Strongyloidiasis Clinical Presentation
- Author: Pranatharthi Haran Chandrasekar, MBBS, MD; Chief Editor: Burke A Cunha, MD more...
History and Physical Examination
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 and can survive decades undiagnosed.
Symptomatic infections typically manifest in gastrointestinal, pulmonary, and dermatologic systems. 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.
Acute infection is generally characterized by gastrointestinal (GI) and pulmonary symptoms, whereas chronic infection is characterized by skin involvement.
Severe strongyloidiasis (hyperinfection, disseminated disease) may be insidious; occasionally, symptoms may have an abrupt onset. Fever is almost always present in disseminated disease.[34] 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. Thus, a diagnosis of severe strongyloidiasis should be suspected with unusual GI or pulmonary symptoms or an unexplained Gram-negative bacilli sepsis.
Gastrointestinal manifestations
Gastrointestinal symptoms are vague, including epigastric abdominal cramping, indigestion, anorexia, weight loss, nausea, vomiting, chronic diarrhea, constipation, pruritus ani, bloating and, rarely, small bowel obstruction. Strongyloides is an important cause of failure to thrive and cachexia in immunocompetent children.
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 in chronic infections and has been successfully treated by deworming.
Prolonged malabsorption of both fat and protein can lead to a celiac-like syndrome, characterized by steatorrhea, hypoalbuminemia, and peripheral edema, such as a syndrome of infantile infection caused by S fulleborni 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 kwashiorkor-like appearance (with ascites and pleural effusions) due to hypoalbuminemia ("swollen baby" sickness).
In severe hyperinfection syndrome or disseminated disease, abdominal symptoms are similar to those of chronic infection, but they are more severe. 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. Bloody stools and/or blood diarrhea may occur along with severe abdominal pains. Massive GI tract bleeding has also been reported.[35]
Pulmonary manifestations
Symptomatic pulmonary strongyloidiasis that results from migrating larvae is observed in 10% of patients. Initial infection may trigger wheezing[36] and mild cough.
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.
In severe (disseminated) disease, pneumonitis may cause hemoptysis and difficulty in breathing. In addition, cough, hemoptysis, dyspnea, wheezing, pleuric pain, tachypnea can occur, and acute respiratory distress syndrome (ARDS) may require mechanical ventilation.
Dermatologic manifestations
Skin penetration by infective larvae can elicit ground itch, a cutaneous eruption of pruritic papulovesicular lesions. Typically, skin penetration is on the feet but may be at any site that contacted infected soil (eg, around the anus [within 12 cm] or anywhere on the trunk and thighs).
Larva currens (racing larvae), the pathognomonic rash of Strongyloides infection, is an intensely pruritic linear or serpiginous urticarial rash that may consist of 1 or more such bands and creeps 5-15 cm/h up the body. The rash, likely an allergic response to the migrating filariform larvae, often manifests as a pruritic wheal or linear urticaria. This dermatologic manifestation may last hours to days but in autoinfection cycles can recur over weeks, months, and years. 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. Excoriation and impetigo are common.
Rarely, in disseminated strongyloidiasis, a rapidly progressive, diffuse, petechial purpuric eruption may be present secondary to vessel injury during larval migration.[37] Characteristic purpuric periumbilical skin lesions should raise the suspicion for its diagnosis; it often portends a fatal outcome in cancer patients.[38] There have also been case reports of multiple atypical dermatologic presentations in hyperinfection cases.[39]
Neurologic and other manifestations (severe strongyloidiasis)
An altered mental status, focal seizures, meningitis, brain abscess or nuchal rigidity may indicate central nervous (CNS) involvement. Symptoms of meningitis may include headache, nausea, vomiting, and, in extreme cases, coma.
Granulomatous hepatitis and parasitic invasion of the heart, kidney, peritoneum, lymph nodes, pancreas, prostate, ovaries, thyroid, or parathyroid may be present in disseminated disease.
A case report demonstrated infertility as a presentation for disseminated strongyloidiasis with larvae found in ejaculate and conception occurring after treatment. Another patient experienced years of recurrent abdominal pain and fever with recurrent eosinophilic oophoritis who had positive strongyloides serology and clinical response to treatment.[40]
Complications
Strongyloidiasis can lead to gastrointestinal (GI), pulmonary, dermatologic, neurologic, and other complications, as well as death.
GI complications include the following:
GI hemorrhage: 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
- Malabsorption
- Intestinal obstruction,[41] perforation, and infarction
- Eosinophilic oophoritis[40]
- Appendicitis[42]
- Peritonitis
- Obstructive jaundice
- Ileus
- Pneumatosis intestinalis
Pulmonary complications include the following:
- Asthma or exacerbation of preexisting obstructive pulmonary disease
- Pneumonitis
- Respiratory failure,[33] acute respiratory distress syndrome (ASDS)
- Alveolar hemorrhage
- Pleural effusion
- Granulomatous lung disease
Dermatologic complications include larva currens, purpura of the trunk and proximal extremities, and chronic urticaria.
Neurologic complications include meningitis due to enteric bacteria and brain abscess.
Vascular complications include hyperinfection syndrome presenting as bacteremia (occasionally recurrent) due to enteric microorganisms (eg, Escherichia coli, Klebsiella pneumoniae, Enterococcus species including vancomycin-resistant E faecium, Streptococcus bovis).
Renal complications can rarely include nephrotic syndrome[43] (eg, minimal-change nephrotic syndrome[44] ). Resolution of the proteinuria occurs after administration of antihelmintic therapy with ivermectin. Incidence of nephrotic syndrome in children in the developing world is increased in those with underlying strongyloidiasis.[45] In addition, the syndrome of inappropriate antidiuretic hormone (SIADH) has been observed in patients with severe Strongyloides infection.[46]
Rarely, a musculoskeletal complication such as reactive arthritis may occur.
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