Konrad L. Davis
Helminthic (worm-related) pulmonary infections are caused by either roundworms (nematodes) or flatworms, which include flukes (trematodes) and tapeworms (cestodes). Although helminthic infection is ubiquitous in nature, human helminthic lung disease is relatively infrequent in North America. The diagnosis is usually considered in travelers returning from endemic regions. The parasites reach the lungs by hematogenous spread or direct migration, and disease is caused by either the parasites themselves or by the host’s immune response to helminthic antigens. Pulmonary manifestations vary from asymptomatic to catastrophic. Nearly all helminthic life cycles require a phase of growth externalized to their host. The four modes of transmission to a human host include fecal–oral, transdermal, vector-borne, and predator–prey.
The principal pathologic nematodes include Ascaris, hookworm species (Ancylostoma duodenale and Necator americanus), Strongyloides, and Filaria. Ascaris lumbricoides is among the most common intestinal nematodes in the world, infecting approximately 25% of the global population. Though found predominately in the tropics, it also infects up to 4 million people living in the southern United States, especially in rural areas. Humans are infected by ingestion of contaminated soil or food that contains the Ascaris egg, which then hatches in the gastrointestinal tract. The larvae subsequently migrate through the venous system to the lungs, where they enter the alveoli and ascend the tracheobronchial tree. The worms are then swallowed, where they are returned to the intestine to mature into adult worms capable of reproduction just 2 to 3 months after initial ingestion.
Pulmonary disease results from a hypersensitivity response to migrating larvae. The manifestations are usually limited to transient pulmonary infiltrates and peripheral eosinophilia. A few patients develop the stigmata of Löffler syndrome (mild fever, cough, dyspnea, wheezing, sternal pain, and mild hemoptysis associated with migratory pulmonary infiltrates and peripheral eosinophilia). This typically occurs 1 to 2 weeks after egg ingestion. Secondary bacterial pneumonia is common, and mechanical airway obstruction has been described in the presence of a high worm burden.
Eosinophilia and elevated serum immunoglobulin E (IgE) levels are common. Chest radiographs may show patchy consolidation or diffuse miliary infiltrates. Sputum is rich in eosinophils and in crystallized protein from fragmented eosinophils (Charcot–Leyden crystals). Eggs are rarely found in the sputum but may be recovered from gastric aspirates. The diagnosis can be made by demonstration of Ascaris eggs in the stool within 3 months of a self-limited eosinophilic pneumonitis. Serum serologies are available, but their use is mainly as a research tool in endemic areas. Preferred treatment includes albendazole (400 mg single oral dose) or mebendazole (100 mg twice daily for 3 days).
The hookworms, Ancylostoma duodenale and N. americanus, infect humans through direct penetration of skin by larvae found in moist contaminated soil. The geographic distribution is worldwide and includes the southeastern Unites States (N. americanus). As with Ascaris, the hookworm larvae migrate to the lung through the venous system and can produce a self-limited Löffler syndrome (see above) before they inhabit the small intestine. Also similar to ascariasis, the stool examination may not be positive for up to 2 months after the pulmonary symptoms develop. Symptoms are usually self-limited, and treatment for pulmonary complaints is generally not necessary, but inhaled bronchodilators may provide symptomatic relief. Eradication of the parasite can be achieved with mebendazole (100 mg two times a day for 3 days or a 500-mg single dose) or albendazole (400-mg single oral dose).
Strongyloides stercoralis is endemic in tropical and subtropical areas and in the southeastern United States. A relatively unique feature of Strongyloides stercoralis is its ability to complete its life cycle entirely within the human (termed “autoinfection”), potentially leading to a substantial worm burden. Although the acute and chronic stages generally produce only mild symptoms in normal hosts, in immunocompromised conditions (AIDS, corticosteroids, and malignancy), it can be devastating. Strongyloides migrate hematogenously to the lungs after the larvae penetrate the skin. From here, they ascend the tracheobronchial tree and are swallowed. In the duodenum, they mature and produce larvae, some of which can penetrate the colonic mucosa or perianal skin, resulting in autoinfection.
The initial skin penetration by strongyloides may lead to local inflammation, edema, and a serpiginous erythematous track that rarely comes to medical attention. The gastrointestinal manifestations include duodenitis, abdominal pain, and malabsorption that can be seen with high worm burdens. The pulmonary manifestations in the immunocompetent patient include cough, wheezing, and a recurrent pneumonitis. Peripheral blood eosinophilia is not necessarily present. Asthma induced by chronic strongyloidosis will paradoxically worsen with corticosteroid administration.
In the immunocompromised host (e.g., those using corticosteroids), the colonic penetration of filariform larvae occurs unchecked and can widely disseminate to lungs, liver, central nervous system, and other organs. This so-called hyperinfection syndrome carries an extremely high mortality (>90%). The pulmonary manifestations at this stage include adult respiratory distress syndrome (ARDS) or secondary bacterial infections caused by enteric Gram-negative bacilli translocating with the worms.
The diagnosis of Strongyloides infection is often made by examination of multiple stool specimens (as a single stool sample has a low sensitivity, roughly 25%). Enzyme-linked immunosorbent assays (ELISA) are about 90% sensitive and have a negative predictive value of 95% in some populations. In hyperinfection syndrome, strongyloidosis has been diagnosed by examination of sputum or cerebrospinal fluid. Ivermectin (200 μg/kg/day for 2 days) is preferred over albendazole (400 mg twice daily for 3 days) for treatment.
Filariasis is caused by a nematode infection of the lymphatics and subcutaneous tissue. The most common filarial species include Wuchereria bancrofti, Brugia malayi, and Brugia timori
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