Microsporidia are pathogens increasingly being recognized worldwide as an important cause

of life-threatening infections in solid organ and bone marrow transplant recipients.1 They are well known to cause disseminated infection in AIDS but have only recently been reported in non-HIV-infected populations especially transplant recipients. The majority of infections are with Enterocytozoon bieneusi and Encephalitozoon intestinalis.2 Disseminated Encephalitozoon infections are considered rare in non-HIV-infected individuals and are usually detected post-mortem because of high mortality rates, low level of clinical suspicion and difficulty in isolating learn more the pathogen. We present a non-HIV-infected, renal transplant recipient with disseminated Encephalitozoon infection which was detected and treated successfully with Albendazole. This is the first such case to be reported in Australia. The patient is a 57-year-old indigenous Australian man with end-stage

renal disease presumed secondary to diabetic nephropathy on haemodialysis since 2002, who received a deceased donor, poorly matched, renal transplant in April 2010. He received standard immunosuppression with Tacrolimus 0.1 mg/kg BD, Mycophenolate Mofetil 1000 mg BD, Prednisolone and Basiliximab induction. He developed mild vascular rejection on day 7 (Banff 2a), for which he received pulsed methyl prednisolone of 1 gram daily for three consecutive days. A subsequent renal transplant biopsy on day 19 demonstrated residual vascular rejection, for which he was treated with anti-thymocyte globulin, 200 mg daily for three consecutive days. AZD5363 in vivo Following this, his creatinine stabilized (110 mmol/L) and a repeat biopsy on day 35 did not show any evidence of rejection. He was then discharged home (Northern Territory) under the care of his treating nephrologist with Trimethoprim/Sulfamethoxazole

prophylaxis. click here In the following months he required hospital admission and treatment for cutaneous Rhizoctonia bataticola infection and subsequent fungemia, Cytomegalovirus (CMV) colitis and pulmonary Mycobacterium bovis infection. In June 2011, he presented to his local hospital with community acquired pneumonia and he was transferred to an intensive care unit (ICU) of a tertiary care centre following deterioration of his pulmonary function. He was febrile at 38.5°C, tachycardic, normotensive but hypoxemic with fine inspiratory crackles bilaterally, requiring intubation and ventilator support. He was pancytopenic and chest radiograph showed bilateral interstitial infiltrates. He was treated with broad spectrum antibiotics including Ticarcillin/Clavulanic acid and Meropenem and he also received Vancomycin and Azithromycin during this period. At this point all immunosuppressive therapy except corticosteroids was stopped. He underwent a broncho-alveolar lavage, which did not reveal any organisms including mycobacteria.