AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

INTRODUCTION

Section 2 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Background

Two species of hookworms commonly infect humans, Ancylostoma duodenale and Necator americanus. These species are found throughout the tropics and subtropics. The distribution of each species significantly overlaps that of the other.

Hookworms are estimated to infect more than 740 million people around the world, but most people who are infected are asymptomatic.¹ These worms are much smaller than the large roundworm, Ascaris lumbricoides, and the complications of tissue migration and mechanical obstruction so frequently observed with roundworm infestation are less frequent in hookworm infestation. The most significant risk of hookworm infection is anemia secondary to loss of iron (and protein) into the gut.

Pathophysiology

A duodenale and N americanus are small, off-white worms. Males are 8-11 mm in length, and females are 10-13 mm. The sexes cannot be distinguished by the naked eye. Hookworm larvae emerge from passed eggs within 24 hours and molt once to an infective filariform larval stage in another 24 hours. After molting, larvae are able to penetrate intact skin. This rapid external portion of the hookworm life cycle is different from that of the roundworm, Ascaris, whose eggs require 3 weeks in the soil before becoming infective.

Walking barefoot in soil contaminated with feces (the source of hookworm eggs and larvae) is the most common method of exposure. After skin penetration, the venous circulation carries larvae to the pulmonary bed, where they lodge in pulmonary capillaries. Within 3-5 days, the larvae break through into alveoli and travel up the ciliary escalator from the lungs into the bronchi, the trachea, and the pharynx. Upon reaching the pharynx, larvae are swallowed and gain access to the GI tract. Once in the GI tract, worms attach to the wall of the intestine and begin to feed on the blood of the host. A N americanus adult worm consumes approximately 0.3 mL of blood per day, while the A duodenale consumes approximately 0.5 mL of blood each day. Chronic loss of blood and serum proteins leads to hookworm anemia and impaired nutrition.

Eggs begin to appear in the stool approximately 6-8 weeks after initial infection with N americanus and as long as 38 weeks after initial infection with A duodenale. The lifespan of the worm is up to one year for A duodenale and up to 5 years for N americanus.

Frequency

United States

Hookworm infection is rare in the United States.

International

The prevalence of infection is as high as 80% in lesser-developed countries with moist tropical climates but is only 10-20% in areas with drier climates.

Mortality/Morbidity

Hookworm infection is rarely fatal, but anemia can be significant in heavily infected individuals. Children and pregnant women with physiologically low iron reserves may suffer greater complications from hookworm anemia. Pulmonary complaints such as cough or wheezing are generally less common than in A lumbricoides infection.

Age

Children are infected more commonly and more heavily than adults. This is because children are more likely than adults to come in direct contact with fecally contaminated soil that contains infective larva.

CLINICAL

Section 3 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

History

• Most infected individuals are asymptomatic.
• In the first 7-10 days following infection, patients may notice "ground itch" (ie, itchy papules where the skin was penetrated by larvae).
• Infected patients are not directly contagious because eggs require a brief period outside the body to hatch into their infective larval form.
• Patients may have a history of wearing open footwear or walking barefoot in endemic areas.
• Early symptoms - Larval migration phase (1-5 d)
• • The onset of ground itch with localized maculopapular eruption ("ground itch") is noted.
  • Low-grade fever may occur.
  • Migration of worms through the lungs may produce a mild cough.
  • Pulmonary inflammatory response can lead to wheezing.
• Late symptoms
• • GI discomfort secondary to irritation may occur as the worms pass into the gastrointestinal tract.
  • Hookworm anemia is usually due to iron deficiency and does not develop until iron reserves are depleted.
  • • About one half of the iron expelled by the worm is resorbed; the remainder is lost.
    • A large worm burden and a history of poor iron intake increase the likelihood of significant anemia.
    • The symptoms of anemia often include fatigue and dyspnea. In rare cases, anemia may provoke ischemic symptoms such as angina or claudication.
    • In high prevalence areas, all anemic patients have hookworms; however, not all patients infected with hookworms have hookworm anemia.

Physical

Physical findings in the early (larval migration) and late (established GI infection) stages of the disease are different.

• Early infection (larval migration)
• • Small, pruritic papules are observed at the larval skin entry site (usually feet).
  • Wheezing may be triggered when the worms first break through from the venous circulation into the pulmonary air spaces.
• Established infection (adult/GI phase)
• • Mild abdominal tenderness
  • Pallor (hookworm anemia)
  • Pale conjunctiva (hookworm anemia)
  • Tachycardia (hookworm anemia)

Causes

The larvae enter through bare skin upon exposure to fecally contaminated soil that contains infective larva.

DIFFERENTIALS

Section 4 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

WORKUP

Section 5 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Lab Studies

• Early infection (larval migration phase)
• • A differential may reveal eosinophilia (1000-4000 cells/mcL).
  • In the early phase, the stool examination is normal.
• Established infection (adult/GI phase)
• • In patients with mature infection, eggs may be seen during stool examination.
  • If eggs are not seen, the likelihood of clinically significant infection is very low.
  • When infection is suspected, stool should be promptly evaluated because eggs hatch into infective larvae within 24 hours.
  • Laboratory findings may be consistent with iron deficiency anemia.
• Hookworm anemia
• • A CBC count may demonstrate iron deficiency anemia.
  • Stool examination may demonstrate significant number of hookworm eggs.
  • Other causes of iron loss and blood loss should be excluded.

Imaging Studies

• In the larval migration phase, a patchy infiltrate may be revealed by chest radiography.
• Imaging studies are not helpful once infection is established in the gut.

Other Tests

• Stool should be examined for ova and parasites. However, because egg laying may be delayed, stool examination should not be considered a sensitive test for identifying hookworm infection. Stool examinations may need to be repeated.

TREATMENT

Section 6 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Emergency Department Care

• Larval migration phase
• • Wheezing and cough are managed with inhaled beta agonists.
  • Steroids may cause pulmonary symptoms to become exacerbated, particularly in patients with Strongyloides infection.
• Early infection (ground itch)
• • Thiabendazole may be used topically to attack migrating larvae.
  • Larvae are susceptible to antihelminthic therapy (see Medication).
• Established infection (adult/GI phase)
• • Effective antihelminthic therapy is available.
  • Need to treat hookworm anemia (ie, iron deficiency anemia).

Consultations

• Specialty consultation is not necessary unless anemia is severe. The primary physician must monitor anemia treatment.

MEDICATION

Section 7 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

The list of drugs used to treat parasitic infections is varied and extensive. The treatment of parasitic infestations is based on the specific parasite and the particular phase of the disease.

Drug Category: Anthelmintics

Parasite biochemical pathways are quite different from those of the human host. This difference permits effective treatment using directed pharmacologic agents in relatively small doses.

FOLLOW-UP

Section 8 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Further Inpatient Care

• Inpatient care may be warranted for patients with severe anemia.

Deterrence/Prevention

• Household contacts of small children in rural areas are at risk of infection through fecal contamination of soil.
• Skin contact with fecally contaminated soil should be avoided.
• Shoes should be worn in endemic areas.
• Family members may be screened to identify those who are infected but are asymptomatic.

Complications

• Iron deficiency anemia may occur.

Prognosis

• Prognosis is excellent with proper treatment.

Patient Education

• Encourage good personal hygiene.

MISCELLANEOUS

Section 9 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical/Legal Pitfalls

• Failure to consider parasitic disease in any patient presenting from an endemic area

REFERENCES

Section 10 of 10

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

1. Stoltzfus RJ, Dreyfuss ML, Chwaya HM. Hookworm control as a strategy to prevent iron deficiency. Nutr Rev. Jun 1997;55(6):223-32. [Medline].
2. Bell DR. Soil transmitted helminths. In: Lecture Notes on Tropical Medicine. Blackwell Scientific Publications; 1985:165-92.
3. de Silva NR, Brooker S, Hotez PJ. Soil-transmitted helminth infections: updating the global picture. Trends Parasitol. Dec 2003;19(12):547-51. [Medline].
4. Freedman DO. Intestinal nematodes. In: Gorbach SL, Bartlett JG, Blacklow NR, eds. Infectious Diseases. WB Saunders Company; 1992:2003-8.
5. Gilles HM. Intestinal nematode infections. In: Hunter's Tropical Medicine. WB Saunders Company; 1984:620-46.
6. Hotez PJ, Brooker S, Bethony JM. Hookworm infection. N Engl J Med. Aug 19 2004;351(8):799-807. [Medline].
7. Hotez PJ, Pritchard DI. Hookworm infection. Sci Am. Jun 1995;272(6):68-74. [Medline].
8. Medical Letter, Inc. Drugs for parasitic infections. Med Lett Drugs Ther. The Medical Letter. Available at http://www.medletter.com. Accessed March 12, 2006.
9. Nawalinski TA, Schad GA. Arrested development in Ancylostoma duodenale: course of a self-induced infection in man. Am J Trop Med Hyg. Sep 1974;23(5):895-8. [Medline].
10. Rizzitelli G, Scarabelli G, Veraldi S. Albendazole: a new therapeutic regimen in cutaneous larva migrans. Int J Dermatol. Sep 1997;36(9):700-3. [Medline].
11. Sakti H, Nokes C, Hertanto WS. Evidence for an association between hookworm infection and cognitive function in Indonesian school children. Trop Med Int Health. May 1999;4(5):322-34. [Medline].

Article Last Updated: May 6, 2008