+1 Recommend
0 collections
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Intestinal strongyloidiasis and hyperinfection syndrome

      1 , , 1 , 1 , 2
      Clinical and Molecular Allergy
      BioMed Central

      Read this article at

          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.


          In spite of recent advances with experiments on animal models, strongyloidiasis, an infection caused by the nematode parasite Strongyloides stercoralis, has still been an elusive disease. Though endemic in some developing countries, strongyloidiasis still poses a threat to the developed world. Due to the peculiar but characteristic features of autoinfection, hyperinfection syndrome involving only pulmonary and gastrointestinal systems, and disseminated infection with involvement of other organs, strongyloidiasis needs special attention by the physician, especially one serving patients in areas endemic for strongyloidiasis. Strongyloidiasis can occur without any symptoms, or as a potentially fatal hyperinfection or disseminated infection. Th 2 cell-mediated immunity, humoral immunity and mucosal immunity have been shown to have protective effects against this parasitic infection especially in animal models. Any factors that suppress these mechanisms (such as intercurrent immune suppression or glucocorticoid therapy) could potentially trigger hyperinfection or disseminated infection which could be fatal. Even with the recent advances in laboratory tests, strongyloidiasis is still difficult to diagnose. But once diagnosed, the disease can be treated effectively with antihelminthic drugs like Ivermectin. This review article summarizes a case of strongyloidiasis and various aspects of strongyloidiasis, with emphasis on epidemiology, life cycle of Strongyloides stercoralis, clinical manifestations of the disease, corticosteroids and strongyloidiasis, diagnostic aspects of the disease, various host defense pathways against strongyloidiasis, and available treatment options.

          Related collections

          Most cited references108

          • Record: found
          • Abstract: found
          • Article: not found

          Epidemiological and clinical interaction between HTLV-1 and Strongyloides stercoralis.

          Strongyloides stercoralis is the most common human parasitic nematode that is able to complete a life cycle and proliferate within its host. The majority of patients with strongyloidiasis have an asymptomatic infection or mild disease. However, when autoinfection occurs, a high number of infecting larvae can gain access to the bloodstream by penetrating the colonic mucosa leading to a severe hyperinfection and the development of disseminated strongyloidiasis. The human T cell lymphotropic virus type 1 (HTLV-1) predominantly infects T cells and induces spontaneous lymphocyte proliferation and secretion of high levels of type 1 cytokines. Strongyloides stercoralis patients with HTLV-1 co-infection have a modified immunological responses against parasite antigens and co-infection has clinical implications for strongyloidiasis. The high production of IFN-gamma observed in patients co-infected with HTLV-1 and Strongyloides stercoralis decreases the production of IL-4, IL-5, IL-13 and IgE, molecules that participate in the host defence mechanism against helminths. Moreover, there is a decrease in the efficacy of treatment of Strongyloides stercoralis in patients co-infected with HTLV-1. Alterations in the immune response against Strongyloides stercoralis and the decrease in the efficacy of anti-parasitic drugs are responsible for the increased prevalence of Strongyloides stercoralis among HTLV-1 infected subjects and make HTLV-1 infection the most important risk factor for disseminated strongyloidiasis.
            • Record: found
            • Abstract: found
            • Article: not found

            Interleukin 4 is important in protective immunity to a gastrointestinal nematode infection in mice.

            Parasitic helminths typically induce components of immediate-type hypersensitivity, including elevated serum IgE, eosinophilia, and mucosal mast cells. These responses are T-cell-dependent and associated with rapid expulsion of parasitic worms from a sensitized host; existing experimental systems have failed to define the precise role of cytokines in these responses. We report here that anti-interleukin 4 or anti-interleukin 4 receptor antibodies block the polyclonal IgE response to a parasitic nematode, Heligmosomoides polygyrus, and abrogate protective immunity to the infection. In contrast, anti-interleukin 5 antibody prevented H. polygyrus-induced eosinophilia but did not prevent protection. These data provide evidence that a specific cytokine affects the physiology and survival of a parasitic nematode in the host.
              • Record: found
              • Abstract: found
              • Article: not found

              Complicated and fatal Strongyloides infection in Canadians: risk factors, diagnosis and management.

              Strongyloidiasis, which is caused by the nematode Strongyloides stercoralis, is a common and persistent infection, particularly in developing countries. In the setting of compromised cellular immunity, it can result in fulminant dissemination with case-fatality rates of over 70%. The majority of new Canadian immigrants come from countries where Strongyloides is highly endemic; therefore, the burden of Strongyloides may be underappreciated in Canada. Because early diagnosis and therapy can have a marked impact on disease outcome, screening for this infection should be considered mandatory for patients who have a history of travel or residence in a disease-endemic area and risk factors for disseminated disease (e.g., corticosteroid use and human T-lymphotropic virus type I infection).

                Author and article information

                Clin Mol Allergy
                Clinical and Molecular Allergy
                BioMed Central (London )
                30 May 2006
                : 4
                : 8
                [1 ]Department of Internal Medicine, Quillen College of Medicine, East Tennessee State University, VA Building 1, Johnson City, Tennessee, USA
                [2 ]Division of Allergy and Immunology, James H. Quillen Veterans Affairs Medical Center, Johnson City, Tennessee, USA
                Copyright © 2006 Vadlamudi et al; licensee BioMed Central Ltd.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                : 2 February 2006
                : 30 May 2006



                Comment on this article