Category Archives: public health

The Black Death in the Ottoman Empire and Ragusan Republic


Nükhet Varlık. Plague and Empire in the Early Modern Mediterranean World: The Ottoman Experience 1347-1600. Cambridge University Press, 2015.

Zlata Blažina Tomic and Vesna Blažina  Expelling the Plague: The Health Office and the Implementation of Quarantine in Dubrovnik, 1377-1533. McGill-Queens University Press, 2015.  [Dubrovnik = Ragusa]. [An English edition of  Blažina-Tomić, Zlata. Kacamorti i kuga. Utemeljenje i razvoj zdravstvene službe u Dubrovniku. [The Cazamorti and the Plague: Founding and Development of the Health Office in Dubrovnik] Zagreb: HAZU, 2007.]

Comparing the Ragusan Republic to the Ottoman Empire is a little like comparing an ant to an anteater, but nevertheless they managed to coexist as neighbors throughout the plague years. They were both carved out of the relic of the Byzantine empire. If you have never heard of the Ragusan Republic, that is probably because the city of Ragusa is now called Dubrovnik and the republic was limited to that small coastal area of modern Croatia. It was one of the smallest city states of the Mediterranean world. On the other hand, by 1600 the Ottoman Empire included almost all of what had been the Eastern Roman Empire or Byzantine Empire.

It seems natural to assume that the larger, more powerful nation should be able to do everything better, but when it comes to public health the opposite is often true. Quarantines are much easier to develop and maintain in a smaller state with limited points of access like Ragusa. The fact that smaller wealthy states often have better health care does not prevent contemporaries from still expecting the larger state to do better. Expectations are rarely realistic. The Ottoman empire was not well understood by contemporary Europeans and the growth of the empire over the 14th and 15th centuries terrified them. The second plague pandemic hit the Ottoman empire at least as hard as elsewhere and yet, it continued to grow. This alone gives the Ottoman experience a unique position in plague history.

Each book naturally is focused on their unique contributions to plague studies. Varlık reconstructs the movements of the plague on a grand scale as it ebbed, flowed, and pulsed through the Ottoman empire by 1600 encompassing about a third of the Mediterranean rim. It has become clear that we can not understand the Black Death without the Ottoman experience. Tomic and Blažina provide a microhistory of the public health and medical practices in the single city of Ragusa (Dubrovnik). They remind us that even in a city that was extremely diligent with their quarantine measures, security and economics often trump public health and that medical care was a contracted service to meet the needs of city administrators.

Turning to the Ottoman empire first, Varlık has to begin with some damage control on assumptions about the Ottomans. She made me grateful that I don’t have any assumptions about the Ottomans to be be undone; sometimes its good to be a blank slate. This is an important chapter for historians who deal with opinions of 14th centuries sources and their impact on subsequent historiography.  For most of us, the Ottoman experience during the Black Death as been a black hole in history– until now.

Her chapter on the natural history of the plague in Ottoman lands is a gold mine of information on fleas and hosts. It is clear that there were plenty of black rats in Constantinople at the onset of the Black Death and Istanbul in subsequent epidemics. Fleas and lice were such a common way of life that people who did not have fleas or lice were considered suspect of either being lepers or having foul body odor! (p. 34) This is the kind of historical evidence we need for most regions of the world with plague histories.

In most of the book, Varlık traces the trajectory of the plague to Constantinople / Istanbul and the rest of the Ottoman empire ultimately through four phases. When the Black Death first arrived, Constantinople was still part of the Byzantine empire and the Ottomans were a small Anatolian group. This was followed by three phases of plague activity from the time the Ottoman’s conquered Constantinople, renaming it Istanbul. In the first phase (1453-1517), the Ottomans were besieged by plague imported from the West in multiple ‘waves’. Remarkably, it did not check population or urban growth. Plague pulsed in and out of the empire’s regional networks during the second phase (1517-1570). By the third phase (1570-1600), Istanbul has transformed to a plague hub reflecting its centralizing role in the empire. She finished the last section of the book with a discussion of new understandings of the plague and social experience of the Ottomans during the plague.

Varlık looks forward to others examining other contemporary major states like the Hapsburg empire for comparative analysis. Personally, I look forward to a comparison between the first pandemic in the Roman/Byzantine Empire and the second pandemic among the Ottoman Empire. It is essentially the same territory, both seated from Constantinople / Istanbul. Did Roman Constantinople have the same ‘capital effect’ that Varlık outlines in this book?  An obvious difference being that the Ottomans waxed during the second pandemic, while Byzantium waned from the first pandemic onward. What role, if any, did the plague have in their polical trajectories? The rise of the Ottomans straight through the second pandemic should make people pause in their eagerness to claim the first pandemic doomed the Roman empire.  Or did their political trajectories explain how plague was transmitted within or through the respective empires? I suspect the later is the right question. I rather suspect, as Varlık shows here, that the plague is reflecting social and political changes rather than causing those changes. And, this does not diminish the importance of the plague in any way.

Pivoting to the Ragusan Republic, the scale has shrunk so much that it seems like a different world (even though the Ottoman’s had hegemony over Ragusa for part of the period covered). The entire Ragusan Republic was perhaps on par with a medium size Ottoman city. Comparing the differences in attitude toward each other between Ragusa and Istanbul in these two books is interesting. The Ragusan Republic had a peculiar organization owing to its foundation by a group of Byzantine businessmen, who created a state to allow their business and lifestyle to continue but with little if any political or religious ambitions.  Due to its small size it had to contract most professionals like physicians, surgeons, and clergy from outside the republic, primarily from Italy. Their position on the frontier between Christendom and Islamic lands gave them unusual religious independence especially considering they had to import their clergy.

Ragusa’s primary claim to plague fame is having established the first quarantine zone to protect the city of Ragusa. Fair enough, though as small as the republic was, the protected zone was limited to the city of Ragusa itself with its peripheral islands used for isolation of the sick and quarantine of the suspected. Their plague program had to be set up and maintained while business continued in the city. Ragusa was too small to stop imports. It couldn’t feed itself, much less keep its economy moving enough to pay for the security it needed, with its port closed. They were in constant fear that the plague would make them vulnerable to conquest by their neighbors.

Tomic and Blažina utilize a unique archive of government actions and contracts for health services to reconstruct the health care program of Ragusa. Their interaction with the physicians they contracted for services was fascinating. First, physicians never were in control or even had a significant influence on the function of the health office. They were contracted like any other professional. During plague outbreaks, they granted leaves of absence to the regular physicians that they valued. They were apparently too important to risk during the plague (p. 173). They then contracted specific plague physicians (medi pestis) who were only allowed to evaluate suspected plague cases and treat those who had plague. I previously wrote about one of their plague doctors here. They were not allowed to do other services and had to live in essentially quarantined due to their contact with possible plague victims. These plague doctors were paid by the state and were required to treat people of all classes the same, so the poor could expect to have the same attention as the wealthy. Ragusa’s health office was an experiment in socialized medicine. Those interested in the evolution of public health should be interested in this book.

Between these two books the eastern Mediterranean can begin to take the pivotal place that its geography suggests it must have in understanding the second plague pandemic. In the 15th and 17th century the Ottoman Empire linked together the three continents all ravaged by the pandemic. In the decades leading up to 1600 when Istanbul became a plague hub, it reflected Istanbul’s essential role in controlling all movement within the empire and thus within this connecting zone between the three continents. Tracking the plague may well inform political and economic history as well as the history of health in this critical region.

Challenging Virgin Soil Epidemic Assumptions 

The depopulation of Native Americans during the 16th to 18th centuries, one result of the ‘Columbian Exchange’, has been held up as the ultimate example of virgin soil epidemics. The emphasis put on the ‘virginity’ of the native population, bordering on biological determinism, has absolved the colonial powers of a multitude of sins. Some archaeologists and historians of early North America have begun to challenge the emphasis placed on the virulence of the new pathogens in the native population without minimizing the depopulation itself. They have uncovered multiple additional factors that led to such a drastic loss of native Americans.

Chiaves la florida, 1584
Chiaves la florida, 1584

I recently finished Paul Kelton’s Epidemics and Enslavement: Biological Catastrophes in the Native Southeast, 1492-1715 (2007) and it was illuminating. He is covering the area of the modern Carolinas, Georgia, northern Florida, and Alabama and contiguous frontiers. This area was colonized by the Spanish, English and the French toward the Mississippi. These infant colonies set off an extensive reorganization of native tribes as trade goods shifted the balance of power throughout the region.

The colonial powers were initially interested in resource extraction over building large colonies. This region had only two easily exploitable resources — deer skins and slaves. This sparked a period of nearly constant intra-tribal warfare and the creation of confederations for protection.

Kelton shows that native depopulation did not occur solely due to epidemics, but due to a set of actions taken by the colonial powers primarily in Carolina. In the first century of the English colonies, native tribes became dependent upon trade good especially guns, powder and shot that were paid for with deer skins and captives. Moreover, the English wanted primarily women and children as captives. Eventually this led to a gender imbalance in most tribes preyed upon for captives. This made it nearly impossible for the tribes to recover from severe epidemics. Having enough women of reproductive age is absolutely necessary for population recovery after an epidemic or any other sudden population loss.

Kelton does not look at human genetic analyses but this makes me think of population analyses in Central and South America where native mtDNA lineages (via matrilineal only) are common but native Y chromosomes are very rare. Many female captives would become wives to immigrant men and their offspring are advantaged over all North American native children. Kelton never really explores the destination of native captives/slaves but implies that many went to markets outside of the English colonies. He implies that it was primarily when native captives were exhausted that Carolina turns to more African slaves.

As the tribes disintegrated from the stresses of warfare and slave raiding, they reorganized into the confederations we are more familiar with, like the Cherokee, Creeks, and Choctaw. None of the groups existed before the colonial period.  In the process of reformation many villages were abandoned. They resettled in a tighter configurations and some built palisades for the first time. In the past many of these settlements were claimed to have been depopulated by epidemics.

Natives in the south-east were primarily farmers who supplemented their diet with venison, fish and other salvaged sources of protein. Without domestic animals for protein, their nutrition was maintained by a precarious balance of crops liable to be disrupted by climate and social disruption. Evasion of slave raiding parties made it difficult to grow crops (most maize) and gather supplementary wild food (deer, fish, oysters, fruit/berries etc). Famine coupled with enteric disease has to be a significant factor in any explanation of native depopulation.  Even before 1492, native populations showed signs of nutritional stress and short lifespans, sometimes with average lifespans in the low twenties.

I’ve focused on non-epidemics causes of depopulation so far because this was the newest material to me. Kelton postulates that malaria was the first epidemic disease to spread among the native population. Malaria is likely to have become entrenched in wetlands early, but how quickly it spread is more questionable and he seems to minimize its demographic impact.  From my own research on the mid-Mississippi valley, malaria makes its first appearance in the records with the arrival of the English even though the French and Spanish had been in the valley long before.

Smallpox is generally considered the most dangerous pathogen of the Columbian Exchange. Kelton acknowledges that smallpox first came to the Spanish missions in Florida and Georgia, but asserts that these epidemics were limited to the mission system. Native North Americans did not have the population density or extensive trade networks found in Mexico and further south. He shows that smallpox (and perhaps measles) did not begin to spread between tribal groups at distance from the colonial settlements until the English facilitated native enslavement system, always done through native partners, developed. By the mid-18th century, native tribes stopped cooperating with the British to sell captives creating a more direct confrontation between the European colonies and all native groups, and increasing the importation of African slaves.

Supposed virgin soil epidemics have been an attractive explanation for demographic collapses in part because it comparatively simple, absolving humans of more responsibility. Humans are portrayed as being victims of biology. Finding other causes does not clear new pathogens of a significant role in native depopulation. Epidemics remain an integral piece of the puzzle, but only a piece.

Reference: Paul Kelton, Epidemics and Enslavement: Biological Catastrophe in the Native Southeast, 1492-1715. Lincoln & London: University of Nebraska Press, 2007.

Changing the Plague-Flea Transmission Paradigm

The old paradigm is dead! Long live the new paradigm!

X. cheopis, the rat flea
Xenopsylla cheopis, the rat flea

Rebecca Eisen, David Dennis, and Kenneth Gage just published an article gathering all the evidence that should put an end to the blocked flea model  as the only significant method of plague transmission.  They summarize the data proving that unblocked fleas can and do transmit Yersinia pestis at levels that readily cause infection in rodents and humans. They call all transmission by unblocked fleas early phase transmission (EPT), even in flea species that never block.

Important findings summarized:

  • The blocked flea model –  that only a biofilm blocked Xenopsylla cheopis which can not eat so it tries to aggressively feed and  regurgitates high numbers of Yersinia pestis into the bite site – is insufficient to account for either epizootics or large human outbreaks. Blocked fleas do transmit the plague but are simply insufficient to account for the speed and volume of epizootic and epidemic transmission.
  • Transmission can occur as quickly as the very next blood meal taken by the flea, at times within 1-2 hours. Y. pestis does not need to replicate in the flea for transmission to occur. This makes it much more likely that the flea will survive long enough to transmit the infection.
  • Early phase transmission has been experimentally observed to cause infections after exposure to a single Oropsylla montana flea. Therefore, exposure to large numbers of unblocked infected fleas is not required for transmission. Epidemiologic findings suggest that most US cases come from bites from a single or at most a few fleas, and this is consistent with findings around the world where fleas that do not block are primary vectors.
  • Many reservoirs of plague are maintained by fleas that never block. Prairie dog reservoirs in the western US and great gerbil reservoirs in central Asia are both maintained by fleas that are never blocked by a biofilm.
  • “In short, EPT was observed in all flea species evaluated at varying temperatures. Transmission occasionally occurred as early as 3 h post-infection but usually was observed over 1-4 dpi [days post infection]. Although all flea species tested were capable of EPT, efficiency in these studies varied among species, suggesting that some fleas are likely to be more important than others in the rapid spread of plague in nature, especially those that are both efficient transmitters and abundant on susceptible hosts.” (p. 3)

  • Strains of Y. pestis that can not form a biofilm transmit as effectively by EPT as biofilm competent strains. Virulence factors that are necessary for biofilm production are not necessary for EPT.
  • EPT – compared to a contaminated “dirty needle” – is a mechanical form of transmission that “requires no modification or multiplication of the pathogen in the vector for transmission to occur” (p. 4).
  • In the pre-antibiotic era, many human bubonic plague infections and all septicemic and pneumonic cases would have produced bacteremia levels sufficient to infect fleas for EPT. In the 71 fatal plague cases recorded by the CDC between 1956 and 2013, 86.8% were either primary or secondary septicemic cases.
  •  “Epidemic support in favor of interhuman flea borne transmission comes from records of limited bubonic plague outbreaks in isolated rural communities under exceptional circumstances of heavy human flea infestations, high familial attack rates, and a lack of evidence for concurrent rat-flea borne plague. … [studies in Africa, the Middle East and the Andes mentioned]… Based on epidemiologic pattern of person to person spread, especially the high attack rates among contacts of the sick, an absence of domestic rats, and an unusual abundance of P. irritans infesting villages and their homes, investigators concluded that the outbreak resulted from infective bites by P. irritans.” (p. 7-8)

  • They note that interhuman plague transmission by pulex irritans has been documented early in the 20th century and supported by laboratory experiments. As covered here a year ago, infected Pulex irritans were recovered from the homes of plague patients in Madagascar in 2013. They end with a call for more work on P. irritans to evaluate its role in modern and historical human epidemics.

It is worth noting here that throughout the article they cite many studies using many different fleas. EPT studies have also been demonstrated  for mouse fleas (Aetheca wagneri Baker)  and cat fleas (Ctenocephalides felis).  I’ve never really understood why studies of historic plagues often overlook mice as a source of fleas.

I also have to add that mechanical transmission by the flea makes a lot of evolutionary sense.  It gives evolution a place to start tinkering. ‘Good enough’ is the stuff of evolution! Optimization only occurs after a very long evolutionary process, and may never be achieved. The fact that X. choepis evolved a method (via bioflim blockage and regurgitation [LPT]) to keep transmission going longer does suggest that the rat flea has been historically important to Y. pestis evolution. Obviously mechanical transmission has also allowed Y. pestis to expand into areas and exploit new opportunities where a more complicated, required transmission system would have been an obstacle.

Experiments proving that EPT is possible have been scattered over the last 50 years! And, yet the old paradigm still reigned. Why? Obviously there has been a lack of communication within science and between science and the humanities. It would really be helpful for a historian of 20th century science to look into how this could have happened.


Eisen, R. J., Dennis, D. T., & Gage, K. L. (2015). The Role of Early-Phase Transmission in the Spread of Yersinia pestis. Journal of Medical Entomology, tjv128–10. Advanced access, Aug. 19, 2015. (Open access)