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.

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

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

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

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

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

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

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

Works cited

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

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

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

Previous posts in the series

Part 1

Part 2

Part 3

Part 4

“Spillover” by David Quammen

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

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

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

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

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

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.

“Fool Me Twice” by Shawn Lawrence Otto

Science denial, I fear, is here to stay. Almost half of Americans believe in creationism. Anti-vaccination sentiment is going strong, despite record pertussis outbreaks. Academics are even leaving their jobs, in part, because of the terrible anti-intellectual attitude in this country. It’s depressing and demoralizing–so what does one do about it? Shawn Lawrence Otto’s “Fool Me Twice” offers an analysis.

Otto’s book is good stuff. He devotes the first quarter or so of the book to understanding how we got to where we are regarding science denial and anti-science attitudes. It’s a nice introduction, moving from Galileo up to modern day, and covering the intersections of science and religion, as well as the “two cultures” thinking. He uses these chapters to argue that science is inherently political, and that scientists need to engage in the public like in the good ol’ days past. Otto argues that today, partisan politics and shock jocks have pushed us further away from valuing science, and scientists are left wondering what they can do to compete against the money and influence that industry wields.

To do this, Otto creates something of a roadmap. It’s probably suggestions many of us in the field have heard before in publications such as Unscientific America and elsewhere, but it never hurts to hear it again. Engage. Talk to churches and other community organizations. Run for office. Be inclusive and avoid identity politics. Don’t be alarmist. Frame your message. Talk about *how* one does science rather than just the findings and the facts. While this is great stuff, he spends less time discussing the difficulties of actually, y’know, *doing* this as a scientist (though he does talk a bit about the Sagan effect early in the book, and so doesn’t completely ignore the problems that scientists can have when they do more communication and outreach).

Not surprisingly, he also brings up the importance of Science Debate, of which Otto is the CEO. Otto notes that candidates are questioned much more on religious issues than on scientific ones, and Science Debate can serve as a non-partisan platform to get important science questions answered by candidates. In 2008, both candidates did respond to a list of 14 questions. How much did it matter in the long run? Probably not a lot, but at least it did get candidates to think about important scientific issues and put ideas down in writing for the public.

In the end, I found “Fool Me Twice” a thought-provoking but dense book. I also wonder who Otto’s intended audience was. One back-of-the-book blurb reads “Before you vote in the next election, read Shawn Lawrence Otto’s “Fool Me Twice.” Bill Nye’s blurb also enthuses, “Here’s hoping some voters and Congress members take [Otto] seriously–soon.” Nice thought, but I can’t see the average voter picking up this book. There are portions within where even I found difficult to get through–his discussion of post-modernism, for example, probably would be fine for those with more grounding in philosophy and familiarity with its terminology, but again it got me thinking about target audience and how many would be able to connect the dots without giving up on the book at that point (and thereby missing out on a lot of the good stuff to come in later chapters). Maybe I’m too cynical. I do hope, however, that at least a number of scientists–especially those just wading into the waters of communication and science politics–do pick up the book, and dog-ear some of the important pages and suggestions as I have done. Otto has hope for a more scientific American future. I hope he is right.