Hookworm disease – symptoms, treatment, prevention

The duodenal hookworm (Ancylostoma duodenale) and the American necator (Necator americanus) cause similar clusters of clinical symptoms known as hookworm disease.

The incidence of hookworm disease

Hookworm and American necator infections occur in tropical and subtropical zones virtually all over the world. It is estimated that the total number of people infected is 580-740 million. The highest incidence is observed in sub-Saharan Africa, East and Southeast Asia, Oceania, South and Central America. Infection usually occurs in rural areas because of a warm and humid climate, inadequate sewage disposal and barefoot walking.

People contract the hookworm disease through the percutaneous route. The larvae present in the soil actively penetrate during skin contact with the ground. Oral infection is also possible, especially with Ancylostoma duodenale. Children are most often infected in endemic regions, and multiple infections may occur throughout their lives.

Etiology

The duodenal hookworm and the American necator are nematodes 5-13 mm long, they live in the human digestive tract from several months to several years. Females lay several thousand eggs every day. Rabdite-like larvae hatch in moist soil, which after two extrusions transform into filaria-like larvae capable of infecting humans.

Hookworm disease – the mechanism of its origins

After penetrating through the skin, the larvae move towards the venous vessels, and then are transported to the lungs, where they enter the lumen of the bronchial tree, from where they are expectorated and swallowed together with bronchial secretions. In the digestive tract, the larvae mature, attach themselves to the wall of the small intestine and parasitize there. In the case of infection through the digestive tract, the larvae do not migrate, but they transform into mature forms in the digestive tract.

As they pass through the skin, the larvae secrete certain substances, such as:

  1. anticoagulants,
  2. proteolytic enzymes,
  3. immunomodulatory.

The presence of larvae in the lungs causes the accumulation of eosinophilic cells in the course of a toxic-allergic reaction, which sometimes leads to the formation of infiltrates with a pathogenesis similar to that of ascariasis.

Hookworm disease – symptoms

Clinical symptoms in hookworm disease may accompany the migration of the larvae through the skin, passage through the lungs, and parasitization in the gastrointestinal tract, however in over 90% of all infected, the course is asymptomatic. At the site of penetration of the invasive larvae, there may be pruritus and changes in the form of lumps. Massive invasion through the lungs may be manifested by coughing, shortness of breath and bronchospasm. The parasitization of the worm in the gastrointestinal tract can cause abdominal pain and mild diarrhea.

In hookworm infection the characteristic clinical symptom is iron deficiency anemia. It is believed that even an invasion of twenty individuals of this species can cause symptoms of anemia. On the other hand, children may have protein and energy deficiencies characterized by impaired psychomotor development.

How to recognize hookworm disease?

The diagnosis is confirmed by the detection of hookworm eggs in the stool. Significant eosinophilia is often present in the peripheral blood.

Differential diagnosis

Other causes of anemia should be considered. Gastrointestinal and respiratory symptoms should be differentiated from ascariasis and nematode, although mixed infections are very common in endemic areas.

Hookworm disease – treatment

In patients with hookworm disease, albendazole is administered in a single dose of 400 mg or mebendazole in a dose of 2 times 100 mg for 3 days. In cases of significant anemia, iron supplementation is used.

The treatment success rate is high and the prognosis is good.

Literature

1. Bethony J., Brooker S., Albonico M., Geiger S.M., Loukas A., Diemert D., Hotez P.J.: Soil-transmitted helminth infections: ascariasis, trichuriasis, and hookworm, Lancet 2006; 367: 1521-1532.

Source: J. Cianciara, J. Juszczyk, Infectious and parasitic diseases; Czelej Publishing House

Leave a Reply