Category Archives: climate

Landscapes of Disease Themed Issue

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For the last couple years, I have been writing about a landscape-based approach to the study of infectious disease in general and historic epidemics in particular. When I first wrote about Lambin et al.’s now classic paper “Pathogenic landscapes” nearly three years ago, I did not know then that it would be so influential in my thinking or that the Medieval Congress sessions would be so successful. In the fall of 2014, Graham Fairclough and I began talking about ways that this first congress session could be represented in the journal he edits, Landscapes. This issue is a departure from their usual approach to landscape studies so I would like to thank Graham Fairclough for entrusting me with a whole issue. It has been a challenge for both of us, and I am proud of our product.

This issue represents the wide variety of studies that can be done all contributing to an understanding of past landscapes of disease. One of the reasons why I like the phrase landscape of disease, rather than simply landscape epidemiology, is that it opens up the array of disciplines that can be involved. In the study of diseases of the past, humanistic approaches can be as valuable as scientific methods. Both are required to build a reasonably coherent reconstruction of the past. Science and the humanities need to act as a check and balance on each other, hopefully in a supportive and collegial way.

The issue was published online a couple days ago. Accessing the journal through your library will register interest in the journal with both your library and the publisher, and would be appreciated. By now the authors should (or will soon) have their codes for their free e-copies if you do not have access otherwise.

Table of Contents

Landscapes of Disease by Michelle Ziegler. An introduction to the concept of ‘landscapes of disease’ and the articles in the issue. (Open access)

The Diseased Landscape: Medieval and Early Modern Plaguescapes by Lori Jones

The Influence of Regional Landscapes on Early Medieval Health (c. 400-1200 A.D.): Evidence from Irish Human Skeletal Remains by Mara Tesorieri

Malarial Landscapes in Late Antique Rome and the Tiber Valley by Michelle Ziegler

Epizootic Landscapes: Sheep Scab and Regional Environment in England in 1279-1280 by Philip Slavin

Plague, Demographic Upheaval and Civilisational Decline: Ibn Khaldūn and Muḥammed al-Shaqūrī on the Black Death in North Africa and Islamic Spain by Russell Hopley

plus seven book reviews. Enjoy!

 


Lambin, E. F., Tran, A., Vanwambeke, S. O., Linard, C., & Soti, V. (2010). Pathogenic landscapes: Interactions between land, people, disease vectors, and their animal hosts. International Journal of Health Geographics, 9(1), 54. http://doi.org/10.1186/1476-072X-9-54

A winter’s worth of work

Its well into spring now and my blogging has perhaps hit an all time low. I have been working on a project that I will write about more later this year. I’ve been reading a lot about environmental history, not the usual material for this blog. Some of it is listed below. It’s a sample of the kind of thing that I need to be read to understand disease in the past. I think it will be worth it eventually even if pollen diagrams and geology diagrams are not very exciting. 

I do have quite a few ideas for new posts, so I will be back…soon. 

A sampling of some of my recent reading:

Büntgen, U., Myglan, V. S., Ljungqvist, F. C., McCormick, M., Di Cosmo, N., Sigl, M., et al. (2016). Cooling and societal change during the Late Antique Little Ice Age from 536 to around 660 AD. Nature Geoscience, 1–7. http://doi.org/10.1038/ngeo2652

Mitchell, P. D. (2015). Human Parasites in Medieval Europe: Lifestyle, Sanitation and Medical Treatment. Advances in Parasitology (Vol. 90, pp. 389–420). Elsevier Ltd. http://doi.org/10.1016/bs.apar.2015.05.001

Mitchell, P. D. (2016). Human parasites in the Roman World: health consequences of conquering an empire. Parasitology, 1–11. http://doi.org/10.1017/S0031182015001651

Brogolio, G.P. 2015. Flooding in Northern Italy during the Early Middle Ages: resilience and adaption, in Post-Classical Archaeologies. 5: 47-68.

Galassi FM, Bianucci, R., Gorini, G., Giacomo M. Paganotti. G.M., Habicht, M.E., and Rühli, F.J. 2016. The sudden death of Alaric I (c. 370–410AD), the vanquisher of Rome: A tale of malaria and lacking immunity, European Journal of Internal Medicine. http://dx.doi.org/10.1016/j.ejim.2016.02.020 [Ahead of Print]

Mensing, S. A., Tunno, I., Sagnotti, L., Florindo, F., Noble, P., Archer, C., et al. 2015. 2700 years of Mediterranean environmental change in central Italy: synthesis of sedimentary and cultural records to interpret past impacts of climate on society, in Quaternary Science Reviews, 116(C), 72–94.

Sadori, L., Giraudi, C., Masi, A., Magny, M., Ortu, E., Zanchetta, G., & Izdebski, A. 2015. Climate,  environment and society in southern Italy during the last 2000 years. A review of the environmental, historical and archaeological evidence, in Quaternary Science Reviews, 1–16.

Li, Y.-F., Li, D.-B., Shao, H.-S., Li, H.-J., & Han, Y.-D. (2016). Plague in China 2014—All sporadic case report of pneumonic plague. BMC Infectious Diseases, 1–8. http://doi.org/10.1186/s12879-016-1403-8

Statskiewicz, A. (2007). The early medieval cemetery at Aschheim-Bajuwarenring: A Merovinigan population under the influence of pestilence? In Skeletal series and their socio-economic context (pp. 35–56).

The Spotty History of Chicken Pox

For its extreme antiquity, the virus that causes chicken pox has a surprising sparse documented history.  The earliest clear reference to the virus is actually to an emergence of its latent form as shingles, also called zoster. The ancient Greeks called it zoster after the word for girdle, while shingles comes from the latin word cingulus (belt) both referring to the most common site of emergence along peripheral nerves of the back that wrap around the abdomen. There are many theories, but as far as I know, no one has successfully explained how it got the name chicken pox.

It was not until histological and immunological investigations in the early twentieth century that the relationship between the primary phase infection, chicken pox (varicella), and the emergence of the latent virus as shingles (zoster) was confirmed. Into the 18th century, chicken pox and smallpox were commonly confused as a severe and mild form of the same disease. There are subtle differences between the rashes than can distinguish them. Chicken pox produces watery pustules that concentrate on the head and trunk of the body, while smallpox lesions become hard and dimpled and are concentrated on the appendages.  Chicken pox lesions are sparse or absent from the palms of the hands and soles of the feet, while these areas are often heavily covered by smallpox lesions. But, both diseases can cause lesions anywhere in the body including internal cavities and both can leave deep scars. Chicken Pox 1 They are also, of course, distinguished by their mortality rates. Smallpox has a mortality rate of around 30%, while chicken pox has a mortality rate of less than 1%. However, pregnant women and immune compromised patients are at high risk for life threatening complications from chicken pox. The blisters can also develop secondary bacterial infections that can become life threatening. Unlike chicken pox, smallpox requires a constant supply of non-immune hosts to persist in a community.

Viral Lifecycle

The lifecycle of the varicella virus is ideal for persisting in small communities over many generations without outside introduction. It is primarily transmitted as a respiratory virus, but it can also be transmitted by contact with fluid from the blisters. Both routes are critical. Respiratory transmission allows it to spread rapidly while contact with blisters transmission allows it to persist in the community (more on this below).

As the virus enters the body it replicates for 10 to 21 days before the chicken pox rash of virus-filled blisters appears. Meanwhile, some of the virons are infecting the peripheral nerves where the virus becomes dormant (latent). A couple days before the rash appears people feel unwell with fatigue, headache and potentially a fever, and they become contagious by coughing or sneezing. By spreading the virus before the rash appears, they spread the virus far and wide before the disease is recognized and isolated.

The blisters usually appear first on the scalp and on the trunk of the body with the number of blisters increasing with increasing age of the person. Young children can have as few as a dozen or less, while adults can have thousands of blisters. Over one to two weeks,  the immune system gains the upper hand and the pustules scab over. Once the rash is scabbed over, the person is no longer contagious.

The length of time it takes for the rash to stop depends completely on the strength of the immune system. The virus can remain dormant in the peripheral nerves for 50 years or more emerging when either the peripheral nerves become inflamed (often by injury) or immune suppression develops. It re-emerges as shingles (zoster), a highly painful, high-density group of blisters that break out along the line of the peripheral nerve they come from, usually spinal peripheral nerves. It will look something like a whip mark of blisters wrapping around the body from the back to the front. Fluid from these blisters can cause chicken pox in non-immune people. This is a generational persistence strategy. In small communities, the virus persists by being transmitted from an elder’s shingles to children born after the last epidemic.

Life long immunity usually follows recovery from chicken pox.  Young children who only have a few lesions in their first infection can contract chicken pox a second time. It is also possible for vaccinated people to develop a usually mild case of chicken pox. In the United States vaccine acceptance is high enough that many people under age 25 have never seen a case of chicken pox. There is little doubt that if vaccination coverage wains, chicken pox will quickly become endemic again.

Origins and Evolution

The ancestral  Varicella-Zoster Virus (VZV), that causes chicken pox and shingles, co-evolved with apes, hominids and humans. Along with VZV, its closest alphaherpesvirus relatives herpes simplex 1 (HSV1, ‘cold sores’) and herpes simplex 2 (HSV2, genital herpes) have a common ancestor that is approximately 120 million years old. If the age estimates for the herpes phylogenetic tree are accurate, the evolution of the alphaherpesviruses  (VZV, HSV1, HSV2) coincides with the split of Africa from the supercontinent Godwanaland.

VZV has the ideal lifecycle to persist in small, isolated groups of humans, allowing it to easily survive through all three human epidemiological transitions. Latency and re-emergence in elders allowed the virus to survive in small hunter-gatherer groups, and continues to remain an advantage today. This process was observed in action on the small mid-Atlantic island of Tristan de Cunha where the population of about 200 people only experienced chicken pox outbreaks after an elder first exhibited shingles (Grose, 2012).

Phylogeny of VSV supports its origin in Africa before humans left the continent and subsequent spread through the world. Regionalism has likely occurred because VZV viruses undergo few replications per infection before they become latent so there is little chance for mutation or recombination between the clades (though it does occur).  Once many more sequences are available correlations between VZV evolution and human migration should become more clear. The history of the chicken pox virus still has a long way to go. As a DNA virus, it is possible that it may be found in ancient DNA but as a virus with a low mortality rate, it will be extremely difficult to find specimens with a high enough viral copy number to detect. Those rare mummies found with pox scars should be tested for both the smallpox virus and varicella-zoster virus. Regardless we must be careful distinguishing smallpox and chicken pox in the historic record.

References:

Grose, C. (2012). Pangaea and the Out-of-Africa Model of Varicella-Zoster Virus Evolution and Phylogeography. Journal of Virology, 86(18), 9558–9565. doi:10.1128/JVI.00357-12

Schmidt-Chanasit, J., & Sauerbrei, A. (2011). Evolution and world-wide distribution of varicella–zoster virus clades. Infection, Genetics and Evolution, 11(1), 1–10. doi:10.1016/j.meegid.2010.08.014

Wood, M. J. (2000). History of Varicella Zoster Virus. Herpes : the Journal of the IHMF, 7(3), 60–65.

Centers for Disease Control and Prevention (CDC): Chicken Pox (Varicella) Information portal. Last updated February 26, 2014.

CDC, Varicella: People at High Risk for complications. Nov. 16, 2011.

Conger, Cristen.  “How Chicken Pox Works”  11 March 2008.  HowStuffWorks.com. <http://health.howstuffworks.com/skin-care/problems/medical/chicken-pox.htm&gt;  24 May 2014.