Strongyloidiasis overview On the Web
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Strongyloidiasis is an infection caused by a roundworm (nematode), Strongyloides stercoralis. Transmission occurs predominantly in tropical and subtropical areas but can also be found in countries with temperate environments including the southeastern U.S. Infection is contracted via direct contact with contaminated soil during agricultural, domestic, and recreational activities. S stercoralis in humans usually produces an asymptomatic chronic infection of the gastrointestinal tract that can remain undetected for several decades. Usually there are no unique clinical symptoms to suggest infection, although abdominal bloating and eosinophilia are common in many infected patients. In some patients a disseminated or hyperinfection syndrome can develop with the dissemination of larvae to extra-intestinal organs, and that can result in mortality rates exceeding 90%. Risk factors and predisposing conditions include immunosuppressive therapies with corticosteroids and other medications, HTLV-1 infection, organ transplantation, immune reconstitution syndrome, hematologic malignancies (lymphoma), tuberculosis, and malnutrition. Diagnosis is generally made by the detection of larvae in the stool. Ivermectin, thiabendazole, and albendazole are the most effective medicines for treating the infection. Excellent recovery after treatment should be expected in immunocompetent patients.
Strongyloides was first discovered in 1876 by the French physician Louis Alexis Normand while working in the naval hospital in Toulon; he identified the adult worms and sent them to Arthur Réné Jean Baptiste Bavay, chief health inspector, who observed that the worms were the adult forms of the larvae found in stool. In 1883, the German parasitologist Rudolf Leuckart made initial observations on the life cycle of parasite. Belgian physician Paul Van Durme described the mode of infection through the skin. The German parasitologist Friedrich Fülleborn described autoinfection and the mechanism by which strongyloidiasis involves the intestine. Strongyloidiasis was investigated further during the 1940s, as persons who had acquired the infection abroad and then received immunosuppression developed hyper-infestation syndrome.
Strongyloidiasis may be classified as acute or chronic based on the duration of symptoms and as hyper infection syndrome or disseminated strongyloidiasis based on the organ system involvement.
Strongyloides is a soil-transmitted helminth. The principal definitive hosts of S stercoralis are humans, but infection in dogs can also occur. Infection is contracted via direct contact with contaminated soil during agricultural, domestic, and recreational activities. Filariform larvae penetrate the skin and enter a venous or lymphatic vessel. These larvae then migrate to the lungs, where they break out of the capillaries into the alveoli and move to the trachea as they mature. Eventually these larvae gets coughed up and swallowed. Parthenogenetic female worms reside in the lamina propria of the duodenum and the proximal jejunum, where they lay eggs. The eggs hatch into rhabditiform larvae. These larvae migrate into the intestinal lumen and ultimately exit the body with the feces. The free-living rhabditiform larvae may either directly molt into infective (parasitic) filariform larvae that are capable of penetrating the skin of a suitable host or shift to a free-living cycle. In this latter indirect (heterogonic) cycle, molts result in the development of adult male and female worms that mate and produce a generation of offspring whose filariform stage will have the ability to re-enter parasitic life. A small percentage of the rhabditiform larvae molt within the host's intestine into the filariform stage. These tissue-penetrating infective larvae may penetrate the colonic wall or the perianal skin, completing an internal cycle, and maturing into adult females in the small intestine. This process is known as autoinfection and may be the mechanism by which S stercoralis can persist indefinitely in infected hosts. This is a unique characteristic of S stercoralis.
Differentiating Strongyloidiasis from other Diseases
Strongyloidiasis can mimic other worm infections like Ascaris lumbricoides, Trichuris trichiura, hookworm infections (Necator americanus and Ancylostoma duodenale), Enterobius vermicularis (pinworm) and gastrointestinal pathologies such as peptic ulcer disease, intussusception in children, and bile duct stone.
Epidemiology and Demographics
The global prevalence of Strongyloides is unknown, but recent studies estimate that there are between 30–100 million infected persons worldwide, mainly in tropical and subtropical countries. Strongyloidiasis is more common in the pediatric age group (ages 2-10 years).
Common risk factors in the development of strongyloidiasis include immunosuppressive therapies with corticosteroids and other medications, HTLV-1 infection, organ transplantation, immune reconstitution syndrome, hematologic malignancies (especially lymphoma), tuberculosis, and malnutrition
Most fatal infections caused by S.stercoralis can be prevented by early detection and treatment of asymptomatic chronic infections. Screening is highly recommended to detect latent S.stercoralis infection before the start of chemotherapy or immunosuppression/steroid therapy in patients at risk. Repeated stool examination for ova and parasites or agar culture of stool may be the most appropriate approach.
Natural history, Complications, and Prognosis
If strongyloidiasis is left untreated, the infection can disseminate and transform into hyper-infection syndrome which has a mortality rate of 90%. Complications that can develop as a result of strongyloidiasis are disseminated strongyloidiasis (especially in patients with HIV or other immunocompromised conditions ), eosinophilic pneumonia, malnutrition, and malabsorption. With appropriate treatment, people should make a full recovery. Treatment needs to be repeated often. Infections that are severe or widespread often have a poor outcome, especially in people with a suppressed immune system.
History and symptoms
Strongyloides infection can present in various forms. The majority of people infected with Strongyloides are asymptomatic. The symptomatic spectrum of strongyloidiasis ranges from subclinical in acute and chronic infection to severe and fatal in hyper infection syndrome. On acquiring the infection, there may be respiratory symptoms (Löffler's syndrome). The infection may progress to chronic stage with mainly digestive symptoms. On reinfection there may be respiratory, skin, and digestive symptoms. Finally, hyper infection syndrome sets in and cause symptoms in many organ systems, including the central nervous system.
The physical examination findings in strongyloidiasis vary and are usually dependent on the worm burden and the involved organ.
The diagnosis of strongyloidiasis is made by presence of clinical signs and symptoms, eosinophilia, and positive serological findings. Definitive diagnosis of strongyloidiasis is generally made by the detection of larvae in the stool. Sputum examination may rarely be used to identify organisms in cases of hyperinfection. Agar tracking (detection of larval tracks on agar culture plates) has been shown to be more sensitive than the conventional stool examination. However, agar tracking is usually unavailable on a routine basis in clinical microbiology laboratories. Immunodiagnostic tests for strongyloidiasis are indicated when the infection is suspected and the organism cannot be demonstrated by repeated examinations of stool. Enzyme immunoassay (EIA) is currently recommended because of its greater sensitivity (90%). Antibody test results cannot be used to differentiate between the past and current infection. In disseminated cases of strongyloidiasis, larvae can be detected in sputum by simple wet-mount in fluid from a bronchoalveolar lavage (BAL).
X rays can be helpful in the diagnosis of strongyloidiasis. Radiographic findings are variable, depending upon the stage and extent of infection which includes pulmonary infiltrates, when present, may be alveolar or interstitial, diffuse or focal, uni- or bilateral. Lung consolidation, occasional cavitation, and even abscess formation can also be found. Plain abdominal radiographs and contrast studies can reveal worm masses in bowel loops. Chest radiographs are explained by pulmonary migration of the parasites and by different types of bacterial super-infection, particularly gram-negative bacilli.
There are no specific CT findings associated with strongyloidiasis. However, in cases of abdominal obstruction due to worm burden, CT can demonstrate collapsed loops of the bowel distally and radial distribution of several dilated, fluid-filled bowel loops.
There are no specific MRI findings associated with strongyloidiasis.
There are no specific ultrasound findings associated with strongyloidiasis.
Other Imaging Findings
There are no other specific imaging findings associated with strongyloidiasis infection.
Other diagnostic tests
Ivermectin, thiabendazole, and albendazole are the most effective medicines for treating strongyloidiasis infection. Ivermectin is the drug of choice, and albendazole is considered the least effective. Thiabendazole is not generally used in the U.S. due to adverse events, but it is still used in other countries. All patients with strongyloidiasis (even asymptomatic patients) require treatment. Complete obstruction with inadequate decompression, lack of response within an interval of 24-48 hrs, volvulus, intussusception, or perforation should be managed surgically.
Strongyloidiasis is usually managed with medical therapy. However, surgery may be indicated when medical management fails or complications arise.
The prevention of strongyloidiasis is best achieved through improvements in personal hygiene and environmental sanitation.
Secondary preventive measures of strongyloidiasis are similar to primary preventive measures.