More than a billion persons worldwide are infected with one or more species of intestinal nematodes. Table 217-1 summarizes biologic and clinical features of infections due to the major intestinal parasitic nematodes. These parasites are most common in regions with poor fecal sanitation, particularly in resource-poor countries in the tropics and subtropics, but they have also been seen with increasing frequency among immigrants and refugees to resource-rich countries. Although nematode infections are not usually fatal, they contribute to malnutrition and diminished work capacity. It is interesting that these helminth infections may protect some individuals from allergic disease. Humans may on occasion be infected with nematode parasites that ordinarily infect animals; these zoonotic infections produce diseases such as trichostrongyliasis, anisakiasis, capillariasis, and abdominal angiostrongyliasis.
Table 217-1 Major Human Intestinal Parasitic Nematodes
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Table 217-1 Major Human Intestinal Parasitic Nematodes
|Feature||Ascaris lumbricoides (Roundworm)||Necator americanus, Ancylostoma duodenale (Hookworm)||Strongyloides stercoralis||Trichuris trichiura (Whipworm)||Enterobius vermicularis (Pinworm)|
|Global prevalence in humans (millions)||807||576||100||604||209|
|Endemic areas||Worldwide||Hot, humid regions||Hot, humid regions||Worldwide||Worldwide|
|Infective stage||Egg||Filariform larva||Filariform larva||Egg||Egg|
|Route of infection||Oral||Percutaneous||Percutaneous or autoinfection||Oral||Oral|
|Gastrointestinal location of worms||Jejunal lumen||Jejunal mucosa||Small-bowel mucosa||Cecum, colonic mucosa||Cecum, appendix|
|Adult worm size||15–40 cm||7–12 mm||2 mm||30–50 mm||8–13 mm (female)|
|Pulmonary passage of larvae||Yes||Yes||Yes||No||No|
|Incubation perioda (days)||60–75||40–100||17–28||70–90||35–45|
N. americanus: 2–5 y
A. duodenale: 6–8 y
|Decades (owing to autoinfection)||5 y||2 months|
N. americanus: 4000–10,000
A. duodenale: 10,000–25,000
|Principal symptoms||Rarely gastrointestinal or biliary obstruction||Iron-deficiency anemia in heavy infection||Gastrointestinal symptoms; malabsorption or sepsis in hyperinfection||Gastrointestinal symptoms, anemia||Perianal pruritus|
|Diagnostic stage||Eggs in stool||Eggs in fresh stool, larvae in old stool||Larvae in stool or duodenal aspirate; sputum in hyperinfection||Eggs in stool||Eggs from perianal skin on cellulose acetate tape|
Intestinal nematodes are roundworms; they range in length from 1 mm to many centimeters when mature (Table 217-1). Their life cycles are complex and highly varied; some species, including Strongyloides stercoralis and Enterobius vermicularis, can be transmitted directly from person to person, while others, such as Ascaris lumbricoides, Necator americanus, and Ancylostoma duodenale, require a soil phase for development. Because most helminth parasites do not self-replicate, the acquisition of a heavy burden of adult worms requires repeated exposure to the parasite in its infectious stage, whether larval or egg. Hence, clinical disease, as opposed to asymptomatic infection, generally develops only with prolonged residence in an endemic area and is typically related to infection intensity. In persons with marginal nutrition, intestinal helminth infections may impair growth and development. Eosinophilia and elevated serum IgE levels are features of many helminth infections and, when unexplained, should always prompt a search for intestinal helminths. Significant protective immunity to intestinal nematodes appears not to develop in humans, although mechanisms of parasite immune evasion and host immune responses to these infections have not been elucidated in detail.
A. lumbricoides is the largest intestinal nematode parasite of humans, reaching up to 40 cm in length. Most infected individuals have low worm burdens and are asymptomatic. Clinical disease arises from larval migration in the lungs or effects of the adult worms in the intestines.
Adult worms live in the lumen of the small intestine. Mature female Ascaris worms are extraordinarily fecund, each producing up to 240,000 eggs a day, which pass with the feces. Ascarid eggs, which are remarkably resistant to environmental stresses, become infective after several weeks of maturation in the soil and can remain infective for years. After infective eggs are swallowed, larvae hatched in the intestine invade the mucosa, migrate through the circulation to the lungs, break into the alveoli, ascend the bronchial tree, and return—through swallowing—to the small intestine, where they develop into adult worms. Between 2 and 3 months elapse between initial infection and egg production. Adult worms live for 1–2 years.
Ascaris is widely distributed in tropical and subtropical regions as well as in other humid areas, including the rural southeastern United States. Transmission typically occurs through fecally contaminated soil and is due either to a lack of sanitary facilities or to the use of human feces as fertilizer. With their propensity for hand-to-mouth fecal carriage, younger children are most affected. Infection outside endemic areas, though uncommon, can occur when eggs on transported vegetables are ingested.
During the lung phase of larval migration, ∼9–12 days after egg ingestion, patients may develop an irritating nonproductive cough and burning substernal discomfort that is aggravated by coughing or deep inspiration. Dyspnea and blood-tinged sputum are less common. Fever is usually reported. Eosinophilia develops during this symptomatic phase and subsides slowly over weeks. Chest x-rays may reveal evidence of eosinophilic pneumonitis (Löffler's syndrome), with rounded infiltrates a few millimeters to several centimeters in size. These infiltrates may be transient and intermittent, clearing after several weeks. Where there is seasonal transmission of the parasite, seasonal pneumonitis with eosinophilia may develop in previously infected and sensitized hosts.
In established infections, adult worms in the small intestine usually cause no symptoms. In heavy infections, particularly in children, a large bolus of entangled worms can cause pain and small-bowel obstruction, sometimes complicated by perforation, intussusception, or volvulus. Single worms may cause disease when they migrate into aberrant sites. A large worm can enter and occlude ...