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Strongyloidiasis

  • Author: Pranatharthi Haran Chandrasekar, MBBS, MD; Chief Editor: Michael Stuart Bronze, MD  more...
 
Updated: Oct 21, 2015
 

Background

Strongyloidiasis is an intestinal infection caused by 2 species of the parasitic nematode Strongyloides. The most common and clinically important pathogenic species in humans is S stercoralis (see the following image). S fuelleborni is found sporadically in Africa and Papua New Guinea. Distinctive characteristics of this parasite are its ability to persist and replicate within a host for decades while producing minimal or no symptoms (individuals with an intact immune system) and its potential to cause life-threatening infection (hyperinfection syndrome, disseminated strongyloidiasis) in an immunocompromised host (60-85% mortality rate).[1, 2, 3]

Rhabditiform larva of Strongyloides stercoralis in Rhabditiform larva of Strongyloides stercoralis in stool specimen (wet mount stained with iodine).

The symptoms related to strongyloidiasis may reflect the nematode's systemic passage, its local cutaneous involvement, or both. 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. Infection is clinically characterized by watery diarrhea, abdominal cramping, and urticarial rash. In malnourished children, strongyloidiasis remains an important cause of chronic diarrhea, cachexia, and failure to thrive.

This condition can also be a health consequence of captivity. During the World War II, allied military personnel held by the Japanese experienced deprivation, malnutrition, and exposure to tropical diseases.[4] Certain tropical diseases have persisted in these survivors, notably infections with S stercoralis, with studies 30 years or more after release documenting overall infection rates of 15%. Chronic strongyloidiasis may produce a linear urticarial larva currens rash, with such individuals at risk of fatal hyperinfection if immunity is suppressed.

Patient Education

Travelers to endemic areas should wear footwear when walking on the beach and other areas with soil. Community education in endemic areas should include sewage management, avoidance of soil contaminated with feces or use of feces for fertilizer, wearing of protective clothing when handling sewage or contaminated soil, and wearing of shoes while outdoors.

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Pathophysiology

The life cycle of Strongyloides stercoralis is complex and unique among the intestinal nematodes. This worm has 2 types of life cycles—a free-living life cycle (rhabditiform larvae) and a parasitic life cycle (filariform infective larvae)—with 3 developmental stages: adult, rhabditiform larva, and filariform larva.

The first type of life cycle 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 type of life cycle 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.

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.

Humans are the principal host of S stercoralis. Dogs, cats, and other mammals can also harbor the worm and may serve as reservoir hosts.

Stage 1

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 or other material contaminated with human feces (fecal-oral route) (see the image below). 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.

First stage, life cycle of Strongyloides stercoral First stage, life cycle of Strongyloides stercoralis. Illustration by Tessa Kalman.

The larvae migrate into the pulmonary circulation via the lymphatic system and venules. 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.

Stage 2

Migration of infective larvae traditionally has been believed to occur via the lymphatic vessels and venules. These larvae reach the pulmonary circulation, where, once in the pulmonary capillaries, the larvae produce hemorrhages, which form the avenue of penetration into the alveolar space. An inflammatory response associated with eosinophilic infiltration follows, and the sequence of events that occurs in the lungs results in pneumonitis. The larvae migrate up the pulmonary tree, where they are swallowed (see the following image) and finally enter the intestine.

Second stage, life cycle of Strongyloides stercora Second stage, life cycle of Strongyloides stercoralis. Illustration by Tessa Kalman.

Stage 3

When they reach the small bowel, they molt twice and mature into adult females (2 mm × 0.05 mm in diameter). (All parasitic adult worms are female.) The parasitic females produce eggs via parthenogenesis. Each adult female may live up to 5 years and continue the reproductive cycle. Their eggs hatch into noninfective rhabditiform larvae within the intestine, which may then be passed through the stool into the environment, where they mature into adult males and females (see the image below). 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.

Strongyloides is the only helminth to secrete larvae (and not eggs) in feces. Typically, larvae appear in feces approximately 1 month (about 28 days) after skin penetration, but the incubation period is unknown. As long as the patient is infected, which can be for several decades, the infection is communicable. The excreted rhabditiform larvae may again live freely in soil or be transformed into filariform larvae awaiting another human host. Alternatively, they may cause autoinfection.

Third stage, life cycle of Strongyloides stercoral Third stage, life cycle of Strongyloides stercoralis. Illustration by Tessa Kalman.

Autoinfection

Autoinfection involves premature transformation of noninfective larvae (rhabditiform, 0.25 mm × 0.015 mm) into infective larvae (filariform, 0.5 mm × 0.015 mm), which can penetrate the intestinal mucosa (internal autoinfection) or the skin of the perineal area (external autoinfection), thus establishing a developmental (parasitic) cycle within the host. Infection can be maintained by repeated migratory cycles for the remainder of the host’s life.

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. The infective filariform larvae reenter the circulation by 1 of 3 methods: (1) The larvae penetrate the mucosa of the colon and cause indirect endoautoinfection; (2) the larvae penetrate the mucosa of the upper small intestine and cause direct endoautoinfection; or (3) 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.

Autoinfection is kept in check by a normal host immune response. However, in patients with impaired cell-mediated immunity, autoinfection may give rise to the 2 most severe forms of strongyloidiasis: hyperinfection syndrome (stage 4) and disseminated strongyloidiasis (stage 5).

Stage 4

The pathophysiology that results from the hyperinfection cycle, which leads to dissemination in a compromised host, is not well understood. Patients receiving high-dose corticosteroids[5] or patients with human T-cell lymphotrophic virus type I ((HTLV-I) are at particularly increased risk.

Hyperinfection syndrome represents an acceleration of the normal life cycle of S stercoralis, leading to excessive worm burden without the spread of larvae outside the usual migration pattern (eg, gastrointestinal tract, lungs) (see the following image). The larvae do not exit the host in feces and instead molt into the infective filariform larva within the intestinal lumen. These larvae are then capable of penetrating the bowel wall and traveling throughout the body.

Fourth stage, life cycle of Strongyloides stercora Fourth stage, life cycle of Strongyloides stercoralis. Illustration by Tessa Kalman.

Stage 5

Disseminated strongyloidiasis involves widespread dissemination of larvae to extraintestinal organs (eg, central nervous system [CNS], heart, urinary tract, endocrine organs), which are outside the realm of the parasite's ordinary life cycle (see the image below). All organs and tissues may be invaded, along with the small intestine. In these severe forms, translocation of enteric bacteria may occur, leading to polymicrobial bacteremia and occasionally meningitis with enteric pathogens. The enteric pathogens may be carried on the filariform larvae or may enter the circulation through intestinal ulcers. The CNS, liver, and lungs are the most common destinations of the autoinfectious larvae.

Fifth stage, life cycle of Strongyloides stercoral Fifth stage, life cycle of Strongyloides stercoralis. Illustration by Tessa Kalman.
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Etiology

Strongyloidiasis is caused by the nematode (roundworm) Strongyloides 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. Other species include S myopotami and S procyonis. These species have animal hosts and are thus responsible for zoonotic infections.[6]

Infections are initiated when exposed skin contacts contaminated soil. Autoinfection commonly occurs allowing infection to persist decades. The longest documented asymptomatic infection was more than 65 years. Hyperinfection is typically triggered by drug-induced or disease-associated defects in cellular immunity, which allows a massive increase in parasite burden and dissemination to nearly all organ systems.

Risk factors for severe strongyloidiasis include the following:

  • Corticosteroid therapy: This is the most important risk factor [5, 7] ; other immunosuppressive agents are also risk factors (eg, chemotherapeutic agents, tacrolimus, tumor necrosis factor [TNF] modulators)
  • Human T-cell leukemia virus type 1 (HTLV-1) infection [8, 9] : HTLV-1, the retrovirus associated with adult T-cell leukemia, has a bidirectional relationship with Strongyloides; coinfection with Strongyloides shortens the preleukemic phase of HTLV-1 infection [10] ; the Strongyloides antigen accelerates leukemogenesis, and treatment of the infection may actually decrease HTLV-1 viral load
  • Hypogammaglobulinemia
  • Malignancy/neoplasms, particularly hematologic malignancies (lymphoma, leukemia): Studies have suggested that Strongyloides infection may be associated with increased incidence of gastrointestinal lymphoma [12]
  • Organ transplantation [13, 14, 15, 16]
  • Malabsorption states and malnutrition
  • Chronic renal failure and end-stage renal disease
  • Diabetes mellitus
  • Advanced age
  • Collagen-vascular disease
  • Chronic alcohol consumption [3]

No evidence exists of direct person-to-person transmission in a household. Strongyloides larvae have been detected in the milk of mothers with chronic infection, suggesting vertical transmission. Evidence in dogs also shows transmission in breast milk.[17] No studies indicating transmammary transmission in humans exist. Cadaveric donors of renal transplants have been implicated as sources of fatal hyperinfection syndromes in transplant recipients.[18]

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.

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Epidemiology

United States statistics

The true prevalence of S stercoralis is likely underestimated, because infection is often subclinical. Strongyloidiasis is uncommon in the United States, although endemic foci exist in rural areas of the southeastern states and the Appalachia region (especially in eastern Tennessee, Kentucky, and West Virginia) and Puerto Rico,[19] with prevalence rates close to 4%. Populations in whom strongyloidiasis is more prevalent include patients in long-term institutionalized care (mental health facilities, prisons), immigrants or refugees from tropical and subtropical countries (eg, Southeast Asia, Africa, Middle East),[20] and persons who were stationed in Southeast Asia during World War II[21] and the Vietnam War.

In one study, Southeast Asian immigrants living in Washington, DC, were found to have a 38% incidence of infection.[22] Similarly, a Canadian epidemiology study of Southeast Asian immigrants to Canada demonstrated infection in 11.8% in the Vietnamese population and a 76.6% seroprevalence in Cambodian immigrants.[23] Sudanese Lost Boys and Girls and Somali Bantu refugees demonstrated 46% and 23% respective seropositive rate.[24] Five percent of Vietnam veterans reporting mild symptoms demonstrated S stercoralis infection.

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% to 90%.[25, 26]

International statistics

Globally, prevalence rates of strongyloidiasis are as high as 40% in certain areas where suitably moist soil and improper disposal of human waste coexist, especially West Africa, the Caribbean, and Southeast Asia, as well as Colombia, tropical sections of Brazil, and temperate sections of Spain.[27, 28] The disease is estimated to affect 100-200 million people worldwide in 70 countries.

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.[29]

Racial and age differences in incidence

No racial predilection is apparent for Strongyloides infection; however, Southeast Asia appears to have the highest endemic percentage, and it is highly prevalent in some tropical Aboriginal communities in Australia.[30] Larva currens is most frequently seen in white patients with an infection acquired in Southeast Asia.

Although Strongyloides infection is represented in all ages, infection may most frequently initially occur in childhood, as children are most likely to play outdoors in contaminated soil with bare feet.[31] Advanced age is also a risk factor for severe strongyloidiasis, because it may be associated with an immunosuppressed state.

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Prognosis

Acute and chronic strongyloidiasis carry a good prognosis in immunocompetent hosts. However, untreated infection can persist for the remainder of the patient's life because of autoinfection. Most immunocompetent individuals who develop strongyloidiasis have asymptomatic chronic infections that result in negligible morbidity. A patient's prolonged absence from an endemic area is no guarantee of freedom from infection.

Severe strongyloidiasis (hyperinfection syndrome and disseminated strongyloidiasis) carries a high mortality rate (up to 80%) because the diagnosis is often delayed. This relates to its nonspecific presentation and the host's immunocompromised status. Death from Strongyloides infection is typically iatrogenic and frequently occurs after an asymptomatic infected person is treated with immunosuppression.[32] Gram-negative sepsis is a common consequence of hyperinfection and carries a 50% mortality rate.[33] 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.

(See Complications under Clinical.)

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Contributor Information and Disclosures
Author

Pranatharthi Haran Chandrasekar, MBBS, MD Professor, Chief of Infectious Disease, Program Director of Infectious Disease Fellowship, Department of Internal Medicine, Wayne State University School of Medicine

Pranatharthi Haran Chandrasekar, MBBS, MD is a member of the following medical societies: American College of Physicians, American Society for Microbiology, International Immunocompromised Host Society, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Coauthor(s)

Hari Polenakovik, MD, FACP, FIDSA Associate Professor of Medicine, Wright State University, Boonshoft School of Medicine

Hari Polenakovik, MD, FACP, FIDSA is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Society for Microbiology, Society for Healthcare Epidemiology of America, European Society of Clinical Microbiology and Infectious Diseases, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Sylvia Polenakovik, MD Internist, Department of Internal Medicine, Sycamore Hospital; Internist, Miami Valley Hospitalist Group, MVH; Clinical Instructor, Wright State University, Boonshoft School of Medicine

Sylvia Polenakovik, MD is a member of the following medical societies: American College of Physicians-American Society of Internal Medicine, Society of Hospital Medicine

Disclosure: Nothing to disclose.

Chief Editor

Michael Stuart Bronze, MD David Ross Boyd Professor and Chairman, Department of Medicine, Stewart G Wolf Endowed Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center; Master of the American College of Physicians; Fellow, Infectious Diseases Society of America

Michael Stuart Bronze, MD is a member of the following medical societies: Alpha Omega Alpha, American Medical Association, Oklahoma State Medical Association, Southern Society for Clinical Investigation, Association of Professors of Medicine, American College of Physicians, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Acknowledgements

Leslie L Barton, MD Professor Emerita of Pediatrics, University of Arizona College of Medicine

Leslie L Barton, MD is a member of the following medical societies: American Academy of Pediatrics, Association of Pediatric Program Directors, Infectious Diseases Society of America, and Pediatric Infectious Diseases Society

Disclosure: Nothing to disclose.

Ramesh A Bharadwaj, MD, Fellow in Infectious Diseases, Detroit Medical Center, Wayne State University School of Medicine

Disclosure: Nothing to disclose.

Emily Anne Carpenter Rose, MD, Fellow in Pediatric Emergency Medicine, Loma Linda University School of Medicine

Disclosure: Nothing to disclose.

Rosalie Elenitsas, MD Herman Beerman Associate Professor of Dermatology, University of Pennsylvania School of Medicine; Director, Penn Cutaneous Pathology Services, Department of Dermatology, University of Pennsylvania Health System

Rosalie Elenitsas, MD is a member of the following medical societies: American Academy of Dermatology and American Society of Dermatopathology

Disclosure: Lippincott Williams Wilkins Royalty Textbook editor; DLA Piper Consulting fee Consulting

Wesley W Emmons, MD, FACP Assistant Professor, Department of Medicine, Thomas Jefferson University; Consulting Staff, Infectious Diseases Section, Department of Internal Medicine, Christiana Care, Newark, DE

Wesley W Emmons, MD, FACP is a member of the following medical societies: American College of Physicians, American Medical Association, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, and International AIDS Society

Disclosure: Nothing to disclose.

Ronald A Greenfield, MD Professor, Department of Internal Medicine, University of Oklahoma College of Medicine

Ronald A Greenfield, MD is a member of the following medical societies: American College of Physicians, American Federation for Medical Research, American Society for Microbiology, Central Society for Clinical Research, Infectious Diseases Society of America, Medical Mycology Society of the Americas, Phi Beta Kappa, Southern Society for Clinical Investigation, and Southwestern Association of Clinical Microbiology

Disclosure: Pfizer Honoraria Speaking and teaching; Gilead Honoraria Speaking and teaching; Ortho McNeil Honoraria Speaking and teaching; Abbott Honoraria Speaking and teaching; Astellas Honoraria Speaking and teaching; Cubist Honoraria Speaking and teaching; Forest Pharmaceuticals Speaking and teaching

Ashir Kumar, MD, MBBS, FAAP, Professor Emeritus, Department of Pediatrics and Human Development, Michigan State University College of Human Medicine

Disclosure: Nothing to disclose.

Mark Louden, MD, FACEP Assistant Medical Director, Emergency Department, Duke Raleigh Hospital

Mark Louden, MD, FACEP is a member of the following medical societies: American Academy of Emergency Medicine and American College of Emergency Physicians

Disclosure: Nothing to disclose.

Antonio Muñiz, MD Professor of Emergency Medicine and Pediatrics, University of Texas Medical School at Houston; Medical Director of the Pediatric Emergency Department, Children's Memorial Hermann Hospital

Antonio Muñiz, MD is a member of the following medical societies: American Academy of Emergency Medicine, American Academy of Pediatrics, American College of Emergency Physicians, American Heart Association, American Medical Association, Society for Academic Emergency Medicine, and Southern Medical Association

Disclosure: Nothing to disclose.

James J Nordlund, MD Professor Emeritus, Department of Dermatology, University of Cincinnati College of Medicine

James J Nordlund, MD is a member of the following medical societies: American Academy of Dermatology, Sigma Xi, and Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Allison J Richard, MD Assistant Professor of Emergency Medicine, Keck School of Medicine, University of Southern California; Associate Director, Division of International Medicine; Attending Physician, Los Angeles County-University of Southern California Hospital Emergency Department

Disclosure: Nothing to disclose.

Robert A Schwartz, MD, MPH Professor and Head, Dermatology, Professor of Pathology, Pediatrics, Medicine, and Preventive Medicine and Community Health, University of Medicine and Dentistry of New Jersey-New Jersey Medical School

Robert A Schwartz, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, and Sigma Xi

Disclosure: Nothing to disclose.

Russell W Steele, MD Head, Division of Pediatric Infectious Diseases, Ochsner Children's Health Center; Clinical Professor, Department of Pediatrics, Tulane University School of Medicine

Russell W Steele, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Immunologists, American Pediatric Society, American Society for Microbiology, Infectious Diseases Society of America, Louisiana State Medical Society, Pediatric Infectious Diseases Society, Society for Pediatric Research, and Southern Medical Association

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Mordechai M Tarlow, MD Clinical Associate, Department of Dermatology, University of Pennsylvania School of Medicine

Mordechai M Tarlow, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, American Society for MOHS Surgery, American Society of Cosmetic Dermatology and Aesthetic Surgery, and Sigma Xi

Disclosure: Nothing to disclose.

Jeter (Jay) Pritchard Taylor III, MD Compliance Officer, Attending Physician, Emergency Medicine Residency, Department of Emergency Medicine, Palmetto Health Richland, University of South Carolina School of Medicine; Medical Director, Department of Emergency Medicine, Palmetto Health Baptist

Jeter (Jay) Pritchard Taylor III, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Robert W Tolan Jr, MD Chief, Division of Allergy, Immunology and Infectious Diseases, The Children's Hospital at Saint Peter's University Hospital; Clinical Associate Professor of Pediatrics, Drexel University College of Medicine

Robert W Tolan Jr, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, Phi Beta Kappa, and Physicians for Social Responsibility

Disclosure: GlaxoSmithKline Honoraria Speaking and teaching; MedImmune Honoraria Speaking and teaching; Merck Honoraria Speaking and teaching; Sanofi Pasteur Honoraria Speaking and teaching; Baxter Healthcare Honoraria Speaking and teaching; Novartis Honoraria Speaking and teaching

Eric L Weiss, MD DTM&H, Medical Director, Office of Service Continuity and Disaster Planning, Fellowship Director, Stanford University Medical Center Disaster Medicine Fellowship, Chairman, SUMC and LPCH Bioterrorism and Emergency Preparedness Task Force, Clinical Associate Professor, Department of Surgery (Emergency Medicine), Stanford University Medical Center

Eric L Weiss, MD is a member of the following medical societies: American College of Emergency Physicians, American College of Occupational and Environmental Medicine, American Medical Association, American Society of Tropical Medicine and Hygiene, Physicians for Social Responsibility, Southeastern Surgical Congress, Southern Association for Oncology, Southern Clinical Neurological Society, and Wilderness Medical Society

Disclosure: Nothing to disclose.

Michael J Wells, MD Associate Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine

Michael J Wells, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, and Texas Medical Association

Disclosure: Nothing to disclose.

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First stage, life cycle of Strongyloides stercoralis. Illustration by Tessa Kalman.
Second stage, life cycle of Strongyloides stercoralis. Illustration by Tessa Kalman.
Third stage, life cycle of Strongyloides stercoralis. Illustration by Tessa Kalman.
Fourth stage, life cycle of Strongyloides stercoralis. Illustration by Tessa Kalman.
Fifth stage, life cycle of Strongyloides stercoralis. Illustration by Tessa Kalman.
Rhabditiform larva of Strongyloides stercoralis in stool specimen (wet mount stained with iodine).
 
 
 
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