Q.F. Ye's research while affiliated with Wuhan University and other places

Background: The aim of this study was to describe the incidence, time of onset, clinical characteristics, and outcomes of Pseudomonas aeruginosa infection after liver transplantation (LT) and to investigate the drug resistance of P aeruginosa to frequently used antibiotics to provide evidence for clinical prevention and therapy. Methods: Patients undergoing LT from January 1, 2003, through June 30, 2015, were considered. We determined the site of infection and the drug susceptibility of P aeruginosa isolates and collected these patients' data to confirm post-LT clinical and laboratory characteristics. Results: Of the 303 patients who underwent cadaveric LT, 15 (5.0%) developed 20 episodes of P aeruginosa infection. All episodes of P aeruginosa infection were early-onset, with the bloodstream being the most common source of infection. The majority (86.7%) of these recipients were in intensive care unit stay, and 7 (46.7%) patients had a body temperature of ≥38°C at the onset of infection and an inappropriate antibiotic therapy. In 14 (93.3%) patients, P aeruginosa infection was nosocomial infection. Platelet numbers of <50 × 10(9)/L and lymphocyte count of <300/mm(3) developed in 33.3% and 46.7% of patients, respectively. Seven (46.7%) deaths were attributable to P aeruginosa infection. Of these 20 P aeruginosa isolates, 10 (50%) each were carbapenem-resistant and multidrug-resistant. P aeruginosa was relatively susceptible to amikacin, levofloxacin, or cefoperazone-sulbactam (resistance rate, 30%). Conclusions: The bloodstream was the most common site of infection; a high body temperature, nosocomial origin, decreased platelet and lymphocyte count occurring in the early period after LT, high antibiotic resistance rate, and high morbidity and mortality rates were the main characteristics of P aeruginosa infection.

Objective We estimated species distribution and frequency of antimicrobial resistance among bacterial pathogens isolated from respiratory tract specimens of renal recipients with acute respiratory distress syndrome (ARDS) due to pneumonia. Methods We retrospectively collected patient demographics and clinical characteristics and microbiologic culture data with the use of standard microbiologic procedures and commercially available tests. Results From January 2001 to August 2014, 320 respiratory tract specimens were obtained from 94 renal recipients with ARDS. Bacterial cultures were positive in 134 specimens from 68 recipients (72.3%), yielding 139 bacterial strains. The most commonly isolated species were gram-negative bacteria (111 isolates) with dominance of Acinetobacter baumanii (29.7%) and Pseudomonas aeruginosa (18.0%). The gram-negative bacteria were relatively resistant to 1st- and 2nd-generation cephalosporin and monocyclic beta-lactam and relatively sensitive to levofloxacin and meropenem, with rates of resistance of 80.2%, 76.6%, 73.9%, 36.0%, and 44.1%, respectively. The gram-positive bacteria, excluding Streptococcus uberis, were sensitive to glycopeptides and oxazolidone. Conclusions Gram-negative bacteria predominated as 79.9% of isolates from respiratory tract specimens of renal recipients with ARDS. The gram-negative bacteria were relatively sensitive to levofloxacin and meropenem and the gram-positive bacteria were sensitive to glycopeptides and oxazolidone.

Objective Acinetobacter baumannii has become a major problem among solid organ transplant (SOT) recipients. The aim of this study was to investigate the distribution, drug resistance, and clinical characteristics of A baumannii infections in SOT recipients. Methods We retrospectively identified 78/1,850 (4.2%) SOT recipients who developed A baumannii infections from January 1, 2003, to April 1, 2015, and evaluated the distribution, drug resistance, and clinical characteristics of these infections. Results Over the study period, 101 episodes of A baumannii infection occurred in 78 SOT recipients, with respiratory tract (37.6%) and blood (35.6%) as the most common sites of infection. Fifty-six episodes of A baumannii infection were accompanied with a serum creatinine level of >1.5 mg/dL. Multidrug resistance (MDR) or extensive drug resistance (XDR) occurred in 83.2%. Antibiotic resistance rate of all A baumannii to 8 of 9 antibiotics investigated was >50%. Seventy-eight percent of A baumannii were carbapenem-resistant. All but one A baumannii isolates tested against polymyxin B were susceptible. There were 40 (51.3%) overall in-hospital deaths and 31 (39.7%) infection-related deaths. Conclusions A baumannii infections are associated with high morbidity and mortality in SOT recipients, and MDR or XDR is common. Prevention measures are essential, and combination therapy of antibiotics are needed to improve the outcomes of SOT recipients with A baumannii infections.

Background A sustained immunosuppressive state in renal transplant recipients is a factor that can contribute to increased incidence of acute respiratory distress syndrome (ARDS) due to pneumonia. ARDS renal recipients with ESKAPE (E. faecium, S. aureus, K. pneumoniae, A. baumannii, P. aeruginosa, and Enterobacter spp.) pneumonia are probably related to high morbidity and mortality. We therefore sought to investigate the frequency of ESKAPE and resistant ESKAPE (rESKAPE) pathogens isolated from respiratory tract specimens of renal recipients with ARDS and determine the risk factors for mortality. Methods A retrospective analysis of ARDS renal recipients with ESKAPE/rESKAPE pneumonia was reviewed. Multiple logistic regression analysis was conducted to identify the independent risk factors associated with infection-related mortality. Results During the study period, 88 ESKAPE pathogens obtained from respiratory tract specimens of 54 ARDS renal recipients were documented including 33 A. baumannii, 24 P. aeruginosa, 17 S. aureus, 6 K. pneumoniae, 8 Enterobacter species, and 0 E. Faecium. Among these ESKAPE organisms, 61.4% (54/88) were antimicrobial resistant. The risk factors for mortality independently associated with ARDS renal recipients with ESKAPE pneumonia were severe ARDS (odds ratio [OR] 4.3 (95% confidence interval [CI] 1.1–16.4), P = .032), serum creatinine level >1.5 mg/dL (OR 4.2 95% CI (1.0–17.9), P = .05) and body temperature less than 38°C (OR 5.0 (95% CI 1.3–19.6), P = .02) at ARDS onset. The independent determinants of mortality were associated with ARDS renal recipients with rESKAPE pneumonia were serum creatinine level >1.5 mg/dL (OR 13.7, 95% CI 1.3–142.1, P = .028) and body temperature less than 38°C (OR 5.5 (95% CI 1.1–26.6) at ARDS onset, P = .035). Conclusions The majority of EPKAPE isolates were antimicrobial resistant. Mortality in ARDS renal recipients with ESKAPE/rESKAPE pneumonia was associated with the severity of ARDS, elevated serum creatinine level, or depressed febrile response at ARDS onset.

Although infections caused by the pathogens Enterococcus faecium, Staphylococcus aureus, Klebsiella pneumoniae, Acinetobacter baumannii, Pseudomonas aeruginosa, and Enterobacter spp (ESKAPE) have recently been identified as serious emerging problems in solid organ transplant, no information in liver transplant (LT) recipients is available. We sought to investigate the risk factors for associated mortality in LT recipients with ESKAPE infections. A retrospective analysis of infection after LT was reviewed. Risk factors for mortality caused by ESKAPE infection were identified. Fifty-three episodes of infections caused by ESKAPE were documented in 51 LT recipients. The main sites of infection were the bloodstream (49.0%), the lungs (33.3%), and the intra-abdominal/biliary tract (17.6%). The risk factors for mortality independently associated with ESKAPE infection were female sex (odds ratio [OR] = 6.6, 95% confidence interval [CI] = 1.1-40.8, P = .042), septic shock (OR = 30.1, 95% CI = 3.7-244.8, P = .001), and lymphocyte counts <300/mm(3) (OR = 20.2, 95% CI = 2.9-142.2, P = .003). To improve the results of LT, more effective therapeutic treatments are of paramount importance when female LT recipients with ESKAPE infection present with septic shock and decreased lymphocyte counts. Copyright © 2014 Elsevier Inc. All rights reserved.

Background Although bacteremias caused by the 6 ESKAPE pathogens (Enterococcus faecium, Staphylococcus aureus, Klebsiella pneumoniae, Acinetobacter baumannii, Pseudomonas aeruginosa, and Enterobacter species) have recently been highlighted as a serious complication in solid organ transplant (SOT), more information is urgently needed. We sought to investigate the frequency and clinical outcomes of ESKAPE bacteremia in SOT and determine the risk factors for mortality.MethodsA retrospective analysis of bacteremia after SOT was reviewed. Risk factors for mortality caused by ESKAPE bacteremia were identified.ResultsEighty-four episodes of bacteremia were caused by ESKAPE strains. Of these strains, 41 were caused by resistant ESKAPE (rESKAPE) organisms. The only factor for bacteremia-related mortality independently associated with ESKAPE was septic shock (odds ratio [OR] = 21.017, 95% confidence interval [CI] = 5.038–87.682, P < 0.001). The factors for bacteremia-related mortality independently associated with rESKAPE bacteremia were septic shock (OR = 16.558, 95% CI = 6.620–104.668, P = 0.003) and age ≥40 years (OR = 7.521, 95% CI = 1.196–47.292, P = 0.031).Conclusions To improve the outcomes of transplantation, more effective therapeutic treatments are of paramount importance when older SOT recipients with bacteremia due to ESKAPE/rESKAPE organisms present with septic shock.

Both mannose-binding lectin (MBL) and ficolin (FCN) interact with carbohydrate structures on microbial surfaces. Polymorphisms at the promoter and exon 1 of the MBL2 gene, which are responsible for low serum levels of MBL, have been shown to play important roles to increase the risk of post-transplant infections. Three gene polymorphisms in the promoter region of FCN2 and 2 in exon 8 (+6424 G > T) are associated with serum levels of FCN2 or binding capacity toward N-acetylglucosamine on microbial surfaces. We prospectively analyzed 81 kidney transplant recipients for 6 well-known functional single-nucleotide polymorphisms in the MBL2 and 5 in the FCN2 gene of the recipients determined by gene sequencing. The bloodstream infections collected prospectively were associated with MBL2 and FCN2 genotypic variants over the first year after kidney transplantation. Multivariate analyses only found an association of recipient QQ + PQ genotypes of MBL2 5'-UTR +4 (odds ratio [OR] = 3.677, 95% confidence intervals [CI] = 1.127-11.998, P = .031) and FCN2 exon 8 Thr 236 Met(+6359 C > T) (OR = 4.917, 95% CI = 1.229-19.667, P = .024) with the incidence of bacteremia. Recipient QQ + PQ genotypes of MBL2 5'-UTR +4 and recipient FCN2 exon 8 Thr 236 Met(+6359 C > T) variants showed significant impacts on the risk of developing bloodstream infections after kidney transplantation.

Pneumonia remains a significant cause of morbidity and mortality after kidney transplantation. The present study was therefore conducted to investigate whether or not the polymorphisms of tumor necrosis factor (TNF)β, interleukin (IL)-10, IL-1β, and IL-1 receptor antagonist (IL-1ra) gene predicted the susceptibility to pneumonia within the first year after kidney transplantation. Subjects comprised 33 kidney transplant recipients with pneumonia and 63 noninfected kidney transplant recipients. Genomic DNA from these 96 kidney transplant recipients was extracted from peripheral blood leukocytes. The regions containing the NcoI polymorphic site at position +252 of TNFβ gene, the RsaI polymorphic site at position -592 of IL-10 gene, and the AvaI polymorphic site at position -511 of IL-1β gene were amplified by polymerase chain reaction (PCR) and subsequently digested with NcoI, RsaI, and AvaI restriction enzyme, respectively. The polymorphic regions with intron 2 of the IL-1 ra gene (IL-1 RN) containing variable numbers of a tandem repeat of 86 base pairs, were amplified by PCR. Univariate analysis showed that recipient IL-10, IL-1β, and IL-1 RN polymorphisms were not associated with the presence of pneumonia (P = .589, .940, and .286, respectively). However, compared with GG genotype, recipient TNFβ +252AA + AG genotype was significantly associated with susceptibility to pneumonia (P = .006). Age of 45 years or older was not significantly associated with susceptibility to develop pneumonia but had a tendency to develop it (P = .119). After adjusting for age of 45 years or older, recipient TNFβ+252 AA + AG genotype (odds ratio = 5.366, 95% confidence intervals = 1.470 - 19.589, P = .011) independently predicted the risk for pneumonia within the first year after kidney transplantation in the multivariate analysis. These results suggested that recipient TNFβ gene polymorphism may be useful in predicting pneumonia, hence identifying individuals who could benefit from preventive treatment and a less potent immunosuppression regimen.

Late severe noninfectious diarrhea in renal transplant recipients can lead to malnutrition and even graft loss. The purpose of this study was to evaluate risk factors associated with this condition and summarize therapy for these patients. For more than 36 months we observed a cohort of 541 recipients who underwent kidney transplantation from January 2001 to June 2007. They were provided a calcineurin inhibitor (CNI) combined with mycophenolate mofetil (MMF). The four group includes a continuous cyclosporine (CsA); a preconversion to tacrolimus and a postconversion group as well as a continuous tacrolimus group. The rate of severe late noninfectious diarrhea was compared among the four groups. Risk factors were analyzed between the diarrhea and nondiarrhea cohorts. Clinical characteristics, efficacy, and safety were observed after modifying the immunosuppressive protocol for late severe noninfectious diarrhea recipients. Twenty-eight recipients presented with late sever noninfectious diarrhea. No patients displayed chronic diarrhea in the CsA (n = 145) or preconversion group (n = 95). The rate of diarrhea was 7.31% in the postconversion and 7.35% in the tacrolimus group. Using multivariate Cox proportional hazards analysis, factors associated with an increased risk of noninfectious diarrhea were cytochrome P450(CYP)3A5 *3/*3 type, chronic renal allograft dysfunction, and patient ingestion of Tripterygium wilfordii Hook F. All diarrheal recipients experienced weight loss, hypoalbuminia, and an increased serum creatinine. All affected patients underwent adjustment of the immunosuppressive regimen to achieve remission. Renal allograft survival in recipients with diarrhea was worse than that in nondiarrheal recipients receiving tacrolimus combined with MMF. Tacrolimus with MMF increased the risk of late severe noninfectious diarrhea among renal transplant recipients compared with hosts treats with CsA plus MMF. The CYP3A5 *3/*3 type, chronic renal allograft dysfunction, and T wilfordii supplementation were high-risk factors for late diarrhea. Prompt adjustment of immunosuppression was an effective, feasible therapy for these patients.

Information on risk factors for mortality among deceased donor liver transplant recipients with bloodstream infections (BSIs) was sought using a retrospective analysis from January 2002 to January 2012. We performed deceased donor liver transplantations in 135 subjects who experienced 77 episodes of BSIs. We assessed risk factors for mortality among 43 of them using univariate and multivariate logistic regression analysis. The 43 recipients (31.9%) who developed BSI showed a mean age of 45.1 (45.1 ± 14.1 years). The majority of infections were nosocomial in origin (97.7%), with more than half being polymicrobial (53.5%). There were 24 deaths among these recipients (55.8%). The univariate analysis identified the following variables as risk factors for BSI-related mortality: polymicrobial (P = .029), platelet count <50,000/mm(3) (P = .02), creatinine > 1.5 mg/dL (P = .008), and septic shock (P < .001). Multivariate logistic regression showed the independent risk factors for mortality to be a serum creatinine > 1.5 mg/dL and septic shock. The risk factors significantly associated with increased mortality in deceased donor liver transplant recipients with BSIs are higher serum creatinine levels and septic shock. Despite appropriate antimicrobial treatment, BSIs accompanied by septic shock or higher serum creatinine levels were associated with high mortality rates. It is therefore essential to protect renal function to reduce the incidence of BSIs.