Plague in Victorian San Francisco–lessons for public health communication

I have a post up today at the Scientific American Guest blog, discussing how an earthquake and denial led to prairie dog plague. It details an outbreak of plague in Victorian San Francisco–the first time plague hit the United States–and the many downstream consequences of that outbreak (which began in 1900 and wasn’t really contained until 1908). While the story is over at SciAm, here I wanted to talk more about why the outbreak became such a public health disaster.

The outbreak was first recognized by Dr. Joseph Kinyoun, a bacteriologist who had been, until his transfer to San Francisco, heading up the United States Hygienic Lab, the precursor to the National Institutes of Health. Charged with inspecting incoming ships, Kinyoun had the power to quarantine ships and their crew in harbor, in an effort to keep plague out (which was already circulating in port cities of Honolulu, Sydney, and Tokyo, amongst others). When Kinyoun first suspected a case of plague, San Francisco merchants quickly banded together to deny any such pestilence in their city. What followed was a mess of ineffective quarantines, fights over scientific data, accusations of “spiking” corpses with plague samples Kinyoun had brought with him from Washington, D.C., and an eventual call for Kinyoun’s execution.

History shows that Kinyoun was right–San Francisco had plague cases, and the plague would continue to smolder for almost a decade. As I note in the post, it still lingers today in squirrels and rodents from the Pacific Ocean inland to the Great Plains. So what went wrong, if Kinyoun clearly had the facts on his side?

Like many scientific issues today, it wasn’t the facts that ended Kinyoun’s career in San Francisco, but his messaging. Admittedly, he was acting without all the knowledge of plague transmission that we have today–it wasn’t confirmed in 1900 that rat fleas were the main vector of the disease from rodents to person, and so Kinyoun couldn’t have been sure his attempts to quarantine Chinatown would be ineffective. Furthermore, in some cases, he was merely obeying orders from his superiors. His boss, Surgeon General Walter Wyman, had recently published a monograph on plague, endorsing the idea that plague selectively targeted Asians due to their particular diets and their poverty.

Still, the way Kinyoun went about attacking those most affected in the initial outbreak–the Chinese immigrants–only served to terrify them and drive plague cases underground. Indeed, when public health officers went door-to-door searching for plague cases, one anecdote notes that a game of dominoes was set up in a home, and all the men stayed perfectly still with dominoes in their hands while officers searched the home for anyone with plague symptoms. Little did they know that a plague corpse was sitting at the card table, “Weekend at Bernie’s” style (1). Other Chinese fled Chinatown, bunking with friends and relatives elsewhere when possible. Threats were made to burn Chinatown (as had recently happened in Honolulu); Kinyoun tried to bar travel by any “Asiatics” on trains or boats leaving the city, clearly a race-based order. Furthermore, even when cases of plague were identified in Chinatown, the very practice of carrying out autopsies was offensive to the Chinese, giving them even more reason to hide their sick and dead rather than cooperate with Kinyoun and other public health authorities.

Kinyoun left the city in 1901, and eventually Rupert Blue was brought in to control the outbreak. Taking lessons from those who’d been there prior (and were unsuccessful), Blue took a much more diplomatic tack. He secured the assistance of a Chinese translator, Wong Chung, and worked within the Chinese community to gain their support. He often downplayed the outbreak–never suggesting it wasn’t happening or wasn’t important, but trying to differentiate hype from supported fact. He worked to clean up Chinatown, both in its housing and in rat infestations, rather than to quarantine infected areas. He noted that plague could occur in many different races, and avoided scapegoating one particular ethnic class. He also reached out to businessmen to educate them, and show how important cleaning up the city was for their bottom lines. He worked with the facts as Kinyoun did, but he recognized the importance of grassroots support in his campaign, and targeted reasons why various factions should support his various anti-plague measures.

In the end, while Kinyoun was practically run out of town on a rail, Blue was given banquets and numerous accolades. He served as the Surgeon General from 1912-1920, and his methods for cleaning up the city led to a decrease not only in plague, but in many infectious diseases. While Kinyoun’s science was sound, Blue managed to break down barriers and work with those who could help him spread his message, and take ownership of the work that needed to be done. He framed* the threat in terms that meant something to the populations he was working with: businessmen and threat to their incomes; immigrants’ threat to health, with promises to respect their culture and help them make their homes cleaner places to live; city and state government, noting the threat to the very reputation of California and San Francisco in the US and around the world. His tactics served him well in 1902-08, and should serve as a reminder to science communicators today as well.

(*I know that term is somewhat tainted in some circles, but bear with me…)

Further reading and references

Chase, “The Barbary Plague”.

Echenberg, “Plague Ports: The Global Urban Impact of Bubonic Plague, 1894-1901.”

Eastern Equine Encephalitis: The Mosquito that bit the Snake

Guest post by Hillary Craddock

Last week a new study regarding Eastern Equine Encephalitis (EEE) was published online (Bingham EEE is a mosquito-borne virus that can cause serious, and sometimes deadly, disease in humans and equines. In warmer parts of North America, the virus is spread year-round, but in areas where mosquitoes get killed off in the winter it has been something of a mystery as to how the virus makes it from year to year. Humans and equines are both dead-end hosts, which means that a mosquito can not be infected from biting an infected person or horse. Researchers in Alabama found that wild snakes in the Tuskegee National Forest were positive for  Eastern Equine Encephalitis virus (EEEV), which could explain how EEE was maintained after the first frosts killed off infected mosquitoes. Essentially, what would happen is that an infected mosquito bites a snake, probably during the summer or early fall, and the snake harbors the virus in its blood during the winter. Then, in the spring, an uninfected mosquito (which overwinters as a larva) bites the snake and acquires the virus. This now-infected mosquito can bite a horse or a human, who can then get sick. (I’m sensing a Chad Gadya theme here. Just me? Ok…)

Amphibians and/or reptiles as the winter reservoir of EEE is not a recent research question. A book, Reptiles as possible reservoir hosts for eastern encephalitis virus, (which I was unfortunately unable to get my hands on, since apparently only the University of Alberta has an available copy) was published in 1961, and another  study in 1980 by Smith and Anderson stated that two New England species of turtles could be infected by the virus. Interestingly enough, a 2012 study by Graham et. al. (same research group as Bingham found that, out of 27 species surveyed, only snakes showed high seropositivity (positive for virus antibodies in the blood), while amphibians, turtles, and lizards had low to no seropositivity. A 2004 study by Cupp, also in Alabama, found that mosquitoes carrying EEEV had fed on amphibians and reptiles in addition to birds and mammals. Now, it’s all well and good to show that a reptile can act as a host, but just because something can be the host doesn’t mean that it is the host in the actual system. The crucial step was testing their hypothesis in a wild population.

And test they did. The researchers were careful to state that the question of snakes acting as reservoir hosts is “unresolved,” but there is “mounting evidence” that snakes are the winter hosts of the virus. Cottonmouths (Agkistrodon piscivorus) were the most common snake sampled, making up 41% of sampled reptiles. They were also frequently seropositive, with 35.4% testing positive for EEEV. Of the five species sampled, one other, the copperhead (Agkistrodon contortrix) was found to be positive. The researchers tested for active infection in addition to antibodies, and found that some snakes were actively infected. This means that, if a mosquito bit the snake, the mosquito could possibly acquire the virus and pass it on to other creatures.

So why am I so excited? When I took my first Emerging Infectious Diseases class in college, the professor explained to us that zoonotic infectious diseases were most likely to jump between closely related species. Granted, I’m using the word “close” loosely here. She meant that diseases were far more likely to jump mammal to mammal or bird to mammal than, say, fish to mammal or reptile to mammal. I was also taught that if you can understand how a disease is transmitted, you’re one step closer to controlling it.

Which answers the ultimate question – so what does this all mean? When we better understand how a disease is transmitted, it’s easier to control it. Further research in other parts of the country is needed to see if snakes are harboring the virus in the North East and Midwest regions, but the implications for disease control are there. If we understand where or when snakes congregate, we might be able to better predict disease dynamics, specifically outbreaks. If the first outbreaks in the summer originate from mosquitoes biting snakes, then it’s possible that scientists could conduct heavier surveillance in areas where snakes are known to congregate. In this case, we have two entire categories of experts – herpetologists (reptile specialists) and wildlife scientists – that public health practitioners can work with to try to control the disease. This paper is amazing because it unlocks a whole new cavalcade of questions and potential solutions.


This post was republished with permission by the author, and was originally published at Mind the Science Gap.

Hillary is a second year master’s student in Epidemiology at the University of Michigan, and she is currently working in influenza research. Her primary interests include zoonotic, emerging, and vector-borne infectious diseases, disaster preparedness and response, and public health practice.

“Rabid” by Bill Wasik and Monica Murphy

Rabies is a disease without a public relations firm. In developed countries, human disease is incredibly rare–we see typically one or two deaths from rabies each year. In contrast, lightning is responsible for about 60 deaths each year. However, worldwide, rabies is another matter. Today is World Rabies Day, a reminder that 55,000 people still succumb to this virus every year–most of them in impoverished regions of Africa and Asia. While cases in the U.S. are typically due to wildlife exposure (rabid bats or even beavers or rabid kitten), infected dogs remain the main vector of infection in most rabies-endemic countries.

In a new book, “Rabid”, Bill Wasik and Monica Murphy have penned an ambitious history of rabies. It’s subtitled, “A cultural history of the world’s most diabolical virus,” and this emphasis makes Rabid unique. Indeed, while the recognition of the rabies virus is just a bit over a hundred years old, Wasik and Murphy trace the infection back to antiquity. The first half of the book is, as promised, a cultural history–4,000 years of literature references to rabies, hydrophobia, “rage” disease, and dog- and bat-borne contagion in places as far-flung as various mythologies (Greco-Roman, Christian, and Egyptian, to name a few); medical literature from Aristotle to Pasteur; and even the vampire myths from medieval times up to Sesame Street’s Count. Wasik and Murphy explore the animal metaphors used for millenia and examine them through the lens of rabies infection, as well as colorfully explain the various (mis)understandings of the virus and rabies epidemiology in ancient texts. Though Rabid is certainly a pop-science book, many portions of the book wouldn’t be out of place in various literature, history, and even religion classes, which again lends to the book’s eclectic flavor.

The latter half of the tale, then, focuses more narrowly on the science of rabies, covering Pasteur’s work toward a vaccine; the (rather late) discovery of bats as the ultimate reservoir of the virus; the challenge to mount vaccination campaigns in resource-poor areas, and the lingering fear of rabies to this day, which is sometimes justified and sometimes not. They also cover the controversy over the Milwaukee protocol as a treatment for symptomatic rabies, and the problem of rabies control.

Finally, Wasik and Murphy note that even today, almost 130 years after the development of the rabies vaccine, control of rabies among the biggest human source of disease–infected dogs–is almost as poor in some places as it was during pre-vaccine England. The methods to control it are, in some cases, also equally barbaric. The introduction of rabies into Bali in 2008 led to a mass cull of dogs, shooting many in the street. Eventually, a science-based vaccination strategy was adopted and seems to be helping, but not before well over 100,000 dogs were culled and several hundred people had been killed by the virus. Rabies may be an ancient disease, but it is a scourge that is still threatening us where government lacks the will and the funding to beat back “the world’s most diabolical virus.”

Did Yersinia pestis really cause Black Plague? Part 5: Nail in the coffin

Despite its reputation as a scourge of antiquity, Yersinia pestis–the bacterium that causes bubonic plague–still causes thousands of human illnesses every year. In modern times, most of these occur in Africa, and to a lesser extent in Asia, though we have a handful of cases each year in the U.S as well.

When Y. pestis was first confirmed as the cause of bubonic plague during an 1894 outbreak in Hong Kong, most people assumed that we also now knew the cause of the 14th-century Black Death, and the later plague outbreaks that resurfaced periodically. However, there has been lingering resistance to the idea that Y. pestis actually caused the Black Death. I covered the reasoning behind this resistance in a series of posts back in 2008, so I’ll just give the Cliff notes version here. Basically, many of those advocating “not Y. pestis” pointed to differences in the epidemiology of the Black Death compared to modern outbreaks of Y. pestis. Today, people are much less likely to die of plague; the outbreaks aren’t nearly as big; and the pneumonic form (which infects the lungs and is therefore able to spread directly person-to-person) seems too rare to account for the number of cases that occurred during the Black Death. Also, they argue that transmission across Europe was much too fast, given that rodents (typically rats) are the disease vector. Instead of Yersinia, some authors have suggested that the Black Death was instead caused by a hemorrhagic fever virus, or perhaps by an unknown microbe that went extinct sometime in the last 600 years.

More recently, we’ve been able to test these claims, using paleomicrobiology to look for molecular evidence of Y. pestis in skeletons that presumably died of plague. Many of these come from mass graves that have been dated to the time of the Black Death–some also have parish or other town records to attest to the timing of the grave. In most cases, investigators found Y. pestis DNA. In a few cases, they didn’t, which led to controversy and charges of contamination in the positive samples.

However, the tide has turned. In 2010 and 2011, three papers came out which, um, put the nail in the coffin for the Y. pestis naysayers. At the time, the papers got press not necessarily because of what they explained, but because the ancient Y. pestis strains looked fairly ordinary–there was nothing obvious to suggest why, from the bacterial point of view, the Black Death was so deadly. However, I hadn’t had a chance to read these closely until now, and one of the punches never made it into the mainstream media. From the discussion section of this paper, the authors note:

Two of the authors (SW and JM) have previously argued that the epidemiology, virulence, and population dynamics of the Black Death were too different from those factors of modern yersinial plague to have been caused by Y. pestis (13). Given the growing body of evidence implicating this bacterium as responsible for the pandemic, we believe scientific debates should now shift to addressing the genetic basis of the epidemic’s unique characteristics.

The reference cited within is this paper, where the authors cast doubt on another group’s finding of Y. pestis DNA in ancient corpses. So it took them 10 years and probably a dozen or more papers, but two “Black Death doubters” have now come around. Score one for the weight of scientific evidence changing minds.

Works cited

Schuenemann VJ, Bos K, DeWitte S, Schmedes S, Jamieson J, Mittnik A, Forrest S, Coombes BK, Wood JW, Earn DJ, White W, Krause J, & Poinar HN (2011). Targeted enrichment of ancient pathogens yielding the pPCP1 plasmid of Yersinia pestis from victims of the Black Death. Proceedings of the National Academy of Sciences of the United States of America, 108 (38) PMID: 21876176

Bos KI et al. A draft genome of Yersinia pestis from victims of the Black Death. Nature, 2011.

Haensch, S et al. Distinct Clones of Yersinia pestis Caused the Black Death. PLoS Pathogens, 2010.

Previous posts in the series

Part 1

Part 2

Part 3

Part 4

“Spillover” by David Quammen

Regular readers don’t need to be told that I’m a bit obsessed with zoonotic disease. It’s what I study, and it’s a big part of what I teach. I run a Center devoted to the investigation of emerging diseases, and the vast majority of all emerging diseases are zoonotic. I have an ongoing series of posts collecting my writings on emerging diseases, and far too many papers in electronic or paper format in my office to count. Why the fascination? Zoonotic diseases have been responsible for many of mankind’s great plagues–the Black Death, the 1918 “Spanish” flu pandemic, or more recently, HIV/AIDS. So you can imagine my delight when I read about Spillover, a new book by David Quammen on zoonotic diseases.

I’ve previously highlighted some of Quammen’s work on this site. That link goes to a 2007 story he wrote for National Geographic on “infectious animals,” which really serves as a preview to “Spillover,” introducing some of the concepts and stories that Quammen elaborates on in the book.

“Spillover” is wide-ranging, tackling a number of different infectious agents, including viruses like Nipah, Hendra, and Ebola; bacteria including Coxiella burnetii and Chlamydia psittaci; and parasites such as Plasmodium knowlesi, a zoonotic cause of malaria. HIV is a big part of the story; Quammen devotes the last quarter or so of the book to tracing the discovery and transmission of HIV from primates to humans, and from 1900 to present-day. He even takes the time to explain the basic reproductive number–something that’s not always a page-turner, but Quammen manages to do it well and without being too tangential to the rest of the story; much more of a Kate-Winslet-in-Contagion than Ben-Stein-in-Ferris Bueller delivery.

Indeed, “Spillover” is somewhat unique in that it doesn’t read quite like your typical pop science book. It’s really part basic infectious disease, part history, part travelogue. Quammen has spent a number of years as a correspondent for National Geographic, and it shows. The book is filled with not only well-documented research findings and interviews with scientists, but also with Quammen’s own experience in the field, which gives the book a bit of an Indiana Jones quality. In one chapter, he details his adventure tagging along with a research team to capture bats in China, entering a cave that “felt a little like being swallowed through the multiple stomachs of a cow.” This was after an earlier dinner in which he describes his encounters with the an appetizer of the “world’s stinkiest fruit” (I’ll keep the description of the smell to myself) with congealed pig’s blood for a main dish (bringing to mind the scooping out of monkey’s brains in “Temple of Doom”–and the various zoonotic diseases that could be associated with those, come to think of it).

Quammen’s book is an excellent, and entertaining, overview of the issues of zoonotic disease–why do they emerge? Where have they come from? How do they spread? The only thing that’s missing is more of a cohesive discussion about what to do about them. However, that’s rather understandable, as we certainly have less of a grasp of this question than we do about the others (and even with some of those, our knowledge is spotty at best). I hope “Spillover” will inspire another generation of future germ-chasers, as “The Coming Plague” did almost 20 years ago.

Summer reading: memoirs in global health and field epidemiology

I know summer is winding down, but there’s still plenty of beach time left and some great books to take along with you. Two giants in the field have recently released memoirs of their respective fights against infectious diseases: William Foege’s House on Fire: The Fight to Eradicate Smallpox and Peter Piot’s No Time to Lose: A Life in Pursuit of Deadly Viruses.

I’ll begin with William Foege. Foege is a native Iowan, an Epidemic Intelligence Service alum, and former director of the Centers for Disease Control and Prevention. His book, as the title suggests, focuses on his role in the fight against smallpox in the 1960s-70s, and primarily his work in Nigeria and India. Realizing that universal vaccination wasn’t going to be possible for a number of reasons, Foege pioneered the implementation of “ring vaccination,” where smallpox cases would be identified and their contacts vaccinated, then those contacts vaccinated, providing “rings” of protection. Hence, the “house on fire” metaphor–one needs to pour water where it will do the most good; on the burning house.

Peter Piot trailed behind Foege by about a decade, starting his scientific investigations in global health after the eradication of smallpox in most countries. Instead, his first field work was with the 1976 Ebola outbreak in Zaire. Piot, a Belgian, was a newly-trained infectious disease doctor, aided in the discovery of the Ebola virus from African samples, and was then sent to assist with the investigation of the outbreak in Belgium’s former colony. The first third of the book details his work in Zaire and sets the stage for the rest of his career, which has focused on sexually transmitted diseases in general and HIV/AIDS in Africa in particular. Piot’s career has included extensive field work, carrying out studies on the ground investigating the epidemiology of HIV, as well as extensive policy work–he was the director of UNAIDS from 1995 until 2008. The final part of the book covers this portion of his career, discussing Piot’s successes and difficulties implementing global AIDS policies.

Both men present harrowing tales of working with deadly viruses in developing countries. Both discuss the difficulty of carrying out ethical research and interventions in places where medicine is more magic and less science. Both mention some perhaps less-than-ideal behavior, either coercing patients to participate (Foege) or hiding their own potential illnesses during the outbreak (Piot), and express frustration at times, detailing not only their successes but also their failures. Both also strongly encourage understanding culture as part of one’s scientific investigations, and to work with local leadership rather than simply swoop in and take over. The books also compliment each other nicely, as Piot describes the first recognition of two novel diseases, while Foege’s work covers the death of smallpox in the natural world.

Is history repeating itself?

This is the fifteenth of 16 student posts, guest-authored by Cassie Klostermann. 

One of the major accomplishments that public health professionals pride themselves in is the reduction of people getting sick or dying from preventable infectious diseases. Unfortunately, these debilitating, historic diseases that health professionals had once thought they had under control are starting to rear their ugly heads once again in the United States (U.S.). One of these diseases that I am referring to is measles. Measles is a highly contagious virus (from the genus Morbillivirus) spread through the air when an infected person coughs or sneezes making measles extremely easy to get by being around someone who is sick with this disease. According to the Centers for Disease Control and Prevention (CDC), if someone has the measles virus they could potentially infect 9 out of 10 people they come in contact with who are not immune (i.e. not vaccinated) to the disease.

Some of the most common symptoms associated with measles are fever, runny nose, and cough which are also very similar to the symptoms of many other diseases. Measles also commonly causes a rash that can cover the entire body. Those who have measles can spread the virus to another person about 4 days before and after the rash shows up. There are also a few more rare but more serious complications that can develop from having the measles virus such as pneumonia and encephalitis and it can also lead to the death of those infected.

The word measles comes from the Middle Dutch word masel meaning “blemish.” The history of measles cases goes relatively far back into history with references of the virus appearing in records as early as 700 AD. In the U.S., before the vaccine was introduced in 1963, there were about 3-4 million cases (essentially every child had had the disease by the time they were 15 years old), about 1,000 people suffered deafness or permanent brain damage (from encephalitis, for example) and around 450 people died from measles each year. By 2000, naturally occurring cases of measles in the U.S. (meaning cases that originated in the U.S. rather than another country) had been eliminated, although there are normally about 50 measles cases per year in the U.S. that come from other countries where measles is endemic (or constantly present in their population) and with increased worldwide travel people need to be more aware of their risk for contracting measles. Throughout the world, there are an estimated 20 million cases leading to about 164,000 deaths from measles each year, which is a great improvement from the 2.6 million deaths that occurred before the measles vaccine was globally used. The number of measles cases, long-term diseases, and deaths caused by measles are going down year by year and much of this progress can be attributed to efforts that provide the measles vaccine worldwide.

While the overall number of measles cases throughout the world are decreasing (mostly from decreasing cases in developing countries) the U.S. and other developed countries are seeing the opposite trend. According to the Notifiable Diseases and Mortality Tables from the Morbidity and Mortality Weekly Report, there were 223 reported cases of measles for 2011 occurring over 17 outbreaks in the U.S. (the average number of outbreaks is 4). This is an increase from previous numbers (63 cases in 2010 and 71 cases in 2009, to name a couple) and the majority of people infected, about 65%, had not been vaccinated against measles even though most of them were eligible to get the vaccine. Out of the measles cases seen in 2011, 90% were traced back to measles viruses seen in endemic countries and brought back to the U.S. where it was spread person to person in the States. Even though historically measles cases have been high in developing countries (especially Africa and Asia) extensive immunization programs have greatly decreased the amount of cases per year. Now European countries are seeing a large increase in their numbers of measles cases since 2009 because the number of vaccinated people has decreased.

The only proven way to effectively protect someone against contracting measles is to get the MMR (measles, mumps, and rubella) vaccine. If you have not been vaccinated then you are leaving yourself vulnerable to getting the diseases included in the MMR vaccine. This issue doesn’t just stop with the individual person, it spreads to everyone that individual comes into contact with. As mentioned above, measles is highly contagious and is spread through the air when an infected person coughs or sneezes so it can easily infect anyone breathing the same air you breath that is also vulnerable to the disease. When people who are vulnerable to getting the disease breathe in the contaminated air, they have a fairly high chance of getting measles and it is important to keep in mind that there are people who cannot get the MMR vaccine because they are either too young (under 12 months old), too sick (i.e. cancer patients), or the elderly who may have lost some of their immunity. For these people, they do not have a choice as to whether or not they get the vaccine, but they still deserve to have some protection from diseases prevented by vaccines. This protection comes from a concept referred to as herd immunity where there are enough people in a community or country vaccinated against a disease so that is unable to be “kept alive” because there not enough vulnerable people for it to pass through. If we are able to keep herd immunity up high enough by having enough people vaccinated against the measles, then the number of measles cases per year could drop back down to the normal 50 per year instead of 220 per year.

Travelers especially need to keep in mind that although a disease, like measles, is usually a rare occurrence in the U.S., this is not the case in many other countries in Europe, Asia, and Africa as examples. People traveling to countries where measles is endemic really should consider being vaccinated because their risk of being infected is much greater due to the higher number of people in the country infected with the disease.

As with anything in medicine, vaccines can cause reactions in rare situations and I urge people to ask their healthcare provider any questions they have regarding the MMR vaccine. I also urge people to receive all of the recommended vaccines they can (unless they have had past allergic reactions to a specific vaccine) because the risk of contracting measles and dying from it is more common than having a more moderate reaction to the MMR vaccine. If you or your kids are eligible to receive the MMR vaccine, please, please get vaccinated and talk to your doctor if you have concerns about an allergic reaction. By getting vaccinated you are not only protecting yourself and your children but also those who are unable to get the vaccine to protect them from the measles. If vaccination rates do not improve, we may very well see case numbers approach historical highs present before the vaccine was used.



Wait, the infamous “Black Death” still plagues the United States?

This is the eighth of 16 student posts, guest-authored by Michelle Formanek. 

For many of us in the scientific world, particularly budding infectious disease epidemiologists like myself, the Plague (or, more dramatically, the “Black Death”) is a prime example of the rapid and devastating spread of an infectious disease. So devastating, in fact, that it wiped out nearly one-third of the population in Europe in the mid-1300’s. That’s roughly equal to 25 million people. It then persisted and has caused various outbreaks throughout history, most notably the Great Plague of London in which 1 in 5 residents died.

So why should be care about the Plague today? Isn’t that old news?

While I will go into more detail about the history of the plague a little later, I first want to mention what prompted me to write about what many people consider to be a no-longer-relevant disease. In order to gauge modern perceptions of the plague, I took a very unofficial survey of friends and family from various backgrounds about what they knew about the Plague. While the knowledge base ranged quite a bit, most were very surprised to hear that we still have cases of the Plague here in the United States.

Yes, you heard me right. The Plague still exists in the United States.

Of course, due to increased knowledge and antibiotic therapy, we no longer see the sweeping epidemic that caused so much turmoil throughout history. Nevertheless, an Oregon man is currently suffering from a rare case of the “Black Death.”

According to reports, a stray cat bit the unidentified man while he was trying to pull a mouse away from the cat. (I won’t even begin to speculate as to why this man was attempting to steal a mouse away from what was likely a very hungry stray cat, but that’s another story.) Several days later the man began to feel ill and presented to the hospital with symptoms typical of the Plague. These included fever, swollen lymph nodes and stomach pain. It has since progressed to bleeding mouth, nose and anus, and dying tissue.  Although the CDC has yet to confirm the diagnosis, all signs point to the Plague.

Only 10-15 people report becoming ill with the disease each year in the United States; this man is the fifth person in Oregon since 1995.

The Plague is caused by the bacterium Yersinia pestis., a rod-shaped bacillus that can live in various species of animals including rats, mice, squirrels, cats, prairie dogs, camels, and rabbits, among others. Yersinia pestis can then be transferred to humans through direct contact with infected animals, bites from fleas that have previously fed on infected animals (this is most common), or human-to-human through the air. Historically, the high population of small rodents and their flea friends in urban areas were attributed to the rapid spread of the disease.

While the Bubonic plague may be the most well known form of the disease, there are actually three different types of the Plague.  The Bubonic plague is the most common form and is characterized by buboes – painful, swollen lymph nodes – in the groin, armpit or neck. Septicemic plague occurs when the bacteria begins to spread in the bloodstream. Lastly, the most infectious form of the disease is Pneumonic plague. This advanced stage strikes when the bacteria can be passed from person to person through airborne droplets coughed up from the lungs. Bubonic plague is fatal roughly half the time, while Septicemic and Pneumonic are almost uniformly fatal without antibiotic treatment.

The man in Oregon was first believed to be suffering from Bubonic plague, but is now beginning to show signs of Septicemic plague, meaning it has entered his bloodstream and is able to reach all different parts of the body.  Luckily, antibiotics are effective in the treatment of the Plague if given early enough. Without antibiotics, 1 in 7 people infected end up dying.

So you may be asking yourself, as I did, where a deadly disease like this came from in the first place. The puzzling start of the epidemic went something like this:

“The Black Death arrived in Europe by sea in October 1347 when 12 Genoese trading ships docked at the Sicilian port of Messina after a long journey through the Black Sea. The people who gathered on the docks to greet the ships were met with a horrifying surprise: Most of the sailors aboard the ships were dead, and those who were still alive were gravely ill. They were overcome with fever, unable to keep food down and delirious from pain. Strangest of all, they were covered in mysterious black boils that oozed blood and pus and gave their illness its name: the “Black Death.” The Sicilian authorities hastily ordered the fleet of “death ships” out of the harbor, but it was too late: Over the next five years, the mysterious Black Death would kill more than 25 million people in Europe–almost one-third of the continent’s population.”

Unfortunately, the cause of the disease was not discovered until 1894, long after it swept through Europe with alarmingly high death rates. People had their ideas about what was causing the Black Death, but no one could actually figure it out. Some believed it was the spirit escaping the eyes of a sick man and infecting the nearest healthy person, others believed it was God’s way of punishing those who had sinned.  Citizens were so panicked that they went to extreme lengths to avoid contracting the disease, even so far as to completely abandon loved ones who got sick. More details here.

As mentioned before, antibiotics can be extremely effective in fighting this bacteria. As of right now, the Oregon man is still fighting for this life, but thanks to modern medicine, his chances of living are fairly high. The man likely contracted the disease from the cat; however, the cat died shortly after and its remains have since been sent to the CDC for testing.  Who knew that a stray cat in the Northwest U.S. could have possibly been harboring bacteria that once had the potential to wipe out entire cities. Fortunately, modern medicine is on our side.

So is the re-emergence of the Plague something that we should really be concerned about? Probably not. But it never hurts to be informed.