Opening the Plague Files

Book Citation: A.P. Cook & N.D. Cook.  The Plague Files: Crisis Management in Sixteenth-Century Seville.  Louisiana State University Press, 2009. 296 pp. ISBN: 978-0-8071-4360-5.

Topic:
Public Health Crisis Management

Time and Place:
Seville, Spanish Empire, 1579-1581.

Audience: 

Those interested in history, crisis management, public health, and political science; written for a general audience.

Discussion:

The Plague Files is an intensive history of the daily challenges and crises dealt with by the royal governor and city council of Seville from 1579 to 1582.  As its title implies, this book is about crisis management and it stays true to this focus. Seville was faced with two very different pandemics, influenza and plague, within the same year compounded by food shortages, economic pressures, response funding difficulties, response fatigue, and the potential of civil unrest. If you ever wondered what it would be like for plague and an influenza pandemic to go (sequentially) head to head in the same population, Seville in 1579-1580 is your ideal test population.  The challenges and limitations of both quarantine and a cordon sanitaire are highlighted throughout the book.

I was impressed by their case investigation and surveillance system.Workers were contracted and paid based on their service, so detailed reports were filed to justify their pay from the plague commission. Using these reports, the authors were able to trace the detailed steps of case investigators as they tracked exposed people and textiles that they viewed as contagious. Dispatched surveillance officers also had to file detailed reports of their efforts and findings to draw their pay. The Count of Villar, the royal governor, handed out penalties including jail time for officials and others who were deemed negligent in their duties.

It was fascinating to see how their concepts of contagion played into their public health response. Textiles were the gravest concern for controlling plague contagion inside the city walls. The trail of dead owners of some clothing or bedding seems to justify their concern. Yet, there is no evidence of personal protective equipment/behavior or concern over grain storage. On the other hand, the city was on the verge of starvation much of the time so they couldn’t be very choosy about grain shipment or storage. Physicians were advisers to the Plague Council but not central to the decision-making process. Most were hired to work for the duration of the plague, often one per hospital or outlying village. The Plague Council was primarily concerned with controlling movements of people, and  providing and paying for the poor and destitute who they knew were kindling for an explosive outbreak. Diagnosis was the physicians most useful duty to the plague council. Plague diagnoses were complicated by concurrent outbreaks of influenza, typhus, other ‘common fevers’ (possibly malaria), and malnutrition. There is no doubt that the plague with all its classic symptoms was the primary pathogen.

One of my take home lessons from The Plague Files is how long and relentless a plague outbreak could be. Response fatigue was a critical problem for everyone. People just get tired of the restrictions and become conditioned to the steadiness of death. Unlike the short, sharp influenza mortality, plague deaths often trickled in at less than ten per week for months punctuated by spikes of death.

Historical  & Scientific Content:

This microhistory draws almost entirely  from a cache of primary source documents in Seville’s Municipal Archive. Surprisingly, quotes from these documents are very short. The focus on Seville is so intense context is often lacking.

The science is anecdotal and kept at the level of sixteenth century understanding. They don’t apply modern understanding of plague or influenza.  Medical treatment is discussed vaguely; few specific treatments are detailed. For example, the council paid for apothecaries to stock and provide plague medicines but the authors didn’t discuss what they stocked or if they had difficulty obtaining medicines. It appears that there was no standard treatment or medication used in the region. They don’t make an effort to accumulate data or do any standard epidemiological analysis. By the end of the book I was craving some data. The volume of anecdotal evidence does provide plenty of evidence that diagnosis was not very secure for many individuals complicating data classification.  Historical epidemiologists will have to cope with other concurrent diseases, significant for plague outbreaks that last months to over a year. Ironically in the case of Seville, I suspect a standard epidemiological chart of total deaths vs time would have highlighted the difference between influenza and plague.

References, Illustrations, and Usability

It has a full bibliography but minimal footnotes, mostly to primary sources. I suspect that it would be fairly difficult to look for more information based on their footnotes and access to the primary sources.  They appear to have made minimal use of the secondary sources, or at least there are very minimal footnotes to them. It does have a glossary for Spanish terms; all quotes are translated. The illustrations were okay. It could have used a few more local maps fit into the text where appropriate.

I recommend this book primarily for biosecurity and crisis managers. Its usefulness to the sciences and humanities is primarily for anecdotal information.

The Landscape of Super-Spreading

Super-spreading individuals and disease hot spots have been known for over a century, but rarely have they been considered together. Sara Paull and colleagues [1] have pulled together all of the recent work the ecology of disease hot spots and transmission heterogeneity (super spreading) to explore the continuum between individual transmission heterogeneity and the landscape of disease, otherwise known as disease ecology. Hawley and Altizer [2] have developed the interrelationships further to the cellular level by linking disease ecology directly to ecological immunology, examining the effects of the environment on the immune system of  host populations. Taken together, these fields can be developed into a continuum of macro to micro landscapes  with transmission heterogeneity, better known as  super-spreading, at its center.

Adapted from Hawley and Altizer (2011). (Click to enlarge)

Disease Ecology

Disease ecology is the study of pathogens in the context of their dynamic environment. Unlike most medical experiments conducted in vitro, removing or stabilizing as many variables as possible, disease ecology seeks to understand the place of the pathogen in an an open, responsive environment with an unknown number of variables [3]. In disease ecology, multiple hosts and vectors of zoonotic diseases are considered together as a complex system. It is normal for the system to respond in unpredictable ways and for multiple stable states to be possible; the human gut microbiome consists of up to a thousand bacterial species that can come to at least three stable states (enterotypes) unrelated to easily identified variables (age, gender, ethnicity, etc.) [3].

Some of the basic areas of disease ecology include understanding the multiple hosts of a pathogen including factors effecting the lifecycle of the hosts, ecological drivers, endemic/enzootic and epidemic/epizootic dynamics,  characterization of the rural or urban landscape, and transmission dynamics. The US Environmental Protection Agency (EPA) defines an ecological driver as any biotic or abiotic factor that causes change to the ecological landscape. Ecological drivers can be as diverse as invasive species, climate change or changes to a man-made landscape. Transmission dynamics is also a basic factor in disease ecology.

Transmission Heterogeneity

Transmission between hosts is rarely, if ever, a uniform process. Extreme cases of transmission heterogeneity, where a small number of individuals are responsible for most successful transmissions, are called super-spreaders. These super-spreaders are major factors in epidemic dynamics of an increasing number of human pathogens. Drilling down into why transmission dynamics are heterogeneous yields a variety of causes.

Species level transmission heterogeneity has led to the recognition of ‘amplifying species’ that act as super-spreaders within the landscape.  American Robins as preferential hosts and transmitters of West Nile Virus are a classic example of an amplifying species [1]. Presumably changes in the landscape could alter the degree to which each possible host species contributes to the overall transmission within the environment and which host becomes the amplifying species. It would naturally follow that not all possible vectors are equally responsible for disease transmission. For example, we know that rat fleas, cat fleas, human fleas and possibly human lice can all transmit Yersinia pestis, but they are not equally responsible for transmission.

Landscape contributes to transmission heterogeneity as well. Studies have shown that oak tree vulnerability to sudden oak death syndrome varied with tree genotype but in field tests temperature and rainfall differences  mattered more than the genetics of individual trees [1]. These landscape characteristics go beyond the classical definitions of disease ‘hot spots’. Typical hot spots are defined as areas where there is higher pathogen levels or more amplification hosts [1].  For example, buffalo wallows and sites of buffalo deaths can become anthrax hot spots. Human have created animal disease hot spots; chronic wasting disease is increased among Colorado mule deer near human settlements rather than more remote areas [1]. In Belize, agricultural run-off alters the aquatic plant communities increasing breeding efficiency of the malaria vector Anopheles vestitipennis [1]. Some environmental hot spots can be so strong that they are “analogous to superspreaders” [1].

Which comes first, the hot spot or the super-spreader? Paull et al  note that “logically, superspreaders create hotspots of transmission around them, and hosts in a disease hotspot, by definition, experience an increased infection pressure as compared with others in the population” [1]. Ultimately what really matters is understanding why there is increased transmission. Does the ‘hot spot’ move with the hosts or is it tied to a locality or architectural structure? Some ‘hot spots’, like ships, are capable of moving although the increased transmission is tied to a piece of architecture. Likewise, some types of air conditioning systems can become ‘hot spots’ for Legionellosis, but redesign of the air conditioning system eliminates the ‘hot spot’.

Ecological Immunity

Ecological immunity takes factors of disease ecology and heterogeneous transmission particularly to the cellular and molecular level. For example, high testosterone levels suppress the male immune system (in birds and rodents) while triggering behavior that increases their territory and contact rates making them behavior super-spreaders [1,2]. It has been suggested that testosterone levels could be “a common driver of superspreading phenomena, broadly linking within- and among-host processes across vertebrate host taxa” [2].

The role of the environment and immunologic costs intersect when we look at seasonal effects and nutritional needs of the immune system. Malnutrition depresses the immune system directly and indirectly through hormones like leptin. The cost of immunity comes home when we realize that leptin intentionally cripples the immune system as part of the starvation response. Seasonal effects are easier to understand in animals that have a more defined seasonal pattern of migration, or a defined mating period [2]. Yet human infectious disease fluctuates with the season; influenza being a prime example of a disease with seasonal fluctuations.

Coinfections are also best understood for their impact at the cellular level of the immune system. The cost of the immune response makes immune trade-offs necessary during coinfections.  Focus has zeroed in on a classic immune trade-off between production of T-helper 1  and T-helper 2 cells as at least a partial explanation of poor prognosis for  helminth (worm)  and an intracellular pathogen coinfections [2].  Several studies have now shown that HIV infections progress faster if there is a helminth coinfection [2]. Likewise, in African buffalo helminth infections correlate with tuberculosis vulnerability and rapid progression; “Joelles et al (2008) found evidence for a direct trade-off between circulating levels of IFNγ (Th1 response) and eosinophils counts, their measure for Th2-type response in buffalo” [2]. To decrease vulnerability and improve prognosis for HIV and tuberculosis, treatment for helminths should become a priority.

What constitutes immune fitness must also be reevaluated in light of ecological immunity findings. The high cost of immune defenses are such that unnecessary defenses for the current environment are generally not maintained [2]. Likewise, costs and trade-offs may make it necessary for the immune system to develop tolerance to some pathogens deemed low risk to fight other greater risk challenges. Hawley and Altizer  note that “a ‘competent’ immune system may employ tolerance strategies, making immune ‘competence’ difficult to assess via infection outcome alone” [2].

Today we are only at the very beginning of understanding complex disease ecologies. For zoonotic diseases the impact of ecological drivers and enzootic dynamics all around the world make the identification of the best predictors an imperative. Yet, outbreak prediction will remain an imprecise science, not unlike the prediction of hurricanes or volcanic eruptions.  Increased surveillance will remain key to a rapid response and epidemic mitigation.

References:

[1] Paull, S., Song, S., McClure, K., Sackett, L., Kilpatrick, A., & Johnson, P. (2012). From superspreaders to disease hotspots: linking transmission across hosts and space Frontiers in Ecology and the Environment, 10 (2), 75-82 DOI: 10.1890/110111

[2] Hawley, D., & Altizer, S. (2011). Disease ecology meets ecological immunology: understanding the links between organismal immunity and infection dynamics in natural populations Functional Ecology, 25 (1), 48-60 DOI: 10.1111/j.1365-2435.2010.01753.x

[3] Pepper, J.W. & Rosenfeld, S. (2012). The emerging medical ecology of the human gut microbiome, Trends in Ecology & Evolution, 27 (7) 384. DOI: 10.1016/j.tree.2012.03.002

American World War II Plague Posters

National Museum of Health and Medicine

These posters were found in the Otis Historical Archives National Museum of Health & Medicine flicker site housing photos and graphics from the National Museum of Health and Medicine in Washington, DC. These government produced World War II  images are now public domain.

If you look closely at the faces on the fleas, the poster to the left appears Japanese and the flea below resembles Hitler. These posters must reflect an unease that biological warfare was possible on all fronts. By placing the face of the enemy on disease vectors, the military wants the soldiers to associate disease with biological warfare rather than natural sources.

Japanese Use of Plague during World War II

I’ve been reading Sheldon Harris’ Factories of Death: Japanese Biological Warfare, 1932-1945, and the American Cover-up. (Rev. ed, 2002), considered the definitive book on biological warfare in the Pacific theater during WWII. My primary interest is in Japanese research and use of plague in their biological warfare program.  Since this blog is, in part, a research tool, this post is a collection of notes taken specifically on plague, though the book covers a much wider program. If you ever wondered why plague is a category A bioterrorism agent, what follows will go a long way in explaining.

Lt. Gen. Shiro Ishii (1892-1959) of Unit 731, the biological warfare unit of Imperial Japan.

Lt. Gen. Shiro Ishii was the primary organizer, promoter and director of the Japanese biological warfare (BW) program. He was involved at all levels from pitch-man to the Japanese military and academia to personally supervising research on human subjects. He began his work research in the potential of biological weapons in the late 1920s.

One of Ishii’s first facilities was called the Zhong Ma Castle in Beiyinhe northern Manchuria. Initially their test subjects were trouble makers among the Chinese population: criminals, communists, and other suspicious persons. Ishii began by focusing on plague, glanders and anthrax. Subjects were injected with the pathogen and the course of their disease was monitored; all were extensively autopsied. (p. 33-34) There are numerous reports of autopsies being carried out on the unconscious, as in  not yet dead.

In 1939 the stressed Japanese military allowed Ishii to send several BW attacks  against Soviet forces in the Nomonhan region. Details of the mission refer to the contamination of water supplies with typhoid but plague, cholera and dysentery effected both Japanese and Soviet troops during the campaign. Harris is unclear whether these were effects of biological weapons operations or naturally occurring outbreaks. (p. 97-98) In 1942 a Soviet defector to Germany claimed that Soviet biological weapons were field tested during combat in Mongolia (/Manchuria) and that a there was a major plague epidemic at that time. (p. 98) With both sides attempting biological warfare and with the level of technology at the time, it is unlikely that it will be possible to unravel outcome of either the Japanese or Soviet efforts.  The Japanese BW program was developed primarily with a future war against the Soviets in mind, as Japan planned to take land north of Manchuria. The intent of the BW program was to give Japan an advantage over the vast population and natural resources of China and the Soviet Union.

Shiro Ishii built an extensive network of facilities in China for the purposes of research and testing. Some details of these units in respect to plague activity follows:

• Unit 731 was the primary unit under Ishii’s command based at his specially built facility at Ping Fan outside of Harbin, Manchuria. The scale of Ping Fan was enormous. Here Ishii built his dream facility complete with four boilers capable of producing one ton of  culture media each sterilized in fourteen autoclaves, ‘Ishii cultivators’ each capable of producing 30 kilograms of bacterial cell mass, and the capacity to maintain  plague, cholera, typhoid and paratyphoid, dysentery, anthrax, gas gangrene, tetnus, and glanders. Ping Fan was also equipped with the capacity to mass produce fleas and its own fleet of airplanes for experiments. (p. 69) After the war Maj. Gen. Kawaashima Kiyochi boasted that Ping Fan could produce 300 kg of plague monthly in addition to other pathogens. (p. 69)

Manchuria, today split between Russia and China. (Public domain image from the CIA’s World Fact Book via Wikipedia Commons.)

• Unit 731 conducted ‘field tests’ throughout northern and eastern China from late 1939 to 1942. They specialized in spreading pathogens by contaminated water and food. They tested cholera, typhoid, paratyphoid, and especially anthrax and plague. They were reported to start epidemics and then enter villages claiming to vaccinate against the epidemic, except that they would inject the pathogen instead. Their experiments involved introducing pathogens by unusual routes such as ‘vaccine’ injections including cholera bacteria. In a Soviet war crimes trial, testimony was given that Ishii’s forces handed out special chocolate bars laced with anthrax to Chinese school children “with unavoidable side effects”‘. (p. 99)

• Unit 731  gave special attention to plague, spreading plague infected rats widely throughout China and experimenting with spreading plague through fomites like contaminated fountain pens or canes. When a full scale epidemic broke out, Japanese soldiers would force an evacuation of the village and burn it to the ground. An American missionary Archie Crouch reported seeing Japanese plains drop odd bombs that spread what looked like wheat over the city of Ningbo and plague erupted just days later. Chinese officials tried to combat the plague with isolation, quarantine and burning the most infected part of the city but over 500 people died of plague and other agents spread by Ishii’s forces. Outbreaks of plague continued in the region of Ningbo until as late as 1959 (p. 101-103).  The city of Quzhou was also subjected to bombs that scattered, soy beans and rags contaminated with plague, cholera, typhoid and possibly anthrax. Bacteriologist Qui Mingxuan lived in the city as a child, and put the death toll for the six years after the first plague outbreak in 1940 at 50,000. Qui noted that there was no history of plague in Quzhou before 1940. (p. 102) In August 1942 plague was sprayed over the village of Congshan in the Zhejiang Province.  Rats began to die in droves two weeks later and over the next two months 392 out of 1200 residents died of bubonic plague. (p. 103) For unexplained reasons, after 1942 Unit 731 stopped large field tests and began to concentrate on more direct human experimentation in controlled environments. Harris estimates that by the end of 1942, “the casualty count in the open tests surely fell into the six figure range” (p. 104).

• Enough credible reports made their way out of China to convince the Allies that Japan was conducting biological warfare. (p. 100-103) In addition to reports coming out of China, American investigators found ampoules of cholera in Burma that locals reported where dropped from planes by the Japanese. In September 1944, Thailand also experienced a plague although there had been no recent plague activity in the area. The Thais and Americans both concluded that these outbreaks in Burma and Thailand were acts of biological warfare by Japan. (p. 226)

• The facility at Nanking, operated by Unit Ei 1644 under the direction of Tomosada Masuda, was a mass production site for bacteria (cholera, typhus, and plague), rodents and vectors. Nanking specialized in flea production for plague experiments. It was also a training site for bacteriologists to conduct biological warfare, producing about  900  from 1941-1943 (p. 142-143)

• Unit 100 in Changchun region worked on plague among other pathogens from 1940 to 1945. Although plague outbreaks had occurred in the region previously, several large suspicious outbreaks that took thousands of lives occurred from 1940 to the end of the war. Unit 100 used these outbreaks as cover for widespread experimentation on villagers.  Injecting slum dwellers with plague under the guise of vaccines against the plague was one of their notable practices. They then relocated about 5000 survivors and burned the slum to the ground. As the war was coming to a close, the order came to destroy all evidence, buildings and people. None of the test subjects or Chinese workers escaped. Some of the infected animals were released into the countryside after the official surrender possibly triggering outbreaks of plague, anthrax and glanders in 1946, 1947 and 1951. (p. 126-133)

• At the Anda test facility in northern Manchuria, Chinese test subjects were tied to open air stakes and bombs containing either an anthrax slurry or plague infected fleas were exploded around them in an attempt to infect them. There is some evidence that anthrax worked slightly better than the plague because the fleas did not handle the exploding bomb well (!). By 1944 they were working on developing means for spreading pneumonic plague and other respiratory pathogens. Fortunately, they were still unsuccessful by the end of the war. (p. 88-90) Ishii would later brag to US war dept. interrogators that he developed a porcelain bomb that successfully disseminated plague (p. 247).

At the beginning of the war, the American biological weapons program was the least developed of all the major combatants. The US military was eager to repair this deficit. American offensive and defensive biological warfare research began at Fort Detrick, Maryland, in 1942. Plague was one of many different pathogens worked on during the war. (p. 210) After the Japanese surrender, American officials were much more interested in extracting intelligence from cooperative Japanese researchers, including Shiro Ishii, than in pursuing justice for the Chinese or even American POWs that were victims of their experiments. To insure cooperation Shiro Ishii was given immunity from prosecution and no one was ever brought to the war crimes trials in Tokyo for biological warfare.  I will leave issues of justice and the cover-up to journalists and political historians.

I do have to take issue with Harris’ assertion that Shiro Ishii was a good microbiologist. He may have been a good pitch-man, organizer and military man but not necessarily a good biologist or physician.  First, I can’t accept that anyone racist enough to mentally justify this work was a competent biologist, much less a physician. Designing and carrying out these ‘experiments’ are the sign of an unstable mind. Methodologically,  ‘try absolutely everything you can think of and something might work’ is not good science, not even in wartime. Even if allied programs did similar things, it is still not good science. He thought more like an engineer than a biologist. The innovation that started his career and gained military attention was the development of a water filtration system to prevent cholera for the military. From a strategic point of view, biological weapons were incredibly risky in the 1940s before the discovery of penicillin and other effective antibiotics. The Japanese military actually had to reign them in out of fears of blow-back. Considering what the Japanese military was willing to do during World War II, this says a great deal.

Plague at the Siege of Caffa, 1346

The first stage of the Black Death among Europeans was said to begin with the whoosh of a Mongol trebuchet. Gabriele De’ Mussi, a lawyer from near Genoa writing in about 1348, is believed to have recorded the account of the earliest use of plague as  weapon of war at Caffa in 1346.

Mongol siege with trebuchet. Edinburgh University Library via Wikipedia Commons.

“The dying Tartars, stunned and stupefied by the immensity of the disaster brought about by the disease, and realizing that they had no hope of escape, lost interest in the siege. But they ordered corpses to be placed in catapults and lobbed into the city in the hope that the intolerable stench would kill everyone inside. What seemed like mountains of dead were thrown into the city, and the Christians could not hide or flee or escape from them, although they dumped as many bodies as they could into the sea. As soon as the rotting corpses tainted the air and poisoned the water supply, and the stench was so overwhelming that hardly one in several thousand was in a position to flee the remains of the Tartar army. Moreover one infected man could carry the poison to others, and infect people and places with the disease by look alone. No one knew, or could discover, a means of defense.” (Horrox, p. 17).

As Mark Wheelis observes in his 2002 article, infected corpses flung into the fortress by trebuchet are a plausible means of infecting the inhabitants. It is not unlikely that corpses would be flung into fortresses, as a terror tactic, with or without disease. Imagine being besieged for months and then having rotting corpses flung at you. By choosing the strongest smelling corpses, it is likely that when they were hurled they came down hard and very sticky. Body fluids can certainly spread Yersinia pestis to people with abrasions and the mess these would have caused upon landing would draw rats from within the fortress. Rats will feed on dead corpses. Direct contact may account for more medieval cases of plague that it is generally credited; in the United States, direct contact is the likely form of transmission for 20% of cases between 1970 and 1995 (Wheelis, 2002).  Wheelis suggests that this had an additional bonus,  helping the Mongols (Tartars)  deal with the mortuary problem that plague always causes. While it is possible that rat transmission brought the plague into the fortress, there is no reason to doubt Gabriele De’ Mussi’s association between the flung corpses and the beginning of the outbreak.

Gabriele De’ Mussi is also revealing his own thoughts about contagion and transmission. Following the miasma theory of contagion, infection is passed through the contamination of the air and water/food. According to Gabriele De’ Mussi, “intolerable stench would kill everyone inside”; the contagion is in the foul-smelling air that can also permeate and therefore contaminate food or water. Although he recognized that it could be transmitted person to person, it was done “by look alone”. Without understanding germ theory, they could not understand what was actually being passed but did recognize respiratory and oral routes of transmission.

Using corpses to foul land or water is a method of biological warfare that is probably as old as warfare itself. If you read all of Gabriele De’ Mussi’s account, he is not really condemning the Tartars (Mongols) as doing anything out-of-bounds or evil. To Gabriele, God was striking down both the Tartars and the Christians. It is unclear if the Tartars were using the corpses as a tactic of biological warfare  or as an act of terrorism and desperation, a ‘share the pain’ or revenge tactic.   Gabriele De’ Mussi says “realizing that they had no hope of escape, lost interest in the siege” and then began to fling the corpses. At this point the Tartars had nothing more to lose. Unlike virtually every other biological warfare strategy, the Tartars did not have to be concerned with the greatest risk of biological warfare, blow-back, that is, the infection of your own army. Although many Italians fled the fortress, it remained under Italian control and the Tartars did abandon their siege (Wheelis, 2002).

Far from blaming the Tartars, Gabriele De’ Mussi places the responsibility for bringing the plague to the Mediterranean squarely on his own people, the Genoese and Venetians.

“among those who escaped from Caffa by boat were a few sailors who had been infected with the poisonous disease. Some boats were bound for Genoa, others for Venice, and to other Christian areas. When sailors reached these places and mixed with people there, it was as if they had brought evil spirits with them: every city, every settlement, and their inhabitants, both men and women, died suddenly. … We Genoese and Venetians bear responsibility for revealing the judgements of God. Alas, once our ships had brought us to port we went to our homes. And because we had long been delayed by tragic events, and because among us there were scarcely ten survivors from a thousand sailors, relations, kinsmen and neighbors flocked to us from all sides. But, to our anguish, we were carrying darts of death. While they hugged and kissed us we were spreading poison from our lips even as we spoke.” (Horrox, p. 18-19)

Wheelis argues that Gabriele De’ Mussi must be mistaken that a single or few ships fleeing from Caffa brought the plague to Europe.  He notes that the spread into the Mediterranean shown in the figure below took too long for a direct voyage from Caffa to Italy. Wheelis points out that this is probably the work of multiple streams of infected ships. He also suggests that caravan routes over land did spread plague to the south of Caffa, though as his maps shows, not nearly as effectively as by sea. Wheelis concludes that “the siege of Caffa, for all its dramatic appeal, probably had no more than anecdotal importance in the spread of the plague, a macabre incident in terrifying times.” Perhaps, but Gabriele De’ Mussi’s rhetoric may be read in other ways.

Transmission from Caffa. (Wheelis, 2002)

Gabriele De’ Mussi deploys a dizzying array of rhetorical devices to express the trauma and tragedy of the plague. He is inconsistent in his point of view, sometimes writing as through he were at Caffa or on the fleeing ship, other times writing from  a distance. As Wheelis notes, Gabriele De’ Mussi did not leave Italy during this years. The entire treatise is wailing to God over the tragedy, and at times talking directly or even conversing with God. When Gabriele De’ Mussi writes that “we Genoese and Venetians bear responsibility for revealing the judgements of God”, he is not referring to a few refugees. This seems to be an indictment of an entire people and could reflect transmission of the plague through the Italian trading network. It should also be considered that ships carrying refugees from the East had a powerful symbolic importance to Italians. Mythologically, the Romans claimed descent from Aeneas who led refugees from Troy to Italy where they won a home. Just as refugees from the East founded the Roman people, Italians fleeing from the East have now brought destruction to Italy and all of Europe. Gabriele De’ Mussi does not mention Aeneas, Troy or the founding of Rome but simplifying his story of plague transmission to a few refugees fleeing from the East makes his story more powerful.

Although refugees from Caffa may have only been one stream of disease transmission, ships from Caffa could have been important for two reasons. First, ships from Caffa could have been a primary disease stream even if they didn’t directly reach Genoa or Venice. Following what we now know about super-spreading phenomena a few ships stopping at multiple ports could radically effect transmission dynamics as plague entered Europe. Additionally, at least in Genoa and possibly Venice, the events at Caffa and its refugees formed a foundation narrative for a tragedy of biblical proportions. A few survivors from Caffa who eventually made their way home, possibly changing ships multiple times, may have arrived about the same time as the plague with horror stories of the plague in ships and ports along their route.

References:

Wheelis M (2002). Biological warfare at the 1346 siege of Caffa. Emerging infectious diseases, 8 (9), 971-5 PMID: 12194776

Horrox, R. ed & trans. (1994) The Black Death. Manchester Medieval Sources series. Manchester and New York: Manchester University Press.

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Paul Slack’s Plague: A Very Short Introduction

Book Citation: Paul Slack. (2012) Plague: A Very Short Introduction. Oxford: Oxford University Press. ISBN: 978-0-19-958954-8. Pocket size paperback, 138 pages. $11.95 {#307 of Oxford’s Very Short Introduction series}

Topic: The Plague

Time and Place: Primarily Europe from c. 540- c. 1910

Audience: General audience. Intended as an introduction to the topic for anyone with a college reading level.

Discussion:

A couple of months ago I asked a history of medicine discussion list to recommend a book surveying plague studies to provide a good overview of the field. No one had any suggestions for this monumental task. Little did any of us know that about that time, Paul Slack’s Plague: A Very Short Introduction was being published (on March 24, 2012 according to Amazon) almost simultaneously with that conversation. When I first saw this book advertised I thought how could such a small book (pocket-size or easily purse size) at only 138 pages be worth much. Almost out of desperation, I ordered it. I am so glad that I did. Slack’s Plague proves that a book does not have to be long or packed with data to provide a good introduction to such a long-lasting and complicated topic.

Covering the entire history of plague and looking for the presence or absence of trends over 1500 years sets this book apart from most books on plague. Naturally, the Black Death and its aftershocks dominate but he makes an effort to continually use examples from the Plague of Justinian and less commonly the Third pandemic. Although he clearly approaches the plague as a historical topic, he gives adequate space to the discussion of the science of causes and nature of the pandemics. I think his best chapter is on plague’s role in the development of public health. This is a book that I will reread and study for quite a while to come.

Narrative grade: A.
Slack, an emeritus professor of social history, writes with the elegance and confidence of a senior scholar introducing but also assessing a field he has intimately known as a teacher and researcher for his entire career. While acknowledging areas of debate, he writes in very clear and even bold statements without the litter of caveats for every possible exception.

Historical Content grade: A

Slack covers all of the primary historical questions using plenty of examples without being tempted to follow them off track. One area that could have received more attention is medical care, which is only mentioned in passing along with the black death experience or the public health chapter.  He writes with clear thesis statements and well supported arguments. As a topic introduction, this is not a book that will provide data or even data summaries. Primary sources are translated and specialist terminology is avoided.

Scientific Content grade: A-

Scientific content is presented at the right reading level and with a rational discussion of the debates. This book was written before the full sequencing of a Yersinia pestis from East Smithfield in London. Slack is firmly on the side of Yersinia pestis and its continuous history.  He does not attempt to cover plague as a biological weapon or the modern status of plague.

References and Usability grade: B

The note system is rather strange and doesn’t follow any system that I am familiar with. It has an extensive ‘further reading’ section rather than a bibliography.

Illustrations: B

Figures, maps and graphs were okay for the size of the book.

Outlining a Project: Human Plague

I’ve had a bit of a blogging slump lately. I came back from the medieval congress with too many things on my mind to settle down to write a post. Nevertheless, it has been a productive couple of weeks. I’ve been working on an outline for one of the book projects that I mentioned quite a while back. I think its time to share some of those plans. I’m eager for feedback, criticism, suggestions… It won’t hurt my feelings at all and will be much appreciated! So here goes with the outline.

Working title: Human Plague: Natural History & Crisis Management

Introduction

Part I: A Natural History of Yersinia pestis

1. Origin, Evolution and Biogeography (also including bacteriology and reservoirs)

2. Anatomy of an Epidemic (transmission and epidemiology)

3. Natural History of an Infection (diagnosis, pathophysiology, immunology)

Part II: Crisis Management

4.Government Response (legal, economic, & political)

5. Medical Care

6. Mortuary Care

7. Children and the Plague

8. Crises of Faith and Response

9. Scapegoating the Other

10. Signs of Resilience

Part III: Modern Concerns

11. Weaponizing the Plague

12. Plague Today

Appendix: Chronology

The theory here is that the first part is a natural history from the point of view of biologists, public health, and medicine. ‘Human plague’ because a natural history of Yersinia pestis or ‘the plague’ would primarily be about rodents. These chapters will work in the entire history of human plague from evolution of the bacterium in central Asia to its movements for the next 1500 years. Certainly most of the epidemiology will include pre-modern epidemics.

The second maybe two-thirds of the planned book is influenced by my biosecurity training. It’s hard to think about the plague without thinking about the 1500 years of crisis management with the same organism. I expect that this section will change dramatically as I work on it. This outline is really just some of the elements of crisis management: government reaction, medical care, mortuary care, special populations (here represented by children), religious crises as the most evident social impact, and religious and racial persecution, and evidence of resilience.

The last section is pretty self-explanatory. It will review evidence of plague as a biological weapon and continuing concerns that it will be used as a weapon. It will end with an assessment of where we are today with plague as re-emerging disease.

My goal is to write this at about the same level of technical difficulty as this blog. I hope that it is useful to all of the many disciplines involved in plague research and response in the sciences and humanities.

It seems like I’m trying to put an awful lot in one book but I don’t really have a baseline to judge that by. Feedback would be much appreciated in the comments below or by email!