eMedicine Specialties > Dermatology > Parasitic Infections

Strongyloidiasis

Author: Robert A Schwartz, MD, MPH, Professor and Head, Dermatology, Professor of
Pathology, Pediatrics, Medicine, and Preventive Medicine and Community Health, UMDNJ-
New Jersey Medical School
Coauthor(s): Mordechai M Tarlow, MD, Clinical Associate, Department of Dermatology,
University of Pennsylvania School of Medicine
Contributor Information and Disclosures

Updated: Jun 16, 2010

Introduction

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.

Consequences of captivity include health effects, including strongyloidiasis. Allied military

personnel held by the Japanese during the World War II experienced deprivation, malnutrition,
and exposure to tropical diseases.1 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.

Also see the eMedicine article Strongyloidiasis.2

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%.3 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%.4,5

International

Strongyloidiasis is endemic in tropical and subtropical countries.6 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.7

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.8
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

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

o 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.

o 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

o 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.

o 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

o Cutaneous features

A rapidly progressive, diffuse petechial and purpuric eruption may

occur.

The cause is the massive migration of filariform larvae into the

skin.
 o 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.9,10 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.11

Physical

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

Acute infection

o 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.

o Systemic findings

Wheezing may occur.

The patient may have a fever.

 Epigastric tenderness may be present.

Chronic infection

o 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.

o Systemic findings

Examination findings are usually normal.

Epigastric tenderness may be preset, and weight loss may occur.

Severe disseminated infection

o 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.

o 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.12

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.

o Infections are reported among veterinarians and laboratory workers who

work in temperate climates and are exposed to larvae from horses.

o 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:

o Use of immunosuppressive agents

o Malignancy

o Other infections, particularly HIV infection and other immunosuppressive

infections13

o Collagen-vascular disease

o Diabetes mellitus

o Malnutrition

o Advanced age
 In patients who were exposed to the parasite, the likelihood of Strongyloides
should be carefully assessed before immunosuppressive therapy is begun.