AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Further Reading
• References

INTRODUCTION

Section 2 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Further Reading
• References

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 it 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

Section 3 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Further Reading
• References

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 celiaclike 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 kwashiorkorlike 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.

DIFFERENTIALS

Section 4 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Further Reading
• References

Other Problems to be Considered

Anaphylaxis
Sepsis
Transient pulmonary eosinophilic syndrome

WORKUP

Section 5 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Further Reading
• References

Lab Studies

• Peripheral eosinophilia (>500 cells/µL) is often the only abnormal laboratory test result found in patients with chronic strongyloidiasis, and it probably represents an immune response to larvae migrating through host tissues. However, this finding may be absent in the immunocompromised host. Peripheral leukocytosis may occur in the early stages of the infection.
• Stool examination reveals the characteristic larvae. Because female S stercoralis organisms release as few as 50 eggs per day, multiple stool specimens using various concentrating techniques may be required to detect minor or chronic infections. The sensitivity of 3 routine stool specimens by direct examination is 50% and is nearly 100% if 7 or more serial specimens are analyzed. Stool examination findings are negative during the early phase of infection (until the parasites reach the gut and begin to produce eggs). Unlike the eggs of other parasitic nematodes, the eggs of S stercoralis are not usually found in the feces; instead, they embryonate within the intestine and develop into larvae, which are deposited in the soil.
• • Several specialized stool culture techniques have been advanced that exploit the ability of S stercoralis to enter a free-living cycle of development. In all of these methods, fecal material is cultured in a vessel for approximately 1 week, during which filariform larvae crawl out of the stool suspension.
  • In the standard test tube (Harada-Mori) method, stool is spread onto a filter paper strip and is cultured in a test tube containing a little water; filariform larvae appear in the water after 7-10 days.
  • Cultures can be grown in Petri dishes that contain water or solid agar.
  • Charcoal fecal culture (26°C) for 1 week, using the Baermann concentration method, is best for detecting hatched larvae. Availability of this cumbersome test in clinical practice is highly variable. False-positive test results can occur in patients with hookworm infection.
  • Other techniques of detection include examining for characteristic larval tracts on nutrient agar plates.
• A string test (Entero-Test) or duodenal aspiration can be performed when results of stool examinations are negative for larvae; however, results may be negative if larvae are located too far down in the lower intestine. The reported sensitivity ranges from 40-90%. The Entero-Test capsule (HDC Corp, San Jose, Calif) consists of a textured string within a gelatin capsule. One end of the string is taped to the cheek and the capsule is swallowed; after several hours or overnight the terminal portion of the string ideally unravels into the duodenum. If it does, the end of the string should be bile stained, and mucous secretions can be wiped onto a slide using gloved hands. Examination of the slide should reveal larvae.
• Serodiagnosis can be helpful but is not readily available, and false-negative results may occur. Several immunodiagnostic assays have been developed, including skin testing with larval extracts, indirect immunofluorescence using killed larvae, filarial complement fixation testing, indirect agglutination testing, radioallergosorbent testing for specific immunoglobulin E, gelatin particle indirect agglutination (GPIA), Western blot analysis, and enzyme-linked immunosorbent assay (ELISA) for immunoglobulin G antibodies. With the greatest accuracy for diagnosis of strongyloidiasis,⁷ ELISA testing has been shown to detect the disease in approximately 85-90% of patients. ELISA can be performed at the National Institutes of Health (Laboratory for Parasitic Diseases) and the Centers for Disease Control and Prevention. However, results may not help distinguish acute from prior infection, making the test less helpful in endemic areas. Cross-reaction with the antigen of filarial worms may occur.
• In disseminated Strongyloides infection, larvae can be recovered from extraintestinal sites, including sputum, bronchoalveolar fluid, and in some cases, cerebrospinal fluid.
• Children with S fulleborni infection shed eggs rather than larvae in the feces, and the infection is easily diagnosed using microscopic techniques.

Imaging Studies

• Radiography may be useful in individuals exhibiting either pulmonary or GI tract symptoms.
• In pulmonary strongyloidiasis, fine miliary nodules or diffuse reticular interstitial opacities may be seen on chest radiographs or CT scans. In severe cases, bronchopneumonia (either segmental or lobar opacities) may be seen. In these patients, clinical progression to acute respiratory distress syndrome may occur. Occasionally, pulmonary effusions may occur. Lung cavitation and abscesses have been described in association with secondary bacterial infection.
• Radiographic findings associated with GI tract strongyloidiasis include duodenal edema, with irregular mucosal folds, ulcerations, and strictures. Occasionally, strictures and ulcerations may be present, mimicking inflammatory bowel disease.

Procedures

• Upper and lower GI tract endoscopy has identified many features, ranging from normal-appearing mucosa to frank colitis or duodenitis.
• With CNS involvement, lumbar puncture may reveal evidence of meningitis, with increased neutrophils and protein concentration and a reduced glucose level in cerebrospinal fluid.

TREATMENT

Section 6 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Further Reading
• References

Medical Care

All persons found to harbor Strongyloides organisms should be treated, even if they are asymptomatic, because of the risk of hyperinfection. In addition, Strongyloides species are the hardest worms to eradicate. Treatment of early infection is with symptomatic support because specific therapy is more effective once intestinal infection is established.

Benzimidazoles (thiabendazole, mebendazole, and albendazole) are antihelmintic agents that disrupt energy production in the parasites. The final common pathway of the benzimadole is inhibition of beta-tubulin polymerase, which causes disruption of cytoplasmic microtubule formation. These antihelmintics not only kill adult gut-dwelling stages of the parasite but sterilize the larvae and eggs. 

Thiabendazole is the most commonly administered agent but a number of side effects makes it less desirable. Ivermectin inhibits neurotransmission in nematodes by stimulating the release of gamma-aminobutyric acid-dependent neurotransmission. Eradication rates with ivermectin are as high as 97%. Ivermectin and thiabendazole have shown to be superior to albendazole. Ivermectin is becoming the drug of choice in many countries due to more favorable side effects compared with albendazole.^{8, 9} 

Posttherapy stool examinations are recommended to verify Strongyloides eradication and to exclude other parasitic infections. Patients with hyperinfection and disseminated disease should be treated with ivermectin. In this select group of patients, ivermectin should be administered daily until symptoms have resolved and until larvae have not been detected for at least 2 weeks.

• Beta 2–agonist inhalers may be needed for wheezing.
• Anthelmintic therapy is poorly effective against larvae and is more effective once established infection occurs.
• Corticosteroid therapy must be avoided because hyperinfection and death may occur.
• In patients with wheezing, the use of leukotriene synthesis inhibitors may worsen infection because leukotrienes are shown to play a potential role in the immunity against Strongyloides infection.
• Treatment may have to be repeated or the duration prolonged in patients with hyperinfection syndrome. Relapses may occur despite proper therapy.
• Secondary bacterial infections that occur with hyperinfection, such as sepsis or meningitis, are treated using broad-spectrum antimicrobials based on culture results.

Surgical Care

Surgical intervention may be required in the rare instance of bowel obstruction or infarction.

Consultations

Consultations with specialists in infectious diseases, pulmonology, gastroenterology, and surgery may be helpful, depending on the clinical presentation.

MEDICATION

Section 7 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Further Reading
• References

Several anthelmintic drugs are available for established infection. Thiabendazole, the original benzimidazole, remains a good therapeutic agent for strongyloidiasis, despite an erratic efficacy rate and significant adverse effects. Albendazole and mebendazole have been used in patients with S stercoralis infection but results have varied. Ivermectin has been used recently and has been shown to be more effective than albendazole. Patients with hyperinfection and disseminated disease should be treated with ivermectin. In these patients, ivermectin should be administered daily until symptoms have resolved and larvae have not been detected for at least 2 weeks.

Drug Category: Anthelmintics

The effectiveness of these agents against larvae is poor; they are more effective once established infection occurs.

FOLLOW-UP

Section 8 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Further Reading
• References

Further Outpatient Care

• Individuals with immunosuppression or hyperinfection syndrome should have close follow-up care.

Deterrence/Prevention

• Persons in household contact with patients are not at risk for infection.
• Proper disposal of human excreta substantially reduces the prevalence of strongyloidiasis.
• A vaccine has been developed that is effective against infective-stage filariform larvae in mice. Further studies in humans are required to confirm these findings.

Complications

• Mortality rates of up to 80% can occur in patients with hyperinfection syndrome who are immunocompromised despite aggressive treatment and supportive measures. 
• Life-threatening GI bleeding has been described in a patient with hyperinfection syndrome. The bleeding was found to be from microaneurysms ("berry aneurysms") in the superior and inferior mesenteric arteries.
• The syndrome of inappropriate antidiuretic syndrome has been observed in patients with severe Strongyloides infection.¹⁰
• Eosinophilic oophoritis has been associated with strongyloidiasis.¹¹
• Minimal-change nephrotic syndrome has been described in patients with strongyloidiasis.¹² Resolution of the proteinuria occurred after administration of antihelmintic therapy with ivermectin.
• Complete resolution of duodenal obstruction due to infestation of Strongyloides has been reported with ivermectin administration.¹³
• Two cases of appendicitis due to Strongyloides infection have been reported.¹⁴
• See the Gorgas Courses in Clinical Tropical Medicine for an instructive case.

Prognosis

• Prognosis is excellent if the patient is not immunocompromised.
• In patients who are immunocompromised, hyperinfection can occur, severe symptoms may develop, and death may ensue. Mortality rates are as high as 80% in immunocompromised patients with hyperinfection.

Patient Education

• Control measures used to prevent exposure are paramount to reduce prevalence of the disease. Educate at-risk individuals regarding risk of infection from walking barefoot in areas where soil may be contaminated.
• Educate individuals regarding sanitary disposal of human waste products.

MISCELLANEOUS

Section 9 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Further Reading
• References

Medical/Legal Pitfalls

• Diagnosis relies on keeping an index of suspicion because no distinctive clinical features exist, and ancillary laboratory, imaging, or endoscopic findings often are nonspecific.
• Obtaining a good travel and residence history and considering the possibility of strongyloidiasis in any immunocompromised patient who experiences sudden deterioration are important.
• Delay in diagnosis frequently results in death despite vigorous treatment.
• Complete eradication of the parasite before the initiation of immunosuppressive therapy is essential in patients with uncomplicated infections to ensure that hyperinfection syndrome does not develop.

FURTHER READING

Section 10 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Further Reading
• References

For more information, see images 17, 30, and 57 at the McGill Faculty of Medicine Web site.

REFERENCES

Section 11 of 11

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Further Reading
• References

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29. Horton J. Albendazole: a review of anthelmintic efficacy and safety in humans. Parasitology. 2000;121 Suppl:S113-32. [Medline].
30. Igual-Adell R, Oltra-Alcaraz C, Soler-Company E, Sanchez-Sanchez P, Matogo-Oyana J, Rodriguez-Calabuig D. Efficacy and safety of ivermectin and thiabendazole in the treatment of strongyloidiasis. Expert Opin Pharmacother. Dec 2004;5(12):2615-9. [Medline].
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Article Last Updated: Jan 28, 2008