Granny’s mean pot of bushmeat stew

Left to right, Granny Beck, my Grandma June, and Great-Great Grandma Bertha, circa 1961. Who knows what was on the menu that day.

My Great-Grandpa and Granny Beck were, in some ways, ahead of their time. My Grandpa’s mom and step-dad, they both went through scandalous divorces and then switched partners with another couple, Granny Orpha marrying Wade and my Grandpa’s dad Lee marrying Wade’s ex-wife, Edna. Orpha and Wade raised 5 of Orpha’s boys together, and had a daughter after the divorce/remarriage.

By the time I was born, my Granny Beck was in her 80s, and I have only vague recollections of going over to visit her at her home. But I remember hearing about her cooking. I was a picky eater anyway, and my mom once told me she was always afraid to eat Granny Beck’s stew, because it could be rabbit, it could be ‘possum, it could be squirrel, it could be groundhog…you just never knew. I never ate anything over there.

Grandpa Beck used to have coon dogs, and would bring home anything that the dogs would catch. My great-aunt affirmed my mom’s recollection of Granny Beck’s cooking (and Grandpa Beck’s eating):

My mom did cook some pretty weird things. We always had wild game such as rabbit and pheasant, but I do remember when she cooked a raccoon (I didn’t try it!). My dad was the one that would eat anything, and I do mean anything! We used to bring him such things as chocolate covered ants, pickled pigs feet, and pickled rooster combs. He loved them!

Over the weekend, my neighbor sent along some meat packages for us. He had recently gotten back from another hunt and bagged his third deer of the season (you’re allowed four per year in my county). He was grilling when my partner stopped over on the way home, and sent some ground deer (I think–I’ve not opened the package yet), deer steaks, and a still-warm hunk of a deer heart, well done.

Deer assortment
Various deer parts brought over by my neighbor this weekend.


All of this is to say that we can eat some really weird things here in the “civilized,” first-world, developed United States.

Why bring this up now? The current Ebola outbreak has brought out all kinds of biased to outright racist views of Africa and disease. Because it’s postulated that the outbreak started with the consumption of or contact with an infected animal—possibly a fruit bat, which the index family noted they do hunt—people have come out of the woodwork to pontificate on how those in Guinea and other countries “brought this on themselves” because of their consumption of “bushmeat,” and that they’re so uneducated and backwards to eat that in the first place–because really, how could people eat that stuff, especially when it could be diseased?

Prominent magazines run pictures of butchered meat and primates with headlines that are intended to scare and “other.”

People judge harshly, partly because of bush meat consumption:

“Is it time that we drag ignorant, superstitious third world Africans kicking and screaming into the 21st century or should we stop giving aid to Africa and let them fend for themselves? Would the later propel the former?”

Even though we do the same. damn. thing. in the United States.

“Bushmeat” is the name given to pretty much any kind of wild game hunted in Africa–bats (obviously a concern given their possible role in Ebola spread and maintenance of the virus); primates; birds, duikers, lizards, crocodile, various rodents, even elephant, and more.

What do we call “bushmeat” in the US? Or just about everywhere else?

Just “wild game,” or some variation thereof.

In the U.S., we hunt thousands of deer, elk, pheasant, turkey, rabbit, and other animals every year. There are even wild game restaurants that cater to those tastes (though many “wild game” species are actually farmed to some degree). Yet even the bushmeat page at United States’ Fish and Wildlife Service ignores the hunting that goes on in the United States, noting that:

Here in the United States, we have laws that control the preparation, consumption, and trade of meat, ensuring that animals are treated appropriately, kept healthy, and sold legally. This is not the case in some countries in Africa and other parts of the world.

This seems to refer mostly to domestically-raised meats, as it’s much harder to police the treatment, health, and sale of hunted animals. Though one needs a license to hunt many animals and generally to fish, laws vary from state to state. Here in Ohio, though a hunting license or permit needs to be obtained for most types of hunting or trapping, and there may be limits on the number of animals of certain species one can kill per season (such as deer and turkey), for most animals, there’s merely a daily limit (6 squirrels, 4 rabbits, etc. per day). For other animals, including fox, raccoon, skunk, opossum, weasel, crow, groundhog, and coyote, there is no daily bag limit. So one could, conceivably, feed themselves fairly well on just a diet of wild game if they had the time and inclination to do so.

Of course, most people in the U.S. don’t get our food this way. We look at Daryl Dixon of the Walking Dead and his squirrel-hunting prowess as something that could carry one through the zombie apocalypse, but not school lunches for a family of 4. We think it’s awesome when he finds an opossum in a cupboard and proclaims, “Dinner!” I’m sure many readers have plans for their own apocalypse survival plan, which likely involve some kind of wild source for food.

But in modern-day Africa, such hunting is somehow “barbaric” and “backward,” regardless of whether it is for sustenance or trade.

Though Ebola has not been identified in wild animals in the US, our animals are far from disease-free. No wild (or domesticated) animal is. We certainly can find Tularemia and Pasturella in rabbits; deer can carry tuberculosis, Brucella, Hepatitis E, and maintain transmission of Lyme disease and potentially Erlichia. Other zoonotic pathogens that could be acquired from a variety of wild animals include Campylobacter, E. coli, plague (mainly in the Southwestern United States); Cryptosporidia, Giardia, avian influenza from waterfowl, rabies (more likely from handling than ingestion); hantavirus, Trichinella, Leptospira, Salmonella, Histoplasma, and I’m sure many more from handling or consumption of wild animals.

Finally, while people malign “bushmeat” hunters in Africa, let’s not forget that almost any source of food can be contaminated with potential pathogens. Even in the United States, 1 in 6 Americans (48 million people) get sick, 128,000 are hospitalized, and 3,000 die of foodborne diseases. Every year. And that’s with our “high standards” for animal husbandry and processing.

So perhaps rather than looking to countries in Africa and judging their food consumption habits as they relate to infection, we should turn a mirror to our own. If we don’t judge Granny Beck for her wild game consumption, neither should we judge those a continent away.

Additional readings

The long and ugly tradition of treating Africa as a dirty, diseased place

If you can’t be a good example, be a warning. How EcoInternet’s #Scicomm #Fail can make you a more culturally aware science communicator

 American Bushmeat

Deadly distrust

Gregg Mitman’s article in the September 17th New England Journal of Medicine, “Ebola in a Stew of Fear,” is unfortunately all too prescient. Dr. Mitman highlighted “the ecology of fear” in Western Africa. Fear is present on both the part of Westerners (scared of Africa’s yellow fever, malaria, Ebola, its mere “different-ness”), and by native Africans (of whites’ history of colonization and slavery, of medical exploitation dating back well over a century). Fear of each other.

This history of fear, the cultural legacy of decades of mistrust of both Western people and their medical science, played a role in the murders of 8 people working on the Ebola outbreak in Guinea–journalists, medical officers, local administrators, and a preacher who were just trying to educate locals about the virus. The hostile crowd first threw stones at the team, and ended in their brutal deaths. The steps in-between have not been reported.

This is the extreme end of the science and medical denial continuum. We can scoff in America and attribute such horrors to the “brutal, savage Africans,” who cut their daughters and rape virgins to cure AIDS, as I’ve unfortunately already seen in some Twitter comments–some of our notions of “them” not so dissimilar from American colonists of centuries past regarding the slaves they once owned.

We can accept this scape-goating and ignore the West’s own modern-day culpability, with our fake vaccination campaigns that have left others dead in the aftermath; with our movies and popular culture depicting Africans as the West’s guinea pigs, and our shady pharmaceutical dealings that make that characterization all too believable.

No, it isn’t always a battle of Africans against Westerners. In South Africa, former President Thabo Mbeki was deceived by false claims about the relationship between HIV and AIDS that he had read on the internet, suggesting that HIV was not the cause of AIDS, and that  Western science should be distrusted in favor of traditional herbal remedies recommended by his health minister, such as garlic and beetroot. Because of his suspension of Western medical treatments, an estimated 330,000 South Africans died prematurely from HIV/AIDS between 2000 and 2005 , and at least 35,000 babies were born with HIV infections that could have been prevented.

Denialism kills. Distrust kills. Fear kills.

Here in the U.S., Natural News, a site run by the self-dubbed “Health Ranger,” Mike Adams, ran a piece this past summer suggesting that journalists and scientists who defended genetically-modified organisms (GMOs) were similar to Nazis, accelerating “heinous crimes being committed against humanity” and collaborating with an “with an anti-human regime,” and that such individuals should be named as such for future crimes:

“Just as history needed to record the names and deeds of Nazi war criminals, so too must all those collaborators who are promoting the death and destruction caused by GMOs be named for the historical record. The true extent of their collaboration with an anti-human regime will all become readily apparent once the GMO delusion collapses and mass global starvation becomes an inescapable reality.

I’m hoping someone will create a website listing all the publishers, scientists and journalists who are now Monsanto propaganda collaborators. I have no doubt such a website would be wildly popular and receive a huge influx of visitors, and it would help preserve the historical record of exactly which people contributed to the mass starvation and death which will inevitably be unleashed by GMO agriculture (which is already causing mass suicides in India and crop failures worldwide).”

Adams is similarly anti-vaccine, and currently is featuring on his website “11 horrible truths about Ebola the government doesn’t want you to know.” These “truths” include suggesting that infected individuals should avoid hospitals, and that citizens everywhere should prepare for the inevitable quarantine at gunpoint.

The worst part of Adams’ misinformation of this type is that it doesn’t stay within the borders of the U.S.–misinformation on Ebola epidemiology and quack cures like those Adams promotes are also being spread in African nations via Facebook pages and other types of social media

Denialism kills. Distrust kills. Fear kills.

Because of distrust of Western medicine, a recent article noted that parts of Africa have better vaccination rates than many wealthy neighborhoods in Los Angeles–and as a result, 10 babies died in a 2010 outbreak of whooping cough in California.

The deaths of the workers in Guinea show this fear and denial writ large; the purposeful killing of those only wanting to help their local and global neighbors in the face of a terrible epidemic. Those murdered are the latest victims of the most malignant form of distrust. They will not be the last.

Student guest post: Are parasites causing a rise in the global HIV epidemic?

Student guest post by Carrie Ellsworth

During the summer of 2010 I spent two months in Ghana studying a parasite called schistosomiasis. We worked in a small town called Adasawase to determine prevalence and treat the schoolchildren who were infected. We were told that schistosomiasis was not a major health concern for the people in the town because they were often faced with other diseases that had more immediate and severe health consequences than a parasitic infection. It became apparent that if we wanted the people of this small town to take this health threat seriously, we needed to stress the long term health sequelae that could arise due to schistosome infections.

Carrie picture 1

(Personal photo taken in Ghana in 2010)

Our research group decided to implement an educational portion to our schistosomiasis control program. Through a Knowledge Attitudes and Practices survey, we found that most schoolchildren in the town reported learning about health from their teachers in school. We held a meeting with all teachers and administrators from Adasawase to educate them on the transmission, symptoms, and long term implications of schistosomiasis infections. When the possibility of greater transmission of HIV to individuals with schistosomal infections came up in discussion, we suddenly had everyone’s complete attention. You could have heard a pin drop on the cement floor of the school room.

Recently, the BBC reported that over 25% of schoolgirls between the ages of 10 and 14 in South Africa are infected with HIV. The World Health Organization has shown that HIV prevalence is much higher in females living in urban areas than in any other demographic group. More than 2/3 of the world’s population living with HIV/AIDS lives in Sub-Saharan Africa. Many efforts have been made to decrease the prevalence of HIV in Africa but few people have looked at the possibility of a parasitic infection possibly contributing to the transmission of HIV.

Carrie picture 2


Schistosomiasis haematobium is a species of waterborne parasite that specifically affects the urogenital system of infected individuals. When people with S. haematobium urinate in stagnant water, they deposit schistosome eggs. The eggs develop into larvae which then enter a freshwater snail to continue its life cycle and mature. It leaves the snail and matures into its infective stage while in the water. The mature larval form of the parasite burrows through the skin of an individual who has contact with contaminated water. Once inside the body, the mature larva develops into an adult worm and then travels to the blood vessels surrounding the bladder. The male and female will mate to produce eggs which penetrate through the bladder wall and are passed in the urine to continue the cycle.

The treatment for a schistosomiasis infection is an inexpensive anti-helminthic medication called Praziquantel. Common signs of a S. haematobium infection are bloody and cloudy urine. Damage to the bladder wall is inevitable and if the infection becomes chronic, damage to the kidneys can also ensue. Chronic genital sores can develop in females with S. haematobium infections when the schistosome eggs are deposited in the uterus, vulva, cervix, and vagina. These lesions are believed to put the females with S. haematobium infections at a greater risk of contracting HIV. A study conducted in Zimbabwe showed that women ages 20-49, who had genital lesions due to a urogenital schistosomiasis infection, had a 3-fold higher risk of having HIV than women without a schistosomal infection.

There are 207 million cases of Schistosomiasis worldwide, and 112 million of those cases are urogenital Schistosomiasis found in Sub-Saharan Africa. This creates a significant overlap between areas of Africa that are endemic to HIV/AIDS and Schistosomiasis. This has caused many scientists to question whether a greater effort to control S. haematobium infections would be an effective method of decreasing the prevalence and transmission of HIV/AIDS in Africa.

Carrie picture 3


There is a Schistosomiasis Control Initiative (SCI) based out of London which is attempting to implement schistosome control methods in areas that are endemic. A study done in Burkina Faso showed that a single mass treatment with Praziquantel was shown to decrease the prevalence of S. haematobium by 84% in girls and 78% overall for up to 2 years. The WHO has a strategy of mass drug administration (MDA) in which school aged children in areas that have a greater than 10% prevalence of schistosomiasis would receive Praziquantel on a biannual basis, and areas that have greater than 50% prevalence would receive treatment on an annual basis. Treatment with Praziquantel results in a parasitological cure but will not heal genital lesions that have already developed from a S. haematobium infection. For this reason, prophylactic treatment starting at a young age is crucial in using this method as a means to decrease HIV prevalence.
It only costs about 32 cents to treat one child with Praziquantel. In most developing countries Praziquantel is distributed through bulk sales to the government. From there, the government dispenses its allotted Praziquantel out to different programs. The organizations that supply developing countries with Praziquantel include UNICEF and the World Health Organization among many other international organizations. Data has shown that a schistosomiasis infections increase susceptibility to HIV, elevate viral replication, exacerbate immunosuppression and increase transmission of HIV. Due to these findings, greater emphasis on schistosomiasis control is being pursued as a means of decreasing the ever growing HIV/AIDS prevalence in Africa. Widespread distribution of Praziquantel to schoolchildren in countries endemic to both schistosomiasis and HIV/AIDS could potentially prevent 120,000 new cases of HIV/AIDS in the next decade.

If treatment with Praziquantel for one child costs $0.32, then treating 70 million children would cost $22 million for one year. If a 10 year plan was implemented that treated every one of those 70 million children biannually, that would cost approximately $112 million. Compare that with the $18.8 billion that has been proposed to be spent over the next 5 years by the U.S. President’s Emergency Plan for AIDS Relief (PEPFAR). The cost of treating 70 million children for schistosomiasis over a 10 year span is dwarfed by the projected costs of the PEPFAR and could potentially make a significant change in the rising trend of HIV infections in Africa.
All of the research points towards mass treatment with Praziquantel as being the most cost effective and successful method of decreasing the number of schistosomiasis infections and HIV/AIDS transmission. The cooperation between HIV and schistosomiasis control programs is critical in ensuring the success of such a program. Combatting two of Africa’s top health concerns with one simple low cost medication would do wonders for lowering the morbidity and mortality rates of many African countries.

“HIV and AIDS Statistics: Worldwide.” Statistics: Worldwide. AmfAR, Nov. 2012. Web. 10 June 2013. <>.
Hotez PJ, Fenwick A (2009) Schistosomiasis in Africa: An Emerging Tragedy in Our New Global Health Decade. PLoS Negl Trop Dis 3(9): e485. doi:10.1371/journal.pntd.0000485
Hotez, Peter J., Alan Fenwick, and Eyrun F. Kjetland. “Africa’s 32 Cents Solution for HIV/AIDS.” PLoS Neglected Tropical Diseases 3.5 (2009): E430. Print.
“International Strategies for Tropical Disease Treatments – Experiences with Praziquantel – EDM Research Series No. 026: Chapter 5: The International Supply of Praziquantel*: Global Distribution of Praziquantel.”

International Strategies for Tropical Disease Treatments – Experiences with Praziquantel – EDM Research Series No. 026: Chapter 5: The International Supply of Praziquantel*: Global Distribution of Praziquantel. World Health Organization, 2013. Web. 10 June 2013.
Kosinski, Karen C., Kwabena M. Bosompem, Miguel J. Stadecker, Anjuli D. Wagner, Jeanine Plummer, John L. Durant, and David M. Gute. “Diagnostic Accuracy of Urine Filtration and Dipstick Tests for Schistosoma Haematobium Infection in a Lightly Infected Population of Ghanaian Schoolchildren.” Acta Tropica 118.2 (2011): 123-27. Print.
“Schistosomiasis.” World Health Organization. Web. 10 June 2013. <>.
“Schistosomiasis: Epidemiological Situation.” World Health Organization. N.p., n.d. Web. 10 June 2013. <>.
Secor, Evan W. “The Effects of Schistosomiasis on HIV/AIDS Infection, Progression, and Transmission.” Current Opinions on HIV and AIDS 7.3 (2012): 254-59. Print.
Simon, Gregory. “Combined Schistosomiasis and HIV Control Programs: Saving Lives AND Money”. End the Neglect. N.p., 7 May 2013. Web. 11 June 2013. <>.
“South Africa: ‘Over 25% of Schoolgirls HIV Positive'” BBC News. BBC, 14 Mar. 2013. Web. 10 June 2013. <>.
Temple, Bliss. Schistosoma Haematobium (blood Flukes). Schistosomiasis Haematobium (blood Flukes). Stanford University, May 2004. Web. 10 June 2013. <>.

“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.”

Obstetric fistula as a neglected tropical disease

Mahabouba*, age 14, was sold into a marriage as a second wife to a man 50 almost years her senior. Raped and beaten repeatedly, she ended up pregnant, finally succeeding in running away 7 months into her pregnancy. Fleeing to the nearby town, she found that the people there threatened to return her to her husband, so she ran back to her native village in Ethiopia. However, her immediate family no longer lived there. An uncle eventually took pity on her and provided her with housing. When Mahabouba went into labor, lacking resources, she tried to deliver her baby herself. Her pelvis was still too small for the baby’s head to pass through, and she ended up in obstructed labor for 7 days before a birth attendant was finally called in to assist. By this point, the tissue of between the baby’s head and Mahabouba’s pelvis had become necrotic due to lack of blood flow. The baby was stillborn and Mahabouba had developed a fistula–a hole had formed between the tissue in her vagina and her rectum. She had no control of her waste elimination, and couldn’t even stand up due to damage to her nerves.

Her uncle wanted to help her, but the common belief was that women who experienced such tragedies were cursed by God. She was moved to a hut at the edge of the village and left to fend for herself against circling hyenas. Eventually, still unable to use her legs, she crawled to another village searching for help. Found by a missionary, she was taken to the Addis Ababa fistula hospital. The damage to her body was too severe to completely fix, but she received a colostomy which allowed her to at least live in society, and eventually she became a nurse’s aide at the hospital.

Mahabouba’s story, on the grand scale of things, is a success story. It’s estimated that up to 3.5 million women currently suffer from fistulas, with somewhere from 50,000 to 130,000 new cases each year–and most of them go untreated. Because many of these happen in rural areas lacking health care providers, it’s difficult to get at exact numbers, and there is little push to obtain them. A woman quoted in Kristof and WuDunn’s “Half the Sky,” an Australian gynecologist who has worked in Ethiopia for more than 30 years, notes that women with fistulas “are the women most to be pitied in the world…They’re alone in the world, ashamed of their injuries. For lepers, or AIDS victims, there are organizations that help. But nobody knows about these women or helps them.”

A new paper aims to change that. Out today in PLoS Neglected Tropical Diseases, Dr. L. Lewis Wall of Washington University in St. Louis argues that obstetric fistula should be included among the neglected tropical diseases (NTDs), which currently include a variety of infectious conditions. NTDs typically are present in warmer climates, and they disproportionately affect the “bottom billion” of the world’s population–the poorest of the poor. They also lack attention from the research community, particularly when it comes to funding priorities.

Though obstetric fistula isn’t an infectious disease, it certainly fits the other parameters for a NTD. “The emphasis on infectious diseases has meant that other important forms of morbidity and mortality have been neglected,” explained Wall via email. “Surgical services are not high on the list of most public health interventions and infectious disease specialists and public health workers are, in general, ill-equipped to deal with surgical issues or obstetric issues. This would mean focusing attention on a huge category of human need that is also neglected as are the traditonal NTDs and could mean a significant uptick in funding for programs to deal with maternal health generally, and obstructed labor/obstetric fistula particularly.”

Indeed, history has shown that obstetric fistulas are fairly easy to prevent and treat, given the proper medical personnel and training. Once common in the United States (the Waldorf-Astoria hotel in Manhattan sits on the site of the first fistula hospital in the U.S.), Wall points out that they are now rare enough here that they merit case reports in the medical literature. Why are they so uncommon? Primarily, very few women in the U.S. are so unattended in childbirth that they would go days in labor without intervention. Rather, most would have a Cesarean section to remove the baby and thus the fistula wouldn’t develop in the first place. Access to this intervention is severely lacking in women in developing countries. “The Cesarean rate in the United States is over 30% (for various reasons) but in many African countries, the rate is less than 1%; well below the 6% needed to meet minimal maternal health needs,” points out Wall.

For women who do develop fistulas, surgical treatment has a high success rate–and is cheap. One of the tragedies of obstetric fistula is that the surgery to treat the injury in many cases costs only around $420–for less than the cost of a fancy TV, you could give a woman back her life. Still, that’s far above what most women in developing countries can afford to pay. Furthermore, even if every woman could afford treatment, “the surgical capacity to treat current fistula cases is woefully inadequate; probably only 10,000 cases per year, with 3-10 times that many new cases,” says Wall.

Unfortunately, there are painfully few treatment centers in developing counties. In addition to the facility in Ethiopia, Dr. Wall is also one of the founders of the Danja fistula center in Niger, which opened its doors earlier this year. There are others scattered throughout continent, but given the rarity of surgical expertise and the frequency of obstetric fistula, the need far outpaces the personnel available. Nevertheless, early attention and surgical intervention are both needed. Wall notes, “The most important thing is identifying prolonged labor and intervening before a fistula develops. There are pilot studies using village health workers to identify women who do not delivery in a timely fashion and to route them to centers for more advanced obstetric care, but these are few and far between. There are programs to train emergency medical technicians who can perform Cesarean sections without being fully qualified doctors; there has been some success with this. With rare exceptions, however, fistula surgery requires surgical skill, long training and experience, so healthcare systems must develop the capacity to perform this kind of work, even when patients are not popular or wealthy enough to ‘pay’ for services.”

While obstetric fistula mirrors many other NTDs, there is one way it is also unique–it affects women solely, and particularly very young women (age 12-14) whose bodies have not developed enough to safely bear children. Maternal health is already a sorely underfunded area of research. Every day, even in 2012, 800 women die from causes related to pregnancy and childbirth, and 99% of those are in developing countries, particularly in rural areas. A midwife working in Ethiopia and quoted in “Half the Sky” lamented, “If this happened to men, we would have foundations and supplies coming in from all over the world.” The inclusion of obstetric fistula into the umbrella of NTDs could open up new funding streams and awareness, and bring us one step closer to this goal.

*Mahabouba’s story is told in “Half the Sky” by Nicholas Kristof and Sheryl WuDunn, pages 93-97, as well as in this New York Times article. Other women’s stories can be found at this site.

Works cited and further reading

Wall, LL (2012). Obstetric Fistula Is a “Neglected Tropical Disease” PLoS Neglected Tropical Diseases, 6 (8) Link

Kruk et al. (2007) Economic evaluation of surgically trained assistant medical officers in performing major obstetric surgery in Mozambique. BJOG.

White et al. (1987) Emergency obstetric surgery performed by nurses in Zaïre. Lancet.

Wilson et al. (2011) A comparison of clinical officers with medical doctors on outcomes of caesarean section in the developing world: meta-analysis of controlled studies. BMJ.

Kristof and DuWunn (2009). Half the Sky: Turning Oppression into Opportunity for Women Worldwide. Knopf, New York.

Ebola: Back in the DRC

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.

Pigs with Ebola Zaire: a whole new can o’ worms

Ebola has long been associated with wildlife. From the early days, bats were viewed as a potential reservoir (though it wasn’t confirmed that they actually harbored the virus until 2005). Contact with wild animals–particularly primates which were butchered for food–was also long thought to be a risk factor, and now we know that primates can become ill with Ebola and pass the virus to humans.

What hadn’t been examined until 2008 were pigs. I mean, it’s not exactly the animal you associate with central Africa, where many of the Ebola cases have been concentrated. However, pigs are much more plentiful in the Philippines, where another Ebola subtype–Ebola Reston–is thought to lurk. The Reston strain actually was first documented in the United States, where twice it was associated with outbreaks in primates originating from the Philippines. When the facility in the Philippines was closed down in 1997, Reston disappeared for 11 years–until it surfaced in pigs in 2008.

The ecology of Ebola Reston in the Philippines isn’t known–unlike African Ebola strains (and their cousin, Marburg), no bats have been caught in that country and tested positive for the virus, though they probably serve as a reservoir of the virus in the Philippines just as they do in Africa. So it was a huge surprise when pigs from that country tested positive for Ebola Reston–and so did 6 of their human caretakers, suggesting cross-species transmission. (I should note here that the Reston strain has yet to be linked to any symptomatic infections in humans–the pig farmers who tested positive probably had no idea they’d been infected and did not show any clinical signs of illness). Pigs hadn’t previously been linked to any Ebola infection, so this brought in a whole other wrinkle when it came to Ebola transmission–the possibility of being exposed to Ebola via contaminated food, and the potential for pig populations to harbor the filovirus (and transmit it to their caretakers, as we have seen with outbreaks of Nipah and Hendra viruses).

A new study delves further into Ebola in pigs. Instead of using the Reston strain, they use the much-more-deadly Zaire strain. This is the one that movies are made about; the one which can cause outbreaks so nasty that they kill up to 90% of those who are infected. Why use Zaire instead of the Reston strain–the one which has actually infected pigs in nature? Well, the researchers wanted to find an animal that’s easier to work with than primates (there are all kinds of very strict regulations when it comes to working with non-human primates), so if pigs could work as a good model for human Ebola disease, that would make studying the virus just a bit easier. (In any case, for any live Ebola work, it still needs to be done in a biosafety level 4 environment, meaning complete spacesuits and the whole works).

The authors did 2 studies. In the first, they inoculated 6 pigs with Ebola Zaire, via a combination of intranasal, intraocular, and oral routes of infection. (Interestingly, no injection, which can be a key way Ebola is spread). They had an additional 2 pigs that they inoculated the same way with a saline solution, and housed them separately from the Ebola-inoculated animals. The goal of this experiment was to look at the pathogenesis of a virulent Ebola strains in the pig model. The infected animals all developed fevers and respiratory disease, with some internal hemorrhaging and evidence of airway replication by Ebola. Infectious virus was found at low levels in nasal washes and oral and rectal swabs; one animal also had a low level of virus in the blood. Higher levels of virus were found in various organs, including the heart and bladder, while the highest levels were found in lung tissue.

In the second experiment, they inoculated 3 new pigs in the same fashion, but then added in 4 additional (uninoculated) animals to stay with them, and kept 2 additional control animals in a separate area so that they could investigate pig-to-pig transmission of the virus. They did find viral RNA from the mucosa of all contact animals, and infectious virus was detected from 2 of 4, demonstrating that the virus can be passed among pigs. Not stated in the article was if the authors thought this was due to direct contact with respiratory secretions among the pigs, or via airborne transmission (a much more concerning route of transmission, as in humans, Ebola Zaire doesn’t seem to transmit well via air–typically it’s spread via close direct contact and bodily fluids).

Notably, pigs didn’t seem to develop severe systemic disease from Ebola, as primates do–the main symptoms exhibited were respiratory, which the pathology supports (finding little virus in the blood, but a lot in the lungs). This suggests that even for Ebola Zaire, infection in a pig could be mistaken for other respiratory diseases, such as influenza or PRRS virus (porcine respiratory and reproductive syndrome virus, which the initial pigs in the Phillipenes were co-infected with). So, Ebola may be circulating even more than we realize in the pig population, disguised by its commonplace symptoms.

A commentary published in tandem with the research article ponders the issue of foodborne Ebola, suggesting that this is a remote possibility and noting that butchering infected animals in the wild in Africa has certainly spread the virus. However, solely eating meat as a means of infection hasn’t been reported, and cooking likely destroys any risk (similar to influenza viruses). Like influenza virus, Ebola doesn’t seem to survive long in most environments, but it’s also noted that differences in African food storage (with little refrigeration) versus more typical cold storage may affect that as a risk factor, possibly prolonging the life of the virus when held in the cold. I think foodborne transmission is unlikely, but it can’t be completely ruled out right now.

Because of the respiratory symptoms, does this mean Ebola could enter the population via meat from animals that farmers don’t consider very ill, or put butchers at a heightened risk of infection during slaughter? This to me is more concerning than simple foodborne transmission. With Reston, at least no human symptoms have been observed, but if pigs (and potentially other animals?) can present with Ebola Zaire as a rather generic respiratory infection…well, that could spell trouble in a lot of different ways. It means that telling individuals to simply avoid sick-looking primates (and bats) is going to be even more woefully inadequate than it already is. Plus, it raises the remote-but-not-completely-outside-the-realm-of-possibility of someone intentionally spreading the virus via animals that are infected in this manner.

Science fiction? Maybe. Probably. Hopefully. But this research opens the door on many new lines of investigation and once again, raises even more questions.

Kobinger GP, Leung A, Neufeld J, Richardson JS, Falzarano D, Smith G, Tierney K, Patel A, & Weingartl HM (2011). Replication, Pathogenicity, Shedding, and Transmission of Zaire ebolavirus in Pigs. The Journal of infectious diseases PMID: 21571728

Ebola in Uganda: current and past outbreaks

Via H5N1 and other sources, there’s at least one new Ebola case in Uganda:

The rare and deadly Ebola virus has killed a 12-year-old Ugandan girl and health officials said on Saturday they expected more cases.

The girl from Luwero district, 75 km (45 miles) north of the capital Kampala, died on May 6, said Anthony Mbonye, the government’s commissioner for community health, in the first outbreak of the virus in Uganda in four years.

“Laboratory investigations have confirmed Ebola to be the primary cause of the illness and death. So there is one case reported but we expect other cases,” he said.

Though we’ve known about Ebola in Africa since 1976, Ebola wasn’t recognized in Uganda until a bit over 10 years ago. Now, this is the third outbreak in this amount of time. 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.

I couldn’t find any other details about the current outbreak–how she was infected, if she’s actually the index case or if there were previous deaths that have not yet been confirmed. (The girl died at the hospital–previous deaths may have gone unrecognized if they had died at home). I’m sure more details will be coming in the next days and weeks. What we’re left with now is the knowledge that in 11 years’ time, Uganda is now on its third Ebola outbreak. These have occurred in 3 different areas of the country (Gulu is toward the north, Kampala region in the south near Lake Victoria, and Bundibugyo in the southwest, almost due west of Kampala) and with 2 different strains (thus far). This again feeds my morbid fascination with the virus–what does this mean about Ebola reservoirs in Uganda? Are these cases bat-acquired? Other wildlife? Spillover from other countries, as suggested with the 2000-1 outbreak? As always, Ebola outbreaks tend to raise more questions than they answer.

[UPDATE: via Crawford Killian, CDC says current outbreak is due to Sudan strain.]