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Dracunculiasis
SECTION C Other Tissue Nematode Infections
118 Dracunculiasis Donald R. Hopkins
KEY FEATURES • Human dracunculiasis manifests as an ulcer on the skin, with the nematode Dracunculus medinensis protruding through the lesion. • It is an incapacitating disease of poor residents in rural areas without access to safe drinking water. It severely affects agricultural productivity and school attendance. • Infection occurs after ingestion of freshwater copepods or inadequately cooked aquatic animals that contain the larval worm. Acute manifestations begin about 1 year after infection with the formation of a skin blister, accompanied by redness and irritation (burning sensation); this is usually preceded by fever and allergic symptoms, including intense generalized itching. • The intense skin irritation prompts the patient to seek relief by immersing the lesion in water. The blister breaks and an ulcer-like lesion develops with the anterior end of the parasite exposed. This allows the adult female worm to discharge larvae into the water. • Lesions occur on the lower extremities, including the ankle or foot in about 90% of cases, but the parasite can exit from anywhere on the body. • Abscesses can occur if the worm is broken during manual extraction or if they die before exiting the body and calcify. Chronic manifestations of arthritis, synovitis, and muscle and tendon contractures with resultant ankylosis of the limb are rare. • Synonyms include Guinea worm disease, dracontiasis, and dracunculosis.
INTRODUCTION Dracunculiasis is caused by the nematode Dracunculus medinensis, and is a disabling disease of poor rural residents in parts of three countries in Africa.1,2 D. medinensis has been known since ancient Egyptian times, and the life cycle of the parasite was fully described by Alexei Fedechenko in 1870.3 Infection manifests with the emergence through a lesion on the skin of 2- to 3-foot (≈1 m)-long worms; it has an enormous adverse impact on agricultural production and school attendance. Infection is close to being eradicated.
EPIDEMIOLOGY AND ERADICATION During the nineteenth and twentieth centuries, dracunculiasis was common in much of southern Asia and in North, West, and East Africa. The Dracunculiasis Eradication Program began in 1980; in 1986 an estimated 3.5 million cases occurred annually in India, Pakistan, and 16 African countries.4 Transmission of dracunculiasis in Yemen was confirmed during 1994, and the World Health Organization (WHO) declared the Central African Republic to
878
have indigenous transmission in 1996, making it the twentieth endemic country.5 South Sudan, the twenty-first endemic country, became independent of Sudan in 2011. By 2017, only 30 cases were reported, from Chad and Ethiopia (Fig. 118.1).1,2 Disease in Asia was eradicated in 1997. People usually become infected when they drink water containing tiny freshwater copepods called cyclops or water fleas, which act as intermediate hosts and harbor infective larvae.6 Since 2012 there has been increasing evidence of an unusual life cycle of D. medinensis in Chad, involving a paratenic host in fish, frogs, or other aquatic animals and predominately affecting domestic dogs, with occasional infections of humans who eat infected, inadequately cooked aquatic animals.7,8 When ingested copepods are killed by the digestive juices in the stomach, the larvae are released and move to the small intestine, where they penetrate the intestinal wall and migrate to the connective tissues of the thorax.6 Male and female larvae mature and mate 60 to 90 days after infection. Over the next 10 to 14 months, gravid female worms mature, reaching lengths of 70 to 100 cm (2–3 feet), and slowly migrate to the surface of the body (Fig. 118.2), where they become visible through ulceration. On contact with freshwater, powerful contractions cause a loop of the worm’s uterus to break and discharge a swarm of motile larvae. Contraction of the worm and discharge of larvae may be repeated if the lesion is again submerged in water, until the entire brood of larvae is discharged. Motile free-swimming larvae are ingested whole by copepods and mature in the body cavity in about 2 weeks. Stagnant sources of drinking water such as ponds; cisterns; pools in dried-up river beds; and shallow, unprotected, hand-dug wells commonly harbor copepods and are the usual sites of infection transmission. Seasonality varies according to location. In endemic countries in the Sahel area of Africa (Chad, Ethiopia, South Sudan), transmission usually peaks during the rainy season at mid-year (May– September). This is because stagnant surface sources of water are more common in these areas during the 5- to 6-month-long rainy season. The seasonal emergence of the worm often coincides with harvest or planting seasons, and thus significantly affects agricultural productivity and school attendance. Most cases usually occur in older children and working-age adults.
NATURAL HISTORY, PATHOGENESIS, PATHOLOGY, AND CLINICAL FEATURES Infected people remain asymptomatic for approximately a year after infection, until the mature female worm approaches the skin and forms a painful papule in the dermis. This papule can become a blister within 24 hours or may enlarge for several days before blistering (Fig. 118.3). The blister is accompanied by redness and induration, and is usually preceded by systemic symptoms of low-grade fever and allergic symptoms (erythema, urticarial rash, intense pruritus, dizziness, nausea, vomiting). The lesion produces intense irritation and burning, inducing the patient to seek relief by immersing the affected limb in water, where the blister breaks, allowing the adult worm to discharge larvae into the water (Fig. 118.4). Eighty to ninety percent of lesions occur on the lower extremities, including the ankle or foot. However, worms can exit from
879
CHAPTER 118 Dracunculiasis
Guinea Worm Reduction Over Time
1986
118
2017
Fig. 118.1 Guinea worm reduction from 1986 to 2017.
4
1 Emerging worm
2
Copepods First-stage larve
3 Fig. 118.2 Life cycle of Dracunculus medinensis. (Courtesy, Encyclopedia Britannica, Inc., © 1996.)
Third-stage larve
880
PART 6 Helminthic Infections
Fig. 118.3 Blisters caused by Dracunculus medinensis and rupture of blisters resulting in skin lesions with protruding Guinea worms. (Courtesy, Elizabeth Long, The Carter Center.)
anywhere on the body, including the head, upper extremities, buttocks, and genitalia. More than one worm may emerge from a given patient either simultaneously or sequentially over a period of weeks or months. As the worm emerges through the skin lesion, the affected person pulls it out slowly and carefully (because of inflammation and pain), usually by winding a few centimeters of the worm each day on a small stick. This very painful process may last many weeks. Pain and other symptoms may lessen with the rupture of the blister, but pyogenic organisms invariably invade the superficial lesion and worm tract and aggravate the condition (see Fig. 118.4). If the worm breaks during extraction and the remaining part retracts into the tissue, an intense inflammatory reaction occurs, with pain, swelling, and cellulitis along the worm tract and usually the formation of an abscess. The reported period of incapacitation ranges from 2 to 16 weeks (average 8.5 weeks)9–16 and more than half of a village’s population may be affected at the same time. In addition to the blisters and skin lesions, secondary bacterial infections can lead to sepsis, abscesses, septic arthritis, contracture of muscles near joints, or even tetanus.17 Chronic manifestations are due to inflammation of the joints, with signs and symptoms of arthritis, synovitis,18 and muscle and tendon contractures with resultant ankylosis of the limb.19 Migration of the worms to the retroperitoneum and from the retroperitoneum to the subcutaneous tissue in the leg sometimes results in aberrant (ectopic) locations such as the pancreas, lung, periorbital tissues, testis, pericardium,20 and the spinal cord, producing compression21 as well as focal abscess formation.
PATIENT EVALUATION, DIAGNOSIS, AND DIFFERENTIAL DIAGNOSIS No serodiagnostic tests are available to detect an incubating Guinea worm. Diagnosis is based on the clinical history and findings with an appropriate exposure. The blister fluid is bacteriologically sterile and initially contains polymorphonuclear leukocytes and later lymphocytes, eosinophils, and macrophages. Larvae are always present in the fluid, and white blood cells adhere to them.6 With time, the blister and worm tract often become secondarily infected. Differentiation between human and zoonotic species of Dracunculus (which rarely affect humans) requires morphologic
Fig. 118.4 Pyogenic organisms invade the superficial lesion and worm tract, aggravating the condition. (Courtesy, The Carter Center.)
examination of adult male worms (which are rarely available). Therefore efforts are underway to map the genome of the Guinea worm’s DNA in order to ascertain the infecting parasite’s species. Although there are several zoonotic species of Dracunculus, only medinensis is specific to humans. A molecular tool is now available to differentiate between D. medinensis and other tissue-dwelling nematodes, including other Dracunculus species that may rarely infect humans.22 Work on determining the genome of D. medinensis is ongoing at the Centers for Disease Control and Prevention, Wellcome Trust Sanger Institute, and Vassar College (Eberhard ML, personal communication).
TREATMENT There is no curative drug or vaccine against dracunculiasis. Infected people do not develop immunity. Applying wet compresses to the lesion may relieve pain during the worm’s emergence. Placing an occlusive bandage on the wound keeps it clean and may help to keep the patient from contaminating sources of drinking water. Oral analgesics and anti-inflammatory medicines can be administered to alleviate pain and inflammation. Topical antiseptics or antibiotic ointment may minimize the risk of secondary bacterial infections, reduce inflammation, and permit removal of the worm by gentle traction over a number of days. Systemic antibiotics can be used in established infections. Patients usually recover completely, but repeated infections occur.
PREVENTION Prevention of dracunculiasis includes educating the at-risk population about the disease and avoidance measures. These measures include filtering drinking water to remove copepods, preventing infected people from entering water intended for drinking, cooking aquatic animals well, and tethering infected dogs. Developing safe sources for drinking water is also a key feature of control.
REFERENCES
1. Hopkins DR, Ruiz-Tiben E, Weiss AJ, et al. Progress toward global eradication of dracunculiasis — January 2017–June 2018. MMWR Morb Mortal Wkly Rep 2018;67:1265–70. 2. World Health Organization. Dracunculiasis eradication: global surveillance summary 2017. Wkly Epidemiol Rec 2018;93:305–20. 3. Fedchenko AP. Concerning the structure and reproduction of the Guinea worm (Filaria medinensis L.). Proceedings of the Imperial Society of the Friends of Natural Sciences, Anthropology, and Ethnography. Vol 8 (in Russian), 1870, Reprinted in. Am J Trop Med Hyg 1971;20: 511–23. 4. Watts SJ. Dracunculiasis in Africa: its geographical extent, incidence, and at-risk population. Am J Trop Med Hyg 1987;37:119–25. 5. World Health Organization. Dracunculiasis: global surveillance summary: 1996. Wkly Epidemiol Rec 1997;72:133–9. 6. Muller R. Dracunculus and dracunculiasis. Adv Parasitol 1971;6:73–151. 7. Eberhard ML, Ruiz-Tiben E, Hopkins DR, et al. The peculiar epidemiology of dracunculiasis in Chad. Am J Trop Med Hyg 2014;90:61–70. 8. Eberhard ML, Yabsley MJ, Zirimwabagabo H, et al. Possible role of fish and frogs as paratenic hosts of Dracunculus medinensis in Chad. Emerg Infect Dis 2016;22:1428—30. 9. Belcher DW, Wurapa FK, Ward WB, et al. Guinea worm in southern Ghana: its epidemiology and impact on agricultural productivity. Am J Trop Med Hyg 1975;24:243–9. 10. Khan HD, Aminuddin M, Shah CH. Epidemiology and socio-economic implications of dracunculiasis in eleven rural communities of District Bannu (Pakistan). J Pakistani Med Assoc 1986;36:233–9. 11. Smith GS, Blum D, Huttley SRA. Disability from dracunculiasis: effect on mobility. Ann Trop Med Parasitol 1989;83:151–8.
CHAPTER 118 Dracunculiasis
881
12. Watts SJ. Guinea worm: an in depth study of what happens to mothers, families, and communities. Soc Sci Med 1989;29:1043–9. 13. Adeyeba OA, Kale OO. Epidemiology of dracunculiasis and its socioeconomic impact in a village in south-west Nigeria. West Afr J Med 1991;10:208–15. 14. Ilegbodu VA, Ilegbodu AE, Wise RA, et al. Clinical manifestations, disability, and use of folk medicine in dracunculiasis in Nigeria. J Trop Med Hyg 1991;94:35–41. 15. Chippaux JP, Benzou A, Agbede K. Social and economic impact of dracunculiasis: a longitudinal study carried out in two villages in Benin. Bull World Health Organ 1992;70:73–8. 16. Rhode JE, Sharma BL, Patto H, et al. Surgical extraction of Guinea worm: disability reduction and contribution to disease control. Am J Trop Med Hyg 1993;48:71–6. 17. Adeyeba OA. Secondary infections in dracunculiasis: bacteria and morbidity. Int J Zoonoses 1985;12:147. 18. Robineau M, Sereni D. Arthrite aiguë du genou avec presence intraarticulaire de microfilaires de D. medinensis. Évolutions clinique et immunologique compares. A propos d’un cas. Bull Soc Pathol Exot Filiales 1978;71:85–9. 19. el Garf A. Parasitic rheumatism: rheumatic manifestations associated with calcified Guinea worm. J Rheumatol 1985;12:976–9. 20. Kinare SG, Parulkar GB, Sen PK. Constrictive pericarditis resulting from dracunculosis. Br Med J 1962;1:845. 21. Odaibo SK, Agowun IA, Oshagbemi K. Paraplegia complicating dracontiasis. J R Coll Surg 1986;31:376–8. 22. Bimi L, Freeman AR, Eberhard ML, et al. Differentiating Dracunculus medinensis from D. insignis, by the sequence analysis of the 18S rRNA gene. Ann Trop Med Parasitol 2005;99:511–17.
118
118 Dracunculiasis Donald R. Hopkins
KEY FEATURES • Human dracunculiasis manifests as an ulcer on the skin, with the nematode Dracunculus medinensis protruding through the lesion. • It is an incapacitating disease of poor residents in rural areas without access to safe drinking water. It severely affects agricultural productivity and school attendance. • Infection occurs after ingestion of freshwater copepods or inadequately cooked aquatic animals that contain the larval worm. Acute manifestations begin about 1 year after infection with the formation of a skin blister, accompanied by redness and irritation (burning sensation); this is usually preceded by fever and allergic symptoms, including intense generalized itching. • The intense skin irritation prompts the patient to seek relief by immersing the lesion in water. The blister breaks and an ulcer-like lesion develops with the anterior end of the parasite exposed. This allows the adult female worm to discharge larvae into the water. • Lesions occur on the lower extremities, including the ankle or foot in about 90% of cases, but the parasite can exit from anywhere on the body. • Abscesses can occur if the worm is broken during manual extraction or if they die before exiting the body and calcify. Chronic manifestations of arthritis, synovitis, and muscle and tendon contractures with resultant ankylosis of the limb are rare. • Synonyms include Guinea worm disease, dracontiasis, and dracunculosis.
INTRODUCTION Dracunculiasis is caused by the nematode Dracunculus medinensis, and is a disabling disease of poor rural residents in parts of three countries in Africa.1,2 D. medinensis has been known since ancient Egyptian times, and the life cycle of the parasite was fully described by Alexei Fedechenko in 1870.3 Infection manifests with the emergence through a lesion on the skin of 2- to 3-foot (≈1 m)-long worms; it has an enormous adverse impact on agricultural production and school attendance. Infection is close to being eradicated.
EPIDEMIOLOGY AND ERADICATION During the nineteenth and twentieth centuries, dracunculiasis was common in much of southern Asia and in North, West, and East Africa. The Dracunculiasis Eradication Program began in 1980; in 1986 an estimated 3.5 million cases occurred annually in India, Pakistan, and 16 African countries.4 Transmission of dracunculiasis in Yemen was confirmed during 1994, and the World Health Organization (WHO) declared the Central African Republic to
878
have indigenous transmission in 1996, making it the twentieth endemic country.5 South Sudan, the twenty-first endemic country, became independent of Sudan in 2011. By 2017, only 30 cases were reported, from Chad and Ethiopia (Fig. 118.1).1,2 Disease in Asia was eradicated in 1997. People usually become infected when they drink water containing tiny freshwater copepods called cyclops or water fleas, which act as intermediate hosts and harbor infective larvae.6 Since 2012 there has been increasing evidence of an unusual life cycle of D. medinensis in Chad, involving a paratenic host in fish, frogs, or other aquatic animals and predominately affecting domestic dogs, with occasional infections of humans who eat infected, inadequately cooked aquatic animals.7,8 When ingested copepods are killed by the digestive juices in the stomach, the larvae are released and move to the small intestine, where they penetrate the intestinal wall and migrate to the connective tissues of the thorax.6 Male and female larvae mature and mate 60 to 90 days after infection. Over the next 10 to 14 months, gravid female worms mature, reaching lengths of 70 to 100 cm (2–3 feet), and slowly migrate to the surface of the body (Fig. 118.2), where they become visible through ulceration. On contact with freshwater, powerful contractions cause a loop of the worm’s uterus to break and discharge a swarm of motile larvae. Contraction of the worm and discharge of larvae may be repeated if the lesion is again submerged in water, until the entire brood of larvae is discharged. Motile free-swimming larvae are ingested whole by copepods and mature in the body cavity in about 2 weeks. Stagnant sources of drinking water such as ponds; cisterns; pools in dried-up river beds; and shallow, unprotected, hand-dug wells commonly harbor copepods and are the usual sites of infection transmission. Seasonality varies according to location. In endemic countries in the Sahel area of Africa (Chad, Ethiopia, South Sudan), transmission usually peaks during the rainy season at mid-year (May– September). This is because stagnant surface sources of water are more common in these areas during the 5- to 6-month-long rainy season. The seasonal emergence of the worm often coincides with harvest or planting seasons, and thus significantly affects agricultural productivity and school attendance. Most cases usually occur in older children and working-age adults.
NATURAL HISTORY, PATHOGENESIS, PATHOLOGY, AND CLINICAL FEATURES Infected people remain asymptomatic for approximately a year after infection, until the mature female worm approaches the skin and forms a painful papule in the dermis. This papule can become a blister within 24 hours or may enlarge for several days before blistering (Fig. 118.3). The blister is accompanied by redness and induration, and is usually preceded by systemic symptoms of low-grade fever and allergic symptoms (erythema, urticarial rash, intense pruritus, dizziness, nausea, vomiting). The lesion produces intense irritation and burning, inducing the patient to seek relief by immersing the affected limb in water, where the blister breaks, allowing the adult worm to discharge larvae into the water (Fig. 118.4). Eighty to ninety percent of lesions occur on the lower extremities, including the ankle or foot. However, worms can exit from
879
CHAPTER 118 Dracunculiasis
Guinea Worm Reduction Over Time
1986
118
2017
Fig. 118.1 Guinea worm reduction from 1986 to 2017.
4
1 Emerging worm
2
Copepods First-stage larve
3 Fig. 118.2 Life cycle of Dracunculus medinensis. (Courtesy, Encyclopedia Britannica, Inc., © 1996.)
Third-stage larve
880
PART 6 Helminthic Infections
Fig. 118.3 Blisters caused by Dracunculus medinensis and rupture of blisters resulting in skin lesions with protruding Guinea worms. (Courtesy, Elizabeth Long, The Carter Center.)
anywhere on the body, including the head, upper extremities, buttocks, and genitalia. More than one worm may emerge from a given patient either simultaneously or sequentially over a period of weeks or months. As the worm emerges through the skin lesion, the affected person pulls it out slowly and carefully (because of inflammation and pain), usually by winding a few centimeters of the worm each day on a small stick. This very painful process may last many weeks. Pain and other symptoms may lessen with the rupture of the blister, but pyogenic organisms invariably invade the superficial lesion and worm tract and aggravate the condition (see Fig. 118.4). If the worm breaks during extraction and the remaining part retracts into the tissue, an intense inflammatory reaction occurs, with pain, swelling, and cellulitis along the worm tract and usually the formation of an abscess. The reported period of incapacitation ranges from 2 to 16 weeks (average 8.5 weeks)9–16 and more than half of a village’s population may be affected at the same time. In addition to the blisters and skin lesions, secondary bacterial infections can lead to sepsis, abscesses, septic arthritis, contracture of muscles near joints, or even tetanus.17 Chronic manifestations are due to inflammation of the joints, with signs and symptoms of arthritis, synovitis,18 and muscle and tendon contractures with resultant ankylosis of the limb.19 Migration of the worms to the retroperitoneum and from the retroperitoneum to the subcutaneous tissue in the leg sometimes results in aberrant (ectopic) locations such as the pancreas, lung, periorbital tissues, testis, pericardium,20 and the spinal cord, producing compression21 as well as focal abscess formation.
PATIENT EVALUATION, DIAGNOSIS, AND DIFFERENTIAL DIAGNOSIS No serodiagnostic tests are available to detect an incubating Guinea worm. Diagnosis is based on the clinical history and findings with an appropriate exposure. The blister fluid is bacteriologically sterile and initially contains polymorphonuclear leukocytes and later lymphocytes, eosinophils, and macrophages. Larvae are always present in the fluid, and white blood cells adhere to them.6 With time, the blister and worm tract often become secondarily infected. Differentiation between human and zoonotic species of Dracunculus (which rarely affect humans) requires morphologic
Fig. 118.4 Pyogenic organisms invade the superficial lesion and worm tract, aggravating the condition. (Courtesy, The Carter Center.)
examination of adult male worms (which are rarely available). Therefore efforts are underway to map the genome of the Guinea worm’s DNA in order to ascertain the infecting parasite’s species. Although there are several zoonotic species of Dracunculus, only medinensis is specific to humans. A molecular tool is now available to differentiate between D. medinensis and other tissue-dwelling nematodes, including other Dracunculus species that may rarely infect humans.22 Work on determining the genome of D. medinensis is ongoing at the Centers for Disease Control and Prevention, Wellcome Trust Sanger Institute, and Vassar College (Eberhard ML, personal communication).
TREATMENT There is no curative drug or vaccine against dracunculiasis. Infected people do not develop immunity. Applying wet compresses to the lesion may relieve pain during the worm’s emergence. Placing an occlusive bandage on the wound keeps it clean and may help to keep the patient from contaminating sources of drinking water. Oral analgesics and anti-inflammatory medicines can be administered to alleviate pain and inflammation. Topical antiseptics or antibiotic ointment may minimize the risk of secondary bacterial infections, reduce inflammation, and permit removal of the worm by gentle traction over a number of days. Systemic antibiotics can be used in established infections. Patients usually recover completely, but repeated infections occur.
PREVENTION Prevention of dracunculiasis includes educating the at-risk population about the disease and avoidance measures. These measures include filtering drinking water to remove copepods, preventing infected people from entering water intended for drinking, cooking aquatic animals well, and tethering infected dogs. Developing safe sources for drinking water is also a key feature of control.
REFERENCES
1. Hopkins DR, Ruiz-Tiben E, Weiss AJ, et al. Progress toward global eradication of dracunculiasis — January 2017–June 2018. MMWR Morb Mortal Wkly Rep 2018;67:1265–70. 2. World Health Organization. Dracunculiasis eradication: global surveillance summary 2017. Wkly Epidemiol Rec 2018;93:305–20. 3. Fedchenko AP. Concerning the structure and reproduction of the Guinea worm (Filaria medinensis L.). Proceedings of the Imperial Society of the Friends of Natural Sciences, Anthropology, and Ethnography. Vol 8 (in Russian), 1870, Reprinted in. Am J Trop Med Hyg 1971;20: 511–23. 4. Watts SJ. Dracunculiasis in Africa: its geographical extent, incidence, and at-risk population. Am J Trop Med Hyg 1987;37:119–25. 5. World Health Organization. Dracunculiasis: global surveillance summary: 1996. Wkly Epidemiol Rec 1997;72:133–9. 6. Muller R. Dracunculus and dracunculiasis. Adv Parasitol 1971;6:73–151. 7. Eberhard ML, Ruiz-Tiben E, Hopkins DR, et al. The peculiar epidemiology of dracunculiasis in Chad. Am J Trop Med Hyg 2014;90:61–70. 8. Eberhard ML, Yabsley MJ, Zirimwabagabo H, et al. Possible role of fish and frogs as paratenic hosts of Dracunculus medinensis in Chad. Emerg Infect Dis 2016;22:1428—30. 9. Belcher DW, Wurapa FK, Ward WB, et al. Guinea worm in southern Ghana: its epidemiology and impact on agricultural productivity. Am J Trop Med Hyg 1975;24:243–9. 10. Khan HD, Aminuddin M, Shah CH. Epidemiology and socio-economic implications of dracunculiasis in eleven rural communities of District Bannu (Pakistan). J Pakistani Med Assoc 1986;36:233–9. 11. Smith GS, Blum D, Huttley SRA. Disability from dracunculiasis: effect on mobility. Ann Trop Med Parasitol 1989;83:151–8.
CHAPTER 118 Dracunculiasis
881
12. Watts SJ. Guinea worm: an in depth study of what happens to mothers, families, and communities. Soc Sci Med 1989;29:1043–9. 13. Adeyeba OA, Kale OO. Epidemiology of dracunculiasis and its socioeconomic impact in a village in south-west Nigeria. West Afr J Med 1991;10:208–15. 14. Ilegbodu VA, Ilegbodu AE, Wise RA, et al. Clinical manifestations, disability, and use of folk medicine in dracunculiasis in Nigeria. J Trop Med Hyg 1991;94:35–41. 15. Chippaux JP, Benzou A, Agbede K. Social and economic impact of dracunculiasis: a longitudinal study carried out in two villages in Benin. Bull World Health Organ 1992;70:73–8. 16. Rhode JE, Sharma BL, Patto H, et al. Surgical extraction of Guinea worm: disability reduction and contribution to disease control. Am J Trop Med Hyg 1993;48:71–6. 17. Adeyeba OA. Secondary infections in dracunculiasis: bacteria and morbidity. Int J Zoonoses 1985;12:147. 18. Robineau M, Sereni D. Arthrite aiguë du genou avec presence intraarticulaire de microfilaires de D. medinensis. Évolutions clinique et immunologique compares. A propos d’un cas. Bull Soc Pathol Exot Filiales 1978;71:85–9. 19. el Garf A. Parasitic rheumatism: rheumatic manifestations associated with calcified Guinea worm. J Rheumatol 1985;12:976–9. 20. Kinare SG, Parulkar GB, Sen PK. Constrictive pericarditis resulting from dracunculosis. Br Med J 1962;1:845. 21. Odaibo SK, Agowun IA, Oshagbemi K. Paraplegia complicating dracontiasis. J R Coll Surg 1986;31:376–8. 22. Bimi L, Freeman AR, Eberhard ML, et al. Differentiating Dracunculus medinensis from D. insignis, by the sequence analysis of the 18S rRNA gene. Ann Trop Med Parasitol 2005;99:511–17.
118