Strongyloides stercoralis

Author: MBLOGSTU

Introduction

S. stercoralis causes strongyloidiasis and is the fourth most important intestinal nematode infection in the world.

Although isolated pockets of low endemicity and indigenous sporadic infections have been found in many temperate areas, S. stercoralis infection predominantly occurs in humid tropical regions.

The specific impact of chronic infection on human health is difficult to evaluate in populations with widespread enteric diseases, other parasitoses, and malnutrition. However, strongyloidiasis is not generally believed to be a major cause of morbidity worldwide.

Infection in humans usually produces an asymptomatic chronic disease of the gastrointestinal tract that can remain undetected for decades.

In immunocompromised patients – especially those receiving corticosteroids – hyperinfection can develop with dissemination of larvae to extraintestinal organs, resulting in mortality rates as high as 85%.

Epidemiology

The worldwide prevalence of strongyloidiasis is inconsistent with estimates ranging between 3 million and 100 million people infected.

S. stercoralis is probably present in virtually all tropical and subtropical regions.

The high prevalence has been attributed to agricultural activities.

The infection has also been found intermittently in institutionalized individuals and in patients at cancer centers in several North American locations where the parasite is not endemic in the general population.

Considering its long persistence in the host and relatively high prevalence in some tropical/subtropical populations, physicians in industrialized countries should consider strongyloidiasis in immigrant or refugee patients born in developing regions, as well as in individuals from known local areas of endemicity.

Morphology

Additional morphological details were not provided in this presentation.

Pathogenesis

Chronic strongyloidiasis is sustained by a relatively low and stable number of adult worms that reside harmoniously in the host’s intestine and survive via well-regulated autoinfection. Autoinfection is mediated by host cell–mediated immunity; when immunosuppression occurs, more autoinfective larvae complete the cycle and the adult worm population increases (hyperinfection).

Eventually, the extraordinary number of migrating larvae deviates from the canonical route (intestine → venous bed → lungs → trachea → intestine) and disseminates to other organs—including the meningeal spaces, brain, liver, kidneys, lymph nodes, and cutaneous/subcutaneous tissues—causing hemorrhage, inflammation, and the implantation of gram-negative bacteria brought from fecal material. This disseminated strongyloidiasis is nearly always fatal.

Some investigators propose that S. stercoralis may reach an "optimal" population size in the small intestine. With a low initial infective dose, a higher rate of intraluminal molting (autoinfection) occurs until this optimal size is reached.

During the early phase of infection, the host mounts an immune response against all tissue stages of the parasite. Although this response may not eradicate all parasites, it limits their population. In individuals with impaired immunity (e.g., agammaglobulinemic patients, HTLV-I-infected subjects, severely malnourished children), larger numbers of parasites can develop. However, complete dysregulation is rare since the worms partially regulate their own growth.

The administration of exogenous or endogenous corticosteroids may increase ecdysteroid-like substances in host tissues (including the intestinal wall where adult females reside), which can act as molting signals for eggs or rhabditiform larvae—transforming them into excessive numbers of filariform larvae.

Once an intestinal population becomes very large (e.g., around 100,000 adult worms), it expands rapidly even at low molting rates, and simply discontinuing steroids is insufficient to halt the growth, eventually leading to the host’s death.

Clinical Manifestations

Gastrointestinal Manifestations

Patients may report epigastric abdominal pain, postprandial fullness or bloating, and heartburn. Brief episodes of diarrhea alternating with constipation can occur, and occult blood is occasionally detected in stools. Massive colonic and gastric hemorrhage have also been reported.

Physical examination is often normal or shows only mild abdominal tenderness. Rarely, chronic strongyloidiasis may resemble inflammatory bowel disease, particularly ulcerative colitis.

In disseminated strongyloidiasis, gastrointestinal manifestations intensify. Hyperinfection is marked by profuse diarrhea due to erosions, ulcerations, and edema in the small and large intestinal mucosa, resulting in malabsorption, exudation, altered motility, a predisposition to bacterial enterocolitis, and eventually paralytic ileus.

Pulmonary Manifestations

In chronic infections, the low number of larvae passing through the lungs often produces no significant respiratory symptoms. In contrast, disseminated strongyloidiasis typically features pulmonary issues—especially diffuse bronchopneumonia and intra-alveolar hemorrhage (which may be severe enough to cause death). Filariform larvae, and occasionally rhabditiform larvae and even eggs, may be found in respiratory secretions.

Neurologic Manifestations

Uncomplicated strongyloidiasis is not generally associated with neurologic symptoms. However, in disseminated disease, gram-negative polymicrobial meningitis is the most frequent central nervous system complication, and larvae have been identified in cerebrospinal fluid in some cases. Less commonly, cerebral and cerebellar abscesses containing S. stercoralis larvae may develop.

Cutaneous Manifestations

Two types of skin manifestations have been noted:

• Urticarial Rashes: Possibly resulting from sensitization to parasite antigens.
• Migratory Serpiginous Dermatitis (Larva Currens): Caused by the subcutaneous migration of filariform larvae.

Other Systemic Manifestations

Other manifestations include:

• Arthritis: Uncommon and associated with local deposition of immune complexes containing S. stercoralis antigens.
• Cardiac Arrhythmias/Arrest: Exceedingly rare, attributed either to direct myocardial damage by migrating larvae or to electrolyte imbalances from severe diarrhea.
• The presence of larvae in semen and genital lesions, as well as multivisceral damage, have also been documented.

Overall, the infection is associated with a higher degree of severity in immunocompromised individuals.

Laboratory Diagnosis

Confirmation of strongyloidiasis depends on recovering and identifying adult worms, larvae, or eggs from the stool, duodenal material, or sputum. Fecal specimens may sometimes be negative—even after routine ova and parasite examinations and concentration procedures—because larval counts can vary from day to day.

Duodenal content sampling (using methods such as the Entero-test) is sometimes employed when stool examinations are negative, although its efficacy is debated.

Special techniques like the Baermann, Harada-Mori, and Petriplate culture methods can enhance larval recovery from large stool samples. To differentiate Strongyloides filariform larvae from hookworm filariform larvae, examine the tail under a microscope; Strongyloides larvae have a slit in the tail, whereas hookworm larvae have a pointed tail.

Serological tests (including ELISA, IHA, and IFA) and skin tests are useful for diagnosis, and eosinophilia along with imaging techniques may also support the diagnosis.

Key Points in Diagnosis

• Recovery of rhabditiform larvae from the stool is the standard method.
• If stool examination is negative, the Entero-test is recommended.
• Various concentration and culture methods can assist in larval recovery.
• Eggs are rarely seen in the stool but may be recovered from duodenal contents.
• In very heavy infections, eggs, larvae, and even adult worms may be recovered in the stool.