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Fig. 12.8 Hookworm disease: statue (A) and child (B) from Costa Rica with typical stance caused by malnutrition and severe hookworm infection. (Courtesy of Dr. Herman Zaiman and Muriel Jones).

Clinical Characteristics

It is of paramount importance from a clinical standpoint that hookworm infection and hookworm disease be differentiated. The former term refers to patients with mild infections and no symptoms, whereas hookworm disease is applied to those patients with symptoms and anemia. In previous times, all symptoms of a patient with hookworm infection were attributed to the worm itself, but it is now known that many symptoms are the result of concomitant illnesses, especially malnutrition and other parasitic infections.

It is convenient to classify the disease into two phases clinically; namely, the phase of migration and development, and the symptomatic phase coinciding with the appearance of eggs in the feces. In the migratory phase, pruritus, erythema and vesiculation will occur once the filariform larvae have penetrated the skin of the feet or hands. This is known as "ground or dew itch" in people who go barefoot. Secondary pyogenic infection may occur at these sites. Within 1 to 2-weeks, pulmonary symptoms may develop which are usually mild and transient, consisting of a dry cough, sore throat, asthmatic wheezing and slight fever. A chest x-ray will usually be negative. Sputum examination may reveal occult blood, eosinophils and rarely migrating larvae. The pulmonary symptoms, as well as peripheral eosinophilia, are more pronounced and of longer duration with A. duodenale than with N. americanus infection. In the former, an enteritis with uncontrollable diarrhea and foul stools may last indefinitely.

Most patients, especially indigenous people, with hookworm infection remain asymptomatic after the larvae have reached the small intestine and may remain so for prolonged periods, depending on the severity and duration of the infection and the nutrition and natural resistance of the individual. Europeans, Americans and other expatriates, especially children, who have recently arrived in an endemic area may develop minor anemia with fatigue, lassitude and eosinophilia with a light infection of 100 hookworms or less. Other initial symptoms include dyspepsia, nausea and epigastric distress, which may be relieved by specific anthelmintic therapy.

In untreated patients with heavy infections (indigenous as well as immigrants), symptoms can become increasingly severe from the time of oviposition onward. As iron deficiency anemia develops and worsens, the patient may become indolent and have weakness, palpitations, fainting, dizziness, dyspnea, mental apathy and headache. There may be constipation or diarrhea with occult blood in the stools or frank melena, especially in children; there is often an urge to eat soil or pica. Overwhelming hookworm infections may cause listlessness, coma and even death, especially in infants under a year of age. In advanced stages of the disease, the blood hemoglobin may be as low as 1 gm/100 ml and occasionally, especially with A. duodenale infection, peripheral eosinophilia may reach 90-100% with or without leukocytosis. Connor autopsied 3 patients in Uganda with advanced hookworm disease, all of whom had hemoglobin levels of 0.8 to 2 gm/100 ml. The woman with 0.8 gm Hgb had walked to hospital, where she was unfortunately treated with packed cell transfusions rather than oral iron and anthelmintics. The transfusions precipitated acute heart failure and she died within a few minutes.

Indeed, hookworm anemia is a common cause of cardiac failure in the tropics and can be confused with rheumatic carditis. In Kampala, Uganda, hookworm disease accounted for 47% of the male and 69% of the female admissions for anemia (Knight, 1973). Although there are many causes for anemia in the tropics, such as malaria, hemoglobinopathies, and lack of adequate dietary iron or folate, hookworm infection is easily the most common cause, often in association with pregnancy. In chronic advanced infections with associated malnutrition, there is hypoproteinemia as well as marked anemia (Fig. 12.8). The skin is pale, the face puffy, the feet and ankles swollen, and there may be generalized edema or even ascites. There is a high output reversible failure with tachycardia, hypotension and hemic murmurs heard over the enlarged heart. There may also be renal manifestations simulating nephritis.

Reports from Puerto Rico and India conclude that steatorrhea is a direct result of hookworm disease. However, other investigators in Uganda (East Africa) and Nigeria (West Africa) suggest that hookworm infections rarely, if ever, cause malabsorption and steatorrhea. It is suggested that the associated hypoalbuminemia is the cause of the enteropathy. It is possible that at least some of the infections in Puerto Rico and India may be complicated by tropical sprue, which is common in those areas but is extremely rare in Africa. Most investigators in Africa have found few microscopic changes in the intestinal mucosa, and any such changes generally revert to normal after treatment. The general impression from the literature is that the major result of hookworm disease in humans, at least in most countries, is not malabsorption but anemia, malnutrition, retarded development and stunted growth, and cardiac enlargement, with or without failure. The cause of the edema in severe infections is a concomitant loss of protein and chronic malnutrition.

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