Ascariasis infects approximately 25% of the world’s population.^1,² It is prevalent in warm countries and areas of poor sanitation and is endemic to the southern United States. Ova can remain infective for several years. They are sensitive to temperatures higher than 65° C or lower than 20° C, direct sunlight, and organic solvents. Ascaris lumbricoides reaches up to 40 cm and is characterized by a constricted area at the junction of the first and middle thirds. The golden brown ovoid eggs measure 60 by 40 mcm.

Transmission and Life Cycle

Ascariasis is transmitted by ingesting mature eggs from contaminated soil or in conjunction with human feces used as fertilizer. Infection may cross into nonendemic areas through vegetable transport and tainted water. Children frequently contract the disease by playing in dirt.

Fertilized eggs become infective in soil 3 to 4 weeks after excretion. When the eggs are swallowed, the larvae hatch in the duodenum, penetrate the intestinal wall, and migrate through the portal venous system to the liver. The larvae migrate through the right side of the heart, the lungs, and into the tracheobronchial tree. Over 2 weeks, the larvae are carried up the trachea to the larynx, where they move into the esophagus and are swallowed a second time, to reach the small intestine, where they mature. Female Ascaris worms lay eggs 2 to 3 months after ingestion and produce up to 240,000 eggs per day. The life span of Ascaris is 6 months to 1 year. Ascaris coexists with Trichuris trichiura in the United States, predominantly in the Appalachian Mountains.

Presenting Signs and Symptoms

Many patients are asymptomatic or have mild symptoms, and the infection ends after expulsion of the adult worms. Ectopic migration is possible, and it causes severe clinical manifestations. The pulmonary larval migration occurs 9 to 12 days after egg ingestion and may manifest with cough, bloody or mucoid sputum, pleurisy, and fever.

Eosinophilia develops during this pulmonary migration and may manifest as eosinophilic pneumonitis, known as Loeffler syndrome. Chest radiographs may demonstrate small, rounded infiltrates that are transient and usually resolve after several weeks. Loeffler syndrome is seen mainly in ascariasis, but it also may occur in other parasitic infections such as hookworm infestation and strongyloidiasis. Allergic reaction can occur with reinfection. Two to 3 months after ingestion, the parasite matures in the small intestine and can cause abdominal pain, nausea, vomiting, anorexia, diarrhea, constipation, volvulus, or intussusception. Biliary obstruction and intestinal inflammation can manifest as an acute surgical abdomen, mimicking acute appendicitis or cholecystitis. Liver abscesses and pancreatitis are possible when the female worm migrates up the common bile duct. Protein malnutrition and intestinal obstruction are more likely to occur in heavily infected children rather than in adults.

Diagnosis and Medical Decision Making

The diagnosis can be made from the passage of worms in the stool or by finding eggs in the feces. A single stool specimen sent for ova and parasite examination is usually sufficient. As the worm transverses the esophagus, it may be coughed out. In eosinophilic pneumonitis, larvae may be isolated from sputum or gastric aspirate.

Gastrointestinal radiographic examination may visualize adult worms on contrast studies, ultrasound scans of the pancreatic-biliary system, plain abdominal films, and endoscopic retrograde cholangiopancreatography (ERCP). ERCP can be therapeutic in extracting worms. Serologic antibody tests include complement fixation, precipitin, agar gel diffusion, immunoelectrophoresis, and the radioallergosorbent test.

Intestinal Roundworms: Necator and Ancylostoma (Hookworms)

Epidemiology

Hookworm infestations of Ancylostoma duodenale prevail in southern Europe, northern Asia, and North Africa, whereas Necator americanus is the main species affecting the Western Hemisphere and equatorial Africa. Worldwide, 1 billion persons are believed to be infected with hookworms.³ The frequency of infection is a general indication of the local level of hygiene and sanitation. Disease burden from hookworms results in iron-deficiency anemia and hypoproteinemia.

Transmission and Life Cycle

Hookworm infection is contracted by penetration of the skin or oral mucosa by filariform larvae. Persons who walk barefoot on contaminated soil or who eat contaminated vegetables become infected. Transplacental infection and transmammary infection are also possible. Eggs are passed in the stools to the soil, where they hatch into rhabditiform larvae that develop into filariform larvae. The larvae penetrate the skin or mucosa directly and reach the alveoli through the circulation. The larvae then ascend the airway, enter the esophagus, are swallowed, and reach the small intestine, where they mature.

Adult worms use hooks to attach to the intestinal mucosa, and they suck blood directly from the host. The time frame from skin invasion to egg appearance is 6 to 8 weeks. Ancylostoma adults live on average for 6 to 8 years, and the life span of Necator ranges from 2 to 5 years, but both species of worms can survive for more than a decade.

Presenting Signs and Symptoms

Presentation includes rash, cough, low-grade fever, abdominal pain, diarrhea, generalized weakness, weight loss, heme-positive stools, and eosinophilia. Early larval invasion of the skin causes pruritus and erythematous maculopapular or vesicular dermatitis, known as “ground itch.” Sensitized hosts may have serpiginous tracts as larvae migrate through the subcutaneous tissue, similar to cutaneous larva migrans.

Transient pneumonitis can occur as larvae travel through the lungs. Epigastric pain, inflammatory diarrhea, and eosinophilia may develop with early intestinal invasion. Loss of plasma protein results from malabsorption and increased intestinal permeability and may cause anasarca.

Chronic hookworm infection leads to iron deficiency. In malnourished patients, infection can cause severe anemia and growth delay. Infection in pregnancy may lead to low fetal birth weights and birth defects. Pica and geophagy are observed in infected children.

Diagnosis and Medical Decision Making

Multiple stool specimens for ova and parasite studies or concentration techniques may be necessary to confirm the diagnosis. The parasite burden may be estimated using the Beaver stool or Kato 50 adult slide smear method. The polymerase chain reaction (PCR) technique can identify a hookworm from a single egg.

Hookworm infection may be confused with pneumonia, anemia, and malnutrition from other causes. Hypochromic microcytic anemia, coupled with eosinophilia or hypoproteinemia, indicates a heavy infection.

Treatment

Oral iron supplementation is usually sufficient to correct mild anemia, although blood transfusion may be needed to correct more severe anemia. Vaccine development is currently under way, based on canine and sheep models.³

Intestinal Roundworms: Strongyloides

Epidemiology

Strongyloides stercoralis is found in the tropics, subtropics, and in temperate areas, and it affects an estimated 55 million to 100 million persons.⁴ Strongyloides is endemic to Southeast Asia, Latin America, the West Indies, Bangladesh, Pakistan, Africa, Spain, and the Appalachian region of the United States. S. stercoralis is an unusual helminth in its ability to replicate within the human host, thus resulting in continuous autoinfection. The infection is often difficult to eradicate, especially in immunocompromised hosts (Box 177.1). The larvae can disseminate and can cause systematic disease and mortality.

Box 177.1 Strongyloidiasis in the Immunocompromised Patient

Immunocompromised hosts are at risk for hyperinfection syndromes, in which filariform larvae cause colitis, malabsorption, ulcerative enteritis, ileus, systemic dissemination, gram-negative sepsis, meningitis, pneumonia, intraabdominal abscess, or acute respiratory distress syndrome. Immunosuppressive therapy, especially glucocorticoids, should be avoided in patients suspected to have Strongyloides infection because hyperinfection and iatrogenically caused fatal outcomes may result. Additional risk factors for hyperinfection and disseminated strongyloidiasis include infection with human T-cell lymphotropic virus-1, solid organ transplantation, hematologic malignant disease, hypogammaglobulinemia, uremia, malnutrition, diabetes mellitus, and chronic alcohol consumption.⁴ Strongyloides does not appear to be a common opportunistic pathogen in human immunodeficiency virus (HIV)–positive patients, and the risk of hyperinfection is not increased with HIV coinfection.⁴

Transmission and Life Cycle

In addition to replication within the human host, Strongyloides can survive in a free-living cycle in soil. The rhabditiform larvae can directly transform into infective filariform larvae or a free-living soil form. The filariform larvae penetrate skin or mucosa, travel to the alveoli, and ascend the airway. The larvae are then swallowed and reach the small intestine. The host has no adult male worms, and the 2-mm female worms reproduce by parthenogenesis, hatching eggs within the intestinal mucosa. Rhabditiform larvae migrate to the intestinal lumen and either pass into the feces or directly transform into filariform larvae and cause autologous reinfection.

Presenting Signs and Symptoms

Patients may be asymptomatic or have mild abdominal discomfort, cough, dyspnea, wheezing, and peripheral eosinophilia. Ten percent of patients present with wheezing as their primary complaint.⁵ If adult worms invade the duodenojejunal mucosa, the symptoms can mimic those of peptic ulcer disease, and small bowel obstruction may occur.

Fluctuating eosinophilia is a common finding. Strongyloidiasis may also manifest with urticaria, usually recurrent along the buttocks and wrists. These urticarial serpiginous eruptions are called larva currens, and they are pathognomonic findings.

Diagnosis and Medical Decision Making

Stool examinations need to be repeated 3 to 5 times. An immunosorbent assay for aspiration or biopsy of duodenojejunal contents is also available. Serum immunoglobulin G (IgG) antibodies can be detected with enzyme-linked immunosorbent assay (ELISA). In disseminated strongyloidiasis, sputum, bronchoalveolar lavage samples, and surgical drainage fluids should be examined for larvae. Eosinophilia greater than 5% or a finding of more than 400 eosinophils/microliter is consistent with Strongyloides infection.⁵

Strongyloidiasis can mimic gastroenteritis, gastritis, colitis, irritable bowel syndrome, asthma, and pneumonia. It may also cause meningitis or sepsis.

Treatment

Strongyloidiasis must be treated to avoid hyperinfection. In patients coinfected with human T-cell lymphotropic virus-1 (HTLV-1), treatment failures are common. A regimen of ivermectin plus thiabendazole or ivermectin plus albendazole is recommended for patients with disseminated disease.

Intestinal Roundworms: Enterobius (Pinworms)

Epidemiology

Enterobiasis is worldwide in distribution and is commonly found in young children. Pinworms are most common in developed countries with temperate or colder climates. The adult worms are 6 to 12 mm in length and 0.3 to 0.5 mm in diameter. The eggs are 50 by 25 mcm and are asymmetrically flattened on one side.

Transmission and Life Cycle

Eggs are ingested orally, hatch in the stomach, and pass through to the intestine, where they invade the glandular crypts. The adult worms live in the cecum and appendix and survive for approximately 2 months. Whether pinworms cause appendicitis is not known. The female pinworm migrates out through the rectum and onto the perianal skin to deposit her eggs. Rarely, the worms invade the abdominal cavity and cause threadworm granulomas of the liver, ovary, kidney, spleen, and lung. Transmission of pinworms occurs by direct anus-to-mouth spread from contact with an infected person. It can also be caused by airborne eggs that are shaken free from contaminated clothing or bed linens. Autoinfection is common because patients scratch the pruritic anal area and then bite their nails or put their fingers in their mouth. The whole cycle takes 2 to 4 weeks.

Presenting Signs and Symptoms

Pruritus ani is the main symptom and varies from mild itching to acute pain, generally worse at night. Pinworm disease is essentially an allergic reaction to the release of eggs and other secreted materials from the gravid female. Associated scratching and excoriation can cause secondary bacterial infection. Vulvitis can occur when pinworms enter the vulva and cause a mucoid discharge with pruritus vulvae. Insomnia, restlessness, loss of appetite, weight loss, irritability, and enuresis may be associated with pinworm infection.

Diagnosis and Medical Decision Making

The eggs are rarely seen in the feces, but they are observed when the adult worms migrate to the anus or vulvar area, particularly at night. The “Scotch tape test” is done by pressing a piece of clear sticky tape against the perianal region and then mounting the tape on a slide. The eggs are identified with light microscopy. Patients usually have no eosinophilia or associated anemia.

Treatment

The entire family is treated simultaneously, to avoid reinfection. All bedding and contaminated clothing should be washed. Fingernails should be kept short. Frequent hand washing and bathing may reduce reinfection. Eradication of the parasite may necessitate repeated courses of treatment.

Tissue Nematodes: Trichinella

Epidemiology

Trichinosis has a worldwide distribution. Eight species of Trichinella infect humans. Trichinella spiralis and Trichinella pseudospiralis are found worldwide. Trichinella nativa is found in the Arctic; Trichinella nelsoni occurs in eastern Africa; Trichinella britovi is found in Europe, Asia, and western Africa; and Trichinella murrelli occurs in North America. Trichinella papuae and Trichinella zimbabwensis have also been identified. Human infection results from ingestion of poorly cooked infected meat, particularly pork. Cattle, horse, dog, and wild game meat are also potential sources.

Transmission and Life Cycle

The encysted larvae are released from their capsule by digestive enzymes in the intestine. The larvae then penetrate the intestinal mucosa and mature into adults. After mating, the male worms die, and the female worms discharge larvae to the tissues. After travelling through the circulation, the larvae encyst in muscle and may calcify. Cysts can be seen in the diaphragm, masseter and intercostal muscles, musculature of the larynx, tongue, eye, and heart, and the brain.

The main methods of infection prevention are thorough cooking and regular meat inspection. Trichinella larvae in meat may be killed by heating to a temperature of 77° C or freezing to 15° C for 3 weeks. Both encysted and free Trichinella larvae remain viable for years.

Presenting Signs and Symptoms

The presenting symptoms depend on the level of infection and the location of the larvae. Two phases are recognized: intestinal and muscular. Enteric invasion may cause diarrhea, fever, nausea, vomiting, and abdominal pain during the first week of infection and is often confused with food poisoning. During the second week, the larvae migrate into the muscles and cause hypersensitivity reactions with fever, eosinophilia, rash, headache, cough, and myalgias.

Cardinal clinical findings of trichinellosis include cachexia, edema, splinter hemorrhages, dehydration, ongoing fever, and pruritus. Myocarditis, encephalitis, nephritis, congestive heart failure, pneumonitis, hemiplegia, severe pain, psychiatric disturbances, and epilepsy may develop and lead to death.

Diagnosis and Medical Decision Making

Eosinophilia is a hallmark of trichinellosis. No relationship exists between the level of eosinophilia and the clinical course of disease. Other laboratory manifestations of trichinosis include leukocytosis and elevated creatine phosphokinase, lactate dehydrogenase, and myokinase levels. The diagnosis is made by identification of larvae in blood or tissue. Serologic assays are available, including ELISA, indirect immunofluorescence, and latex agglutination. The circulating antibody can be detected by serologic tests between 2 and 4 weeks after infection. Immunofluorescence is positive 2 to 3 weeks after infection. If serologic test results are equivocal, larvae may be found in muscle by trichinoscopy. This procedure is performed during the muscular phase approximately 7 days from onset of symptoms with samples taken from the deltoid, biceps, gastrocnemius, or pectoralis major muscle.

Trichinosis resembles many conditions: typhoid, encephalitis, myositis, and tetanus. Trichinosis may also be confused with collagen disorders such as periarteritis nodosa and rheumatoid arthritis.

Treatment

For light infections, supportive therapy with analgesics, rest, and antipyretics usually suffices. Patients with severe hypersensitivity reactions such as myositis, myocarditis, and central nervous system (CNS) disease may benefit from corticosteroids tapered over 2 to 3 weeks. Corticosteroids are not indicated for mild disease because the use of these agents can increase the number of circulating larvae.

Tissue Nematodes: Filaria

Epidemiology

Filarial nematodes are estimated to infect 170 million persons.¹ Four main species cause most serious infections: Wucheria bancrofti, Brugia malayi, Onchocerca volvulus, and Loa loa. W. bancrofti is found in Africa, South America, Asia, the Pacific islands, and the Caribbean. Brugia species are found mainly in Southeast Asia, Asia, and Indonesia.