Microsporidia are currently considered emerging pathogens responsible for life-threatening infections in organ transplant recipients. diagnosis of other syndromes such as chronic fever of unknown etiology. INTRODUCTION Microsporidia are ubiquitous obligate intracellular opportunistic parasites recently related to fungi capable of infecting a wide range of vertebrate and invertebrate hosts (2 12 Within microsporidia 8 genera and 14 species have been associated with human infections among which and are the most commonly reported (12). These opportunistic pathogens cause a variety of systemic and nonsystemic diseases with chronic diarrhea as the most common clinical manifestation although the spectrum of diseases caused by them is broad and includes eye respiratory renal and central nervous system infections (12). Most microsporidial infections have been reported to occur in severely immunocompromised individuals mainly HIV/AIDS patients but cases in HIV-negative people including travelers and elderly people are constantly increasing (11 27 Additionally the number of non-HIV-infected patients with other forms of immunosuppression is also increasing. Among these organ transplant recipients (OTR) have recently been considered a group of patients at risk for these pathogens (22). To date only 21 cases of microsporidiosis in solid organ transplant (SOT) and bone marrow transplant (BMT) recipients who were HIV negative have already been explained (4 13 19 20 22 23 28 34 40 44 49 In these individuals diarrhea is the most frequent medical manifestation and the varieties mainly LY2140023 involved (Table 1). Moreover you will find three retrospective studies in which microsporidia have been reported to occur in transplant individuals (25 35 46 Liguory and collaborators analyzed microsporidial illness in stool specimens from 100 individuals obtained over a 6-yr period (1994 to 2000) and they found 8 organ transplant recipients (6 renal 1 liver and 1 heart-lung) who have been positive for (25). Rabodonirina and collaborators inside a retrospective study carried out in France found 23 instances of microsporidiosis in transplant individuals including 3 who experienced already been explained in the literature between 1993 and 2001 (35). Recently ten Hove and collaborators performed a retrospective phylogenetic analysis on isolates of collected between 2003 and 2004 and they included five kidney transplant recipients that were positive for this microsporidian (46 47 Table 1. Microsporidiosis in transplant recipientsin two renal transplant recipients from Gran Canaria Spain and we review the published instances of microsporidiosis in SOT and BMT recipients. Case Reports Patient 1. A 66-year-old male who received a renal transplant in April 2009 was admitted to the nephrology unit of the Hospital Universitario Insular de Gran Canaria (Spain) for severe leucopenia (1 0 cells/mm3) and abundant liquid diarrhea in July of the same yr. He experienced LY2140023 a history Rabbit Polyclonal to MARCH3. of chronic renal failure secondary to a nephroangiosclerosis arterial hypertension and a heart attack. Immunosuppressive therapy consisted of steroids tacrolimus and mycophenolate mofetil (MMF). This treatment as well as valganciclovir and septrim was suspended after admittance to the hospital due to the LY2140023 suspicion of pharmacologic toxicity. No viral or bacterial pathogens had been within the feces samples. The colonoscopy was regular. Cytomegalovirus (CMV) antigen in colonic mucosa was positive. Calcofluor white (48) and improved trichrome (53) discolorations showed buildings evocative of microsporidial spores in feces examples (Fig. 1). The individual was treated with three dosages of LY2140023 filgrastrim fluid diet plan and therapy control. The scientific symptoms vanished and the individual was discharged afebrile with a standard LY2140023 white bloodstream cell count number and normal bowel motions. Fig. 1. LY2140023 (a) Microsporidial spores stained using a improved trichrome stain from individual 1. Club 5 μm. (b) PCR amplification from the rDNA coding area filled with the 243 bp from the It is of toxin was discovered in fecal examples. Fecal smears demonstrated microsporidial spores stained by calcofluor white (48) and improved trichrome (53) discolorations. The medical symptoms disappeared after initiation of fluid therapy diet control and metronidazole treatment. Normal bowel practices and renal function were recovered. Two weeks later on the patient showed episodes of.