Current Diagnosis & Treatment in Infectious Diseases

Section VII - Parasitic Infections

86. Nematodes

James M. Steckelberg MD

Walter R. Wilson MD

Essentials of Diagnosis

  • Intestinal nematodes: demonstration of characteristic eggs or parasites in stool.
  • Bloodstream nematodes (filariasis): clinical diagnosis can be made; fresh blood smear may be confirmatory.
  • Tissue nematodes: clinical diagnosis can be made; skin snip or other tissue examination may show organism.

General Considerations

Nematodes (roundworms) are nonsegmented, tapered, bilaterally symmetrical, cylindrical organisms that have complete digestive tracts and reproduce sexually. Although > 500,000 species of nematodes have been described, only a small number are commonly encountered as human parasites. Most nematodes have complex life cycles, sometimes involving several larval forms and intermediate hosts or free-living stages. The pathogenic nematodes may be categorized as primarily intestinal or extraintestinal tissue parasites (Box 86-1).



Worldwide, more than 1 billion people are infested with Ascaris lumbricoides, the causative agent of ascariasis or roundworm. More than 4 million people are estimated to be infected in the United States. Infection occurs predominately in the southeastern states and more commonly in younger children, and it is associated with lower socioeconomic status. The organism is acquired through ingestion of embryonic forms of the worm, which are found in fecally contaminated soil. After ingestion, the embryonic eggs hatch in the small intestine, and the larvae undergo a tissue migration phase. During the migration, the larvae penetrate the intestinal wall and travel intravenously to the pulmonary alveoli. In the lungs, the organisms provoke a cough, are swallowed by the host, and subsequently mature into the adult worm in the small intestine. A single adult female ascarid may produce 200,000 ova daily, which are shed in the feces.

Clinical Findings

The majority of ascarid infections are asymptomatic. During larval migration, eosinophilic pneumonia with mild fever, cough, wheezing, pulmonary infiltrates, and peripheral eosinophilia may be seen. Heavier worm loads may result in intestinal obstruction or symptoms caused by migration of the adult worm outside of the small intestine, most commonly into the common bile duct, causing biliary obstruction and associated complications. Rarely, adult worms may be expelled from the anus, nose, or mouth.

Differential Diagnosis

During tissue and pulmonary larval migration, other causes of pulmonary infiltrates with eosinophilia, including hookworm and strongyloides infection, as well as Löffler's syndrome, asthma, and allergic bronchopulmonary aspergillosis, should be considered. Heavy intestinal infection may cause obstruction that mimics other mechanical causes of bowel obstruction. Migration into the biliary system or appendix may be confused with acute cholecystitis, appendicitis, acute abdomen, or biliary obstruction caused by other more common causes.


All patients with ascariasis should be treated, even if asymptomatic, to prevent biliary migration and obstruction (Box 86-2). Ascarids should be treated first in mixed parasitic infections, and they should be treated before general anesthesia because of the risk of inducing migration of hypermotile worms. In some cases, endoscopic removal of worms may be indicated. Stools should be reexamined 2 weeks after therapy and treatment repeated as necessary.

BOX 86-1 Nematodes Pathogenic in Human1


·  Ascaris lumbricoides

·  Ancylostoma braziliense or A. caninum (dog and cat intestinal hookworms; cutaneous larva migrans in humans)

·  Enterobius vermicularis (pinworm)

·  Ancylostoma duodenale (“Old World”), Necator americanus (“New World”) (hookworms)

·  Strongyloides stercoralis

·  Trichuris trichiura (whipworm)

·  Capillaria philippinensis (intestinal capillariasis)

·  Trichostrongylus spp.

·  Anisakiasis (larval fish nematode)

Tissue dwelling

·  Wuchereria spp. (lymphatic filariasis)

·  Brugia spp. (lymphatic filariasis)

·  Loa loa (African eye worm)

·  Mansonella spp.

·  Onchocerca volvulus

   Other tissue nematodes

·  Dracunculus medinensis (Guinea worm)

·  Trichinella spiralis

·  Toxocara spp. (larval stages–visceral larva migrans)

·  Angiostrongylus cantonensis (meningitis)

1 A particular nematode's presence is extremely dependent on the geographic location. For example, tissue–dwelling nematodes are uncommon or nonexistent in the United States.


Prognosis is generally excellent, although reinfection is possible. In rare cases, obstruction of the small intestine by a mass of worms may cause an acute abdominal syndrome. In addition, obstruction of the common bile duct may cause acute biliary colic.


Roundworm infection can be prevented by avoiding ingestion of fecally contaminated soil. Measures to accomplish this include hygienic disposal of fecal waste, avoidance of the use of night soil and proper washing of foods contaminated by soil, hand washing, and avoidance of pica.


Also known as pinworm, infection by Enterobius vermicularis is the most common helminth infection in the United States. Enterobiasis is typically found in clusters of individuals living in close proximity, such as families or institutionalized groups. It is particularly common in school-age children. Adult females migrate nocturnally to the perianal areas, where eggs are deposited and subsequently distributed to fingers, fingernails, bedding, nightclothes, and other areas. Ingestion of the embryonated eggs results in development of intestinal adult worms in 1–2 months.

Clinical & Laboratory Findings

Many infections are asymptomatic. In symptomatic patients, nocturnal anal pruritus and interrupted sleep are typical. Laboratory tests are normal; eosinophilia is not seen with enterobiasis. Although adult worms that resemble small threads may be seen with the naked eye, diagnosis is usually made by documenting eggs in the perianal area in the early morning, before bathing or defecation. This can be done by pressing cellophane tape in the perianal area and examining the tape under the microscope or by using a commercial collection system such as the Swube (Becton Dickinson). Stool examination for eggs is usually not helpful.

Differential Diagnosis

Enterobiasis should be distinguished from other causes of perirectal irritation, including pruritis ani, rectal fissures, moniliasis, hemorrhoids, and strongyloidiasis, among other conditions.


Treatment suggestions are given in Box 86-2.


Prognosis is excellent, although reinfection is common in the setting of continued exposure.


Reinfection is common in households with an infected person; examination for asymptomatic carriers and simultaneous treatment of all infected household members may be required. Household members should practice hand washing before meals and after defecation and should launder bedding and bedclothes to eliminate environmental eggs.


Hookworm infestation is caused by Ancylostoma duodenale or Necator americanus. After hookworm eggs are passed in stool, the larvae hatch and mature in soil, where they become infective after 1 wk. Human infection occurs after direct penetration by larvae of the host's skin, usually through the feet. The hookworm larvae then enter venules and are carried to the lungs, where they penetrate into alveoli. From the alveoli, the larvae migrate to the trachea. They induce cough and are swallowed by the host. The larvae mature into adult worms in the small intestine. Hookworms attach to intestinal mucosa by means of teeth and a well-developed mouth, and they feed on blood and nutrients sucked from the host. Humans are the only known hosts.

BOX 86-2 Treatment of Selected Intestinal Nematode Infections


First Choice

Second Choice


·  Pyrantel pamoate, 10–11 mg/kg once

·  Mebendazole, 200–500 mg once (light infection) up to 100 mg twice daily for 3 d

·  Albendazole, 400 mg once (light infection) up to 400 mg once daily for 3 d

·  Ivermectin, 100–200 µg/kg once daily for 32 d

·  Piperazine, 75 mg/kg once daily for 2 d

·  Levamisole, 150 mg once


·  Pyrantel pamoate, 10–11 mg/kg once

·  Mebendazole, 100 mg once, repeat in 2 wk

·  Albendazole, 400 mg once, repeat in 2 weeks

·  Pyvinium pamoate, 5 mg/kg once, repeat in 2 weeks


·  Pyrantel pamoate, 10–11 mg/kg once daily for 3 d

·  Mebendazole, 100 mg twice daily for 3 d

·  Albendazole, 400 mg once (Ancylostoma1) or once daily for 3 d (Necator1)



·  Albendazole, 400 mg/d once or twice daily for 3–7 d, may repeat in1 wk

·  Ivermectin, 200 µg/kg once daily for 2 d

·  Thiabendazole, 25 mg/kg twice daily for 3 d; continue for 5–7 d in disseminated infection


·  Albendazole, 600 mg once

·  Mebendazole, 100 mg twice daily for 3 d

·  Oxantel pamoate, 15 mg/kg once

1Ancylostoma, “Old World” hookworm: Necator, “New World” hookworm.

Clinical & Laboratory Findings

The initial allergic reaction to larval skin penetration and migration is known as “ground itch,” and is manifested by intense pruritus and vesicular or maculopapular dermatitis. Patients may experience cough, wheezing, fever, and pulmonary infiltrates during pulmonary migration. Peripheral eosinophilia may be marked. During the intestinal phase, which may last several years, heavy worm burdens may result in protein malnutrition and iron deficiency anemia.

Differential Diagnosis

Early in infection, strongyloidiasis, cutaneous larva migrans, contact dermatitis, scabies, and other causes of pruritic dermatitis, especially of the extremities, should be considered. Later, other causes of eosinophilic pneumonia should be considered, including A lumbricoides and Strongyloides stercoralis infections, as well as Löffler's syndrome. Chronic intestinal infestation, with nonspecific gastrointestinal symptoms, may mimic a multitude of gastrointestinal conditions and other causes of iron deficiency.


Re-treatment at 2-wk intervals may be necessary to reduce the worm burden to low levels (see Box 86-2). Because light infections are usually asymptomatic, complete eradication may not be therapeutically necessary. In patients with iron deficiency, supplemental iron therapy (eg, ferrous sulfate, 200 mg 3 times daily for several months, followed by 200 mg daily until iron stores are repleted) may be necessary.


Prognosis with treatment is excellent.


Infection by S stercoralis (threadworm) is especially notable because the worm is parthenogenetic and larvae mature to an infective stage within the intestinal lumen. As a consequence, sequential generations of worms may persist in a single host over many years. Immunocompromise caused by organ transplantation, corticosteroid therapy, hematologic malignancies, or other conditions may result in massive autoinfection, termed the hyperinfection syndrome. Surprisingly, human immunodeficiency virus infection does not appear to increase susceptibility for hyperinfection.

Like other intestinal nematodes, the life cycle of S stercoralis is complex. The initial infection occurs through penetration of the skin by soil-borne free-living infectious larvae. The larvae ultimately reach the proximal intestine via blood-lung migration. Eggs from adult worms hatch in the intestine, producing larvae that may (i) reinfect the same host, (ii) pass to a new host directly via skin penetration, or (iii) give rise to soil-borne free-living adults that may, in turn, produce infectious larvae.

Clinical & Laboratory Findings

Many patients with chronic but low worm burden infections are asymptomatic or have irregular intestinal symptoms. During initial skin penetration, local skin irritation, pruritic dermatitis, urticaria, and serpiginous tracts (“larva currens”) may be seen. During pulmonary migration, symptoms and signs of infection are similar to those of other nematodes that travel through the lung; that is, dry cough, wheezing, low-grade fever, dyspnea, and hemoptysis. Symptoms of chronic intestinal infestation are varied and nonspecific, and they may include bloating, abdominal distension, dyspepsia, epigastric pain, pruritus ani, diarrhea, and flatulence. In immunocompromised patients, hyperinfection syndrome may be manifested by gastrointestinal ulceration, peritonitis, ileus, biliary obstruction, cholecystitis, or hepatic granulomas. Invasion of extraintestinal organs, including meningitis, central nervous system invasion, pericarditis or myocarditis, or pleuritis, may also occur. Gram-negative or polymicrobial bacteremia with sepsis may complicate hyperinfection syndrome.

Diagnosis of strongyloidiasis is made by examination of stool or duodenal aspirate for S stercoralis larvae. Larvae may be present in stool only intermittently. Eggs of S stercoralis are rarely seen in stool specimens.

Differential Diagnosis

The myriad of presentations and potential tissue sites of S stercoralis requires a high index of suspicion for diagnosis. Chronic intestinal symptoms may mimic dyspepsia, irritable-bowel syndrome, inflammatory-bowel disease, malabsorption, sprue, giardial infection, or other causes of chronic or recurring diarrhea. Epigastric pain may resemble peptic ulcer disease. During tissue migration, eosinophilia, pulmonary infiltrates, wheezing, and cough may suggest nematode or ascarid infections as well as asthma, hypersensitivity pneumonitis, allergic bronchopulmonary aspergillosis, or Löffler's syndrome. Hyperinfection syndrome may mimic sepsis or bacteremia caused by enteric organisms from other causes, such as aortoenteric fistula.


Eradication is the goal of therapy (see Box 86-2). When immunosuppression can be anticipated, such as in patients being evaluated for organ transplantation, screening for S stercoralis and eradication should occur before immunosuppression.


In immunocompetent hosts, prognosis is good. Severe infection with multiple complications may occur in immunocompromised hosts with hyperinfection syndrome.


Trichuriasis or whipworm is caused by Trichuris trichiura. These small (30- to 50-mm–length) whiplike nematodes attach to the mucosa of the large intestine, especially the cecum; there is no extraintestinal phase. Infection occurs by ingestion of infective eggs from soil contaminated with feces; 2–4 wk of maturation in soil are required for the larvae within the eggs to become infective; thus, direct person-to-person transmission does not occur.

Clinical & Laboratory Findings

Mild to moderate worm burdens are usually asymptomatic. Heavy infections (> 30,000 eggs/g of feces) may be asymptomatic or cause nonspecific abdominal complaints, including abdominal cramping, bloating, distension, nausea, vomiting, flatulence, diarrhea, or tenesmus. Rectal prolapse and appendiceal obstruction with appendicitis are rare complications of strongyloidiasis. Eosinophilia is common; iron deficiency anemia may be seen with heavy infections that result in chronic occult blood loss.


Treatment of symptomatic trichuriasis is outlined in Box 86-2.


Prognosis is excellent.



Lymphatic filariasis is a bloodstream and lymphatic infection caused by the filarial nematodes Wuchereria bancrofti, Brugia malayi, and Brugia timori. The disease is endemic in the tropics and subtropics of both hemispheres. A mosquito serves as an intermediate host and vector; the peak blood parasitemia and optimum time of the day or night for obtaining blood smears differ in various parts of the world, corresponding to the feeding pattern of the local mosquito vectors. After deposition by mosquitoes of infectious microfilariae into humans during a blood meal, 6–12 mo are required before adult worms mature and begin producing numerous circulating microfilariae to continue the life cycle. Symptoms of acute disease generally occur 8–16 mo after infection in nonindigenous peoples, but the incubation period may be longer in indigenous peoples.

Clinical & Laboratory Findings

Indigenous persons with filariasis are often asymptomatic. In the first few years after infection, variably present clinical manifestations include recurrent episodes of lymphangitis, notable for progression proximally to distally, unlike typical bacterial lymphangitis. These episodes may be accompanied by high fever and resolve within 7–10 d. Epididymitis or orchitis may occur intermittently. Other patients, especially travelers, may have allergic symptoms including urticaria, rashes, and eosinophilia. Chronic infection may result in lymphatic insufficiency, with lymphedema involving the extremities or external genitalia. Hydroceles may also occur. The term elephantiasis refers to advanced changes of chronic lymphedema, including subcutaneous thickening, skin hyperkeratosis, and fissuring.

Tropical pulmonary eosinophilia refers to a syndrome of nocturnal cough and wheezing with diffuse miliary chest x-ray infiltrates, eosinophilia, elevated immunoglobulin E concentrations, and high antifilarial antibody titers. The syndrome is caused by sequestration of W bancrofti or B malayi microfilariae in the lungs and responds to treatment with diethylcarbamazine citrate (DEC).

Diagnosis of filariasis is usually clinical in endemic areas. Confirmation requires demonstration of microfilaria in filtered blood samples, the timing of which should be adjusted to match the nocturnal or diurnal periodicity of the peak parasitemia in the region in which the infection was acquired. The organisms adapt their periodicity to local time zones, but this requires 10–14 d.

Microfilariae are more commonly seen in the bloodstream during the early stages of disease (1–2 years after infection) and are rare in the bloodstream during the lymphatic obstructive stage of disease. Administration of 50 mg of DEC may result in positive blood smears immediately (within 1 h) after administration in otherwise smear-negative individuals. Serologic testing may also be helpful, but both false positive and false negative test results occur.


Symptomatic treatment of acute filarial lymphangitis (eg, antihistamines and aspirin) may be helpful in reducing the intensity of symptoms. DEC is an effective microfilaricidal drug, but the adult worms require a longer course of therapy and sometimes multiple courses of therapy to be eradicated. DEC (2 mg/kg) is administered 3 times daily for 2–3 wk. Allergic reactions (eg, fever, urticaria, or lymphangitis) to injured parasites may occur early in therapy; some authorities suggest smaller doses of DEC (50 mg on the first day, increasing to full dosage over 3–4 d) to minimize these reactions. Antihistamines may also be of benefit. Nonspecific side effects include headache, vertigo or dizziness, malaise, fever, or myalgias. Onchocerciasis should be excluded before DEC treatment. DEC is available in the United States from Lederle Laboratories (800-934-5556).


Because transmission depends on mosquito vectors, control measures are directed at reducing mosquito populations and reducing the number of bites by mosquitoes.



Loiasis (African eye worm infection) occurs in rainy areas of central and West Africa. The filarial parasites are transmitted by the bite of an infected Chrysopsspp. horsefly. Organisms mature in the subcutaneous tissues, where adult worms may live for more than a decade and release microfilariae into the circulation.

Clinical Findings

Adult worms migrate through subcutaneous tissues at rates ≤ 1 cm/min. This may be asymptomatic, or, especially when migration occurs around or across the eye, noted as conjunctivitis or eyelid edema. Calabar swellings are subcutaneous edematous areas of 3–10 cm that are nonerythematous and do not pit; local pain, pruritus, and mild fever may be present. Calabar swellings are transient, resolving after 2–3 d or 1 wk, only to reappear at irregular intervals in different locations. Calabar swellings do not necessarily contain worms at the time that they appear.

Symptoms of loiasis vary depending on the host. Indigenous populations typically have relatively mild symptoms or are asymptomatic even though they are microfilaremic. Travelers typically have a more symptomatic course, with an increased number and severity of Calabar swellings, marked eosinophilia, leukocytosis, hypergammaglobulinemia, and elevated immunoglobulin E antibodies.



Treatment is with DEC, 3 mg/kg 3 times daily for 21 d. Localized inflammatory reactions to dying adult worms in tissues are common. In patients with microfilaremia, reactions may be more severe including severe neurologic complications and death. Gradually escalating doses of DEC and in some patients systemic corticosteroids may be used. Ivermectin and albendazole have been investigated as alternative therapies to DEC.


Infection with Onchocerca volvulus causes African river blindness, which is the second leading cause of blindness worldwide. Onchocerciasis is transmitted by the Simulium spp. blackfly and is found in equatorial West, central, and East Africa and portions of Central and South America. Larval forms penetrate the skin after the bite of the blackfly, where they mature into adults in the subcutaneous tissues. Microfilariae from mature females migrate back to the dermis where they are ingested by blackflies to continue the life cycle.

Clinical Findings

Cutaneous and connective tissue manifestations of onchocerciasis include the formation, usually within a year, of mobile nodules encapsulating the adult worms in a fibrous tissue mass. Multiple nodules may be present in subcutaneous or connective tissues, especially over bony prominences. Depigmentation, wrinkling, and thickening of skin may be seen with chronic infection. Visual loss is the most serious complication. The earliest eye lesions are punctate keratitis associated with microfilariae within the cornea and anterior chamber. Iridocyclitis and posterior synechiae may develop, which may result in a fixed and distorted pupil. Lesions of the posterior chamber of the eye are less common, including optic atrophy and choroiditis.

Diagnosis is suspected clinically and confirmed by examination of a skin snip obtained without anesthesia from the shoulder or buttock areas, demonstrating microfilariae. Adult worms may be found in biopsied or excised nodules. Slit-lamp examination of the cornea or anterior chamber of the eye may demonstrate microfilariae. Microfilariae are identifiable in urine in 17%–30% of patients > 10 years old.


The treatment of choice is ivermectin, 150 5g/kg orally as a single dose, which kills microfilariae but is less effective against adult worms. Treatment is repeated at 3-mo intervals for 2–3 years. Diethylcarbamazine has been used historically but is less effective and more toxic than ivermectin, and it is no longer recommended by the World Health Organization. Cutaneous nodules, especially on the scalp, may be surgically excised.



Trichinella species are unique among the tissue-dwelling nematodes in that there is no intermediate arthropod vector stage. Trichinella nematodes parasitize carnivores. Adult worms parasitize the small intestine; infective larvae are released and migrate from the intestine to muscle tissues in the host, where the larvae encyst and remain viable and infectious for several years. When the host tissues are eaten, the cyst walls are digested and the larvae again mature within several days in the intestine of the new host, perpetuating the life cycle. Normal hosts of Trichinella spp. include swine, rats, bears, foxes, walrus, and other carnivorous mammals. Humans are an incidental host. Cooking meat to 55°C core temperatures or freezing (-15°C) for 3 wk kills Trichinella spp. larvae.

Clinical & Laboratory Findings

Mild infection is usually asymptomatic. Early (1 wk) after infection, gastrointestinal symptoms predominate, including diarrhea, nausea or vomiting. After the second week, during the muscle invasion stage, systemic symptoms predominate including fever, myalgias, and malaise in most patients. Periorbital edema with conjunctival chemosis and edema of the eyelids is characteristic and common. Symptoms last between 4 and 8 weeks. Rarely, myocarditis or encephalitis may complicate the clinical course. In the laboratory, eosinophilia after the 10th day, sometimes marked, is characteristic, as is elevated immunoglobulin E. Serum creatine phosphokinase and lactic dehydrogenase concentrations reflect myositis. Trichinella serology becomes positive at ≥ 3 wk after infection.


Treatment for trichinosis remains controversial and is primarily supportive. If ingestion is known to occur within 24 h, albendazole (400 mg twice daily, (60 days), mebendazole (200–400 mg 3 times daily for 3 days, then 400–500 mg 3 times daily for 10 days), or thiabendazole (25 mg/kg/day for 1 wk) has been proposed to prevent infection. The drug is not beneficial for established infection or muscle larvae. No specific therapy has been unequivocally demonstrated to be of benefit during the muscle invasion stage.


Spontaneous recovery is the rule, although full recovery may require weeks to months. Death, typically from myocarditis, encephalitis, or pneumonitis, is rare.



The incidence of human trichinosis has declined in developed countries with measures designed to reduce the prevalence of trichinosis in hogs. Trichina in wild game (or pork) can be killed by thorough cooking (internal temperature > 62°C) throughout all parts of the meat or to > 56°C for > 15 min, freezing < -15°C for ≥ 20 d, or gamma radiation.


Toxocariasis, or visceral larva migrans, is a syndrome caused by invasion of human extraintestinal tissues by larvae of Ascaris spp. for which humans are not the usual host of the adult worms. Toxocara canis, commonly found in dogs, is the most commonly implicated species; Toxocara catis (cats) and Belascaris procyonis (raccoons) have also been implicated. Puppies can be infected transplacentally or transmammarily. Pregnancy in dogs reactivates latent infections in the bitch. Animals harboring adult ascarids in the intestine shed copious numbers of eggs into the environment. The eggs become infectious after 3–4 wk and are highly resistant to harsh environmental conditions. Toxocara eggs may remain infectious for months to years. Human infection results from ingestion of eggs from fecally contaminated soil, as may occur for example in children with pica. Direct transmission from pets to humans does not occur, because the eggs require maturation in soil before they become infective.

In young animals, ingested eggs hatch in the intestine and the larvae migrate through extraintestinal tissues, including liver and lung. Larvae induce coughing and are swallowed and then mature into adults in the small intestine to complete the life cycle, which resembles that of A lumbricoides in humans. In older animals, humans, and other hosts such as mice or rats, larvae also hatch from ingested eggs and invade extraintestinal tissues, but the larvae are unable to fully mature and may continue to persist and migrate in tissues as “second-stage” larvae for ≤ 6 months. If these second-stage larvae are ingested by a dog or cat, the larvae may complete their life cycle and develop into adult intestinal worms. Eosinophilic granulomas caused by toxocariasis most often involve the liver or lungs; brain, eye, muscle, and skin involvement has also been reported.

Clinical & Laboratory Findings

Visceral larva migrans is predominately seen in children < 7 years old, and it may be associated with pica. Most cases appear to be asymptomatic. When present, symptoms are variable and depend on the organ systems involved but may include fever, cough or wheezing, and urticarial rash or skin nodules. Hepatomegaly is relatively common. Splenomegaly, lymphadenopathy, and evidence of myocarditis are less common.

Marked leukocytosis, sometimes exceeding 100,000 leukocytes/µl, and hypereosinophilia are common in visceral larva migrans. Polyclonal hypergammaglobulinemia and anti-A or anti-B antibodies to isohemagglutinin antigens (cross-reacting to T canis larval antigens) may occur. An eosinophilic spinal fluid pleocytosis may occur with central nervous system involvement. Chest x-ray abnormalities may be seen in one-third of patients. Toxocara serology may be helpful in confirming the diagnosis, but it should be remembered that in some populations the background prevalence of seropositivity in patients without clinically apparent visceral larva migrans may be high. Identification of larvae in tissue biopsy samples is diagnostic, but not sensitive. Stool examination is not usually helpful.

Ocular visceral larva migrans deserves special consideration. Infection of the eye with Toxocara larvae usually presents as a solitary finding in patients with no known history of visceral larva migrans and without concurrent multifocal, systemic symptoms or signs. The ocular findings are typically a unilateral posterior or peripheral eosinophilic inflammatory mass. Serologies may be negative. The ocular lesion may be mistaken for a retinoblastoma.


No specific therapy has been proven effective. In many cases, symptoms are self-limited and supportive, symptomatic treatment is all that is required. Treatment with a variety of antihelminthic agents has been tried with limited success. These agents include albendazole, thiabendazole, mebendazole, diethylcarbamazine, or ivermectin. Corticosteroids may be of benefit in some patients, especially subconjunctival applications in ocular visceral larva migrans.

Prevention & Prognosis

Puppies, kittens, and household dogs and cats, especially when pregnant or nursing, should be screened and treated as necessary to prevent transmission to humans. Pica should be prevented. Most cases are self-limited although symptoms may persist for months to several years.


Dracunculiasis, or guinea worm infection, is caused by infection by the tissue nematode Dracunculus medinensis. The parasite has been widely distributed in the Indian subcontinent, the Arabian Peninsula, and certain areas of West and central Africa north of the equator. Human infection is acquired by drinking water that contains tiny copepods (Cyclops spp.; “water fleas”) that carry the infectious third-stage larvae. The larvae migrate to subcutaneous connective tissue, usually in the lower extremities, where they develop into adult worms over an extended incubation period that can last up to a year. The adult female may reach 60–80 cm in length. When the extremities are exposed to water, the head of the gravid female protrudes through an ulceration in the host's extremity, a loop of uterus prolapses and discharges large numbers of first-stage larvae into the water. These are ingested by copepods to complete the life cycle.

An active eradication program by the World Health Organization has led to a dramatic reduction in the incidence of dracunculiasis world-wide. Because no nonhuman reservoir is recognized, the disease may be eradicable in the near future.

Clinical Findings

A peripheral chronic cutaneous ulceration, from which the worm may protrude, is the hallmark of dracunculiasis. A local painful, stinging or burning papule may be the first indication of impending ulceration. Generalized symptoms including fever, nausea, vomiting, dyspnea, urticaria or pruritus, or periorbital edema may be associated with development of ulceration. Ulcers on the foot frequently prevent ambulation and may result in long-lasting deformity and secondary infection (including ankle or knee joint infection). Tetanus may also complicate dracunculiasis. Dead or dying worms may result in intense inflammatory reactions. Diagnosis in endemic areas is based on the typical clinical findings.


No specific antihelminthic therapy is available to kill adult worms. Mechanical removal of worms has been practiced for centuries. General treatment is focused on controlling complications, including bed rest, elevation of the affected extremity, wound care, and antibacterial therapy for secondary bacterial wound infections. Metronidazole, 250 mg orally 3 times daily, mebendazole, 400–800 mg orally daily, or thiabendazole 25 mg/kg twice daily may be helpful in promoting the expulsion of the worm, as is immersion of the affected limb in water several times daily.


Noncontaminated drinking water is the key to prevention of dracunculiasis. The World Health Organization prevention program has focused on provision of clean drinking water by using tube wells, hand pumps, or cisterns, by treating drinking water supplies with temephos (to eliminate the copepods), or by boiling water. Water can also by filtered to remove particles > 100 5m.


Markell EK et al: Medical Parasitology, 7th ed. W.B. Saunders, 1992.

Strickland GT (editor): Hunters Tropical Medicine, 7th ed. W.B. Saunders, 1991.