Trichosporon asahii as a prospective pathogen in solid organ transplant recipients.

Trichosporon spp. is not an important factor of mycotic infections in immunocompetent patients. It may be a cause of invasive mycoses with a high mortality rate in patients undergoing solid organ transplantation. We have analysed the antifungal agents' susceptibility of Trichosporon asahii and its frequency of occurrence as a prospective etiological agent of infections in liver, kidney and simultaneous pancreas-kidney transplant recipients. Clinical specimens (urine, blood, peritoneal fluid and swabs) were obtained from patients hospitalised in the Institute of Transplantation Medicine, Department of General and Transplantation Surgery, Medical University of Warsaw in 2005 and 2006. Microbiological tests were performed in Mycological Laboratory, Department of Microbiology, Medical University of Warsaw. A total of 475 strains of yeast-like fungi were isolated from clinical specimens taken from 263 liver, kidney and simultaneous pancreas-kidney transplant recipients and from 26 organ donors. Trichosporon asahii was found in 26 clinical samples taken from 18 patients and one organ donor. Positive cultures were obtained from 22 urine samples, one stoma fluid, one wound swab, one tracheal aspirate and one ejaculate. Isolates of Trichosporon asahii were found in 6% of total positive mycological cultures in the solid organ transplant recipients. Among cultured strains, 11 isolates were resistant to fluconazole, four to itraconazole and three of them demonstrated resistance to amphotericin B.

Enzymatic variability of Candida krusei isolates in a course of fungal infection in a liver transplant recipient.

Transplant recipients are at high risk of fungal infections. The main site of fungal infections in patients undergoing liver transplantation is the abdominal cavity. One factor determining the pathogenicity of fungi is their ability to secrete hydrolytic enzymes. The aim of this study was to assess the enzymatic activity of Candida krusei, which caused an infection in a liver transplant recipient. The clinical specimens included swabs of throat, nose, and two drains, as well as bile, stool, and abdominal cavity aspirate. The yeast-like fungi isolated were identified by an ID 32 C test (bioMérieux) and their enzymatic activity assayed with the use of an API-ZYM test. Two biotypes of C. krusei were identified, depending on the source of the clinical specimen. The C. krusei isolates cultured from a throat swab, a nasal swab, and one of the drains secreted esterase lipase C8 (enzyme IV) and valine arylamidase (enzyme VII), in contrast to those isolated from the bile, abdominal cavity fluid, another drain, and stool. Characterization of two biotypes of C. krusei isolates cultured from different clinical samples from several infection sites indicated an ability of C. krusei to adapt to variable environmental conditions.

Algorithm of clinical protocol lowering the risk of systemic Mycosis infections in allografts recipients.

The aim of the study was to describe a diagnostic protocol to lower the risk of a mycotic invasive infection among allotransplant recipients and to suggest the use of preoperative prophylaxis and/or empiric therapy. We chose a group of 268 allograft recipients with transient or constant yeast colonization or confirmed yeast infection. Among 7744 clinical samples, 475 were positive for fungi. We used conventional fungal laboratory diagnosis, enzymatic activity tests, serologic tests, molecular diagnosis of samples from sterile body sites, and histopathologic examinations. The following clinical samples were examined: blood samples; swabs from mouth lesions, throat, and rectum; and sputum, urine, and fecal samples from kidney transplant recipients and simultaneous pancreas-kidney transplantation recipients who are highly predisposed to mycotic infections. We established microbiologic criteria of a systemic mycosis and principles to distinguish colonization from infection.