AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

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

INTRODUCTION

Section 2 of 10  

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

Background

Fulleborn first described strongyloidiasis in 1926. The parasitic helminth Strongyloides stercoralis causes this disease. This nematode is unique in its ability to complete its life cycle in humans. It may cause infection over a period as long as several decades. The symptoms related to strongyloidiasis may reflect the nematode's systemic passage, its local cutaneous involvement, or both. Individuals with an intact immune system may have minimal or no symptoms. In contrast, those with a compromised immune system may develop a rapidly fatal infection (eg, hyperinfection syndrome, disseminated strongyloidiasis). During chronic uncomplicated infections, the larvae may migrate to the skin, where they can cause cutaneous strongyloidiasis, known as larva currens because of the quick migratory rate of the larva.

The Medscape Emerging and Reemerging Infectious Diseases Resource Center may be of interest, as may the eMedicine Infectious Diseases article Strongyloidiasis.

Pathophysiology

Strongyloidiasis is typically acquired when the infective filariform larvae penetrate the skin during contact with contaminated soil, although ingestion of filariform larvae via the fecal-oral route can also result in infection. The larvae are transferred through the circulation to the lungs. From the lungs, they ascend to the glottis via the bronchi and are subsequently swallowed. In the duodenum and jejunum, the larvae burrow into the mucus membrane, where, after molting, the female worm produces eggs by parthenogenesis, which yields noninfective rhabditiform larvae. These larvae can be passed in the stool and become infective filariform larvae, or they can develop into adults in the external environment and produce rhabditiform larvae. In the external environment, the rhabditiform larvae can complete the free-living cycle, or they can become infective filariform larvae with the potential to penetrate the skin of another individual.

Autoinfection occurs when noninfective rhabditiform larvae prematurely transform into infective filariform larvae (ie, before leaving the body) and reenter the circulation by 1 of 3 methods. For the first, the larvae penetrate the mucosa of the colon and cause indirect endoautoinfection. For the second, the larvae penetrate the mucosa of the upper small intestine and cause direct endoautoinfection. For the third, the larvae penetrate the perianal skin and cause exoautoinfection. The last method has been associated with the development of larva currens.

After entering the circulation, the larvae are carried to the lungs, where the cycle repeats itself. This mechanism accounts for the chronicity and frequent recurrence of the disease in patients who no longer live in areas in which the disease is endemic.

In immunocompromised hosts, larvae may migrate beyond the normally controlled internal pathways, with widespread dissemination to the extraintestinal regions, including the CNS, heart, urinary tract, endocrine organs, and skin. Millions of filariform larvae reach the skin by means of the circulation or direct invasion from body cavities; they can migrate through all levels of the dermis and involve the subcutaneous tissue.

Frequency

United States

Strongyloidiasis is relatively uncommon. Endemic foci exist in rural areas of the southeastern United States and Appalachia, with prevalence rates close to 4%. Infections acquired in the United States, while not usually associated with larva currens, are not clinically silent; the infected individuals usually have a chronic relapsing illness of mild to moderate severity. Among veterans of the US military forces who served in Southeast Asia, the prevalence of larva currens in those with confirmed strongyloidiasis is high, with studies showing a range of 30-90%.

International

Strongyloidiasis is endemic in tropical and subtropical countries. The worldwide prevalence is approximately 35 million cases, and rates are as high as 40% in certain regions, including Southeast Asia, Latin America, and the Caribbean basin. The international prevalence of larva currens among patients with strongyloidiasis varies, with rates in the range of 30-90% in Southeast Asia. High rates of larva currens are also reported in Latin America. A stool and serosurvey for S stercoralis conducted in a community in the Peruvian Amazon region found strongyloidiasis due to S stercoralis in the stool of 69 (8.7%) of 792 participants.¹

Mortality/Morbidity

In patients who are immunocompromised, disseminated strongyloidiasis may develop. If it does, it is commonly fatal; the mortality rate may be as high as 80%. Therefore, patients at risk must be identified before immunosuppressive therapy is begun.

Race

No racial predilection is recognized; however, it is highly prevalent in some tropical Aboriginal communities in Australia.²

Sex

No sex predilection is reported.

Age

Infection can occur in individuals at any age, although infection is more common during childhood than at other times. Advanced age is a risk factor for severe strongyloidiasis because it may be associated with an immunosuppressed state.

CLINICAL

Section 3 of 10  

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

History

Strongyloides infection is associated with cutaneous and systemic signs and symptoms that can be categorized by the stage of disease. Infection can be asymptomatic, can cause a wide variety of clinical syndromes, or can result in death. 

• Acute infection
• • Cutaneous features
  • • The patient may report a mild eruption at the site of larval penetration, usually on the feet.
    • Most often, the area is also pruritic. This rash has been referred to as ground itch.
  • Systemic features
  • • Pulmonary symptoms caused by the migration of larvae through the lungs may result in coughing, shortness of breath, and fever.
    • GI symptoms include epigastric discomfort, nausea, vomiting, and diarrhea.
• Chronic infection
• • Cutaneous features
  • • Larva currens, or creeping infection, is a form of cutaneous larva migrans specific to Strongyloides infection; it is a result of autoinfection. The eruption begins in the perianal region and rapidly spreads, causing intense pruritus. Episodes usually last several hours, and patients can remain free of symptoms for weeks or months between episodes. Evidence of larva currens may appear soon after infection with Strongyloides organisms, or it may first appear many years (often decades) later. Because of autoinfection, episodes may continue for many years.
    • Excoriation and impetigo are common.
    • Chronic urticaria is also described in a small percentage of patients with strongyloidiasis. This usually resolves after 1 or 2 days.
  • Systemic features
  • • Most patients are asymptomatic or have only vague abdominal complaints.
    • Symptoms may include burning or cramping, nausea, vomiting, diarrhea, constipation, and weight loss.
• Severe disseminated infection
• • Cutaneous features
  • • A rapidly progressive, diffuse petechial and purpuric eruption may occur.
    • The cause is the massive migration of filariform larvae into the skin.
  • Systemic features
  • • Abdominal symptoms are similar to those of chronic infection, but they are more severe.
    • Bloody stools may occur along with severe abdominal pains.
    • Pneumonitis may cause hemoptysis and difficulty in breathing.
    • An altered mental status or a stiff neck may indicate CNS involvement.
• Severe strongyloidiasis is a risk in every corticosteroid-treated patient who has traveled to a soil-infested country, even if the contact was decades earlier.^{3, 4} This diagnosis should be suspected with unusual GI or pulmonary symptoms or an unexplained Gram-negative bacilli sepsis.
• Cutaneous manifestations in disseminated strongyloidiasis are infrequent; characteristic purpuric periumbilical skin lesions should raise the suspicion for its diagnosis. If often portends a fatal outcome in cancer patients.⁵

Physical

Strongyloides infection is associated with cutaneous and systemic signs and symptoms that can be categorized by the stage of disease.

• Acute infection
• • Cutaneous findings
  • • A local pruritic eruption develops in the area of larval penetration, which usually occurs on the foot.
    • This eruption may consist of erythematous macules and papules or acute urticaria, and it is often accompanied by excoriation.
  • Systemic findings
  • • Wheezing may occur.
    • The patient may have a fever.
    • Epigastric tenderness may be present.
• Chronic infection
• • Cutaneous findings
  • • Larva currens is an intensely pruritic linear or serpiginous urticarial lesion, which typically begins within 12 cm of the anus. The lesions may consist of 1 or more such bands, which migrate intermittently and rapidly at a rate as fast as 15 cm/h.
    • Similar lesions may also occur on the groin and trunk, and areas of involvement on the thighs and upper body have been described as well.
    • Excoriation and impetiginization are common.
  • Systemic findings
  • • Examination findings are usually normal.
    • Epigastric tenderness may be preset, and weight loss may occur.
• Severe disseminated infection
• • Cutaneous findings
  • • Petechial and purpuric lesions rapidly expand; these may be accompanied by pink macules and papules.
    • The eruption is diffuse and may consist of serpiginous streaks in a reticulated pattern.
  • Systemic findings
  • • GI findings include abdominal tenderness; distension; and hyperactive, hypoactive, or absent bowel sounds.
    • CNS infection manifests as an altered mental status or meningismus.
    • Pulmonary involvement may result in coughing, respiratory distress, wheezing, or crackles.
    • General signs of severe infection include fever, chills, and shock.
• However, most patients who are immunocompetent have few or no symptoms.

Causes

The parasite responsible for strongyloidiasis is S stercoralis. Other species in the genus Strongyloides include Strongyloides myopotami and Strongyloides procyonis. These species have animal hosts and are thus responsible for zoonotic infections.

• S stercoralis infection is usually contracted by penetration of the larvae into the foot. Barefoot contact with sand or soil that is contaminated with human feces in endemic areas accounts for many infections.
• Zoonotic infections by Strongyloides species are similarly contracted by contact with sand or soil that contains infected animal droppings, including feces from raccoons and nutria.
• • Infections are reported among veterinarians and laboratory workers who work in temperate climates and are exposed to larvae from horses.
  • Zoonotic forms of Strongyloides infection can also produce creeping skin eruptions identical to those of S stercoralis infection.
• Risk factors for severe strongyloidiasis include any cause of an immunosuppressed state, including the following:
• • Use of immunosuppressive agents
  • Malignancy
  • Other infections, particularly HIV infection and other immunosuppressive infections⁶
  • Collagen-vascular disease
  • Diabetes mellitus
  • Malnutrition
  • Advanced age
• In patients who were exposed to the parasite, the likelihood of Strongyloides should be carefully assessed before immunosuppressive therapy is begun.

DIFFERENTIALS

Section 4 of 10  

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

Other Problems to be Considered

Human hookworm infection with Ancylostoma duodenale or Necator americanus
Zoonotic infection with S myopotami, S procyonis, Ancylostoma braziliensis, or Ancylostoma caninum

WORKUP

Section 5 of 10  

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

Lab Studies

• Routine blood testing
• • The CBC count usually reveals a normal WBC count in acute and chronic strongyloidiasis. The WBC count may be elevated in severe strongyloidiasis.
  • Eosinophilia of 10-40% is common during acute infection; it may be as high as 75-80%. Eosinophilia also occurs in chronic infection, although it is intermittent and may not be found at all during severe infection.
  • The total serum immunoglobulin E (IgE) level is usually elevated.
  • Severe infection may be associated with anemia, thrombocytopenia, and a prolonged prothrombin time (PT) because of decreased levels of clotting factors.
  • Obtain blood cultures in all patients in whom Strongyloides infection is suspected because enteric pathogens often cause co-infection.
• Stool examination for ova and parasites⁷
• • Definitive diagnosis depends on the microscopic demonstration of S stercoralis larvae in the feces.
  • The larvae resemble those of hookworms, but they can be distinguished by their short buccal cavity.
  • Ova are almost never observed during strongyloidiasis unless severe diarrhea occurs.
  • Several fresh stool specimens may need to be examined before a positive result is found. At least 3 separate examinations on different days are recommended to achieve a sensitivity of approximately 70-80%.
  • Stool samples may be concentrated with zinc sulfate prior to examination to enhance the recovery of larvae. A modified agar plate method is superior to other techniques used for stool examination.
  • Duodenal fluid can be aspirated or examined by using the Enterotest, or the string capsule method. This test offers a higher likelihood of larval recovery than simple stool examination.
• Serologic analysis
• • Although serologic analysis is the most sensitive test for strongyloidiasis (sensitivity, 84-92%), it is not specific, and cross-reactions with other nematode infections are possible. Therefore, microscopic analysis is also necessary for diagnosis.
  • Common serologic tests used in diagnosing strongyloidiasis include the enzyme immunoassay (EIA) and the enzyme-linked immunosorbent assay (ELISA). However, a stool and serosurvey for S stercoralis conducted in a community in the Peruvian Amazon region found the ELISA test had a negative predictive value of 98% and is an excellent screening test for strongyloidiasis.¹
  • Gelatin particle agglutination test (GPAT) and ELISA results were evaluated in endemic regions of Thailand.⁸ In this work, the GPAT was judged to be more practical for screening for strongyloidiasis than the conventional ELISA.
• Often, establishing a diagnosis and confirming a cure of strongyloidiasis is difficult. Strongyloides-specific antibody levels may be used for serological follow-up for strongyloidiasis.⁹ They may indicate reversion to negative serostatus after successful ivermectin therapy, which is frequent.

Imaging Studies

• Systemic infection is associated with findings that may be observed with imaging studies.
• • Alveolar or interstitial infiltrates or pulmonary effusion may be visible on chest radiographs.
  • Severe infection may be associated with loss of the mucosal pattern, rigidity, and tubular narrowing, as depicted on abdominal radiographs.

Procedures

• In acute or chronic infection, skin biopsy is usually neither necessary nor sufficient because parasites are rarely visualized. When they are, speciation is difficult.
• In severe infection, skin biopsy may be useful because filariform larvae are often observed. Obtain specimens from the purpuric eruptions because these areas contain the largest amount of larvae.
• Intestinal colonoscopy may reveal multiple findings, including normal mucosa, moderate inflammation, or severe duodenitis and colitis, particularly in immunosuppressed patients. Histopathologic examination identified larvae in 71.4% of those immunosuppressed by duodenal biopsy.¹⁰ Thus, in addition to stool analysis, endoscopic observation and biopsies are very important.
• Lumbar puncture and cerebrospinal fluid (CSF) evaluation are indicated when CNS involvement is suspected.
• In severe infections, sputum examination or bronchoalveolar lavage is appropriate for the identification of larvae.

Histologic Findings

Skin biopsy is often helpful in severe infection. Larvae can be observed in all levels of the dermis and occasionally in the subcutis. Other findings include edema, extravasated RBCs, and some lymphocytes in the superficial dermis. Larvae range from 9-15 µm in size. They contain a triradiate digestive tract.

Biopsy of the duodenum or jejunum reveals larvae in the lamina propria, where they produce edema, a cellular infiltrate, villous atrophy, or even fibrosis in prolonged infection.

TREATMENT

Section 6 of 10  

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

Medical Care

• The pathogen in strongyloidiasis cannot be extracted from the area of eruption because it is not localized in any single area.
• Anthelmintic therapy is the standard treatment.
• Supportive therapy should be administered as indicated.
• In instances in which co-infection with enteric bacteria is suspected, antibiotic therapy is indicated as well.
• Cyclosporine, an immunosuppressive agent, has anthelmintic activity. To date, no cases of severe strongyloidiasis development have been reported in patients receiving this agent.

Consultations

• Consider consulting an infectious disease specialist.
• To ensure that the optimal larval-detection tests are performed, notify the local microbiology laboratory staff that strongyloidiasis is suspected.
• Physicians in the United States may obtain assistance with serologic testing from the Centers for Disease Control and Prevention (CDC). Send a serum sample with the patient's history and physical examination findings to the state public health laboratory, which will then send the data to the CDC. Be aware that this process is often lengthy.
• Several commercial laboratories in the United States can perform serologic testing within a few days. Two are listed below.
• • Parasitic Disease Consultants
    PO Box 616
    2177 Flintstone Drive, Suite J
    Tucker, GA 30084
    770-496-1370
    (This facility performs ELISA for Strongyloides detection.)
  • Specialty Laboratories
    2211 Michigan Avenue
    Santa Monica, CA 90404
    800-421-4449 or 310-828-6543
    (These laboratories perform EIA for Strongyloides detection.)

Diet

No specific diet is required.

Activity

The patient's activity does not need to be limited when a cutaneous or systemic infection exists, unless severe disseminated infection occurs.

MEDICATION

Section 7 of 10  

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

The goals of pharmacotherapy are to eradicate the infection, reduce morbidity, and prevent complications.

The medications listed below are available from the CDC Drug Service, Centers for Disease Control and Prevention, Atlanta, GA 30333 (404-639-3670 during business hours, 404-639-2888 during evenings and weekends).

Drug Category: Anthelmintics

Parasitic biochemical pathways are sufficiently different from those of the human host to allow selective interference by chemotherapeutic agents in relatively small doses.

FOLLOW-UP

Section 8 of 10  

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

Further Outpatient Care

• Continue serial sampling of the stool or duodenal aspirates at intervals of 2-3 months to ensure complete eradication of the parasite.
• Serologic studies can be used to monitor the response to therapy.
• • Perform these tests 4-8 months after anthelmintic therapy is completed.
  • Strongyloides titers should decrease to low or undetectable levels 6-18 months after treatment. If titer has not decreased sufficiently, additional therapy may be necessary.

Deterrence/Prevention

• Infection is prevented by avoiding direct skin contact with soil containing infective larvae. Instruct travelers to endemic areas to wear footwear when walking on the beach and other areas with soil.
• Identify patients at risk and perform appropriate diagnostic tests before they begin immunosuppressive therapy.
• No accepted prophylactic regimens exist, and no vaccines are available.
• A wise practice is to search for S stercoralis larvae before initiating immunosuppression in anyone who has traveled to an endemic area, even if it was decades earlier.⁴

Complications

• Cutaneous complications of strongyloidiasis include larva currens and chronic urticaria. Cutaneous complications in immunocompromised patients with severe infection include purpura and petechia.
• Many systemic complications are possible; these can be divided by system.
• • GI complications include intestinal obstruction, perforation or infarction, malabsorption, hemorrhage, ileus, jaundice, and peritonitis.
  • Respiratory complications include pneumonitis, alveolar hemorrhage, pleural effusion, exacerbation of preexisting pulmonary disease, granulomatous lung disease, and adult respiratory distress syndrome (ARDS).
  • Neurologic complications include meningitis and cerebral abscess.
  • Renal and musculoskeletal complications are rare.

Prognosis

• Acute and chronic strongyloidiasis have a good prognosis. However, untreated infection can persist for the remainder of the patient's life because of autoinfection. A patient's prolonged absence from an endemic area is no guarantee of freedom from infection.
• Severe infection or dissemination is commonly a fatal event, and it is often unresponsive to therapy.¹¹

MISCELLANEOUS

Section 9 of 10  

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

Medical/Legal Pitfalls

• Infected immunocompromised patients are at high risk of developing severe disseminated disease.² Strongyloides infection should be excluded prior to commencing immunosuppressive therapies in patients from endemic areas. Appropriate diagnostic procedures must be performed.
• Imported strongyloidosis should be considered in travelers to and immigrants from endemic areas.¹²

REFERENCES

Section 10 of 10

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

1. Yori PP, Kosek M, Gilman RH, Cordova J, Bern C, Chavez CB, et al. Seroepidemiology of strongyloidiasis in the Peruvian Amazon. Am J Trop Med Hyg. Jan 2006;74(1):97-102. [Medline].
2. Johnston FH, Morris PS, Speare R, McCarthy J, Currie B, Ewald D, et al. Strongyloidiasis: a review of the evidence for Australian practitioners. Aust J Rural Health. Aug 2005;13(4):247-54. [Medline].
3. Fardet L, Genereau T, Poirot JL, Guidet B, Kettaneh A, Cabane J. Severe strongyloidiasis in corticosteroid-treated patients: case series and literature review. J Infect. Jan 2007;54(1):18-27. [Medline].
4. Guyomard JL, Chevrier S, Bertholom JL, Guigen C, Charlin JF. [Finding of Strongyloides stercoralis infection, 25 years after leaving the endemic area, upon corticotherapy for ocular trauma]. J Fr Ophtalmol. Feb 2007;30(2):e4. [Medline].
5. Salluh JI, Bozza FA, Pinto TS, Toscano L, Weller PF, Soares M. Cutaneous periumbilical purpura in disseminated strongyloidiasis in cancer patients: a pathognomonic feature of potentially lethal disease?. Braz J Infect Dis. Oct 2005;9(5):419-24. [Medline].
6. Meamar AR, Rezaian M, Mohraz M, Hadighi R, Kia EB. Strongyloides stercoralis hyper-infection syndrome in HIV(+)/AIDS patients in Iran. Parasitol Res. Mar 31 2007;[Medline].
7. Sato Y, Kobayashi J, Toma H, Shiroma Y. Efficacy of stool examination for detection of Strongyloides infection. Am J Trop Med Hyg. Sep 1995;53(3):248-50. [Medline].
8. Sithithaworn J, Sithithaworn P, Janrungsopa T, Suvatanadecha K, Ando K, Haswell-Elkins MR. Comparative assessment of the gelatin particle agglutination test and an enzyme-linked immunosorbent assay for diagnosis of strongyloidiasis. J Clin Microbiol. Jul; 2005;43(7):3278-82. [Medline].
9. Page WA, Dempsey K, McCarthy JS. Utility of serological follow-up of chronic strongyloidiasis after anthelminthic chemotherapy. Trans R Soc Trop Med Hyg. Nov 2006;100(11):1056-62. [Medline].
10. Kishimoto K, Hokama A, Hirata T, Ihama Y, Nakamoto M, Kinjo N, et al. Endoscopic and histopathological study on the duodenum of Strongyloides stercoralis hyperinfection. World J Gastroenterol. Mar 21 2008;14(11):1768-73. [Medline].
11. Fasih N, Irfan S, Sheikh U, Beg MS. A fatal case of gram negative bacterial sepsis associated with disseminated strongyloidiasis in an immunocompromised patient. J Pak Med Assoc. Feb 2008;58(2):91-2. [Medline].
12. Nuesch R, Zimmerli L, Stockli R, Gyr N, Christoph Hatz FR. Imported strongyloidosis: a longitudinal analysis of 31 cases. J Travel Med. Mar-Apr 2005;12(2):80-4. [Medline].
13. Amer M, Attia M, Ramadan AS, Matout K. Larva currens and systemic disease. Int J Dermatol. Jul-Aug 1984;23(6):402-3. [Medline].
14. Gonçalves AL, Machado GA, Gonçalves-Pires MR, Ferreira-Junior A, Silva DA, Costa-Cruz JM. Evaluation of strongyloidiasis in kennel dogs and keepers by parasitological and serological assays. Vet Parasitol. Jun 20 2007;147(1-2):132-9. [Medline].
15. Markell EK, John DT, Krotoski WA. Markell and Voge's Medical Parasitology. 8^th ed. Philadelphia, Pa: WB Saunders; 1999:287-93.
16. Milder JE, Walzer PD, Kilgore G, Rutherford I, Klein M. Clinical features of Strongyloides stercoralis infection in an endemic area of the United States. Gastroenterology. Jun 1981;80(6):1481-8. [Medline].
17. Pacanowski J, Santos MD, Roux A, LE Maignan C, Guillot J, Lavarde V, et al. Subcutaneous ivermectin as a safe salvage therapy in Strongyloides stercoralis hyperinfection syndrome: a case report. Am J Trop Med Hyg. Jul 2005;73(1):122-4. [Medline].
18. Pelletier LL Jr. Chronic strongyloidiasis in World War II Far East ex-prisoners of war. Am J Trop Med Hyg. Jan 1984;33(1):55-61. [Medline].
19. Pelletier LL Jr, Gabre-Kidan T. Chronic strongyloidiasis in Vietnam veterans. Am J Med. Jan 1985;78(1):139-40. [Medline].
20. Polenakovik H, Polenakovic S. Strongyloidiasis. eMedicine from WebMD [serial online]. March 24, 2006;Available at http://www.emedicine.com/med/topic2189.htm.
21. Roeckel IE, Lyons ET. Cutaneous larva migrans, an occupational disease. Ann Clin Lab Sci. Sep-Oct 1977;7(5):405-10. [Medline].
22. Smith JD, Goette DK, Odom RB. Larva currens. Cutaneous strongyloidiasis. Arch Dermatol. Aug 1976;112(8):1161-3. [Medline].
23. Stone OJ, Newell GB, Mullins JF. Cutaneous strongyloidiasis: larva currens. Arch Dermatol. Nov 1972;106(5):734-6. [Medline].
24. von Kuster LC, Genta RM. Cutaneous manifestations of strongyloidiasis. Arch Dermatol. Dec 1988;124(12):1826-30. [Medline].

Article Last Updated: May 2, 2008