaria. The geographic highlights either document transmission events or major steps in the study of malaria, smallpox and leprosy.

Malaria deaths in the United States, 1870 census.

At the height of its expansion, there are few places on earth that malaria did not penetrate. Today malaria is found primarily in tropical regions but that wasn’t always so. The map to the right illustrates the malarial deaths listed in the 1870 US federal census. Malaria once was endemic, at one time or another, in most of the United States east of the Mississippi River and around the Gulf of Mexico. Likewise it was endemic in parts of 19th century Britain. In temperate regions of the world it is the humans who carry the parasite through the winter and infect the spring mosquitoes. Contrary to general knowledge, most malaria in the United States dwindled long before the arrival of DDT. Improving the standard of living and eliminating unnecessary standing water are the most important ways to decrease malaria. Early American physician Benjamin Rush knew this over two centuries ago.

 

Did India and China Escape the Black Death?

One of the few things everyone studying the plague can, I think, agree on is the importance of plague dynamics in Asia. Genetic diversity and biogeography suggest that Yersinia pestis evolved in East Central Asia (S. Russia, Mongolia, N. China) and spread along the Eurasian steppe from the Caspian Sea in Kazakstan to the Mongolia very early, perhaps even before it became a human pathogen [1]. The orange labeled clones in the diagram below represent Y. pestis clones that branched off of the main stem before Y. pestis was a human pathogen. These clones only infect voles [2]. They are spread in a wide belt along the Asian steppe but as these are modern clones, we can’t be sure how early this spread occurred. Pandemic Yersinia pestis, ‘the plague’, could have emerged anywhere along this wide Asian belt. Note the red clones (the “Medievalis biovar”) shadow the Silk Road.

Yersinia pestis isolates across modern Asia. (Li et al, 2009) Click to enlarge

The three main pandemics probably arose from different localities  as clones were slowly spread along the Silk Road and endemic foci emerged and expanded [1,2]. The Plague of Justinian is first recorded in Pelusium Egypt, but it probably arrived via canals linking it to the Red Sea and ultimately the Indian Ocean. The Black Death is first recorded at Caffa on the Black Sea. The third (modern) pandemic began in southern China (purple clones on the figure). Not unsurprisingly it is difficult to trace these pandemics back to an endemic site since as a primarily rodent pathogen, Yersinia pestis can move without effecting humans.

The Black Death (1347-1352) draws all the attention because of its scope and scale, the amount of evidence, and the intensity of its legend. In some parts of the world, legend is nearly all we have (or have so far). Although the scientific evidence points toward an Asian origin for Yersinia pestis, there is precious little documentary evidence of it in Asia before modern times (17th century onwards).

George Sussman set out to examine the evidence of the Black Death in India and China in the current edition of the Bulletin of the History of Medicine. What he found in both enlightening and yet mystifying.

Western legends of the Black Death in the Far East go back to contemporary 14th century accounts of the plague in Europe and the Middle East [3]. Witnesses of the Black Death fueled by traveler’s stories imagined that all the known world was stricken, embellishing their writing accordingly. For the most part, modern historians have accepted their accounts of plague in China and India without scientific or historical evidence from China and India themselves. Sussman notes that McNeill’s influential Plagues and Peoples argues that plague foci in the Indian Himalayas and in central Africa are much earlier and more likely to be the source of the first plague pandemic (6th century) than the endemic strip along the Eurasian Steppe that McNeill dated to the 14th century [3]. Modern genetic diversity and biogeography points toward just the opposite with the eastern Asian steppe (Mongolia/N. China) being the original focus and the African focus dating to about the 14th-15th century [1]. There isn’t much evidence that the Indian Himalayan site is very old at all. We clearly need to learn a lot more about the Indian Ocean trade routes in Antique and Medieval periods to understand how the plague reached Pelusium in the 6th century and southern Africa by the 14th century.

So what evidence is there for plague in India before the third pandemic? During the 14th century northern and central India was ruled by Islamic sultans based in Delhi who kept close ties with the Central Asian peoples they came from and with the Middle Eastern centers of Islam [3]. They were well-connected diplomatically, economically and culturally with both Central Asia and the Middle East, areas that were both devastated by the Black Death and its successive waves. Yet there is no evidence of the plague in 14th century India [3]. Origins aside, this is strange, for there to be no record of plague even at ports makes me suspicious of the completeness of the written records. I would expect small local epidemics in ports, even if it couldn’t get traction in the countryside.  Sussman argues that the Indian subcontinent may have been the only area of Eurasia to have population growth during the 14th century [3].

Plague is unambiguously described in the Deccan of India in the early 17th century. It first came to the attention of Emperor Jahangir in Hindustan in 1616 [3]. The annals of the Emperor Jahangir record the third year of the winter plague with mad and dying rodents in January 1619 [3]. The annals include an interesting story of a cat contracting the plague from a mouse and passing it on to a girl who triggered a larger outbreak.

“After this the grain (dana) of the plague (a bubo) appeared in the girl, and from excess of temperature and increase of pain she had no rest. Her colour became changed—it was yellow inclining to black—and the fever was high (tap muhriq gardid). The next day she vomited and had motions, and died. Seven or eight people in that household died in the same way, and so many were ill that I went to the garden from that lodging. Those who were ill died in the garden, but in that place there were no buboes. In brief, in the space of eight or nine days seventeen people became travellers on the road of annihilation”.(Sussman, p. 337-338)

He is describing a case of secondary pneumonic plague that then spread throughout the household. The development of secondary pneumonic plague in a child can be especially damaging because more people will come to care for a child than an adult. In this case, mouse to cat to child to family doesn’t require any fleas at all. The cat got the plague from biting the sick mouse, the child got the plague from playing with the cat and passed it on to her family. The lack of buboes in the last people to die suggest that at some point in the transmission bubonic plague became pneumonic, probably in the child.

So plague is firmly established in 17th century India, but not in the 14th century during the Black Death pandemic. While I expect that we may yet find evidence of small outbreaks, there not does appear to have been a large epidemic. Why that was is unknown. Perhaps a combination of geographic isolation, climate, vector availability and sheer luck.  Turning to neighboring China, the picture becomes more complicated.

As I’ve already mentioned, Yersinia pestis genetic diversity and biogeography suggests that it has been in northern China long before any of the pandemics. With the wide-spread of early clones, the pandemic does not necessarily have to begin where there is the greatest genetic diversity.

Sussman notes that in the third pandemic the large northern outbreak was marmot-derived pneumonic plague while the southern outbreak was rat-derived bubonic plague [3]. This is still the case today. A marmot derived outbreak of pneumonic plague occurred in northern China as recently as 2009. If plague in northern China is usually pneumonic plague from marmots, I’m not surprised that they did not have a specific name for the disease. Pneumonic plague does not produce unique enough symptoms to differentiate from other rapidly lethal respiratory diseases.

The Yuan dynasty controlled China and Mongolia during the first half of the 14th century. This period coincided with a concerted withdrawal from the greater Mongolian world most of whom had by this time converted to Islam [3]. It was a time of great turbulence: famines, epidemics, natural disasters, political unrest, as the last remnants of the Mongol empire in China devolved to regional warlords and the Ming Dynasty began to develop [3]. Record keeping during this devolution is sporadic and uneven, but it does show three rounds of massive epidemic in 1330- 1350 each taking over 60% of at least regional populations. Unfortunately medical descriptions of the disease(s) have not survived [3]. Sussman’s analysis of the overall Chinese population during the early to mid 14th century is that the losses are comparable to the 25-30% loss in Europe that is directly credited to the Black Death [3]. Given the ancient foci of plague in northern China, this is where we should expect it to come from in the 14th century, and so it does appear to. On the other hand, Sussman notes that the first obvious medical description of plague in China dates to 1644.

Sussman questions whether the 14th century epidemics were plague based on some questionable criteria. He is bothered by the apparent lack of spread of the epidemic to the southwest (where the third pandemic began). He thinks a ‘virgin territory’ epidemic in densely populated China should have easily spread throughout China as it spread throughout Europe.  The European pandemic was the unusual behavior for the plague, not a regional epidemic in China where plague was more ancient than in Europe. In other words, I don’t think that Europe and China were equally ‘virgin territory’ epidemics. The importance of ‘virgin territory’ is probably also being over estimated for Yersinia pestis. Also the terrain in southwestern China is unlike northern China or Europe; it is more tropical. We need to let go of the idea that the second and third pandemic must behave the same. With a sample set of only three pandemics, we surely can not say that there must be one pattern that they will all conform. The lack of medical description also makes Sussman question if it was the plague. However, there is apparently no medical description at all to rule plague out or in. He also finds it unlikely that the plague could have traveled the length of the Eurasian steppe because much of it is so sparsely populated. Yet the first epidemic in northern China occurs in the early 1330s, surely enough time to travel the Silk Road west by caravan or Mongol horsemen. It is also possible that this clone spread along the steppe over several decades or even a century before it erupted at multiple points into large epidemics where the conditions were right and into a pandemic in the west.

Noticeably absent in this discussion is archeological evidence in either India or China. Now that we can identify Yersinia pestis aDNA in remains, hopefully this could be investigated in at least northern China. Unfortunately, I rarely hear about any medieval archaeology from India or China.

World Biomes (click to enlarge)

Plague’s normal biome is semi-arid grassland, shown on this simplified biome map as brown and yellow. From Sussman’s information it appears that the Black Death avoided tropical rainforest biomes (light green). This is not really surprising given its endemic regions. It is the opposite of the third and weakest pandemic. The endemic foci produced by the third pandemic are the usual semi-arid grasslands in the American south-west, Madagascar (which has some savanna), and Brazil.

So in conclusion, what are we left with? First, western reports of plague in the east may be more rhetoric than reality. Even if there were small unrecorded outbreaks in India, there doesn’t seem to be much evidence of population decline. For China, it would help to have more evidence of the nature of the northern epidemic. However, the coincidence and lethality of the epidemic support it being the plague. There is still a lot of work to be done on plague history in southern Asia.

References:

[1] Morelli G, Song Y, Mazzoni CJ, Eppinger M, Roumagnac P, Wagner DM, Feldkamp M, Kusecek B, Vogler AJ, Li Y, Cui Y, Thomson NR, Jombart T, Leblois R, Lichtner P, Rahalison L, Petersen JM, Balloux F, Keim P, Wirth T, Ravel J, Yang R, Carniel E, & Achtman M (2010). Yersinia pestis genome sequencing identifies patterns of global phylogenetic diversity. Nature genetics PMID:21037571

[2] Li Y, Cui Y, Hauck Y, Platonov ME, Dai E, Song Y, Guo Z, Pourcel C, Dentovskaya SV, Anisimov AP, Yang R, & Vergnaud G (2009). Genotyping and phylogenetic analysis of Yersinia pestis by MLVA: insights into the worldwide expansion of Central Asia plague foci. PloS one, 4 (6) PMID: 19543392

[3] Sussman GD (2011). Was the black death in India and China? Bulletin of the history of medicine, 85 (3), 319-55 PMID: 22080795

Cradle of Cholera’s Seventh Pandemic Found

Cholera is a disease of seemingly endless fascination to epidemiologists for good reason. Vibrio cholerae emerged on a global stage in the 19th century just in time for the beginnings of modern medicine to grapple with it and for its transmission to prove the worth of epidemiological work. Although we understand its treatment and transmission well, it is still endemic in several regions, resulting in 3-5 million reported cases per year.

Like other relatively recently emerged pathogens, cholera has come in distinctive waves. Six discrete pandemics occurred between 1817 and 1923, it is believed from what is now known as the classic biotype. From 1923 to 1961 no pandemics occurred but evolution was far from standing still.  The seventh pandemic became apparent in the 1960s as the less severe El Tor biotype, that emerged sometime between 1827 and 1936, began to rapidly spread. The El Tor biotype transmits and survives better in the environment and human host than the classical biotype, including producing more asymptomatic and less severe infections.  El Tor represents an evolutionary leap forward for Vibrio cholerae on every level. We are still in the seventh pandemic. Preliminary characterization of the El Tor biotype’s mobile genetic units revealed too much diversity to reconstruct the pandemic.

Taking advantage of modern complete genome sequences, Mutreja et al (2011) collected and compared the complete genomic sequences of 136 isolates of the El Tor biotype collected over the last 40 years of the seventh pandemic plus 18 previously published genomes of El Tor and Classical biotypes. They were able to track three independent overlapping waves of cholera that are all descended from a 1950s ancestor in the Bay of Bengal. Each of these three descendant lineages left the Bay of Bengal independently for a transcontinental run.

Inferred transmission of the seventh cholera pandemic based on phylology. (Source: Mutreja et al, 2011, doi:10.1038/nature10392) Click to enlarge.

Each of the three waves can be distinguished genetically. The waves can be differentiated by the distinctive version of cholera toxin prophage carried by each clade. In addition, the first wave lacks the antibiotic cluster SXT/R391 and has obtained two VSP-2 genes. The acquisition of the SXT/R391 integrative and conjugative element (ICE) distinguishes the second wave beginning in 1978-1984. O139 strains of cholera are descended from the  second wave clone close to common ancestor of wave 1 and wave 2. The lineages within each wave have become quite complex but remain local enough not to produce waves of their own.

Each of the three waves reflects a clade of cholera that emerged from the Bay of Bengal and spread around the world, evolved into local lineages but then subsequently went extinct in non-endemic areas. Four discernible long distance transmissions have happened with the current outbreak in Haiti being the most recent. The overlapping nature and common source of these distinct waves reinforces the importance of the Bay of Bengal as cholera’s evolutionary cradle.

Considering the importance the Bay of Bengal for cholera, could other pathogens like Yersinia pestis, that has produced similar overlapping pandemic waves, also have an evolutionary cradle?  If so, then a sentinel  system set up around the cradle could give us crucial warning of an oncoming pandemic. The Bay of Bengal also serves as a lesson that knowing of the cradle is a far cry from controlling it.

Mutreja, A., Kim, D., Thomson, N., Connor, T., Lee, J., Kariuki, S., Croucher, N., Choi, S., Harris, S., Lebens, M., Niyogi, S., Kim, E., Ramamurthy, T., Chun, J., Wood, J., Clemens, J., Czerkinsky, C., Nair, G., Holmgren, J., Parkhill, J., & Dougan, G. Evidence for several waves of global transmission in the seventh cholera pandemic. (2011). Nature DOI: 10.1038/nature10392

Safa, A., Nair, G., & Kong, R. (2010). Evolution of new variants of Vibrio cholerae O1 Trends in Microbiology, 18 (1), 46-54 DOI: 10.1016/j.tim.2009.10.003

When Anthrax first came to North America

When pathogens arrived in the Americas is important for understanding the demographic history and biogeography of humans, animals and microbes of the Western Hemisphere. There have been two major periods of human migration to this hemisphere: across the Bering Land Bridge from Asia during the last Ice Age and the arrival of Christopher Columbus in 1492 began a major European and African migration. Although there were probably several minor maritime contacts between the closing of the Bering Land Bridge and 1492, most of these hypotheses are controversial and no pathogens have been linked to those contacts that I know of. So the question often becomes is the pathogen pre-Columbian (pre-1492) or post-Columbian (after 1492)?

Anthrax is a major pathogens of cattle/bison and secondarily humans. We know that it reached epidemic levels on Hispaniola in 1770, as I wrote about earlier, the island where Columbus landed in 1492. The question becomes did it come to the Americas with Columbus (or later Spaniards) and spread out of the Caribbean or had it been in North America before the arrival of the Spanish?

Phylogeography of the primary North American (WNA) Bacillus anthracis clone. TEA = Trans EurAsian (Source: Kenefic et al, 2009)

Phylogenetic analysis of isolates collected from all over North America show a clonal distribution pattern consistent with a northern origin (1).  Bacillus anthracis is a  young species with relatively few clonal lineages and few identified SNPs.  Anthrax’s transmission method by spores means that there are relatively few generations for its overall age.

The Western North American (WNA) clade of Bacillus anthracis is the dominant lineage in the western hemisphere. It in turn is derived from the Trans Eurasian (TEA) clade of the A group of B. anthracis; group A represents about 90% of all strains.  Polymorphisms separating the WNA clade from TEA clade suggest a genetic bottleneck early in the founding of the North American population (1). Commerce has caused local outbreaks and in a few cases the establishment of a local strain from other clades (such as the Ames strain in Texas) (1, 2). The failure of these recent outbreaks and local strains to spread points toward the importance of a native herd animal to spread and maintain it in the environment.

The transmission cycle is accomplished via spores with a slow dispersal method. Northern Canadian outbreaks in the last 50 years suggest that the natural disease cycle produces only 0.28 generations per year (1).  In nature, these spores must wait for the carcase of the dead animal to decay or be preyed upon for the spores to be scattered in the soil or transmitted to scavengers. Humans have been among the most important scavengers of sick and dead animals. Early humans took hides, bones, and even meat from the infected animals. Commerce and use of hides has been the primary means of long distance transport of anthrax throughout the world (2). Anthrax kills its host within about a week, too short of a time period for the sick animal to carry it far from where it was contracted. It seems likely that anthrax was carried to North American over the Bering Straight land bridge (Beringian steppe ecosystem) in hides and other goods by Asians migrants.

American Bison (Source: Jack Dykinga, USDA, Wikipedia Commons)

“Oh give me a home where the buffalo roam and the deer and antelope play…”

A bison wallow at Yellowstone. (Source: Mila Zinkova, Creative Commons via Wikipedia Commons)

Anthrax can infect a wide variety of animals, but in the American bison it has found a nearly perfect host. It is a large herd animal that ranges over a wide region and yet returns to favorite areas (wallows and salt licks). Anthrax spores are kicked up in the dust by hoofed animals and the bison head is angled down toward the ground where it can inhale the spores. (Consider the difference between the orientation of a bison nose vs. a deer or elk.) Perhaps even more importantly bison wallow in shallow depressions, called unsurprisingly buffalo wallows, where they rub their hide in the dirt probably to remove parasites and sooth irritated skin. It is thought that these wallows are key sites in the spread of anthrax. As you can see in the picture to the right, a wallowing bison stirs up a lot of dust probably rubbing cutaneous anthrax into the soil and bison who die in the wallows deposit large numbers of spores there.

Original Bison range map (Source: Simon Pierre Barrette, CC via Wikipedia Commons)

Bison once roamed nearly the length of the North American continent.  The ancestral Holocene bison is represented by the lightest tan area in the diagram to the right, with its descendents the wood bison (medium brown) and plains bison (dark brown). Kenefic et al (2009) predict that anthrax wasn’t introduced until the glaciers withdrew enough to open up a corridor of grasslands into the mid-continent about 13,000 years ago. The movement of humans rather than bison is more critical to the dispersal of the anthrax. As Keneifc et al (2009) point out the  directionality of the evolution of lineages of WNA is distinctly north to south. The bison spread much earlier and more widely than the anthrax areas. I am left wondering about the role of Native American tribes that highly utilized and some followed herds of bison.

Bison areas became prime cattle grazing territory with the arrival of Europeans. Cattle and other domestic animals contract anthrax perpetuating the anthrax as the bison were nearly hunted to extinction. The movement of cattle around the continent further spread the anthrax and introduced some of the smaller regional lineages like the Ames strain in Texas, whose closest match is to strains in China.

Concentration of animals in an area by extensive cattle husbandry amplifies anthrax in an environment. Colonial Haiti would be a prime example of a confined area that was over exploited by cattle ranching and therefore amplified anthrax. On Hispaniola, anthrax is still considered endemic today and its the WNA clade of anthrax (1). We don’t know what it was in 1770 but it seems likely that it originated from contact with the North American continent rather than Europe.

[1] Kenefic LJ, Pearson T, Okinaka RT, Schupp JM, Wagner DM, Hoffmaster AR, Trim CB, Chung WK, Beaudry JA, Jiang L, Gajer P, Foster JT, Mead JI, Ravel J, & Keim P (2009). Pre-Columbian origins for North American anthrax. PloS one, 4 (3) PMID: 19283072

[2] Keim PS, & Wagner DM (2009). Humans and evolutionary and ecological forces shaped the phylogeography of recently emerged diseases. Nature reviews. Microbiology, 7 (11), 813-21 PMID: 19820723

See the previous post: Famine and Epidemic Anthrax, Saint-Dominque (Haiti), 1770