Rudolph's Pediatrics, 22nd Ed.

CHAPTER 324. Ascariasis

John S. Schieffelin and Richard A. Oberhelman

EPIDEMIOLOGY

Ascariasis is caused by the intestinal roundworm Ascaris lumbricoides. The World Health Organization has estimated that more than 800 million people are infected with A lumbricoides, with the largest number of infections occurring in Asia.1,2 In areas of high prevalence, infection rates as high as 95% have been noted. Tropical areas with warm, wet climates favor year-round transmission and are more likely to have high prevalence rates. In the United States, the highest infection rates are among immigrants from developing countries (20–60% infected in some surveys). Young children are infected most frequently, with peak prevalence in children between the ages of 3 and 8 years living in the tropics. Intensity of infection or worm burden typically decreases significantly after the age of 15 years. Infections tend to cluster in families. Individuals may be asymptomatic and shed eggs for years, thus enhancing transmission.

PATHOPHYSIOLOGY

Ascaris is the largest intestinal roundworm that commonly infects humans: females measure 20 to 40 cm long, and males measure 15 to 30 cm long (eFig. 324.1 ).3 The female lays approximately 200,000 eggs daily; eggs are broadly ovoid and 45 to 75 μm by 35 to 50 μm. Fertilized eggs have a 3-layer coat with a bile-stained, mamillated outer shell. Unfertilized eggs are broader and longer (ie, approximately 90 μm by 45 μm) and usually lack the mamillated outer coat (Fig. 324-1).

Eggs are passed in the host’s feces and become infective in the environment only after the first-stage larva molts within the egg (embryonation). The eggs are resistant to drying, low temperatures, and many chemicals. Children often infect themselves and others by playing in the same areas where they eliminate their wastes. Where human wastes are used as fertilizer (eg, Asia), Ascaris infection is especially frequent.

FIGURE 324-1. Fertilized (left) and unfertilized (right) Ascaris egg, 2000× magnification. (Source: http://www.dpd.cdc.gov/dpdx/HTML/Ascariasis.htm. Accessed January 13, 2008.)

When embryonated eggs are ingested and stimulated by enzymes in the duodenum, the larvae emerge, traverse the intestinal mucosa, and enter the mesenteric lymphatics and venules (Fig. 324-2). They then enter the portal circulation and reach the pulmonary vascular bed, perforate the alveolar wall, ascend the respiratory tree to the epiglottis, and are swallowed. The vast majority of ascarids finally settle in the jejunum, where mature worms mate and females begin laying eggs in 2 to 2.5 months. After a life span of 10 months to 2 years, they are passed in the stool.

CLINICAL MANIFESTATIONS

During the period of larval invasion and migration, cough, dyspnea, fever (39.5°C/103.1°F) to 40.5°C/104.9°F), rales, and dullness to percussion of the chest may be evident. Invasion of the respiratory system by migrating larvae results in alveolar hemorrhages, and pulmonary damage may be extensive, especially with large numbers of larvae. Hemoptysis may occur, and larvae may be found in the sputum. Shifting, consolidated infiltrates, and widening of the pulmonary hilum may be seen, and the eosinophil count often is very high (Löffler syndrome). During this phase, other manifestations of hypersensitivity such as urticaria and wheezing may occur with repeated infections. Larvae occasionally may traverse the pulmonary circulation and produce serious lesions in the eye, central nervous system, and kidney, resembling visceral larva migrans caused by Toxocara larvae.

Unless they are numerous, adult worms in the small intestine generally are associated with few symptoms. The most frequently noted symptoms in children are vague epigastric pains, nausea, vomiting, and anorexia. Severe, intermittent, colicky abdominal pain at times may result from partial intestinal obstruction. The more serious problems encountered with Ascaris infection result from migration of adult worms into the bile and pancreatic ducts, where they may induce biliary stone formation, pancreatitis, small intestinal perforation, and complete intestinal obstruction with intussusception. Worms occasionally may migrate cephalad and emerge through the mouth or nose, or migrate posteriorly and pass through the rectum.

FIGURE 324-2Ascaris lifecycle (see text). (Source: http://www.dpd.cdc.gov/dpdx/HTML/Ascariasis.htm. Accessed January 13, 2008.)

Heavy infections may lead to impaired absorption of dietary proteins, lactose, and vitamin A. In addition, there is evidence that ascaris infection is associated with stunting of growth, developmental retardation, and malnutrition. These effects are accentuated in the presence of heavy worm burden and may improve with treatment. Treatment may also lead to improvement in physical fitness and appetite.2,4

DIAGNOSIS AND TREATMENT

Generally, the diagnosis is established by identifying typical eggs of Ascaris in the feces. Eggs are usually abundant, and stool concentration is rarely needed to see them. However, occasionally only unfertilized or decorticated eggs are present in stool samples, and these may be difficult to recognize. If a patient brings a spontaneously passed worm to the clinic, a stool should be examined to ascertain whether any other worms remain. Because ascariasis is associated with asthma and other allergic manifestations, stools should be examined in patients with those symptoms, particularly if they are from an endemic area. Ultrasonography may be useful to diagnose biliary tract invasion. Serologic tests are rarely needed, although the bentonite flocculation test, indirect hemagglutination, and enzyme-linked immunosorbent assays have been useful diagnostic tests in some unusual cases.

Anthelminthic agents available to treat ascariasis are reviewed in Chapter 323 and Table 323-1. Briefly, although not approved by the Food and Drug Administration for the treatment of ascaris, albendazole is the drug of choice given as a single dose of 400 mg to both adults and to children over 24 months.6,7 Albendazole is recommended at a reduced dose of 200 mg for children 12 to 24 months of age, and it has been used in children as young as 12 months without increased reports of side effects.8 Alternatives include mebendazole and ivermectin. Intestinal obstruction is a complication seen most often in young children with a narrow lumen in their distal ileum, and it often responds to medical management: duodenal suction, parenteral fluids, electrolyte correction, and instillation of piperazine (an anthelminthic drug that paralyzes worms) into the duodenal tube. If this fails, the obstructing worms must be removed surgically.

Strategies for control of intestinal helminth infections in developing countries, and of ascariasis in particular, are frequently based on massive countrywide anthelminthic treatment campaigns, usually using albendazole.4,9 The World Health Organization and ministries of health in many developing countries advocate regular (usually annual) population-based treatment for elementary school–aged children, who statistically are at highest risk. In most cases, treatment is administered without screening stool specimens before treatment. This approach is logical in many low-income areas because rates of helminth infection and reinfection are extremely high, single-dose therapy with albendazole is highly effective and well tolerated, and poor sanitation linked with poverty makes environmental control practically and economically unfeasible.