eMedicine Specialties > Pediatrics: General Medicine > Parasitology

Hookworm Infection

Author: Christopher M Watson, MD, Pediatric Critical Care Fellow, Johns Hopkins Hospital; Assistant Professor of Pediatrics, Uniformed Services University of the Health Sciences
Coauthor(s): Patrick W Hickey, MD, FAAP, Assistant Professor of Pediatrics, Uniformed Services University of the Health Sciences; Consulting Staff, Department of Pediatrics, Division of Pediatric Infectious Disease, Walter Reed Army Medical Center
Contributor Information and Disclosures

Updated: Oct 7, 2008

Introduction

Background

Human hookworm infection is a common soil-transmitted helminth infection that is caused by the nematode parasites Necator americanus and Ancylostoma duodenale. Worldwide, hookworms infect an estimated 740 million people, most of whom are asymptomatic.¹ Despite this lack of symptoms, hookworm substantially contributes to the incidence of anemia and malnutrition in developing nations.² The greatest number of cases occurs in the rural tropical and subtropical areas of China and sub-Saharan Africa, followed in number by India, South Asia, and Latin America.¹

The importance of hookworm infection has historically been undermined by the disproportionate number of impoverished people affected and by the insidious nature of the infection. However, this trend has slowly reversed. At the 54th World Health Assembly in 2001, a resolution was passed to encourage antihelmintic treatment in at-risk school-aged children by 2010 in an attempt to control morbidity.² At present, new international efforts are ongoing to reduce the impact of this parasitic infection, with promising progress being made, particularly in the development of a new chemotherapeutics and an effective vaccine.

Pathophysiology

N americanus is the globally predominant human hookworm and the only member of its genus known to infect humans.³ A duodenale is more geographically restricted than N americanus but one of several anthropophilic members of the genus Ancylostoma. Ancylostoma ceylanicum infects canines and felines and causes mild human intestinal illness. Ancylostoma caninum is the canine hookworm and causes eosinophilic enteritis in humans. Ancylostoma braziliense is a canine and feline hookworm that causes cutaneous larva migrans in humans, or creeping eruption, a self-limiting condition characterized by serpiginous burrows as the larvae migrate through the epidermis. Unlike N americanus or A duodenale, these organisms cause zoonotic infections and tend to lead only to mild disease in humans.

N americanus is a small, cylindrical, off-white worm with a life expectancy of 3-10 years.⁴ One worm can cause 0.03 mL of intestinal blood loss per day. The adult male worm measures 7-9 mm; the female worm measures 9-11 mm and lays 3000-6000 eggs per day. A duodenale resembles N americanus in appearance, but its adult life expectancy is only 1-3 years. A duodenale is the larger of the 2 species, with male worms measuring 8-11 mm and adult female worms measuring 10-13 mm. Female members of this species lay upwards of 10,000-30,000 eggs per day.

A duodenale also consumes more blood than N americanus does, ingesting 0.15 mL per worm per day. Although N americanus infects only percutaneously, A duodenale can infect by means of ingestion, and lactogenic transmission during breastfeeding has been proposed. On microscopy, N americanus can be differentiated from A duodenale on the basis of its cutting plates instead of teeth. ⁵

The life cycle of hookworms begins with the passing of hookworm eggs in human feces and their deposition into the soil (see Media file 1 for the hookworm life cycle).^4,6 Larval growth is most proliferative in favorable soil that is sandy and moist, with an optimal temperature of 20-30°C. Under these conditions, the larvae hatch in 1 or 2 days to become rhabditiform larvae, also known as L1.

The rhabditiform larvae feed on the feces and undergo 2 successive molts; after 5-10 days, they become infective filariform larvae, or L3. These L3 go through developmental arrest and can survive in damp soil for as long as 2 years. However, they quickly become desiccated if exposed to direct sunlight, drying, or salt water. L3 live in the top 2.5 cm of soil and move vertically toward moisture and oxygen. Infection of the human host is established when filariform larvae penetrate the skin, typically on the hands or feet. This penetration may cause a local pruritic dermatitis, also known as ground itch. The larvae migrate through the dermis, entering the bloodstream and moving to the lungs within 10 days.

Once in the lungs, the hookworms penetrate the alveoli and are carried to the glottis by means of the ciliary action of the respiratory tract. During pulmonary migration, the host may develop a mild reactive cough, sore throat, and fever that resolve after the worm migrates into the intestines. At the glottis, the larvae are swallowed and carried to their final destination, the small intestine. During this part of the migration, the larvae undergo 2 further molts, developing a buccal capsule and attaining their adult form. Using this buccal capsule, the worms attach themselves to the mucosal layer of the proximal small intestine, including the lower part of the duodenum, jejunum, and proximal ileum. In 3-5 weeks, the adults become sexually mature, and the female worms begin to produce eggs that appear in the person's feces.

Intestinal blood loss secondary to infection is the major clinical manifestation of hookworm infection.⁷ In fact, hookworm disease historically refers to the clinically significant hypochromic, microcytic anemia and the depletion of iron stores resulting from chronic intestinal blood loss secondary to hookworm infection. Attaching to the mucosal layer and using their mouth parts, hookworms rupture the arterioles and venules along the luminal surface of the intestine. The worms ingested and digested some of the blood from the injured mucosa by means of a multienzyme cascade of metallohemoglobinases. Inhibited host coagulation due to a series of anticoagulants directed against factor Xa and the factor VIIa–tissue factor complex, as well as again platelet aggregation, further exacerbate blood loss.

The amount of blood loss and degree of anemia is positively correlated with the worm burden, whereas hemoglobin, serum ferritin, protoporphyrin levels are significantly and negatively correlated with the number of worms.⁴ In addition, because A duodenale consumes more blood per worm than N americanus does, the severity of anemia may differ as a factor of the hookworm species. Because of the clinically significant blood loss and the ingestion of serum proteins, hypoproteinemia may also develop, which clinically manifests as weight-loss, anasarca, and edema.

Despite their small size, large number, and apparent anatomic simplicity, hookworms continue to evade lasting human immune responses. As part of recent public health efforts to reduce rates of hookworm infection, the evoked immune response has been extensively investigated in both human and animal models.^8,9,10 Although hookworm infection stimulates a helper T-cell type-2 response, the role of this response in maintaining or deterring ongoing infection is debated. levels of immunoglobulin G (IgG) increase in the 2-8 weeks after the primary infection. In addition, in naturally infected populations, levels of all 5 subtypes of immunoglobulins appear elevated, with substantial upregulation of polyclonal immunoglobulin E (IgE). Eosinophilia is commonly observed, peaking at 35-65 days after infection. Hookworm infection also appears to cause upregulation of the cytokine interleukin (IL)-10 and is a proposed mechanism of proinflammatory cytokine suppression.¹¹

The persistent nature of hookworm infection supports the theory that hookworms have evolved adaptive molecular mechanisms to achieve a homeostatic balance with the host immune response. Identified components of the hookworm response include calreticulin, antioxidants, and eotaxin metalloproteinase among others.⁹ This modulation of the human immune response by hookworms has also been postulated to reduce the allergenic response of the host, a theory known as the hygiene hypothesis.

Frequency

United States

Once endemic in the southeast United States, hookworm infection is now rare except in high-risk populations, such as international travelers, refugees, international adoptees, and recent immigrants.

International

The absolute number of hookworm infections is highest in China with 203 million followed by sub-Saharan Africa with 198 million.¹ When prevalences are compared, sub-Saharan Africa is highest with 29% of the population infected followed by East Asia, which has a prevalence of 26%. India, South Asia, and Latin America have slightly decreased but still notable infection rates.

Mortality/Morbidity

The mortality rate is low and likely underrecognized because of its insidious nature. Anemia remains the most significant clinical implication of hookworm disease. Because of chronic reinfection, hypoproteinemia, weight loss, edema, and anasarca may also occur. See Special Concerns.

Age

Although children bear a large disease burden, hookworm infection appears to have an atypical distribution of infection by age. Unlike other soil-transmitted helminth infections, such as those due to Ascaris or Trichuris organisms (for which the incidence peaks in childhood), hookworm infection appears to continue to increase throughout childhood until it reaches a plateau in adulthood.⁷

Clinical

History

• Most individuals with hookworm infection are asymptomatic.¹²
• During the first 1-2 weeks after a cutaneous infection, hookworm produces an intensely pruritic dermatitis at the site of infection termed ground itch.¹²
• Wakana syndrome occurs in people who have been infected with a large burden of A duodenale by means of oral ingestion. This syndrome is similar to an immediate-type hypersensitivity reaction characterized by pharyngeal itching, hoarseness, nausea, vomiting, cough, dyspnea, and eosinophilia.⁷
• Mild cough, dysphagia, and fever may occur during pulmonary migration.
• Loeffler syndrome is rare during pulmonary infection. It is characterized by paroxysmal attacks of cough, dyspnea, pleurisy, little or no fever, and eosinophilic pulmonary infiltrates that last several weeks after the initial infection.⁷
• After the worm migrates into the intestines, patients may have nausea, abdominal pain, and flatulence. These symptoms peak 30-45 days after infection.
• Patients with severe anemia may have fatigue, syncope, or exertional dyspnea. They may also have a history of perverted taste and pica.

Physical

• Stunted growth may be observed in children with severe infection.¹³
• An erythematous, pruritic, papulovesicular rash on the palms and soles at the site of initial infection may persist for 1-2 weeks after initial infection.
• During pulmonary migration, cough, fever, and a reactive bronchoconstriction may be observed, with wheezing heard on auscultation.
• Abdominal examination may reveal midepigastric pain on palpation during the period of intestinal involvement.
• Hypoproteinemia may lead to anasarca and peripheral edema.⁴
• Tachycardia, hypothermia, and pallor may be present due to anemia.
• Stools may be bloody or melanotic.

Causes

Poor sanitation and poverty are well-documented risk factors for hookworm infection. High-risk populations include international travelers, refugees, international adoptees, and recent immigrants.¹²

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