eMedicine Specialties > Pediatrics: General Medicine > Parasitology
Strongyloidiasis
Updated: Jan 23, 2009
Introduction
Background
Strongyloides is a helminthic pathogen associated with infection that is clinically characterized by watery diarrhea, abdominal cramping, and urticarial rash. Strongyloidiasis is an extremely common cause of morbidity and mortality worldwide. Most patients are asymptomatic; however, mortality from hyperinfection may occur in immunocompromised individuals.1 If symptomatic, strongyloidiasis generally presents with diffuse nonspecific GI, dermatologic, or respiratory symptoms. In malnourished children, strongyloidiasis remains an important cause of chronic diarrhea, cachexia, and failure to thrive.
Pathophysiology
Strongyloides stercoralis infection is acquired when an individual walks barefoot in contaminated soil. The infective filariform larvae enter the body through the feet by burrowing into the skin. This is facilitated by a potent histolytic protease that is secreted by the organism.
At the portal of entry, the larvae cause petechial hemorrhages, which are accompanied by intense pruritus, congestion, and edema. The larvae migrate into the pulmonary circulation via the lymphatic system and venules. Once in the pulmonary capillaries, the larvae produce hemorrhages, which form the avenue of spread into the alveoli. An inflammatory response associated with eosinophilic infiltration follows, and the sequence of events that occurs in the lungs results in pneumonitis. Larvae migrate up the pulmonary tree, where they are swallowed, and reach the GI system. In the intestine, S stercoralis can produce an inflammatory reaction and induce a malabsorption syndrome when it attaches to the mucosal folds.
The pathophysiology that results from the hyperinfection cycle, which leads to dissemination in a compromised host, is not well understood. Patients receiving high-dose corticosteroids2 or patients with T-cell lymphotrophic virus type I are at particularly increased risk. Impaired cell-mediated immunity seems also to be a risk factor for disseminated disease.
Frequency
United States
Infection by Strongyloides organisms is rare but may occur in the southern and rural southeastern United States and Puerto Rico. The highest prevalence rate is 4%, seen in eastern Kentucky and rural Tennessee. Residents of mental health facilities, prisons, and persons emigrating from other countries (eg, Southeast Asia) are at increased risk of infection.
International
Global prevalence of strongyloidiasis is estimated at 100 million cases. Strongyloides species are distributed worldwide3 but are endemic in tropical and subtropical regions where suitably moist soil and improper disposal of human waste coexist. Worldwide, Strongyloides organisms are most prevalent in Southeast Asia, the sub-Saharan desert, Colombia, tropical sections of Brazil, and temperate sections of Spain.
Mortality/Morbidity
Mortality due to hyperinfection can occur in 30-80% of patients with hyperinfection due to dissemination of Strongyloides. This occurs in patients with immunosuppression due to infection, cancer, radiation therapy, or medication use. Although once thought rare, disseminated strongyloidiasis may be relatively common in high-risk populations and may be frequently misdiagnosed as isolated gram-negative sepsis or acute respiratory distress syndrome.
Race
No racial predilection has been reported.
Sex
No sex predilection has been reported.
Age
Children become infected more commonly because they are more likely to walk barefoot.
Clinical
History
The clinical manifestations of Strongyloides infections vary, depending on the acuity of infection and the underlying host response. The vast majority of patients with strongyloidiasis have uncomplicated disease. As many as 50% of patients remain asymptomatic. Patients who become symptomatic do so shortly after exposure, or they develop late symptoms. Severe symptoms may develop and death may ensue, especially in individuals who are immunocompromised. Classic strongyloidiasis presents in symptomatic patients 3-4 weeks after infestation with GI, pulmonary, and dermatologic symptoms.
- As larvae enter the body, initial manifestations include a transient, pruritic, erythematous, serpiginous eruption (larva currens). Such an eruption represents a local response to a migrating filariform larva. Larvae can move up to 5-10 cm per hour. Eruptions usually occur around the anus or anywhere on the trunk. In an individual who has already been sensitized, a second, creeping, urticarial rash may appear, which is caused by an allergic reaction to the larvae penetrating the skin.
- Symptomatic pulmonary strongyloidiasis that results from migrating larvae is observed in 10% of patients. Migration of the larvae through the lungs produces a pneumonitis that resembles Loeffler syndrome. Symptoms include a productive cough, at times with blood-streaked sputum, dyspnea, and fever. Strongyloidiasis can also produce a clinical syndrome that mimics either asthma or pneumonia.
- The intestinal phase of the disease predominates and presents with epigastric abdominal cramping, indigestion, anorexia, nausea, vomiting, diarrhea, pruritus ani, and bloating. In classic cases, diarrhea is profuse, watery, and mucoid. Periods of alternation between diarrhea and constipation may occur. Malabsorption of fat and vitamin B-12 has been reported and has been successfully treated by deworming.
- In children, prolonged infection can result in chronic diarrhea, vomiting, abdominal distension, anorexia, malnutrition, and failure to thrive.
- Some patients develop chronic disease. Chronic infection is characterized by skin involvement compared with acute infection, which is characterized by GI and pulmonary symptoms. Larva currens is thought to be pathognomonic for strongyloidiasis and is an urticarial serpiginous eruption at the site of parasitic entry. It is usually transient, lasts several hours to days, and typically involves the buttock, thighs, and lower extremities.
- The most significant clinical presentation of strongyloidiasis occurs in patients with hyperinfection syndrome, which occurs primarily in individuals who are immunosuppressed, particularly individuals with hematologic malignancy, autoimmune disease, and malnutrition.
- It may occur in patients receiving immunosuppressive therapy (particularly corticosteroids) or radiation therapy and, occasionally, in patients with acquired immunodeficiency syndrome.
- Other risk factors include chronic alcoholism, burns, hypogammaglobulinemia, organ transplantation, and infection with human T-cell leukemia virus (HTLV-1)4 or human immunodeficiency virus (HIV).
- Invasion of larvae into tissue is potentially massive. As a result, patients present with an exaggeration of the symptoms of established infection found in patients who are immunocompetent.
- In addition, as larvae penetrate the intestinal wall, they may allow enteric flora to escape, causing bacteremia, sepsis, meningitis, and endocarditis.
- Reported presentations include the following signs and symptoms, alone or in combination:
- GI symptoms - Severe abdominal pain, nausea, vomiting, diarrhea, intestinal obstruction, paralytic ileus, intestinal bleeding, malabsorption, eosinophilic ascites, and diffuse peritonitis
- Pulmonary symptoms - Productive sputum, hemoptysis, wheezing, respiratory insufficiency, diffuse bilateral and lobular infiltrates, focal hemorrhages, eosinophilic pleural effusions, diffuse pulmonary alveolar hemorrhages, lung abscess, pneumonitis, and acute respiratory distress syndrome
- Neurologic symptoms - Altered mentation, seizures, meningitis and brain abscess
- Other symptoms - Granulomatous hepatitis and parasitic invasion of the heart, kidney, peritoneum, lymph nodes, pancreas, prostate, ovaries, thyroid, or parathyroid
- Invasion of the CNS may produce symptoms of meningitis, including headache, nausea, vomiting, nuchal rigidity, confusion, focal seizures, and, in extreme cases, coma.
Physical
- Larva currens or other urticarial rash may be seen.
- Lung examination may reveal scattered crackles and wheezing.5 Wheezing has been reported in as many as 10% of patients. Empiric corticosteroid administration used to treat wheezing is problematic because it may cause life-threatening hyperinfection.
- Prolonged malabsorption of both fat and protein can lead to a celiac-like syndrome, characterized by steatorrhea, hypoalbuminemia, and peripheral edema. These children often have cachexia and failure to thrive. Paralytic ileus is occasionally seen. Massive GI tract bleeding,6 obstructive jaundice, necrotizing jejunitis, small bowel infarction, anorectitis, and acute intestinal obstruction have been described.
- Immunosuppression allows the Strongyloides larvae to penetrate the gut wall. Clinically, invasion of larvae can result in diffuse pulmonary infiltrates, CNS involvement, and sepsis due to gram-negative bacilli. Gut flora invade host tissues either through penetration of infective larvae from bowel lumen or through damaged intestinal epithelium. Escherichia coli and Klebsiella species are the most common organisms involved. Severe diarrhea due to the massive increase in infective larvae is observed, often with malabsorption, edema, hepatomegaly, and paralytic ileus. Fatal bowel infarction has been described. Invasion of the CNS by migrating larvae is often accompanied by secondary bacterial infection that results in meningitis or brain abscess.
- A syndrome of infantile infection caused by Strongyloides fulleborni has been described in western Papua New Guinea. These children have diarrhea that becomes protracted in the first months of life, respiratory distress, failure to thrive, protein-losing enteropathy, and a kwashiorkor-like appearance (with ascites and pleural effusions) due to hypoalbuminemia ("swollen baby" sickness). Strongyloides larvae have been detected in the milk of mothers with chronic infection, suggesting vertical transmission.
Causes
Strongyloidiasis is caused by the nematode (roundworm) S stercoralis. The genus Strongyloides is classified in the order Rhabditida, and most members are soil-dwelling microbiverous nematodes. Most of the 52 species of Strongyloides do not infect humans. S stercoralis is the most common human pathogen. The adult female worm is a minute, slender, almost transparent worm that measures approximately 2.2-2.5 mm long and has a diameter of 50 µm. The adult female worm lives in tunnels between the enterocytes in the small bowel of humans.
A parasitic male exists, but it is found only in experimentally infected dogs and has no role in human infections. Parasitic males are shorter and broader than females and are easily eliminated from the intestine. Only adult females are found in infected humans, reproducing by parthenogenesis, in which eggs containing mature larvae are released.
- Humans are the principal host. Dogs, cats, and other mammals also can harbor S stercoralis and may serve as reservoir hosts.
- The life cycle is complex and consists of both a parasitic (homogonic) cycle and a free-living (heterogonic) cycle. Three developmental stages have been identified: adult, rhabditiform larva, and filariform larva (infective). Human infection is acquired by penetration of the skin or mucous membranes by infective filariform larvae, either from autoinfection or from contact with infected soil. Migration of infective larvae traditionally has been believed to occur via the lymphatic vessels and venules. These larvae reach the pulmonary circulation, penetrate the alveolar space, and migrate up the pulmonary tree, where they are swallowed and finally enter the intestine. Compared with hookworms, adult Strongyloides organisms lie embedded in the intestinal folds. The traditional migratory pathway is now perceived to exist in conjunction with an equally significant direct migration from the skin to the duodenum.
- The life cycle of the worm begins when a mature adult female lays eggs, which are embryonated by parthenogenesis within the intestine and develop into noninfective rhabditiform larvae. These are deposited in the soil with human stool. The life cycle has 2 variations.
- The first variation allows development of nonparasitic adults, both males and females, in the soil, which can indefinitely maintain infestation of the soil. This free-living phase is occasionally termed the heterogonic life cycle.
- The second variation allows noninfective new larvae to molt in the human host into infective filariform larvae. Infective larvae can penetrate the intestine and set up a new cycle, commonly termed the hyperinfective or autoinfective cycle. In this setting, unlike in other intestinal nematodes of humans, the larvae can increase in numbers without reinfection from outside. This life-cycle variation is responsible for the decades-long persistence of infection in untreated hosts.
- In patients who are immunocompromised, autoinfection is frequent and causes hyperinfection, with resultant dissemination. All organs and tissues may be invaded, along with the small intestine. In addition, because larvae penetrate the wall of the colon, bacteremia and meningoencephalitis with enteric flora can occur.
- From skin penetration to development of mature female worms in the intestine, the life cycle requires approximately 28 days, but the incubation period is unknown. As long as the patient is infected, which can be for several decades, the infection is communicable.
More on Strongyloidiasis |
 Overview: Strongyloidiasis |
| Differential Diagnoses & Workup: Strongyloidiasis |
| Treatment & Medication: Strongyloidiasis |
| Follow-up: Strongyloidiasis |
| References |
| Further Reading |
| Next Page » |
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Further Reading
For more information, see images 17, 30, and 57 at the McGill Faculty of Medicine Web site. See the Gorgas Courses in Clinical Tropical Medicine for another instructive case.
Keywords
strongyloidiasis, acute intestinal obstruction, acute respiratory distress syndrome, anorectitis, asthma, cachexia, chronic diarrhea, eosinophilic pleural effusions, failure to thrive, granulomatous hepatitis, helminth infection, hyperinfection syndrome, hypoalbuminemia, larva currens, Loeffler syndrome, malabsorption syndrome, necrotizing jejunitis, obstructive jaundice, paralytic ileus, parasitic infection, peripheral edema, peritonitis, pneumonia, small bowel infarction, steatorrhea, Strongyloides fulleborni, Strongyloides stercoralis, S stercoralis, tropical infection
