Figure 195.1 Life cycle of Ascaris lumbricoides. Adult worms live in the lumen of the small intestine. A female may produce approximately 200,000 eggs per day, which are passed with the feces . Unfertilized eggs may be ingested but are not infective. Fertile eggs embryonate and become infective after 18 days to several weeks , depending on the environmental conditions (optimum: moist, warm, shaded soil). After infective eggs are swallowed , the larvae hatch , invade the intestinal mucosa, and are carried via the portal, then systemic circulation to the lungs . The larvae mature further in the lungs (10 to 14 days), penetrate the alveolar walls, ascend the bronchial tree to the throat, and are swallowed . Upon reaching the small intestine, they develop into adult worms . Between 2 and 3 months are required from ingestion of the infective eggs to oviposition by the adult female. Adult worms can live 1 to 2 years. Source: Division of Parasitic Diseases and Malaria, Centers for Disease Control and Prevention, Atlanta, GA. http://www.dpd.cdc.gov/dpdx/HTML/Ascariasis.htm, accessed 13 September 2013.

Most Ascaris infections are asymptomatic. Adult worms may be seen in emesis or stool and are occasionally coughed up or extruded through the nose. Loeffler’s syndrome, characterized by migratory pulmonary infiltrates and peripheral eosinophilia, results from larval migration through the pulmonary parenchyma and may develop within 2 weeks of ingestion. Clinical manifestations include fever, dyspnea, wheezing, and dry cough. Gastrointestinal complications are generally due to a heavy adult worm burden (e.g., intestinal obstruction from worm masses) or to migration of a single adult worm into the bile or pancreatic duct or the appendix. Complications from worms in other organs are rare.

Ascariasis is diagnosed by the demonstration of ova, larvae, or adult worms. Eggs are readily demonstrated in stool. Barium studies occasionally demonstrate adult worms, either by outlining them with barium or by visualizing ingested barium within the gut of the worm. Eosinophilia is not a feature of adult ascariasis but is a common finding during the migration phase.

Because of the potential for worm migration, all infections, whether symptomatic or not, should be treated. When mixed helminthic infections are being treated, Ascaris should always be treated first, because medications may stimulate worms to migrate. Mebendazole or albendazole is appropriate first-line therapy (Table 195.1). Single-dose therapy with either achieves acceptable cure rates.

Trichuriasis

Like ascariasis, trichuriasis is a widely distributed disease. Humans are the only hosts of T. trichiura (whipworm, so named for the characteristic morphology of adult worms). It is most common in tropical climates, with the highest prevalence in children. Human disease may rarely be caused by related species of porcine (Trichuris suis) and canine (Trichuris vulpis) whipworm.

Eggs passed in stool embryonate after 2 to 4 weeks of maturation in soil. There is no tissue (pulmonary) phase; eggs are deposited directly in the cecum, where larvae hatch and mature into adults over several days. Adult worms survive for up to 8 years in the cecum, where they remain attached to the intestinal mucosa. Egg production begins 2 to 3 months after initial infection, with females releasing up to 20 000 eggs per day.

Most infected individuals are asymptomatic. Moderate worm burdens may cause nonspecific gastrointestinal symptoms, including abdominal pain or distension or diarrhea. Heavy worm burdens more often affect children and may lead to profuse bloody diarrhea or rectal prolapse, the hallmark of trichuriasis in endemic areas. Iron deficiency anemia may also be present, but eosinophilia is uncommon.

The diagnosis of T. trichiura infection rests on demonstration of eggs or adult worms. Endoscopy may reveal colitis and the presence of visible worms hanging within the intestinal lumen. Treatment with a 3-day course of mebendazole or albendazole is recommended (Table 195.1), as single-dose therapy leads to suboptimal cure rates.

Hookworm infection

Hookworm infection affects approximately 740 million individuals, with most cases in Asia and sub-Saharan Africa. Disease due to Necator americanus is most common and is found predominantly in tropical climates, whereas Ancylostoma duodenale infection is more geographically restricted, occurring in northern India; North Africa; the Middle East; and parts of China, Southeast Asia, and South America. Prevalence increases throughout early childhood and then plateaus in early adulthood, with worm burden remaining essentially constant (or declining modestly) throughout the life of the infected host. Other hookworm species, including Ancylostoma ceylanicum and Ancylostoma caninum, rarely cause enteritis, whereas Ancylostoma braziliense infection typically causes cutaneous larva migrans.

The life cycle of hookworm resembles that of Ascaris. Eggs are excreted in stool and hatch in soil, and within 7 days larvae become infective. Following penetration of intact skin, larvae migrate through lymphatics to enter the bloodstream and travel to the lungs, ascend the trachea, and are swallowed. Ancylostoma duodenale larvae may also cause infection by the oral route. Within the small intestine, larvae mature into adults and attach themselves to the intestinal mucosa. Ancylostoma duodenale adults survive for up to 1 year, and N. americanus for up to 9 years. Egg production begins 1.5 to 2 months after infection. Females release 5 to 30 000 eggs per day, depending on the infecting species.

An intensely pruritic erythematous maculopapular eruption, “ground itch,” may develop at entry points of filariform larvae. Dermatitis is more likely with repeated exposure and can be complicated by secondary infection. Loeffler’s syndrome may occur 10 to 14 days after infection, and may be accompanied by an urticarial eruption. Nausea, epigastic pain, or abdominal tenderness may be present early in the course of disease and with heavy worm burdens. Infection by the oral route may lead to pharyngeal irritation, hoarseness, cough, and nausea (Wakana disease). The hallmark of hookworm infection is chronic iron deficiency anemia, which results from local blood loss at the site of attachment of the adult worms as well as from their ingestion of blood. The occurrence and severity of anemia depend on the infecting species of hookworm (A. duodenale

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