Toxins A and B are known to be the primary virulence factors of Clostridium difficile. Other potential virulence factors have been identified such as binary toxin (actin-specific ADP-ribosyltransferase toxin, or CDT). A retrospective case-control study was performed in order to identify clinical features and risk factors of C. difficile-associated diarrhoea due to binary toxin-producing strains. Each case (a patient with diarrhoea due to binary toxin-producing strain) was compared with two controls (patients with diarrhoea due to a C. difficile strain that did not produce binary toxin) matched for ward and date of hospitalization. cdtA and cdtB genes were screened by PCR. Production of CDT was studied by Western blotting using an antiserum against Ia and Ib from the Clostridium perfringens iota toxin, and the activity of the binary toxin was assessed using an ADPribosyltransferase assay. Twenty-six cases (14 males and 12 females) were identified in 1999 and 2000. Cases and controls did not differ significantly for sex, age, previous administration of antibiotics or frequency of endoscopic examination. Diarrhoea was community-acquired more often in cases than in controls (65 . 4 vs 35 . 7 %, P ¼ 0 . 017) and more often represented the cause of hospitalization (61 . 5 vs 26 . 2 %, P ¼ 0 . 003). Moreover, diarrhoea in cases was more frequently associated with abdominal pain (63 . 6 vs 39 . 4 %, P ¼ 0 . 07) and with liquid stools (76 . 9 vs 59 . 5 %, P ¼ 0 . 14) than in controls. These results suggest that there could be a correlation between the production of binary toxin and the severity of diarrhoea.
WNA RT-qPCR WNA amplification was performed using the following conditions: 1 Â Invitrogen RT-qPCR buffer mix (Superscript III One step RT-PCR, Life Technologies Corporation, Carlsbad, California), 0.3 mM of each primer (Hc_24_55F: 5 0 -CGTACGACATCATATTAAAAATGA-3 0 and Hc_22_128R: 5 0 -CTTTCTTTAAGGTAGC-CAAAAT-3 0 ), 0.1 mM of probe (Hc_21_79P: 5 0 -FAM-Evaluation of a New RT-qPCR Histoplasma
Background. We sought to determine whether invasive aspergillosis (IA) during the first year after lung transplantation increased the risk of chronic lung allograft dysfunction (CLAD). Methods. We retrospectively reviewed the records of 191 patients who underwent lung transplantation at our institution between January 2013 and December 2017. Screening for Aspergillus was with bronchial aspirates, bronchoalveolar lavage if indicated or during surveillance bronchoscopy, radiography, and computed tomography. We used Fine and Gray multivariable regression to identify potential risk factors for CLAD. Results. During the first posttransplant year, 72 patients had at least 1 deep-airway sample positive for Aspergillus ; 63 were classified as having IA and were included in the study. Median number of endoscopies per patient during the first year was 9 (range, 1–44). Median time from transplantation to first Aspergillus -positive sample was 121 d. Bronchial aspirate samples and bronchoalveolar lavage fluid were positive in 71 and 44 patients, respectively. Aspergillus fumigatus (n = 36, 50%) predominated; bacterial samples were also positive in 22 (31%) patients. IA within 4 mo after transplantation was independently associated with CLAD development (subdistribution hazard ratio, 3.75; 95% confidence interval [CI], 1.61-8.73; P < 0.01) by regression analysis. Survival at 3 and 5 y conditional on 1-y CLAD-free survival was 37% (95% CI, 24%-58%), and 24% (95% CI, 11%-52%) in the IA <4 mo group compared to 65% (95% CI, 57%-73%) and 54% (95% CI, 43%-66%) in the non-IA group and to 69% (95% CI, 58%-83%) and 54% (95% CI, 35%-82%) in the IA ≥4 mo group, respectively ( P < 0.01, logrank test). Conclusions. Our evaluation of de novo IA showed that this infection was most strongly associated with CLAD when found within 4 mo after transplantation.
Objectives: To analyse functional outcome parameters according to antimicrobial treatments after respiratory syncytial virus (RSV)-confirmed infection in adult lung transplant recipients. Methods: A 9-year retrospective multicentre cohort study (2011e19) included adult lung transplant recipients with RSV-confirmed infection. The first endpoint determined new allograft dysfunction (acute graft rejection and chronic lung allograft dysfunction (CLAD)) 3 months after infection. Then baseline and 3 months' postinfection forced expiratory volume in 1 second (FEV 1 ) values were compared according to antimicrobial treatment. Univariate logistic regression analysis was performed. Results: RSV infection was confirmed in 77 of 424 lung transplant recipients (estimated incidence of 0.025 per patient per year; 95% confidence interval 0.018e0.036). At 3 months, 22 recipients (28.8%) developed allograft dysfunction: ten (13%) possible CLAD, six (7.9%) acute rejection and six (7.9%) CLAD. Recipients with the lowest preinfection FEV 1 had a greater risk of developing pneumonia (median (interquartile range) 1.5 (1.1e1.9) vs. 2.2 (1.5e2.4) L/s, p 0.003) and a higher odds of receiving antibiotics (1.6 (1.3e2.3) vs. 2.3 (1.9e2.5) L/s, p 0.017; odds ratio 0.52, 95% confidence interval 0.27e0.99). Compared to tracheobronchitis/bronchiolitis, RSV-induced pneumonia led more frequently to hospitalization (91.7%, 22 vs. 58.0%, 29, p 0.003) and intensive care unit admission (33.3%, 8 vs. 0, p < 10 -3 ). For ribavirintreated recipients (24.7%, 19) and azithromycin prophylaxis (50.6%, 39), 3-month FEV 1 values were not different from untreated recipients. The overall mortality was 2.5% at 1 month and 5.3% at 6 months, unrelated to RSV. Conclusions: At 3 months after RSV-confirmed infection, 22 recipients (28.8%) had new allograft dysfunction. Ribavirin treatment and azithromycin prophylaxis did not prevent FEV 1 decline.
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