Ending Schistosomiasis

Box 1: Neglected Tropical Diseases Neglected tropical diseases bring suffering and death to many millions around the world, but receive very little attention in developed countries. Rather than threatening prosperous and well-informed citizens of nations with good medical services, they attack some of world’s poorest people, who live in isolated rural villages, crowded refugee camps, and urban slums that lack health care, sanitation, and safe water. And not only do these diseases thrive among the poor, they actually promote poverty by weakening, maiming, stigmatizing, and isolating their victims and destroying their ability to work, learn, and contribute to their families and communities. Even more shocking, however, these diseases have well-known, inexpensive, and effective treatments. They exact their terrible toll only because of the world’s neglect and inattention. In addition to schistosomiasis, DCPP is spotlighting two other neglected tropical diseases and the steps that can end the suffering they cause. One of them, trachoma, the major infectious cause of blindness, has already been covered in a feature story (click to read "The End of Blinding Trachoma Among the World's Poor Is in Sight"). The other, leishmaniasis, which brings disfigurement and death, will be covered in a future article. b>

A Disease of Poverty
The resources needed to control schistosomiasis must be considerable. The disease is endemic in 74 countries, with more than 200 million people infected in rural areas and urban slums, according to the World Health Organization. Twenty million suffer severe, disabling, and sometimes fatal effects. Another 120 million have less severe but significant symptoms. Some 85 percent of the infected are in sub-Saharan Africa and an estimated 650 million people overall live in areas with endemic disease. In many such places, schistosomiasis affects a large percentage of children under 14, causing long-term developmental effects.^viii   

In Africa, as throughout the world, according to Susan Watts of the American University in Cairo, schistosomiasis is a “disease of poverty.” Its victims typically lack access to health services, safe water, and education. Furthermore, the disease helps keep them poor by lessening their ability to work, learn, and contribute to their communities.^ix  Most commonly affected are people whose daily activities, such as fishing, washing clothes, farming in irrigated fields, or swimming, bring them into contact with river, lake, or canal water contaminated by the feces or urine of infected people or animals. Even a small number of infected individuals can threaten an entire community with contamination. “The particular dynamics of schistosomiasis transmission, and the need for treatment,” Watts writes, makes the disease’s presence “an indicator of poverty.”^x
 
Schistosomiasis is an infection by flatworms of the genus Schistosoma. These worms inhabit freshwater rivers, lakes, and canals in many parts of the world. After entering the body of a person in contact with contaminated water, they make their way into blood vessels and remain there for years. Five main species cause human disease; each species prefers the vessels of particular organs, where they can cause extensive damage over time. The specific form that the disease takes and the particular harm it inflicts depends on the type of worm involved.  
 
Schistosoma haematobium, found in Egypt and in other parts of Africa and the Middle East, infects the rectum and especially the bladder, causing urinary schistosomiasis, with its characteristic bloody urine. The related S. intercalatum, common in central Africa, affects the spleen, liver, and intestines, causing digestive symptoms and liver disease. S. mansoni, endemic in parts of Africa and the Middle East, as well as in the Caribbean and South America, also causes intestinal disease. Other forms of intestinal schistosomiasis result from S. japonicum, found in China, Southeast Asia, and the western Pacific, and from the closely related S. mekongi of the Mekong Delta in Cambodia and Laos. Japonicum has the further complication of also infecting domesticated animals including cattle, water buffalo, dogs, and pigs. Dogs can also be infected by mekongi.^xi 

Once ensconced in their organs of choice, mated female worms produce a steady stream of eggs, many of which exit their victims’ bodies in urine or feces. If these eggs reach fresh water, they quickly transform into tiny swimming larvae that seek out a particular species of snail as a temporary host. Each species of schistosome has adapted to exploit a particular species of freshwater snail.
 
The larvae that succeed in penetrating a snail then begin a series of transformations.  After several weeks, schistosomes emerge into the water in another larval form capable of swimming for hours or days. Depending on their species, these parasites seek human or other mammalian hosts and continue to mature over two or three months into worms that will live for an average of four to five years.^xii 

The female soon begins laying her eggs, which must pass from the circulatory system through the victim’s tissues in order to reach the bladder or intestines and leave the body. More than half of the eggs never make that passage, however. Instead, they become trapped within the host’s organs, where irritation and inflammation occur as the host’s immune system reacts to the presence of foreign bodies. Over time, this can produce scarring and other damage that may become severe and even fatal, depending on the organs involved and the extent of the harm. 
 
Reversing this damage may be possible early in the disease if the infection is controlled. However, damage eventually becomes permanent even if the original infection is cured. Advanced schistosomiasis, depending on the specific type, can cause intestinal obstruction and deform and even destroy the bladder, kidneys, liver, spleen, and genital organs of both males and females. It greatly increases both the risk of bladder cancer and susceptibility to HIV and other sexually transmitted diseases.^xiii   Early and heavy infection with japonicum b can also cause Katayama fever, characterized by fever, rash, enlarged spleen and liver, bronchial spasms, and perhaps even permanent neurological damage.^xiv

Along with risk to organs, all schistosomiasis victims also suffer subtle harm that can include “impaired cognitive performance, chronic fatigue, and unremitting pain” and contributes to “increased school absenteeism, reduced worker productivity, lowered self esteem, and social exclusion,” notes the World Health Organization.^xv     This occurs even in individuals with relatively light infections and long before organ damage becomes apparent, because the chronic inflammation from the presence of the eggs brings its own harmful consequences. For example, anemia is one of the effects “most firmly associated with schistosomiasis in all its forms,” according to King and Madeline Dangerfield-Cha of Columbia University. “Even light schistosome infection,” they note, is associated with “stunted growth and undernutrition in affected children.” One study showed that Chinese children successfully treated for S. japonicum infection quickly gained “significant” weight. Perhaps more significant, research connects stunting and undernutrition to lower earnings later in life. In addition to affecting learning among 7-to-18-year-olds,” schistosomiasis can impair children’s overall cognitive development.^xvi  

King and Dangerfield-Cha find strong evidence for “a significant long-term carryover effect of childhood schistosomiasis into adult years.”^xvii   Although attention has traditionally focused on the more severe effects, it is now clear that “the years of life lost to schistosomiasis probably account for a very small proportion of the overall DALYs lost to [the disease] compared with the years lost to disability,” note King and co-authors.^xviii

Spreading at a Snail’s Pace
Because the schistosomes must survive both in human (or other mammal) victims and in snails, the disease can only spread in areas where the right mollusks live. Conditions that expand those areas therefore expand the infection’s reach. Schistosomiasis had always affected some of Egypt’s poor, but it became a much greater problem after 1821, when the advent of perennial irrigation boosted agricultural production, the size of the population, and the amount of time that workers spent in contaminated water. Large-scale water projects during the 19th and especially the 20th centuries in many countries, along with increasing use of irrigation, multiplied both snail habitats and the number of schistosomiasis sufferers worldwide.

In addition, ecological changes also affect the type of disease that spreads. Egypt’s Aswan High Dam, constructed during the 1960s and 1970s, produced conditions more favorable to the snails used by S. mansoni and less favorable to those used by S. haematobium, resulting in more intestinal and liver disease and less bladder disease.^xix  China’s massive Three Gorges Dam on the Yangtze River brings huge changes in the local ecology. Yue-Sheng Li of the Hunan Institute of Parasitic Diseases and co-authors, predict that the project “will likely substantially extend the range of the snail habitats and increase schistosome transmission and schistosomiasis cases.”^xx   

Other Chinese scientists fear that global warming will expand snail habitats and spread schistosomiasis into regions of northern China previously protected by temperatures too cold for the snail. Already, climate research has revealed an expansion of the annual period conducive to snail survival between 1950 and 2003. “A warming trend is likely to be one of the reasons contributing to the epidemic increase of schistosomiasis in recent years,” states Yu Shenxian of the Zhejiang Meteorological Institute.^xxi   

On the other hand, an absence of appropriate snails protects regions from schistosomiasis. The trans-Atlantic slave trade, for example, carried schistosomes from Africa to the New World in the bodies of enslaved people, but the worms established themselves and the disease spread only in those continental and Caribbean areas with suitable snails.  Lack of snails also explains why human forms of the disease have not spread into much of India.^xxii

Outwitting the Worm 
The role of snails in the schistosome’s life cycle has made eliminating the mollusks from waterways a favored approach in many attempts at disease control. The complicated, multipart lifecycle of the schistosome was worked out by researchers in the early 20th century, after decades of research following the 1851 discovery by Theodor Bilharz, a German physician, that a parasitic worm caused the disease then known as tropical haematuria. Working at the Egyptian Department of Hygiene in Cairo, he autopsied individuals whose intestines, bladders and other organs showed pathological changes and whose veins yielded ‘a long white parasitic worm’ that Bilharz recognized as new.^xxiii  

Public health officials tried various methods of killing the snails before PZQ arrived on the scene in the 1980s, but snail control efforts generally failed to reduce the number of infected people. Effective modern control methods emphasize widespread use of PZQ, either in entire communities or in particular high-risk populations such as school children. Because reinfection after cure is so easy, however, effective control involves coordinated campaigns to provide appropriate sanitary facilities that break the cycle of contamination, such as latrines, and waste containers on fishing boats. Educating people about the importance of sanitation is also key, as is reducing snail concentrations. In japonicum areas where domestic and farm animals also harbor schistosomes, effective control efforts have included removing livestock from places conducive to infection, sometimes by providing machinery to do the traditional work of oxen or buffaloes.^xxiv

The complex relationship among the worm, the snail, and the human or animal host makes schistosomiasis control a challenging goal, but one that a number of countries have accomplished. The 4,000-year story of schistosomiasis in the Nile Valley is nearing its end. Decades of effort by government agencies have reduced haematobium and mansoni infection rates—once nearly half and more than a third of at-risk populations—to under 2 percent.^xxv  From the time when, according to Disease Control Priorities, “nearly every [rural] boy had blood in his urine by the age of 12, and bladder cancer was the commonest cancer in Egypt, the serious health consequences of schistosomiasis have disappeared.”^xxvi  Success in one of the disease’s most ancient homes shows that, with similar effort, schistosomiasis can become history in afflicted countries everywhere.

 Beryl Lieff Benderly is a prize-winning Washington journalist and author specializing in health, behavior, and science policy. Her articles appear in major magazines and on the Internet, and she is a regular contributor to the Science magazine website. Her eight books include In Her Own Right: The IOM Guide to Women’s Health Issues.
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 ⁱ Tan, S.Y., and A. Ahana. 2007. “Theodor Bilharz (1825-1862): Discoverer of Schistosomiasis.” Medical Journal 48 (3): 184.

ⁱⁱ Hotez, P. J., D. A. Bundy, K. Beegle, S. Brooker, L. Drake, N. de Silva, and others. 2006. In Disease Control Priorities in Developing Countries, 2nd ed., ed. D.T. Jamison, J.G. Breman, A.R. Measham, G. Alleyne, M. Claeson, D.B. Evans, P. Jha, A. Mills, and P. Musgrove, 479. New York: Oxford University Press.

ⁱⁱⁱ (a)King, C. H. 2008. “Schistosomiasis Japonica: The DALYs Recaptured.” PLoS Neglected Tropical Disease 2 (3): e203. (b)King, C. H., K. Dickman, and D. J. Tisch. 2005. "Reassessment of the Cost of Chronic Helmintic Infection: A Meta-analysis of Disability-Related Outcomes in Endemic Schistosomiasis.”  Lancet 365: 1561-69.

^iv King, C. H. 2008.

^v Hotez, P. J., D. A. Bundy, K. Beegle, S. Brooker, L. Drake, N. de Silva, and others. 2006. In Disease Control Priorities in Developing Countries, 2nd ed., ed. D.T. Jamison, J.G. Breman, A.R. Measham, G. Alleyne, M. Claeson, D.B. Evans, P. Jha, A. Mills, and P. Musgrove, 471. New York: Oxford University Press.

^vi (a)King, C.H., and M. Dangerfield-Cha. 2008. “The Unacknowledged Impact of Chronic Schistosomiasis.” Chronic Illness 4: 65-79.  (b) van der Werf, M., S. de Vlas, S. Brooker, C. Looman, J. Nagelkerke,  J. Dik, and others. 2003. “Quantification Of Clinical Morbidity Associated With Schistosome Infection In Sub-Saharan Africa ." Acta Tropica 86 (2-3): 125-139.

 View entire URL here at http://www.sciencedirect.com . 

 ^vii King, C. H. 2008.

^viii (a)World Health Organization (WHO). “Schistosomiasis.” 2007. World Health Organization Fact Sheet. http://www.who.int/mediacentre/factsheets/fs115/en/print.html. (b)Watts, Susan. 2007. “The Social Determinants of Schistosomiasis.  Working Paper 11.” Report of the Scientific Working Group Meeting on Schistosomiasis—Geneva 14-16 November 2005.  World Health Organization, Geneva, . http://www.who.int/tdr/publications/tdr-research-publications/swg-report-schistosomiasis/pdf/swg_schisto.pdf

^ix Watts, Susan. 2007.

^x Watts, Susan. 2007.

^xi Stedman’s Medical Dictionary, 25^th Edition.  Baltimore: Williams & Wilkins, 1990

^xii (a)Sandbach, F.R. 1976. “The History of Schistomiasis Research and the Policy for its Control.”  Medical History 20 (3).  (b) King, C.H., and M. Dangerfield-Cha. 2008.

^xiii (a)King, C.H., and M. Dangerfield-Cha. 2008. (b)Bruun, B., and J. Aagaard-Hansen. 2007. “Working Paper 10: The Sociocultural Contest of Schistosomiasis Control: Current Knowledge and Future Research Needs.” Report of the Scientific Working Group Meeting on Schistosomiasis— Geneva 14-16 November 2005. Geneva : WHO. http://www.who.int/tdr/publications/tdr-research-publications/swg-report-schistosomiasis/pdf/swg_schisto.pdf.

^xiv Doherty, J., A. Moody, and S. Wright. 1996. “Lesson of the Week: Katayama Fever: An Acute Manifestation of Schistosomiasis.” British Medical Journal 313: 1071-1072. http://www.bmj.com/cgi/content/full/313/7064/1071.

 ^xv World Health Organization. 2006. Preventive Chemotherapy in Human Helminthiasis. Geneva : WHO. http://whqlibdoc.who.int/publications/2006/9241547103_eng.pdf. 

^xvi World Health Organization. 2006.

^xvii King, C.H., and M. Dangerfield-Cha. 2008.   

^xviii King, C. H., K. Dickman, and D. J. Tisch. 2005. 

 

 

 

 

 

 

 

 

 

^xix El-Khoby, T., and others. 2000. "The Epidemiology of Schistosomiasis in Egypt: Summary Findings in Nine Governorates."  American Journal of Tropical Medicine and Hygiene 62(20)S.  

^xx Li, Yue-Sheng and others. 2007. “Large Water Management Projects and Schistosomiasis Control, Dongting Lake Region, China." Emerging Infectious Diseases.

^xxi Zhiyong, C. 2007. “Scientists: Warming ‘could increase schistosomiasis’.” Science and Development Network. http://www.scidev.net/en/news/scientists-warming-could-increase-schistosomiasi.html.

^xxii Sandbach, F.R. 1976.

^xxiii Tan, S.Y., and A. Ahana. 2007.

^xxiv Wang, L.D., and others.  2009. “A Strategy to Control Transmission of Schistosoma japonicum in .” New England Journal of Medicine 360: 121-8.

^xxv Youssef, Moustafa Mohamed. 2006. “Working Paper 2: Current Situation and Research Needs for Schistosomiasis Control in .”  Report of the Scientific Working Group Meeting on Schistosomiasis— Geneva 14-16 November 2005. Geneva : WHO. http://www.who.int/tdr/publications/tdr-research-publications/swg-report-schistosomiasis/pdf/swg_schisto.pdf.

^xxvi Hotez, P. J., D. A. Bundy, K. Beegle, S. Brooker, L. Drake, N. de Silva, and others. 2006. In Disease Control Priorities in Developing Countries, 2nd ed., ed. D.T. Jamison, J.G. Breman, A.R. Measham, G. Alleyne, M. Claeson, D.B. Evans, P. Jha, A. Mills, and P. Musgrove, 479. New York: Oxford University Press.