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The incidence and severity of Clostridium difficile infection (CDI) remain high across intensive care units in the United States despite national efforts to decrease this escalating health care burden. Most published literature and guidelines address treatment rather than prevention, yet this approach may be too downstream to limit morbidity and mortality from the disease and its complications. Mechanisms to prevent CDI successfully include reducing modifiable risk factors and minimizing horizontal transmission of C. difficile spores between patients and the health care environment. Because CDI prevention is characterized by a bundled approach, it is difficult to quantify the individual impact of any one element; however, a number of patient- and facility-level strategies can be considered for CDI prevention. Robust hygiene strategies, diagnostic and antimicrobial stewardship, and particular prophylaxis maneuvers such as continuation of oral vancomycin or fidaxomicin in the setting of systemic antibiotics have all demonstrated benefit. The preventive roles of deprescribing acid suppressants, routine use of probiotics, or early fecal microbiota transplantation remain unclear. The focus of this review is to summarize the evidence related to primary and secondary CDI prevention in critically ill adults and provide a concise implementation pathway for clinicians and policymakers.

Cardiovascular implantable electronic device infection (CIEDI) rates are rising. To improve outcomes, our institution developed an online care process model (CPM) and a specialized inpatient heart rhythm service (HRS). This retrospective review compared hospital length of stay (LOS), mortality, and times to subspecialty consultation and procedures before and after CPM and HRS availability. CPM use was associated with shortened time to surgical consultation (median 2 days post-CPM vs. 3 days pre-CPM, p = 0.0152), pocket closure (median 4 vs. 5 days, p

The cardiovascular implantable electronic device (CIED) infection rate is rising disproportionately to the rate of device implantation. Identification of microorganisms that cause CIED infections is not always achieved using present laboratory techniques. We conducted a prospective study to determine whether device vortexing-sonication followed by culture of the resulting sonicate fluid would enhance microbial detection compared with traditional swab or pocket tissue cultures. Forty-two subjects with noninfected and 35 with infected CIEDs were prospectively enrolled over 12 months. One swab each from the device pocket and device surface, pocket tissue, and the CIED were collected from each patient. Swabs and tissues were cultured using routine methods. The CIED was processed in Ringer’s solution using vortexing-sonication and the resultant fluid semiquantitatively cultured. Tissue and swab growth was considered significant when colonies grew on ≥2 quadrants of the culture plate and device was considered significant when ≥20 colonies were isolated from 10 ml of sonicate fluid. In noninfected group, 5% of sonicate fluids yielded significant bacterial growth, compared with 5% of tissue cultures (p = 1.00) and 2% of both pocket and device swab cultures (p = 0.317 each). In infected group, significant bacterial growth was observed in 54% of sonicate fluids, significantly greater than the sensitivities of pocket swab (20%, p = 0.001), device swab (9%, p

Prosthetic valve endocarditis (PVE) is a rare but serious complication of cardiac valve replacement surgery and is associated with high rates of morbidity and mortality. Despite significant advances in our understanding of the pathogenesis and management of this disease process, the rates of undesirable outcomes, including mortality directly attributable to infection, remain unacceptably high. The purpose of this article is to provide an up-to-date review of the changing epidemiology, microbiology and pathogenesis of PVE as well as review state-of-the-art diagnostic approaches and treatment for PVE, including the controversies surrounding the role of surgery for optimal management.

Advancements in our understanding of cardiac conduction abnormalities and pathophysiology of congestive heart failure coupled with innovations in device manufacturing and programming have helped to create a demand for a plethora of newer cardiovascular devices over the past 3 decades. Appropriate use of cardiovascular implantable electronic devices (CIEDs) in carefully selected patients is associated with better survival and significant improvements in quality of life.1 Cardiac resynchronization therapy devices are the newest “breed” to join an existing and growing family of permanent pacemakers (PPMs) and implantable cardioverter-defibrillators (ICDs). The number of cardiac devices implanted each year continues to grow exponentially. Unfortunately, because of the invasive nature of the implantation procedures required for placement of these devices and multiple comorbid conditions in device recipients, the benefits of these devices can be eclipsed by infectious complications. Infection is a very serious and dreadful complication requiring complete removal of the infected device and systemic antimicrobial therapy.2–4 Moreover, the financial cost of managing device infections is enormous. In this article, we review the latest developments pertaining to CIED infections, with a special emphasis on pathogenesis and microbiology. Since their first conceptualization and use in the late 1950s,5 CIEDs have undergone significant enhancements in design and function, and their use continues to rise, with a growing number of indications for placement, improvements in implantation techniques, and enhancements in device programming and monitoring.1 Earlier investigations reported a highly variable CIED infection rate, ranging from 0.13% to 19.9%.6,7 However, a more recent review of case records from the Massachusetts General Hospital reported 21 (1.2%) ICD-related infections among 1700 patients who underwent device implantation procedures.8 In a study by Mela et al,8 CIED infection occurred in 1.8% of 1170 patients who underwent a primary implant, a generator change, …

ObjectiveTo study a cluster ofMycobacterium wolinskyisurgical site infections (SSIs).DesignObservational and case-control study.SettingAcademic hospital.Patients.Subjects who developed SSIs withM. wolinskyifollowing cardiothoracic surgery.MethodsElectronic surveillance was performed for case finding as well as electronic medical record review of infected cases. Surgical procedures were observed. Medical chart review was conducted to identify risk factors. A case-control study was performed to identify risk factors for infection; Fisher exact or Kruskal-Wallis tests were used for comparisons of proportions and medians, respectively. Patient isolates were studied using pulsed-field gel electrophoresis (PFGE). Environmental microbiologic sampling was performed in operating rooms, including high-volume water sampling.ResultsSix definite cases ofM. wolinskyiSSI following cardiothoracic surgery were identified during the outbreak period (October 1, 2008–September 30, 2011). Having cardiac surgery in operating room A was significantly associated with infection (odds ratio, 40;P= .0027). Observational investigation revealed a cold-air blaster exclusive to operating room A as well a microbially contaminated, self-contained water source used in heart-lung machines. The isolates were indistinguishable or closely related by PFGE. No environmental samples were positive forM. wolinskyi.ConclusionsNo single point source was established, but 2 potential sources, including a cold-air blaster and a microbially contaminated, self-contained water system used in heart-lung machines for cardiothoracic operations, were identified. Both of these potential sources were removed, and subsequent active surveillance did not reveal any further cases ofM. wolinskyiSSI.Infect Control Hosp Epidemiol2014;35(9):1169-1175

A 51-year-old woman with diabetes, who immigrated to the USA 22 years ago from Laos, was admitted to the hospital for evaluation of fever, abdominal pain, vomiting and diarrhoea. A workup for acute gastroenteritis revealed a positive stool PCR for Shiga toxin-producing Escherichia coli. Two sets of blood cultures drawn at admission were positive for E coli. A review of her previous medical records revealed the presence of eosinophilia, up to 20%, 14 years prior to that was never investigated. Therefore, stool samples were examined and two of three specimens were positive for Strongyloides stercoralis larvae, confirming the diagnosis of Strongyloides hyperinfection syndrome.

Microsporidia are opportunistic pathogens that usually cause a limited disease in the gastrointestinal tract. Occasionally, they can cause disseminated disease. In solid organ transplant recipients, disseminated disease has been reported only rarely. We describe a 68-year-old woman who presented with fever, cough, and acute kidney injury 6 months after kidney transplantation. Dissemination was confirmed by identification of microsporidial spores in urine and bronchoalveolar lavage fluid. Polymerase chain reaction analysis identified the species as Encephalitozoon cuniculi.

Purpose. Diagnosis of WNV (WNV) relies upon serologic testing which may take several days after the onset of clinical symptoms to turn positive. Anecdotal reports suggest the presence of plasma cells or plasmacytoid lymphocytes in the cerebrospinal fluid (CSF) may be an early indicator of WNV infection.Methods. The CSFs of 89 patients (12 with WNV, 12 with other viral illness{OVI}, and 65 with nonviral illness{NVI}) were compared for the presence of either plasma cells or plasmacytoid lymphocytes.Results. Plasma cells were rarely seen in any of the patients. Plasmacytoid lymphocytes were more commonly seen in WNV (58%) and OVI (50%) than NVI (11%). The differences were significant for WNV versus NVI, but not WNV versus OVI (P<0.001andP=0.58,resp.).Conclusions. A CSF pleocytosis with plasma cells or plasmacytoid lymphocytes was neither sensitive nor specific for the diagnosis of WNV infection.

Improvements in manufacturing and implantation techniques, coupled with an increasing prevalence of atherosclerosis in an aging population, have led to increased utilization of prosthetic vascular grafts. The infection rates of vascular grafts are low. However, when they do occur, high rates of morbidity and mortality can be expected. The purpose of this article is to review the published literature regarding epidemiology, risk factors, pathogenesis, and clinical manifestations of prosthetic vascular graft infections. Moreover, we provide a practical approach to the diagnosis and management of these complicated infections based on empirically grounded evidence.

A 42-year-old woman with uterine fibroids underwent myomectomy. She developed postoperative sepsis and bloodstream infection with Clostridium hathewayi secondary to an infected haematoma. The patient was readmitted after failure of oral antibiotic therapy and underwent intrauterine drainage followed by prolonged parenteral antibiotic therapy. The patient was followed for 1 year and did not have any relapse of infection.