No abstract

Background Risk factors for acquisition of vancomycin-resistant Enterococcus (VRE) include immunosuppression, antibiotic exposure, indwelling catheters, and manipulation of the gastrointestinal tract, all of which occur in liver transplant recipients. VRE infections are documented in liver transplantation (LT); however, only one single center study has assessed the impact daptomycin-resistant Enterococcus (DRE) in this patient population. Methods We conducted a retrospective multicenter cohort study comparing liver transplant recipients with either VRE or DRE bacteremia. The primary outcome was death within one year of transplantation. Multivariable logistic regression analyses were performed to calculate adjusted odds ratios for outcomes of interest. Results We identified 139 cases of Enterococcus bacteremia following LT, of which 78% were VRE and 22% were DRE. When adjusted for total ICU days in the first transplant year, liver-kidney transplantation, and calcineurin inhibitor use, patients with DRE bacteremia were 2.65 times more likely to die within one year of transplantation (aOR 2.648 [1.025-6.840], p = 0.044). Prior daptomycin exposure was found to be an independent predictor of DRE bacteremia (aOR 30.62 (10.087-92.955), p <0.001). Conclusions In this multicenter study of LT recipients with Enterococcus bacteremia, DRE bacteremia was associated with higher 1-year mortality rates when compared to VRE bacteremia. Our data provide strong support for dedicated infection prevention and antimicrobial stewardship efforts for transplant patients. Further research is needed to support the development of better antibiotics for DRE and practical guidance focusing on identification and prevention of colonization and subsequent infection in liver transplant recipients at high risk for DRE bacteremia.

Background The effects of reported beta‐lactam allergies on clinical outcomes have been understudied in lung transplant recipients. We evaluated reported beta‐lactam allergies on clinical outcomes in this population. Methods A single‐center retrospective cohort analysis was performed. One hundred and nine lung transplant recipients were identified and screened for a diagnosis of pneumonia. This cohort was divided into those with a reported beta‐lactam allergy and those without a beta‐lactam allergy. Antibiotic use was compared between groups. We also compared several clinical metrics, including rates of readmission, mortality, Clostridium difficile infection (CDI), allograft dysfunction, and isolation of carbapenem or fluoroquinolone non‐susceptible organisms after treatment. Results Of the 109 lung transplant recipients, 18 (16.5%) were identified as having a reported beta‐lactam allergy. Patients with a beta‐lactam allergy label (BLAL) were found to have decreased utilization of beta‐lactams (p < .001) and a trend toward increased use of carbapenems (p = .062) and aztreonam (p = .080). BLAL patients were found to have higher rates of CDI (p = .049) but were not found to have increased readmissions, mortality, allograft dysfunction, or isolation of carbapenem or fluoroquinolone non‐susceptible organisms. Patients without a BLAL were found to have higher rates of acute kidney injury (AKI) (p = .035). Conclusions Lung transplant recipients with BLAL are more likely to develop CDI, possibly due to increased use of carbapenems. We also found that patients without beta‐lactam allergy were more likely to develop AKI. A multicenter study with a larger sample size might clarify the individual contributions of mutually confounding clinical parameters.

This chapter discusses infection in the neutropenic patient. Patients receiving chemotherapy are at high risk for developing neutropenia and severe infections when their neutrophil count is depressed. Given the lack of inflammatory cells associated with neutropenia, signs of infection may be subtle. Some patients may not mount a fever at all, and the presence of hypotension, tachycardia, or delirium may be the only presenting features of infection. By its very nature, neutropenic fever occurs in those who are immunologically vulnerable and often carry significant infectious comorbidities, such as central venous access, breakdown of the body's physical barriers to infection, and nutritional deficiencies. Therefore, it is not surprising that febrile neutropenia carries significant morbidity and mortality. Researchers have been investigating modalities to help prevent febrile neutropenia, such as the use of colony-stimulating factors, dietary changes, and infection control measures. The chapter focuses on the main causes of infections in febrile neutropenia and selection of antimicrobial therapies.