Generally, patients show a history of travel to endemic areas. Many of them also remember drinking untreated or unfiltered water, eating of vegetables and fresh fruits washed with such water and bathing in water that is potentially contaminated.

Transmission of the disease comes in seasonal variations. In wet areas, most cases occur in the dry season when drinking water is limited and in dry areas, the rainy season sees an upsurge in infection with the increase in availability of surface water.

After physical examination findings indicate the condition, the history of the patient is used to confirm diagnosis.

A blister is formed in the epidermis around the lower extremity by the female worm. Before the formation of the blister, allergic type symptoms like mild respiratory distress, wheezing, urticaria, pruritus, and periorbital edema is present [9]. During this period, some patients may be febrile. The blister becomes erythematous at its periphery as it grows, following the emergence of the head of the worm. Edema occurs around the site of emergence and the burning pain is caused by inflammation of the papule.

The diagnosis is conclusive as soon as the head of the worm is identified within the ulcer.

• Pathologist

  […] and Unit Head of Queensland Paediatric Infectious Laboratory, Sir Albert Sakzewski Viral Research Centre, Royal Children's Hospital Michael D Nissen, MBBS is a member of the following medical societies: American Academy of Pediatrics, Royal College of Pathologists [emedicine.medscape.com]

• Respiratory Distress

  Before the formation of the blister, allergic type symptoms like mild respiratory distress, wheezing, urticaria, pruritus, and periorbital edema is present [9]. During this period, some patients may be febrile. [symptoma.com]

• Nausea

  The female worms move through the personâ s subcutaneous tissue, causing intense pain, and eventually emerge through the skin, usually at the feet, producing oedema, a blister and eventually an ulcer, accompanied by fever, nausea, and vomiting. [web.archive.org]

  Perforation of the skin by the guinea worm, which can be 6 feet long, is accompanied by fever and nausea and vomiting. Infected persons may remain sick for some months. [medicine.academic.ru]

  Symptoms include pruritus, nausea, vomiting, diarrhea, or asthmatic attacks. [connects.catalyst.harvard.edu]

  This is also accompanied by fever, nausea and vomiting. Once a worm has emerged from the body, it must be carefully and slowly removed over several weeks. [unitingtocombatntds.org]

  The worm eventually emerges (from the feet in most of the cases), causing an intensely painful oedema, a blister and an ulcer accompanied by fever, nausea and vomiting. [who.int]

• Leg Pain

  Approximately 1 year after a person acquires infection from drinking contaminated water, the worm emerges through the skin, usually on the leg. [ncbi.nlm.nih.gov]

• Urticaria

  Before the formation of the blister, allergic type symptoms like mild respiratory distress, wheezing, urticaria, pruritus, and periorbital edema is present. [symptoma.com]

  Urticaria, erythema, dyspnea, vomiting, and pruritus are thought to reflect allergic reactions to worm antigens. If the worm is broken during expulsion or extraction, a severe inflammatory reaction ensues, causing disabling pain. [merckmanuals.com]

• Larva Migrans

  African Sleeping Sickness, Sleeping Sickness) Trypanosomiasis, American (Chagas Disease) Visceral Larva Migrans (Toxocariasis, Toxocara Infection, Ocular Larva Migrans) Waterborne Diseases Whipworm Infection (Trichuriasis, Trichuris Infection) Zoonotic [cdc.gov]

  [patient.info] Larva Migrans LARVA MIGRANS CUTANEA (dermatite serpiginosa, anchilostoma del cane e del gatto) LARVA MIGRANS VISCERALE (Toxocariasi) LEISHMANIOSI Viscerale Cutanea Mucosa MALARIA, Trattamento (Plasmodium falciparum, P. vivax, P. ovale e [symptoma.com]

Some of the studies common with dracunculiasis include:

• Serum immunoglobulin levels: Immunoglobulin E (IgE), immunoglobulin G1 (IgG1), and immunoglobulin G4 (IgG4) levels are usually increased. The variability is dependent on the stage of disease.
• CBC count with differential: The WBC count will show elevation even if is slight. The differential common indicator of eosinophilia.
• In rare cases where surgery is considered, a radiologic examination of the lower extremity is important. It helps in identifying calcified worms.

• EEG Slowing

  EEG Slowing Because of slow mobilization in countries with endemic disease, the 1991 WHA goal to eradicate dracunculiasis globally by 1995 was not achieved. [symptoma.com]

• Tissue Nematode

  Dracontiasis Guinea worm infection Dracunculus medinensis Dracunculiasis or guinea or Medina worm infection is caused by the tissue nematode Dracunculus medinensis. This worm has an indirect life cycle with small copepods as intermediate hosts. [parasite-diagnosis.ch]

  [documents.worldbank.org] Other Pathologies Tissue Nematode Dracontiasis Guinea worm infection Dracunculus medinensis Dracunculiasis or guinea or Medina worm infection is caused by the tissue nematode Dracunculus medinensis. [symptoma.com]

  KAZURA, Tissue Nematodes, Including Trichinellosis, Dracunculiasis, and the Filariases, Mandell, Douglas, and Bennett's Principles and Practice of Infectious Diseases, 10.1016/B978-0-443-06839-3.00288-5, (3587-3594), (2010). José Angelo L. [doi.org]

There is no vaccine to prevent dracunculiasis nor is there any medication to treat the disease. However prevention is possible.

Prognosis for this condition is often positive even without treatment. The only danger is when the infection is left untreated.

The disease is caused by drinking water that is contaminated by microscopic arthropods known as copepods. At its peak, the disease was most active in areas that were regarded as some of the poorest in the world which did not have clean water for the inhabitants. Within these areas, stagnant water may still host copepods and these carry larvae of the guinea worm [7].

As at 1986, over 3.5 million individuals spread over 20 countries were infected with guinea worm. By the end of 2004, the entire continent of Asia got rid of the disease [3].

In Australia and North America, there were sporadic cases of the condition predominantly amongst African immigrants from 2000-2005. Many African nations have also reported sporadic cases of the condition since 2006.

Between 2007 and 2008, indigent infections only occurred in specific areas in Niger, Mali, Ghana and Sudan. The disease is endemic in the following countries: Sudan, Mali and Ethiopia. Less than 1,800 cases were reported across the world in 2010 [4].

Today, South Sudan is the major guinea worm disease hotspot. 94% of current cases occur there.

Morbidity/Mortality

Dracunculiasis doesn’t lead to death after primary infection. Death only occurs in instances where secondary infection occurs at the site of the worm’s exit. This often leads to sepsis5. The mortality rate is very low but morbidity remains a major concern in areas where secondary infection is common. Formation of abscess or cellulitis requires immediate attention. The pain from the exit sites of the parasites is often very painful and can leave a patient incapacitated over a few weeks.

The larvae of the parasite develop in Cyclops copepod (water flea). The larvae cause dracunculiasis if the infected Cyclops copepods are not filtered from the water before drinking.

These larvae move to the host's body cavities where the female mates with a male guinea worm. The male dies and is absorbed by the host's body. All of this is completed within 3 months of drinking infected water. The female which contains larvae at this stage, finds its way to the extremities [8].

12 months from the time of drinking the infected water a blister appears in the skin of the host, formed by the female worm. This blister is often seen on the leg or foot and it ruptures within 72 of formation exposing the worm as it emerges.

Dracunculiasis can be transmitted only by drinking contaminated water, so only water free from contamination should be consumed in endemic areas.

Dracunculiasis is a nodular dermatosis that is produced when the Dracunculus parasite develops in the subcutaneous tissue of an individual. It is commonly referred to as the guinea worm disease. Dracunculus medinensis is a parasite which has humans as its only reservoir [1].

The parasite is a very thin and long nematode or roundworm. The parasite enters a host when the individual drinks stagnant water which contains copepods infested with the guinea worm larvae.

One year after the larvae finds a human hosts, the individual begins to feel a painful burning sensation as the female worm forms a blister around the lower limb. Dracunculus medinensis is found in the order Spiruridia which is an order of parasites which include Loa Loa, Brugia Malayi and Wuchereria Bancrofti [2].

Patients and individuals going to endemic areas need to understand that the condition is caused entirely, by drinking contaminated water and this can be prevented by drinking water from sources free from contamination such as boreholes or wells, filtering drinking water with ceramic or sand filters, boiling drinking water and treating water sources with larvicides which kill the copepods [10].

Also, people with emerging guinea worms must be prevented from entering water sources meant for drinking.

1. Centers for Disease Control and Prevention (CDC). Progress toward global eradication of dracunculiasis, January 2005 – May 2007. MMWR Morb. Mortal. Wkly. Rep. 56 (32): 813–7. PMID 17703170.
2. Hopkins D, Richards Jr F, Ruiz-Tiben E, Emerson P, Withers Jr. "Dracunculiasis, onchocerciasis, schistosomiasis, and trachoma". Annals of the New York Academy of Sciences 2008 1136: 45–52. Bibcode:2008NYASA1136...45H.
3. World moves closer to eradicating ancient worm disease". World Health Organization. 2007-03-27.
4. McNeil DG. Dose of Tenacity Wears Down a Horrific Disease. New York Times. 2006.
5. 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. Jul 2005;99(5):511-7.
6. Bloch P, Simonsen PE. Immunoepidemiology of Dracunculus medinensis infections I. Antibody responses in relation to infection status. Am J Trop Med Hyg. Dec 1998;59(6):978-84.
7. CDC. Progress toward global eradication of dracunculiasis, January 2004-July 2005. MMWR Morb Mortal Wkly Rep. Oct 28 2005;54(42):1075-7.
8. Greenaway C. Dracunculiasis (guinea worm disease). CMAJ. Feb 17 2004;170(4):495-500.
9. Hopkins DR, Ruiz-Tiben E, Downs P, et al. Dracunculiasis eradication: the final inch. Am J Trop Med Hyg. Oct 2005;73(4):669-75.
10. Hunter JM. An introduction to guinea worm on the eve of its departure: dracunculiasis transmission, health effects, ecology and control. Soc Sci Med. Nov 1996;43(9):1399-425.