JOURNAL OF THE LOUISIANA STATE MEDICAL SOCIETY
Infective filariform larvae develop in sand or soil by two mechanisms. (1) Vicarious defecation and the improper management of human wastes deposit rhabditiform larvae in sand or soil to develop directly into infective filariform larvae. (2) Alternatively, rhabditiform larvae can develop into free-living and mating male and female adult worms with the fertilized females producing eggs that hatch into rhabditiform larvae that develop into another crop of infective filariform larvae. Figure 2 shows an infective filariform larva in an unstained stool specimen from a patient with strongyloidiasis. Anyone who has walked barefoot (or sat or sunbathed nude) on a tropical beach, soil, or yard contaminated with infective Strongyloides stercoralis filariform larvae is at risk of contracting strongyloidiasis, not only in the tropics, but also in the Southeast U.S.
The Epidemiology of Strongyloidiasis
The world burden of strongyloidiasis is significant. The World Health Organization (WHO) has estimated that up to 100 million people are infected and capable of excreting rhabditiform larvae throughout their lifetimes. 7 In addition to immigrants infected in their native homelands, Southeast Asian war veterans and ex-POWs infected in captivity are another recognized high-risk group for strongyloidiasis. Table 1 1-6 compares the prevalence rates of chronic strongyloidiasis in World War II POWs and in VietnamWar veterans as diagnosedby recommended laboratory tests. Strongyloidiasis is also becoming more common in Western tourists returning from tropical beach vacations in endemic resort regions of the Caribbean, Africa, South America, and Southeast Asia. 8,9 In 2006, Boggild and coinvestigators reported a case series of 43 returning Canadian travelers with strongyloidiasis. 8 The infections were associated with Canadian immigrantsvisitingfriendsandrelatives intheirnativehomelands in 37% of the cases; tourism in 30%; and recent immigration to Canada in 21%. 8 All patients with chronic strongyloidiasis will remain at high risk of developing the hyperinfection syndrome and disseminated strongyloidiasis at some point in their lifetimes, especially if treated with corticosteroids, often for very common pulmonary and rheumatic comorbidities. Several other significant risk factors for precipitating hyperinfection and disseminated strongyloidiasis have now been identified including: (1) endogenous corticosteroids produced by adrenal or pituitary tumors; (2) primary genetic and acquired immunodeficiency disorders; (3) hematologic malignancies; (4) underlying infection with human T cell lymphotrophicvirustype-1(HTLV-1);and(5)chronic,unexplained eosinophilia in developmentally disabled or demented residents of long-term-care facilities. 10-17 The exact mechanisms by which such specific immunosuppressive conditions precipitate hyperinfection and disseminated strongyloidiasis in these high risk groups remain unclear, especially in light of no observed association between the acquired immunodeficiency syndrome (AIDS) and hyperinfection. 10-17
Figure 2: Rhabditiform larva of Strongyloides stercoralis in unstained wet mount of stool. Red arrow points to the genital primordium. Source: United States Centers for Disease Control and Prevention (CDC), DPDx Image Library. No copyright permission required. Available at https://www.cdc. gov/dpdx/strongyloidiasis/index.html.
The Clinical Manifestations of Strongyloidiasis
As noted, Strongyloides stercoralis causes three types of human infections. Acute strongyloidiasis, which if symptomatic, may be associated with transient symptoms including a pruritic, erythematous, urticarial rash at the site of skin penetration, usually on the foot, abdominal pain, anorexia, fatigue, alternating diarrhea and constipation, and tracheal irritation with a dry cough caused by larval migration through the lungs (Loeffler’s syndrome). 9 Chronic strongyloidiasis results from recurrent autoinfections by infective, filariform larvae that penetrate the duodenal mucosa internally (internal autoinfection) or the perianal skin externally (external autoinfection). These bouts of autoinfection may cause intermittent abdominal pain; alternating constipation and diarrhea; pruritus ani; and larva currens, a recurrent serpiginous, maculopapular rash on the buttocks, perineum, thighs, or abdomen caused by filariform larvae migrating through connective tissues. Unless reactivated by conditions that impair the host’s immune response to parasitic infection, chronic strongyloidiasis remains relatively quiescent for decades; interrupted only by bouts of abdominal pain and migratory, maculopapular urticarial rashes (larva currans) during autoinfections that are often ascribed to more common recurrent conditions, such as heartburn and eczema. Lastly, the hyperinfection syndrome occurs in patients with chronic strongyloidiasis who have received corticosteroids. Hyperinfection is caused by an overwhelming number of filariform larvae initially migrating to the lungs and gastrointestinal tract and causing alveolar and gastrointestinal
20 J La State Med Soc VOL 170 JANUARY/FEBRUARY 2018
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