Detection of (1,3)-ß-d-Glucan for the Diagnosis of Invasive Fungal Infection in Liver Transplant Recipients.

Invasive fungal infections (IFI) are complications after liver transplantation involving high morbidity and mortality. (1,3)-ß-d-glucan (BG) is a biomarker for IFI, but its utility remains uncertain. This study was designed to evaluate the impact of BG following their diagnosis. Between January 2013 and May 2016, 271 liver transplants were performed in our institution. Serum samples were tested for BG (Fungitell®, Associates Cape Code Inc., Falmouth, MA, USA) at least weekly between liver transplantation and the discharge of patients. Nineteen patients (7%) were diagnosed with IFI, including 13 cases of invasive candidiasis (IC), eight cases of invasive pulmonary aspergillosis, and one case of septic arthritis due to Scedosporium apiospernum. Using a single BG sample for the primary analysis of IFI, 95% (21/22) of the subjects had positive BG (>80 pg/mL) at the time of IFI diagnosis. The area under the ROC curves to predict IFI was 0.78 (95% CI: 0.73-0.83). The sensitivity, specificity, positive predictive value (PPV) and negative predictive value (NPV) of BG for IFI were 75% (95% CI: 65-83), 65% (62-68), 17% (13-21), and 96% (94-97), respectively. Based on their high NPV, the BG test appears to constitute a good biomarker to rule out a diagnosis of IFI.

Echinocandin Resistance in Candida Species Isolates from Liver Transplant Recipients.

Liver transplant recipients are at risk of invasive fungal infections, especially candidiasis. Echinocandin is recommended as prophylactic treatment but is increasingly associated with resistance. Our aim was to assess echinocandin drug resistance in Candida spp. isolated from liver transplant recipients treated with this antifungal class. For this, all liver-transplanted patients in a University Hospital (Créteil, France) between January and June of 2013 and 2015 were included. Susceptibilities of Candida isolates to echinocandins were tested by Etest and the EUCAST reference method. Isolates were analyzed by FKS sequencing and genotyped based on microsatellites or multilocus sequence typing (MLST) profiles. Ninety-four patients were included, and 39 patients were colonized or infected and treated with echinocandin. Echinocandin resistance appeared in 3 (8%) of the treated patients within 1 month of treatment. One patient was colonized by resistant Candida glabrata, one by resistant Candida dubliniensis, and one by resistant Candida albicans Molecular analysis found three mutations in FKS2 HS1 (F659S, S663A, and D666E) for C. glabrata and one mutation in FKS1 HS1 (S645P) for C. dubliniensis and C. albicans Susceptible and resistant isolates belonged to the same genotype. To our knowledge, this is the first study on echinocandin resistance in Candida spp. in a liver transplant population. Most resistant isolates were found around/in digestive sites, perhaps due to lower diffusion of echinocandin in these sites. This work documents the risk of emergence of resistance to echinocandin, even after short-term treatment.

Psoas abscess and chronic Q fever: a contiguous or hematogenous complication? A case report and literature review.

Few cases of psoas abscesses (PA) during chronic Q fever have been reported, and the route of transmission remains unknown. Here, we report a new case and have performed a systematic literature review to determinate the spreading route of this complication. Medline, EMBASE and Web of Science were searched. Local spreading was supported by endocarditis exclusion, evidence of vascular infection and absence of distantly infected sites. Among 275 retrieved references, 179 were initially rejected, and 85 additional references were rejected after full-text review. A total of 11 studies, reporting 13 cases, were included. Additionally, we reported one new case. A total of 14/14 cases reached Q fever vascular infection diagnostic criteria, and 7/14 provided adequate evidence supporting a causal relationship between Q fever vascular infection and PA. All patients presented aorta defects. In conclusion, Q fever PA results from the spreading of a local infection and occurs specifically in patients presenting a vascular graft or an abdominal aortic aneurysm.