Strongyloides stercoralis larvae exist in two forms: free-living rhabditiform and filariform infective larvae. The cycle starts with the infectious filariform larvae penetrating the skin and traveling via lymphatics or bloodstream to the lungs. After penetrating in the alveoli the larvae continue to migrate up to the airways until

they are swallowed. In the duodenum and proximal jejunum the larvae mature into adult females which live threaded in the intestinal mucosa. The larvae can produce up to 40 eggs a day by mitotic parthenogenesis (i.e., asexual reproduction where development of embryos occurs Ganetespib datasheet without fertilization by a male). Once these eggs hatch, rhabditiform larvae are released. These larvae can either passed in the stools, continuing the soil based cycle, or can cause autoinfection. The autoinfection occurs when the rhabditiform larvae prematurely become the infective filariform larvae in the intestinal lumen, and penetrate in the intestinal mucosa or perianal skin (internal and external autoinfection, respectively). In either case the infective larvae migrate to the lungs and restart selleck chemical the cycle previously described [1, 3, 7]. The autoinfection phenomenon allows S. stercoralis to persist and replicate within a host for decades, with the longest reported period being 65 years [10]. The term “”disseminated disease”" is used to define when the infective larvae migrate, from the intestine,

in massive numbers not only to the lungs but to other organs not involved in the normal helminthic life cycle. In disseminated strongyloidiasis, the mortality

rate can be as high as 70-90% [3]. Several risk factors are associated with the development of disseminated strongyloidiasis, including (1) immune deficiency, (2) hematologic malignacy, (3) steroids administration, (4) HTLV-1 infection, (5) chronic alcoholism, (6) renal failure, (7) transplantation, Lepirudin among others [11]. In disseminated disease, translocation of enteric bacteria may occur, leading to Gram-negative sepsis and/or meningitis. The enteric microorganism can either enter the circulation through intestinal ulcers or be carried by the infective filariform larvae. Fedratinib mouse Approximately, half of Strongyloides infections are asymptomatic [1, 3]. Clinical presentation is extremely variable reflecting the complex life cycle of the parasite. When symptoms develop, gastrointestinal complaints are common. Symptoms are vague and nonspecific and include anorexia, nausea, vomiting, weight loss, abdominal pain, flatulence, and diarrhea. Less frequently, malabsorption syndromes, paralytic ileus, intestinal obstruction and gastrointestinal bleeding, may occur [1–3]. Pulmonary symptoms are rare in uncomplicated strongyloidiasis, but cough and wheezing may be part of initial presentation (Löffler’s syndrome). In disseminated disease respiratory symptoms become more prominent and include dyspnea, tachypnea, pleuritic pain, pleural effusion, and hemoptysis [1, 2, 6].