Tropical Medicine Mission Index of Diseases About Tropical Medicine Tropical Medicine Home Page Tropical Medicine Staff

Next Page

Clinical Characteristics

At the time of initial infection, there may be a quite marked reaction at the site of larval penetration. A few minutes after entry there will be focal erythema, edema, urticaria and petechiae, accompanied by itching. The urticaria is more marked in patients who have already been sensitized by a previous infection.

Around the anus during autoinfection the eruption is linear (larva currens), and the larvae moving under the skin cause a severe pruritus. The appearance may mimic the "creeping eruption" of cutaneous larva migrans.

Many Strongyloides infections are light and associated with few or no systemic signs and symptoms, especially during the period of initial migration through the body. Certain individuals, however, are known to be at risk of developing severe strongyloidiasis, including those who have chronic lung disease, are older than 65 years, have altered cellular immunity, or are using corticosteroids. It appears that gastric acid helps prevent massive S. stercoralis infections and thus achlorhydria, and that the use of antacids or H2 blockers increases the risk of severe infection in patients from endemic areas. Surgically created intestinal blind loops also pose a risk for Strongyloides infection by delayed clearance and overgrowth of intestinal organisms.

Pulmonary symptoms may develop during the migration of the larvae in the lungs. These can vary from an innocuous cough and mild hemoptysis to occasional frank pneumonia or asthma. Bronchopneumonia may be associated with a high eosinophilia similar to Löffler's syndrome or the pneumonitis seen during the larval phase of ascariasis, paragonimiasis, and several other parasitic diseases. Generally, the pulmonary symptoms of strongyloidiasis are milder than might be expected from the underlying pathological process.

However, patients with chronic lung disease, such as asthma, chronic bronchitis, emphysema, or interstitial fibrosis are more prone to develop severe pulmonary strongyloidiasis. The presence of fibrosis, bullae, bronchial mucous plugs, and preexisting infection may delay the transit of filariform larvae through the lungs, permitting them to mature into adult ovipositing worms. This repetition of the worm's entire life cycle within the lungs in some patients can occasionally result in dissemination of the parasite throughout the thorax, causing pulmonary hemorrhage with hemoptysis, pleuritis with hemorrhagic pleural fluid, severe bronchopneumonia, and rarely pericarditis. Peripheral blood eosinophilia is common, except in patients with the hyperinfection syndrome, where there may be suppression of eosinophils by steroids or by associated bacterial infection. Patients with the hyperinfection syndrome may develop adult respiratory distress syndrome (ARDS) with pulmonary insufficiency requiring intubation and mechanical ventilation.

The abdominal symptoms associated with strongyloidiasis depend on the intensity of the infection. Some patients will be asymptomatic. In others, there may be mild, moderate, or severe gastrointestinal complaints relating particularly to the duodenum and jejunum. The symptoms may simulate gastritis or duodenitis with vague midepigastric burning sensation and pain, sometimes crampy and relieved by antacids, but exacerbated rather than relieved by food. There may be nausea, lassitude, and local tenderness. Later, especially with autoinfection, the pain is more diffuse, abdominal distention and discomfort predominate, and vomiting is occasionally present. There may be diarrhea, often watery and with mucous, alternating with constipation. Weight loss, anorexia, and weakness may develop. The clinical presentation may resemble peptic ulceration, giardiasis, hookworm disease, amebiasis, or sprue with loss of weight, fat, protein, and electrolytes. There may be increasing malabsorption of fat and vitamin B 12 with chronic diarrhea and protein-losing enteropathy; this may be reversed with antihelminthic therapy and is thought to be in part an immune-based hypersensitivity with histamine release. If not controlled, this condition may lead to overwhelming, rapid malnutrition and death. Attacks are frequently recurrent, possibly due to autoinfection. The illness readily becomes chronic and must be considered among the many causes of intestinal malabsorption.

In advanced cases, vomiting may become persistent, and there will be ankle edema, dehydration, and cachexia. The liver will enlarge and the skin changes of protein malnutrition (a scaly purpuric rash) may develop with dyspigmentation and desquamation. These severe changes can be reversed by adequate treatment and elimination of the worms. In patients with advanced disease, there may be dissemination of the larvae, as the adult worms and larvae honeycomb the entire wall of the intestine and carry E. coli and other bacteria into the blood stream, producing peritonitis and septicemia.

Treatment with immunosuppressants or steroids often changes a benign course of strongyloidiasis to a malignant one with hyperinfection, pulmonary edema and hemorrhage. Thus, patients considered for immunosuppressive therapy for any reason (eg, malignancy, transplant, arthritis, inflammatory bowel disease) should have strongyloidiasis excluded before starting therapy. The possibility of Strongyloides infection must be considered in patients who develop severe pulmonary and gastrointestinal symptoms while undergoing such therapy. S. stercoralis is but one of many opportunistic organisms which may invade the respiratory and intestinal tracts of patients with AIDS, causing pulmonary edema and hemorrhage and intestinal ulcerations, and thus seriously, and often terminally, complicating this modern scourge of humankind. However, a recent study from South America (Dias et al, 1992) compared strongyloidiasis in AIDS and non-AIDS patients and found a similar prevalence of infection in both groups. Worldwide reports of Strongyloides infection in patients with HIV infection or AIDS remain scarce, except from Africa where reports suggest that dissemination is much more likely in HIV-infected patients.

In summary, the clinical diagnosis of strongyloidiasis is often difficult and delayed largely because the signs and symptoms are nonspecific. The constellation of findings, such as peripheral eosinophilia,bronchospasm, bronchitis or pneumonia, and abdominal pain or diarrhea should suggest the diagnosis in patients from endemic areas. The disease should also be suspected if peripheral eosinophilia develops in those on steroid therapy or who are otherwise immunosuppressed, or if there is a worsening of pulmonary and gastrointestinal signs and symptoms following steroid therapy.

Back to the Table of Contents

Copyright: Palmer and Reeder