Guinea Worm Disease Dracunculiasis

Dracunculiasis (Guinea worm disease) is caused by the nematode (roundworm) Dracunculus medinensis.^[1] During the last 25 years, efforts to eradicate the Guinea worm have resulted in a reduction of more than 99% of worldwide cases of dracunculiasis.^[2]

Life cycle^[1]

• Humans become infected by drinking unfiltered water containing copepods (small crustaceans) which are infected with the larvae of D. medinensis.
• Following ingestion, the copepods die and release the larvae. The larvae penetrate the host stomach and intestinal wall to enter the abdominal cavity and retroperitoneal space.
• After maturation into adults and mating, the male worms die and the females (length is between 70 cm and 120 cm) migrate in the subcutaneous tissues towards the skin surface.
• Approximately one year after infection, the female worm induces a blister on the skin (usually on the lower legs or feet), which ruptures.
• When this lesion comes into contact with water, the female worm emerges for between 1 and 3 weeks and releases larvae. The larvae are ingested by a copepod and then develop into infective larvae.
• Ingestion of the copepods in contaminated water completes the cycle.

Epidemiology

• The 'Dracunculiasis Eradication Program' has been very effective. Reported cases of Guinea worm disease have continued to decrease progressively. There were only 3,190 confirmed cases in 2009 compared with 25,217 cases in 2006 and almost 3.5 million cases in 1986.^[3]
• Asia has been declared free of dracunculiasis since 2005. Dracunculiasis now occurs only in rural, isolated areas of sub-Saharan Africa. Since 2006 only sporadic cases in Africa have been reported.^[4]

Presentation^[2]

• The worm emerges as a whitish filament in the centre of a painful ulcer, which is inflamed, often with a secondary bacterial infection.
• Immediately before blister formation, allergy symptoms often occur, eg wheezing, urticaria, periorbital oedema, giddiness and pruritus, associated with fever.
• Oedema and inflammation occur around the blister, causing further pruritus and burning pain.
• Swelling and pain usually decrease after the blister is opened.
• Lymphadenopathy can occur at any stage of the illness.

Investigations^[1]

• The clinical presentation is so typical that it does not need laboratory confirmation.
• Examination of the fluid discharged by the worm may show rhabditiform larvae.
• FBC: the white cell count is usually slightly elevated with an eosinophilia.
• There are no serological tests available.
• X-rays of the lower limbs may show calcified worms.^[2]

Treatment

• The most common treatment still involves wrapping the worm around a stick at the skin surface, and wrapping or winding the worm a few centimetres each day.
  • This process can take many days, but must be slow to avoid breakage and leaving behind a portion of the worm.
  • Leaving a portion of the dead worm within the host's body increases the risk of infection, and can trigger immune responses, resulting in pain and swelling.
• The worm also can be excised surgically.
• Local cleaning of the lesion, and antibiotics for any bacterial superinfection.
• There is no curative antihelminthic treatment available. Metronidazole or tiabendazole have been used in adults as an adjunct to the extraction process, but one study found that antihelminthic therapy was associated with migration of worms, leading to infection in areas other than the lower extremity.^[2]

Prognosis

Prognosis is usually very good with or without treatment, unless any secondary infection remains untreated.

Prevention

• Drink only water from underground sources free from contamination, eg borehole or hand-dug wells.
• Prevent persons with an open Guinea worm ulcer from entering ponds and wells used for drinking water.
• Always filter drinking water, eg cloth or nylon mesh filter.
• Additionally, unsafe sources of drinking water can be treated with an approved larvicide.