Uganda’s latest Ebola outbreak, which I covered back in July, was just officially declared over on October 5th, a mere two weeks ago. Now today there is a report that three are dead from an outbreak of Marburg virus. That makes 4 Ebola outbreaks and now 2 Marburg outbreaks in the country since 2000.
Guest post by Hillary Craddock
Last week a new study regarding Eastern Equine Encephalitis (EEE) was published online (Bingham et.al.). 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 et.al.) 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 et.al., 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.
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.”
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.
August, 1976. A new infection was causing panic in Zaire. Hospitals became death zones, as both patients and medical staff succumbed to the disease. Reports of nightmarish symptoms trickled in to scientists in Europe and the US, who sent investigators to determine the cause and stem the epidemic. Concurrently, they would find out, the same thing was happening hundreds of miles to the north in Sudan. In all, 284 would be infected in that country, and another 358 in Zaire–over 600 cases (and almost 500 deaths) due to a mysterious new disease in just a few months’ time.
The new agent was Ebola, but remarkably, the outbreaks were unrelated, at least as far as any direct epidemiological links go. No one had brought the virus from Sudan to Zaire, or vice-versa. Molecular analysis showed that the viruses causing the outbreaks were two distinct subtypes, subsequently named for their countries of origin, Ebola Zaire and Ebola Sudan.
While Uganda is currently battling another outbreak of Ebola Sudan, rumors in the past week have suggested that this virus may have spread to former Zaire (now the Democratic Republic of Congo), where Ebola has reappeared 4 additional times since the first discovery there in 1976. It’s now been confirmed that Ebola is again present in the DRC, with an (unconfirmed) 6 deaths. However, it’s not related to the Uganda outbreak. Reminiscent of 1976, the strain that’s circulating currently in the DRC is the Bundibugyo subtype, which was first identified in Uganda in a 2007-8 outbreak in that country, rather than the Sudan type causing the current Ugandan epidemic. Interestingly, every previous outbreak of Ebola in the DRC has been caused by the Zaire type of Ebola, so the appearance of Bundibugyo is a first–though not altogether surprising given that the outbreak province borders Uganda.
Is this just coincidence that Ebola has twice now broken out in two different places at the same time, but with different viral subtypes? Hard to say. Though we can now say it’s fairly likely that bats are a reservoir host for Ebola and other filoviruses, we can’t say for sure that bats are the *only* reservoir. Indeed, we know that some outbreaks have occurred because the index case was in contact with an infected ape or their meat–were these animals originally infected by a bat, or by another source? How does the ecology of an area affect the chances of an outbreak occurring? Were there reasons that humans might be increasingly exposed to the virus in these different areas–Zaire and Sudan in 1976, DRC and Uganda in 2012–at the same time? Weather conditions? Trade/industry? Host migration or dispersal? We know with another bat-borne virus, Nipah, that changes in farming practices led to increased proximity of fruit bats and farmed pigs–allowing pigs to come into contact with virus-laden bat guano, become infected with Nipah, and subsequently transmit the virus to farmers. Things that may seem completely inconsequential–like the placement of fruit trees–can actually be risk factors for viral emergence. Is there a common factor here, or just bad luck? Only additional hard-won knowledge of filovirus ecology will be able to tell.
Uganda just can’t catch a break. They’ve recently been hit with nodding disease, a mysterious syndrome where children repeatedly nod their heads and undergo serious seizures, typically leading to death. Now they’re in the grips of another Ebola outbreak. This will be the fourth time the country has suffered through Ebola since 2000, when the virus was first found in the country:
The first occurred in August of 2000; the first case died in Gulu on the 17th of September. Despite an investigation, doctors were unable to determine where or how she had contracted the disease. Her death was followed by the deaths of her husband, two children, and several other family members. This was reported to the Ministry of Health in October of that year, near the peak of the epidemic. An investigation and intervention to control the disease followed, and the epidemic was declared to be over in January of 2001. A total of 425 patients from 3 villages (Gulu, Masindi, and Mbarara) across Uganda were identified based on symptoms and/or laboratory data. 224 of them died, with a resulting mortality rate of 53%; an eerie echo of the 1976 Ebola outbreak in Sudan. Indeed, sequence analysis showed the infecting strain to be the Sudan subtype of Ebola; the first time this type had surfaced since the 1979 outbreak in Sudan. It is hypothesized that Sudanese rebels, who carried out regular attacks around Gulu, may have accidentally introduced the virus in some manner, though this has not been confirmed.
Ebola returned to Uganda in August of 2007, causing 149 illnesses and 37 deaths until the outbreak was declared over in February of 2008. This mortality (36%) was significantly lower than most Ebola outbreaks. Interestingly, when scientists tested this virus, it also reacted strangely with their assays. Therefore, they determined the entire molecular sequence of the virus, and found that it was a whole new strain of Ebola, which they named Ebola Bundibugyo.
The third outbreak occurred just last year, as a single case in a 12-year-old girl, who died of the infection. I’ve not been able to find any follow-up identifying the 2011 strain, but Uganda has been hit previously by both the Sudan and the novel Bundibugyo strains of Ebola, and the current outbreak has been identified once again as Ebola Sudan.
In the current outbreak, which began in the Kibaale district in western-central Uganda, at least 20 have been affected and 14 have died. As of today, an additional six cases are suspected but not yet confirmed, and it appears to be affecting more than one village in the district. One death has also occurred at Mulago hospital in the capital of Kampala. The individual who died was reported to be:
… a health worker who “had attended to the dead at Kagadi hospital” in Kibale, Health Minister Christine Ondoa told reporters.
She is believed to have travelled independently to Kampala — possibly on public transport — after her three-month old baby died, Ondoa added.
Reports also note that other health care workers are in quarantine as a precaution. In Africa, Ebola has really been able to spread in previous outbreaks for two reasons: breakdowns in barrier nursing within hospitals (not wearing gloves/gowns; reusing needles; lack of handwashing/sanitation, etc.) and ritual funeral practices within villages, which put many family members in contact with the virus as they assist with cleansing the victim. Indeed, it appears that 9 of the deaths in this outbreak have come from a single family, so it’s quite possible many were sickened using this type of practice. However, now that Ebola has been confirmed and people are aware of this, stricter controls over these practices can be implemented, and health care workers are being urged to report any cases that may be Ebola to authorities.
Kampala is a city of a bit over a million people on Lake Victoria, southeast of the Kibaale district. The 2011 case originated from Luwero district, due east of the Kibaale district and north of Kampala. The 2000 outbreak occurred in the Gulu district in the north of the country, and the 2007 outbreak in the Bundibugyo district, in the west and neighboring Kibaale. It would seem that Ebola reservoirs (likely fruit bats) could very well be spread across Uganda’s central region, occasionally spilling over into the human populations and igniting these outbreaks. One story notes that “The site where most of the cases occurred are close to Kibale forest where there are a lot of monkeys and birdlife,” and while bats are not explicitly mentioned, they presumably would also be present. Non-human primates have also been implicated in previous outbreaks of Ebola as an amplifying species.
The reporting of the current outbreak was delayed, as patients didn’t have any noticeable bleeding–rather, diarrhea and vomiting were the main reported symptoms. However, while many reports I’ve seen are characterizing hemorrhagic symptoms as “typical,” these aren’t seen in all patients, and indeed the diarrhea, vomiting, and even hiccups are common symptoms of Ebola infection. As such, Uganda has been playing a bit of catch-up, but has certainly learned since the first (and worst) outbreak in 2000. Hopefully this one will end fairly quickly.
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.
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.
This is the twelfth of 16 student posts, guest-authored by Stanley Corbin.
Disease in wildlife is an important concern to the health and safety of humans and domestic animals. The expanding growth of our nation and resultant land use changes with urbanization has resulted in a shrinking habitat and fragmentation for all animals, including humans. The effects of ecological disruption are universally recognized and adversely effects wildlife through multiple mechanisms.
Hand it to the coyote (Canis latrans) for its ability to exist with humans. The resilience of this animal can be attributed to its natural instincts, remarkable intelligence and survivability. Opportunistic is another word that can be used to define them. Once an animal roaming the mid-west prairies, their territory has expanded throughout the North American continent and beyond. Coyotes demonstrate their wily nature by meeting the challenges of the American landscape.
Progression of coyote range expansion throughout North America and Mexico. (7) Click to enlarge.
Precise population estimates of coyotes in the United States are not available and unclear at best. However, to put it in perspective, the California Department of Fish and Game estimates a population range of 250,000 to 750,000 animals.(1) The greater metropolitan area of Chicago estimates home to between 200-2000 coyotes. (3) The coyote population in New York during the summer is approximately 20,000-30,000. (2) In March 2010, a lone coyote led a police chase through lower Manhattan, deep in New York City.
Coyotes can thrive in suburban settings and even some urban ones creating a concern for public health. A study by wildlife ecologists at Ohio State University yielded some surprising findings in this regard. Researchers studied coyote populations in Chicago over a seven-year period (2000–2007), proposing that coyotes have adapted well to living in densely populated urban environments while avoiding contact with humans. They found, among other things, that urban coyotes tend to live longer than their rural counterparts. (3)
As with most all wild animals, the coyote population represents a reservoir for diseases. Zoonotic (animal to human) diseases in particular are on the rise, comprising 75% of emerging infectious diseases. Viruses, bacteria, fungi, internal and external parasites, and other pestilence are only the headings for what’s out there.
Fortunately, the rabies virus is rather uncommon in coyotes as reported. The only exception was the 1974-1998 rabies epizootic (epidemic in animals) in south Texas. The world’s largest wildlife oral rabies vaccine (ORV) drop, 11.6 million doses covering over 189.6 square miles, was performed beginning in 1995 and led to the total elimination of the domestic dog-coyote (DDC) variant by 2006. (4) A study performed by the USDA, APHIS, Wildlife Services, National Wildlife Research Center concluded; “In Texas, the use of the ORV stopped the northward spread and led to the progressive elimination of the DDC variant of rabies in coyotes”. (5) This campaign was a win for our tax dollars as well. The economic evaluation study yielded “total estimated benefits of the program approximately ranged from $89 million to $346 million, with total program costs of $26,358,221 for the study period”. This represents benefit-cost ratios that ranged from 3.38 to 13.12. (5)
Coyote rabies surveillance reported by the Center for Disease Control (CDC) for 2010 declared 10 confirmed cases. None of these cases were DDC variant, which remains non-detected from the populations. The raccoon variant and skunk variant represented 8 (AL, GA, NC, NJ, NY, NYC) and 2 (CA, CO) cases respectively. (6)These coyote rabies cases were diagnosed from New York City (1) on the east coast to California (1) in the west, confirming the widespread distribution of this terrestrial carnivore. An interesting fact that comes from this data is that the coyote is not a player in the zoonotic rabies front. From a public health concern, a human has a significantly greater chance of contracting the disease from the backyard domestic cat.
Canine Distemper Virus is an enzootic disease (prevalent in an animal population) in the coyote. The neurological form is rightfully confused with a rabies infection as the two appear similar clinically. Humans are not susceptible to the disease, however it is highly contagious to dogs. Greater Yellowstone Park has a dynamic management study to assist with the surveillance of the disease enzootic in the parks coyote population.
The parasitic disease Sarcoptic mange is what gives the animal the “mangy” look. Caused by the mite Sarcoptes scabei, the disease in humans is called Scabies. Severely affected coyotes are unsightly and are perceived as threatening by their appearance. The compromised condition may explain the increased frequency of nesting and scavenging in suburban areas, especially in daylight hours. Coyotes with extensive mange infections are not considered aggressive as concluded by The Cook County, Illinois, Coyote Project.(7) Human infections from animal sources are short-lived and self-limiting due the highly host species-specific nature of the bug.
A recent hot epidemiological study conducted in Santa Clara County, California, identified coyotes as a wildlife reservoir for a disease caused by Bartonella vinsonii subsp. Berkhoffii .(8) The disease in humans is characterized by endocarditis, an inflammation of the interior lining of the heart. The study was prompted by the coyote bite of a child who developed symptoms compatible with Bartonella infection. Among 109 coyotes sampled, 31 animals (28%) were found to be bacteremic and 83 animals (76%) had Bartonella vinsonii seropositve antibodies. The disease is thought to be transmitted by insect vectors (ticks, biting flies, fleas), however further studies are necessary to elucidate additional modes of transmission to humans.(8) Bartonellosis in domestic cats is commonly called “cat scratch fever”, caused by a different species variant of Bartonella. The role coyotes play in this emerging infectious zoonose and public health concern are yet to be resolved.
Additional diseases exist in the coyote populations warranting public health attention. Anyone concerned with coyote interaction and communicable diseases will need to seek information relative to their geographical location. The ubiquitous nature of this animal and the corresponding diseases posing risks to humans and domestic animals respectively are regionally specific.
Coyotes are here to stay. Most every state (excluding Hawaii) has a control program in effect to manage the public health risks and deprivation to human welfare. The Humane Society of the US has issued techniques to resolve coyote conflict and how to discourage coyotes. Project Coyote champions innovative solutions to live in peace with the coyote despite differences, especially in terms of human policy. (9) A collaborated and integrated management approach is required to maintain a balance of needs for this specie of animal and humans. Wildlife specialist Jeffery Green summarizes; “regardless of the means used to stop damage, the focus should be on damage prevention and control rather than elimination of coyotes”. (10)
Pet owners need to adapt to coyote presence and take precautionary measures in securing their animal’s health and safety. Routine core vaccinations and other preventative health care are effective in stopping the transmission of nearly all the important diseases from the coyote to a pet animal.
Coyote attacks on humans are rare; the coyote human avoidance factor is responsible for the low incidence. In the cases of human attacks, approximately 30% were reported as humans feeding coyotes. (8) Additionally, greater than 50% of the human attack cases were in California, (8) where coyotes have a longer history of habituation with humans.
A person who sees a coyote should feel lucky since they avoid humans and are mostly invisible.
The most important advice to prevent human exposure is: do NOT feed coyotes and ensure your environment is NOT coyote friendly. Any attempt to domesticate or habituate the coyote will surely be a kiss of death for its existence. Survival of coyotes is dependent on living side by side but not together with humans.
The “tricksters still run wild and provoke all sorts of all-too-human difficulties, pitting the spirit of the wild against the sturdy values of our American farmers and their need to protect livestock. Somehow we need both”. (11)
Our Canadian neighbors at The Royal Canadian Geographical Society conclude; “the more we cut down habitat and build, the happier the scavenging and opportunistic coyote”. (12)
- L.A. County Department of Animal Care and Control website. Accessed June 15, 2012. Available at: http://animalcare.lacounty.gov/coyote.asp
- New York State Department of Environmental Conservation website. Accesses June 15, 2012. Available at: http://www.dec.ny.gov/animals/9359.html
- World Science website: Thriving under our noses, stealthily: coyotes. Accessed June 13, 2012. Available at: http://www.world-science.net/othernews/060105_coyotefrm.htm
- Texas Department of State Health Service website. Accessed June 12, 2012. Available at: http://www.dshs.state.tx.us/idcu/disease/rabies/orvp/statistics/
- Stephanie A. Shwiff, PhD; Katy N. Kirkpatrick, BS; Ray T. Sterner, PhD. Economic evaluation of an oral rabies vaccination program for the control of a domestic dog-coyote rabies epizootic: 1995-2006. JAVMA, Vol.233, No.11, Dec.1, 2008. Available at http://www.avma.org/avmacollections/rabies/javma_233_11_1736.pdf
- Jesse D. Blanton, MPH; Dustyn Palmer, BA; Jessie Dyer, MSPH; Charles E. Rupprecht, VMD,PhD. Rabies surveillance in the United States during 2010. Vet Med Today: Public Veterinary Medicine. JAVMA, Vol. 239, No. 6, September 15, 2011. Available at: http://avmajournals.avma.org/doi/pdf/10.2460/javma.239.6.773
- The Cook County, Illinois, Coyote Project website. Accessed June 13, 2012. Available at: http://urbancoyoteresearch.com/Coyote_Project.htm
- Chang CC, Kasten RW, Chomel BB, Simpson DC, Hew CM, Kordick DL, Heller R, Piedmont Y, Breitschwerdt EB. Coyotes (Canis latrans) as the reservoir for a human pathogenic Bartonella sp.: molecular epidemiology of Bartonella vinsonii subsp. Berkhoffii infection in coyotes from central coastal California. J Clin Microbiol. 2000 Nov; 38 (11): 4193-200. Available at: http://www.ncbi.nlm.nih.gov/pubmed/11060089
- Project Coyote website. Accessed June 15. 2012. Available at: http://www.projectcoyote.org/programs.html
- Jefferey S. Green, Urban Coyotes: Some Summary Thoughts. Proceedings of the 12th Wildlife Damage Management Conference (D.L. Nolte, W.M. Arjo, D.H. Stalman, Eds. 2007
- Shake-Spear’s Bible.com website; Coyote: An Instant Classic. Post by Roger Strirtmatter, October 25, 2011. Accessed June 13, 2012. Available at: http://shake-speares-bible.com/2011/10/25/coyote-an-instant-classic/
- The Royal Canadian Geographical Society website. Accessed June 13, 2012. Available at: http://www.canadiangeographic.ca/wildlife-nature/?path=english/species/coyote/2
- Personal correspondence; James Wright; Tyler Texas. Retired Texas Department of State Health Service official.
This is the eleventh of 16 student posts, guest-authored by Ilze Berzins.
When one hears the words “food-borne illness”, what comes to mind? For me, I think of a medium rare, pink, juicy hamburger, or something like potato salad that may be made with mayonnaise containing raw eggs, or maybe a fresh green garden salad sprinkled with sprouts. I am sure we have all heard about outbreaks or recalls surrounding these familiar dishes. And the usual suspects contaminating these food stuffs are often bacteria with familiar names such as E.coli or Salmonella. The fear of getting “food poisoning” from these products may encourage us to buy fresh seafood from the grocery store, or order the shrimp or salmon when out at a restaurant instead of steak, thinking seafood might be a safer bet. And of course, aren’t health benefits from seafood supposed to be an added bonus? But not so fast! Believe it or not, one can also become ill when eating, or even just handling, seafood. Gives the phrase “fresh catch of the day” a whole new meaning!
Seafood is a broad term…and no…it is not the game you played as a child that while eating you asked people if they wanted seafood and you opened your mouth (get it? SEE food?). Seafood refers to all species of fish and shellfish, coming from both fresh and saltwater sources. Salmon, snapper, trout, tuna, perch, tilapia are just a few of the fish that come to mind. But what is shellfish? Shellfish consists of a mixed group of mollusks and crustaceans that have a shell or shell-like body covering known as an exoskeleton. For the mollusks, this would include oysters, clams, mussels, abalone, and scallops. And although they don’t have an obvious shell (it is very small or absent), squid and octopus are also in this group. Crustaceans that are edible shellfish include lobsters, shrimp, crabs, and crayfish. Yum.
What can make you sick from eating seafood? There are several main categories including infectious pathogens (parasites, viruses, and bacteria – oh, my!), contaminants (heavy metals such as mercury in the form of methymercury), and drug and chemical residues. These can be synthetic compounds but can also come from natural bio-toxins. One such compound is found in the tissues of small aquatic organisms in overgrowth situations or “blooms” such as in red tide events.
Eating raw or undercooked seafood definitely increases the risk of a food-borne illness, but even just handling or processing seafood can cause problems for humans (7, 10). Topically acquired or contact zoonoses can be acquired through stings, bites, or spine/pincer puncture wounds. Zoonoses are illnesses transmitted from animals to humans. Some groups at risk include commercial fishermen, fish farmers (aquaculture), hobbyists, aquarists working in public display facilities, fish food processors, chefs, and even you when you are preparing dinner! Bacteria are the primary causative agents for zoonotic infections through a contact route. Viruses, fungi, and parasites contact infections have rarely been reported (7, 8). However, I am not quite sure how to classify a recent case report on a “parasite-like” infection by the squid Todarodes pacificus (5). A 63-yr-old Korean woman was reported to have experienced severe pain in her oral cavity immediately after eating a portion of parboiled squid along with its internal organs. She did not swallow the portion, but spat it out immediately. She complained of a pricking and foreign-body sensation in the oral cavity. Twelve small, white spindle-shaped, bug-like organisms stuck in the mucous membrane of the tongue, cheek, and gingival were completely removed. On the basis of their morphology and the presence of sperm, the foreign bodies were identified as squid spermatophores!! Not sure if I would call that “parasite-like”?! I digress! Let’s focus!
There are lots of species of seafood and many reports of associated food-borne illnesses (1,2). Where should we start? In this blog, I will focus on a group within the mollusks, the bivalves. Bivalves are mollusks with two shells including oysters, clams, and mussels. I want to focus on this group because given the propensity of humans to eat raw oysters, eating them raw elevates the risk of acquiring a viral or bacterial food-borne illness. In subsequent blogs, I will review other members of the mollusks, then on to crustaceans, and of course, fish, so stay tuned!
Safety issues for bivalves center around two categories; first, the quality of water in which these animals are grown in, and second, the conditions under which they are harvested, processed, and distributed (1,2,8). In 1925, the Bureau of Chemistry (now the United States Food and Drug Administration) met to establish guidelines for the oyster industry. Attendees resolved to control “the beds on which shellfish are grown” and “the plants in which the shellfish are shucked” (shucking refers to removing the animal from its shell)(11). In the late 1800s and early 1900s, most outbreaks of seafood food-borne illness resulted from sewage contamination in the areas where shellfish were grown (11). From the late 1970s through today, there has been an increased incidence of disease associated with naturally occurring shellfish pathogens (11). There are some that think this trend is suggestive of emerging environmental problems such as increasing water temperatures associated climate change. While the species of pathogen isolated in bivalves may vary with salinity of the water the oysters or clams grow in, it is noted that all of these pathogens increase in numbers with an increase in water temperature (11).
How often do we see illness? In a 10 year study on mollusk shellfish food-borne illness, a total of 2795 cases, with 96 deaths, were documented (11). Oysters accounted for the highest proportion of cases (49%) and death (97%). Shellfish from the East and Gulf costs were equally likely to cause disease. Most from the East Coast were viral contaminated clams, where as on the Gulf Coast, most cases were oysters infected with non-cholera bacteria in the family Vibronaceae.
The naturally occurring bacterial pathogens of concern include Vibrio vulnificus, V. parahaemolyticus, V. mimicus, V. hollisae, and V. furnissi. When eating raw oysters, one might become exposed to V. vulnificus. Incubation can take 1-5 days, though the median time is around 28 hours (3). Symptoms include high fever, chills, nausea, vomiting, diarrhea, and abdominal pain. The ill person can become rapidly dehydrated, and the infection can become systemic (body wide) if bacteria enter the blood. V. vulnificus in some cases can multiply so rapidly that blood vessels may become infected (known as vasculitis), and blood clots can develop which may lead to digit or limb amputation, or even death (3)!
How about from contaminated sources? Viral and bacterial enteric pathogens of public health concern are caused by fecal contamination of the waters from which molluscan shellfish are harvested and of the environment in which they are processed. Pathogens of concern that have been associated with disease include human enteric viruses; hepatitis A, non-A, non-B enteral hepatitis (hepatitis E), unclassified viruses; and such bacteria as Salmonella, Shigella, Campylobacter jejuni, and pathogenic Escherichia coli (11). The group of unclassified viruses includes the Norwalk and Norwalk-like viruses.
Do we stop eating seafood? NO!!! But measures to increase the safety of raw shellfish could be, and are being implemented (11). These measures might include policies on when and where to collect (season, time/temperature), requiring harvest areas near sewage treatment facility outflows to be more closely evaluated (9), and continuing to improvement the technology of sewage treatment. Some aquaculture techniques have included lowering temperatures and controlled purification which involves disinfecting (or purifying) the water in which the bivalves are grown. This may reduce gut bacterial levels but it does not entirely remove them. When processing shellfish, facilities can employ techniques such as rapid chilling and cold storage to reduce overgrowth and contamination. Irradiation of the harvested product has been suggested but has yet to be approved. Laboratory tests to detect contamination are moving beyond traditional culture techniques and include identifying pathogens based on their individual DNA using molecular methods (6). Focusing on identifying groups at risk such as those individuals who are immunocompromised (young, old, ill) and concentrating on the more common agents could help resources go further.
Consumer education is also very important. Prevention strategies should focus on preparation and consumption. Cooking oysters to an internal temperature of 85-90°C will destroy both viruses and bacteria of public health concern. But what if you want to eat them raw? Maybe think about cooking oysters during periods of warm weather and go for raw during colder times of the year! An excellent, comprehensive web site about food safety issues is www.foodsafety.gov . It addresses a variety of audiences including consumers, food professionals and industry workers, and provides the latest news, safety alerts, recalls, and health warnings. The site also allows for individuals to report cases, and it has information for physicians on how to diagnose and manage food-borne illnesses. Other useful sites include www.foodsafetywatch.com and www.fda.gov.
With any food product, it is probably wise to stop and ask “To Eat or Not To Eat?”(4). Stay safe!
- Butt, A.A., Aldridge, K.E., and Sanders, C.V. 2004. Infections Related to the Ingestion of Seafood Part I: Viral and Bacterial Infections. Lancet Infect. Dis. 4: 201-212.
- Butt, A.A., Aldridge, K.E., and Sanders, C.V. 2004. Infections Related to the Ingestion of Seafood Part II: Parasitic Infections and Food Safety. Lancet 4: 294-300.
- Daniels, N.A. 2011. Vibrio vulnificus Oysters: Pearls and Perils. Clin. Infect. Dis. 52 (6):788-792.
- Galson, S.K. 2009. To Eat or Not to Eat: Food Safety in the United States: Practical Applications from the Surgeon General. J. Am. Dietetic Assc. 5(20): 1142.
- Park, G.M., Kim, J.Y., Kim, J.H., Huh, J.K. 2012. Penetration of the Oral Mucosa by Parasite-Like Sperm Bags of Squid: A Case Report in a Korean Woman. J. Parasit. 98 (1): 222-223.
- Huss, H. H., Reilly, A., and Ben-Embarek, P.K. 2000. Prevention and control of hazards in seafood. Food Control 11:149-156.
- Iwamoto, M., Ayers, T., Mahon, B.E., and Swerdlow, D.L. 2010. Epidemiology of Seafood-Associated Infections in the United States. Clin. Microbiol. Reviews 23 (2): 399-411.
- Rabinowitz, P.M., Gordon, Z., Holmes, R., Taylor, B., Wilcox, M., Chudnov, D., Nadkarni, P. and Dein, F.J. 2005. Animals as Sentinels of Human Environmental Health Hazards: An Evidence-Based Analysis. EcoHealth 2: 26-37.
- Vinh, D.C., Mubareka, S., Fatoye, B., Plourde, P., and Orr, P. 2006. Vibrio vulnificus Septicemia after Handling Tilapia sp. Fish: A Canadian Case Report and Review. Can. J. Infect. Dis. Med. Microbiol. 17(2): 129-132.
- Wittman, R.J. and Flick, G.J. 1995. Microbial Contamination of Shellfish: Prevalence, Risk to Human Health, and Control Strategies. Annu. Rev. Public Health 16: 123-40.