Strange and Schafermeyer's Pediatric Emergency Medicine, Fourth Edition (Strange, Pediatric Emergency Medicine), 4th Ed.

CHAPTER 65. Common Parasitic Infestations

Alisa McQueen

Steven Lelyveld

HIGH-YIELD FACTS

• Virtually all organ systems are at risk for parasitic infestation, with symptoms depending on the system(s) involved. Some parasites only begin to produce symptoms months to years after the first exposure.

• Ascaris lumbricoides is the largest and most prevalent human nematode, with an estimated one billion cases worldwide. Albendazole (400 mg orally as a single dose) or ivermectin (150–200 μg/kg orally as a single dose) is curative.

• Enterobius vermicularis (pinworm) affects individuals of all ages and socioeconomic levels, with the most common presentation being that of a toddler or small child with anal itch. Scotch tape, placed sticky side to perianal skin when the child first awakens and viewed under low power may reveal the eggs, but may require repeated sampling.

• Trichuris trichiura (whipworm) lives predominantly in the cecum and can cause malabsorptive symptoms, pain, bloody diarrhea, and fever but is usually asymptomatic. A heavy worm burden may cause a colitis-like picture with rectal prolapse and anemia.

• The hookworms, Necator americanus and Ancylostoma duodenale, are one of the most prevalent infectious diseases of humans. The hallmark of hookworm infestation is the microcytic, hypochromic anemia of iron deficiency.

• The avian schistosome Trichobilharzia ocellata is spread by migratory birds to the freshwater lakes of the northern United States. The cercariae cause dermatitis, known as swimmer’s itch.

Parasitic diseases are ubiquitous. Despite worldwide advances in sanitation, new medications, and the heightened awareness of health care providers, between one-fourth and one-half of the world’s population has a parasitic infestation at any given time. Children’s normal developmental oral exploratory behavior places them at particular risk for acquiring parasites. Travel, immigration, the importation of vectors via international trade, and the increased number of immunocompromised hosts have all led to an increase in disease. (see Chapter 59, Evaluation and Management of the Immunocompromised Patient and Chapter 66, Imported Diseases/Diseases in the Traveling Child). Parasitic diseases endemic to the United States are primarily described here.

Three major groups of parasites cause human disease: helminths, protozoa, and arthropods (Anthropods discussed in Chapter XX in dermatology). Three important subgroups of helminths cause human disease: nematodes (roundworms), cestodes (flatworms), and trematodes (flukes).

Important factors to be elicited in the history are included in Table 65-1. Virtually all organ systems are at risk for infestation, with symptoms depending on the system(s) involved. The varied and often nonspecific symptoms produced (Table 65-2) place parasitic infestation on the expanded differential diagnosis of most patients presenting to the emergency department (ED). Symptoms produced depend on the stage of the parasitic life cycle.

TABLE 65-1

Important Aspects of the History in the Child or Adolescent with Possible Parasitic Infestation

Camping trips

Travel to regions with questionable sanitation and water purification practices or a warm climate

Method of food acquisition and preparation

Exposure to pets and other animals, both domestic and wild

Participation in day care

Living in confined situations

Drug abuse

Sexual abuse

Blood transfusions

TABLE 65-2

Symptoms of Parasitic Disease

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NEMATODES (ROUNDWORMS)

image ASCARIASIS

A. lumbricoides is the largest and most prevalent human nematode, with an estimated one billion cases worldwide; most cases of death are because of intestinal obstruction. Although it is most commonly found in tropical and subtropical climates, it is present throughout the United States. Ascariasis is most common in preschool and early-school age children. From an egg measuring 65 μm by 45 μm, this nematode can grow to a length of 30 cm (Fig. 65-1). After being deposited in the stool, the egg matures over 3 weeks. Upon ingestion, the egg hatches in the small intestine. The larvae burrow through the gut mucosa, enter the bloodstream, and migrate to the lungs. They cause shortness of breath, hemoptysis, eosinophilia, fever, and Loffler pneumonia as they break through the alveoli, migrate up the bronchial tree, and are swallowed. Maturing to the adult form, A. lumbricoides can live freely in the small intestine for up to a year, shedding eggs in the stool. At this stage, it usually remains asymptomatic but can cause gastrointestinal symptoms, including pain, protein malabsorption, biliary duct or bowel obstruction, and appendicitis.

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FIGURE 65-1. Ascaris lumbricoides. (Used with permission from S. Margaret Paik, MD.)

Although stool testing for ova is diagnostic, serologic hemagglutination and flocculation tests are available. Albendazole (400 mg orally as a single dose), mebendazole (100 mg orally twice daily for 3 days or 500 mg orally once) or ivermectin (150–200 μ/kg orally as a single dose) is curative. Dosing is the same in adults and children, though ivermectin is approved only for children weighing 15 kg or more. Piperazine salts (50–75 mg/kg for 2 days) are recommended for ascariasis complicated by intestinal or biliary obstruction, as they cause relatively rapid expulsion of the worms.13 If multiple infestations are present, Ascaris should be treated first, as treatment of other parasites may stimulate a large worm burden to migrate simultaneously, causing obstruction.4 Preventive therapy in endemic regions may be considered.

image ENTEROBIASI

E. vermicularis (pinworm) is present in all parts of the United States and affects individuals of all ages and socioeconomic levels. The most common presentation is that of a toddler or small child with anal itch. The egg is oval, approximately 50 μm by 25 μm in size. It is inhaled or ingested and hatches between the ileum and ascending colon, growing to an adult length of 3 mm to 10 mm. The adult may live and reproduce in the colon for 1 to 2 months. The gravid female migrates to the anus, where it deposits embryonated eggs, usually during early morning hours (Fig. 65-2A). When the host stirs, the adult will migrate back into the body, causing symptoms of pruritus ani, dysuria, enuresis, and vaginitis. Scratching and hand–mouth behavior reinoculates the host, and the cycle repeats. Granulomas of the pelvic peritoneum and female genital tract may occur.

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FIGURE 65-2. A. Pinworms. Multiple tiny pearly white worms are seen at the anus. B. This photomicrograph depicts the eggs of the nematode, or round worm, Enterobius vermicularis, mounted on cellulose tape. (Reproduced with permission from Centers for Disease Control Public Health Image Library.)

Scotch tape, placed sticky side to perianal skin when the child first awakens and then viewed under low power (Fig. 65-2B), is usually diagnostic; but repeated examination may be necessary to find the eggs. Treatment is with albendazole, 400 mg orally, pyrantel pamoate (11 mg/kg), or mebendazole (100 mg).1,5 Each drug is given as a single dose, with a repeat given 2 weeks later to remove secondary hatchings.

image TRICHURIS TRICHIUR

T. trichiura (whipworm) is found in southern Appalachia, southwest Louisiana, and other warm rural areas. The life cycle mimics that of E. vermicularis. The eggs are of similar size and configuration, with the addition of a rounded cap at each pole (Fig. 65-3A). The adult resembles E. vermicularis, with a long whip-like projection at one end (Fig. 65-3B). It lives predominantly in the cecum and can cause malabsorptive symptoms, pain, bloody diarrhea, and fever but is usually asymptomatic. A heavy worm burden may cause a colitis-like picture and rectal prolapse and can be associated with anemia and developmental and cognitive deficits.6 Treatment is with albendazole (400 mg daily for 3 days) or mebendazole (100 mg bid for 3 days). Community control should be considered in heavily endemic areas.1,3

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FIGURE 65-3. A. This micrograph depicts an egg from the “human whipworm,” Trichuris trichiura, the causal agent of “Trichuriasis.” B. This micrograph of an adult Trichuris female human whipworm reveals that its size in centimeters is approximately 4 cm (A and B.) (Reproduced with permission from Centers for Disease Control Public Health Image Library.)

image TRICHINOSI

Trichinella spiralis is found throughout the United States, with increasing prevalence in the Northeast and Mid-Atlantic states. Although less than 100 cases of clinical disease are reported annually, cysts are found at autopsy in the diaphragms of 4% of patients. Current control efforts include laws governing the feeding of swine destined for sale to the public (e.g., treatment of garbage used as feed and recommendations for the preparation of meat in the home).7

Digestive enzymes liberate the encysted larvae that lodge in the duodenum and jejunum, grow, and within 2 days, mature and copulate. The females give birth to living larvae that bore through the mucosa, become blood-borne, and migrate to striated muscle, heart, lung, and brain. Host defenses produce inflammation at each site. Although a classic triad of fever, myalgia, and periorbital edema has been described, symptoms of gastroenteritis, pneumonia, myocarditis, meningitis, and seizures can occur.

Most cases are mild and self-limited. The history and physical examination, along with elevation of muscle enzymes and eosinophilia, may suggest the need for further investigation. Serologic tests are available from the Centers for Disease Control and Prevention. Muscle biopsy is confirmative. Treatment with aspirin and steroids, is initially aimed at reducing the inflammatory symptoms. Mebendazole (200–400 mg tid for 3 days and then 400–500 mg tid for 10 days) or albendazole (400 mg bid for 8–14 days) is indicated for severe disease but may not be effective after encystment.1,7

image HOOKWORM

The hookworms N. americanus and A. duodenale are found between 36-degree north and 30-degree south latitude and are one of the most prevalent infectious diseases of humans, with an estimated one billion individuals affected.7The eggs hatch in the soil, releasing rhabditiform larvae 275-μm long that feed on bacteria and organic debris (Fig. 65-4). They double in length, molt, and may survive as filariform larvae for several weeks. Upon contact, they burrow through the skin, causing pruritus (ground itch), enter the blood, travel to the lung, and are ingested, like A. lumbricoides. Although a broad spectrum of symptoms is possible, the hallmark of hookworm infestation is the microcytic, hypochromic anemia of iron deficiency. Each adult hookworm may ingest up to 0.05 mL of blood a day. Children with chronic hookworm disease may develop a characteristic yellow–green pallor called chlorosis. Although more commonly seen with the dog and cat hookworms (Ancylostoma braziliense), these hookworms can also cause the serpentine track of cutaneous larva migrans (Fig. 65-5). Finding the ova in stool is diagnostic.8Albendazole (400 mg qid for 2–3 days), mebendazole (100 mg bid for 3 days), or pyrantel pamoate (11 mg/kg maximum 1 g qid for 3 days) is recommended. Cutaneous larva migrans is usually self-limited, but topical application of 10% thiabendazole, ivermectin (150–200 μg orally), or albendazole (400 mg qid for 3 days) may hasten resolution.1,3,8

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FIGURE 65-4. This micrograph depicts a hookworm rhabditiform larva, which represents its early, noninfectious immature stage. (Reproduced with permission from Centers for Disease Control Public Health Image Library.)

image STRONGYLOIDIASI

Strongyloides stercoralis (threadworm) is found in southern Appalachia, Kentucky, and Tennessee. Like the hookworm, it penetrates the skin, producing pruritus and cutaneous larva migrans. Pulmonary and gastrointestinal symptoms occur as the larvae migrate. The human is a definitive host. Ongoing autoinfection is slowed by the host’s immune response, but immunocompromised patients and the elderly may suffer fatal infestation. The rise in the acquired immunodeficiency syndrome (AIDS) has been mirrored by a rise in reported cases of Strongyloides infestation, and infestation is increasingly common in patients who are immunocompromised for other reasons such as organ transplantation.9 A definitive diagnosis is made by recovering Strongyloides in stool, sputum, or duodenal aspirate. Ivermectin (200 μg qid for 2 days) is recommended. Albendazole (400 mg bid for 7 days) or thiabendazole (50 mg/kg/d divided bid, maximum 3 g/d for 2 days) may also be used. In disseminated strongyloidiasis, treatment may need to continue for up to 2 weeks1,9,10 (see Chapter 59, Evaluation and Management of the Immunocompromised Patient).

TREMATODES (FLUKES)

Few trematodes are endemic to the United States with one important exception of particular interest to the pediatric emergency physician: the avian schistosome, T. ocellata. Spread by migratory birds to the freshwater lakes of the northern United States, the cercariae cause dermatitis, known as swimmer’s itch. The intense reaction produced by host defenses is treated with heat and antipruritics. Severe cases are treated with thiabendazole cream.11

CESTODES (FLATWORMS AND TAPEWORMS)

Cestodes attach to the gut of the host with hooks or suckers at the head (scolex), from which grow segmented proglottids. Each proglottid is equipped to produce large volumes of eggs, which along with the terminal proglottids, pass in the stool and are ingested by the intermediate host. The eggs hatch into a larval stage, either cysticercus (larva with a single scolex in a fluid-filled cyst), cysticercoid (larva with the single scolex filling the cyst), coenurus (a cyst with grapelike daughter cysts internally containing protoscolices), or hydatid cysts (mature cyst filled with numerous immature cysts), depending on the species. Symptoms are produced as these larvae act as space-occupying lesions or cause inflammation. When the intermediate host is ingested by the definitive host, the larvae attach to the intestine and the cycle repeats.

Four cestodes produce most clinical disease seen in the United States: Taenia solium, Taenia saginatum, Diphyllobothrium latum and Echinococcus granulosus. T. solium (pork tapeworm), and Taenia saginatum (beef tapeworm) infestations are generally asymptomatic and are diagnosed when a parent brings a proglottid to the ED for identification (Fig. 65-6). A history of raw meat consumption may be elicited. Patients occasionally will have gastrointestinal complaints. When T. solium enters the cysticercus phase, it may migrate to the heart, brain, breast, eye, skin, or other solid organ. Subcutaneous nodules, visual field defects, focal neurologic findings, acute psychosis, and obstructive hydrocephalus may develop years after infestation.12 Calcified cysts may be found on plain radiographs, and cysts may be seen as a ring of calcification on computed tomography (see neurocysticercosis below). D. latum (fish tapeworm) is becoming more prevalent with the increased popularity of raw fish. Because D. latum absorbs greater than 50 times more vitamin B12 than Taenia, it causes pernicious anemia.

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FIGURE 65-5. Pruritic cutaneous plaque characteristic of cutaneous larva migrans. (Used with permission from Peter Lio, MD.)

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FIGURE 65-6. Scolex of Taenia solium. (Reproduced with permission from Centers for Disease Control Public Health Image Library.)

Echinococcus granulosus (sheep tapeworm) is found in agricultural countries. Most reported cases are from the southeastern United States. Symptomatology is secondary to hydatid cyst formation with mass effect (Fig. 65-7).

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FIGURE 65-7. Abdominal bulge from intraperitoneal cyst of echinococcosis.

Most tapeworms are treated with praziquantel (5–25 mg/kg once). Echinococcus infection and cysticercosis respond best to albendazole (15 mg/kg/d divided tid for 28 days).1,12

PROTOZOA

image AMEBIASIS (E. Histolytica)

E. histolytica, a water-borne single-cell organism, may cause amebiasis. It is found in epidemic proportion after heavy rain in areas of suboptimal sanitation and among closely confined populations. In addition to ingestion of contaminated water, it may be spread by direct human contact, both sexually and through breast milk. Most patients carry amebas asymptomatically in the cecum and large intestine. Heavy infestations of E. histolytica produce a colitis-like picture. These patients may present with nausea, vomiting, bloating, pain, bloody diarrhea, and leukocytosis without eosinophilia. The amebas live at the base of large flask-shaped ulcers. When the infection is severe, direct inspection will reveal pseudopolyps of normal tissue on a base of ulcerative disease. E. histolytica has the capacity to invade the blood, causing abscess formation in the liver (Fig. 65-8), lung, brain, and breast.4 Diagnosis is confirmed with stool specimen or colonoscopic aspiration. Metronidazole (35–50 mg/kg/d divided tid for 10 days) followed by iodoquinol (40 mg/kg/d divided tid for 20 days) is recommended to eradicate this infestation.1,5,13

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FIGURE 65-8. Abdominal CT scan of a large amebic abscess of the right lobe of the liver.

image GIARDIASIS

The flagellate Giardia lamblia thrives in the relatively alkaline pH of the duodenum and proximal small bowel (Fig. 65-9). Infestation occurs after ingestion of contaminated water or other fecal–oral behavior. It is commonly found in day care centers; among travelers, immunocompromised children, and patients with cystic fibrosis; and in association with hepatic or pancreatic disease. Flatulence, nonbloody diarrhea or constipation, abdominal distention, and pain are common symptoms. Fever, weight loss, and fat, carbohydrate, and vitamin malabsorption can occur. Although cysts may appear in the stool, concentration is variable and serial ova and parasite stool examinations are often required to confirm the diagnosis. Fecal immunoassays are commercially available. Metronidazole (15 mg/kg/d divided tid for 5 days) is recommended.5,13

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FIGURE 65-9. Flagellated, binucleate Giardia trophozoite.

REFERENCES

1. Treatment Guidelines from The Medical Letter. Drugs for parasitic infections. Med Lett Drugs Ther. 2007;5(Suppl):e1.

2. Keiser J, Utzinger J. Efficacy of current drugs against soil-transmitted helminth infections: systematic review and meta-analysis. JAMA. 2008;299:1937.

3. Keiser J, Utzinger J. The drugs we have and the drugs we need against major helminth infections. Adv Parasitol. 2010;73:197.

4. Hesse AA, Nouri A, Hassan HS, et al. Parasitic infections requiring surgical interventions. Semin Pediatr Surg. 2012;21:142.

5. Kucik CJ, Martin GL, Sortor BV. Common intestinal parasites. Am Fam Physician. 2004;69:1161.

6. Stephenson LS, Holland CV, Cooper ES. The public health significance of Trichuris trichiura. Parasitology. 2000;121(Suppl):S73.

7. Gottstein B, Pozio E, Näckler K. Epidemiology, diagnosis, treatment and control of trichinellosis. Clin Microbiol Rev. 2009;22:127.

8. Feldmeier H, Schuster A. Mini review: hookworm-related cutaneous larva migrans. Eur J Clin Microbiol Infect Dis. 2012;31:915.

9. Norsarwany M, Abdelrahman Z, Rahmah N, et al. Symptomatic chronic strongyloidiasis in children following treatment for solid organ malignancies: case reports and literature review. Trop Biomed.2012;29:479.

10. Nissapatorn V, Sawangjaroen N. Parasitic infections in HIV infected individuals: diagnostic & therapeutic challenges. Indian J Med Res. 2011;134:878.

11. González E. Schistosomiasis, cercarial dermatitis, and marine dermatitis. Dermatol Clin. 1989;7:291.

12. Brunetti E, White AC Jr. Cestode infestations: hydatid disease and cysticercosis. Infect Dis Clin North Am. 2012;26:421.

13. Wright SG. Protozoan infections of the gastrointestinal tract. Infect Dis Clin North Am. 2012;26:323.