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Testing of asymptomatic patients for severe acute respiratory coronavirus virus 2 (SARS-CoV-2) (ie, “asymptomatic screening) to attempt to reduce the risk of nosocomial transmission has been extensive and resource intensive, and such testing is of unclear benefit when added to other layers of infection prevention mitigation controls. In addition, the logistic challenges and costs related to screening program implementation, data noting the lack of substantial aerosol generation with elective controlled intubation, extubation, and other procedures, and the adverse patient and facility consequences of asymptomatic screening call into question the utility of this infection prevention intervention. Consequently, the Society for Healthcare Epidemiology of America (SHEA) recommends against routine universal use of asymptomatic screening for SARS-CoV-2 in healthcare facilities. Specifically, preprocedure asymptomatic screening is unlikely to provide incremental benefit in preventing SARS-CoV-2 transmission in the procedural and perioperative environment when other infection prevention strategies are in place, and it should not be considered a requirement for all patients. Admission screening may be beneficial during times of increased virus transmission in some settings where other layers of controls are limited (eg, behavioral health, congregate care, or shared patient rooms), but widespread routine use of admission asymptomatic screening is not recommended over strengthening other infection prevention controls. In this commentary, we outline the challenges surrounding the use of asymptomatic screening, including logistics and costs of implementing a screening program, and adverse patient and facility consequences. We review data pertaining to the lack of substantial aerosol generation during elective controlled intubation, extubation, and other procedures, and we provide guidance for when asymptomatic screening for SARS-CoV-2 may be considered in a limited scope.
To analyze the frequency and rates of community respiratory virus infections detected in patients at the National Institutes of Health Clinical Center (NIHCC) between January 2015 and March 2021, comparing the trends before and during the coronavirus disease 2019 (COVID-19) pandemic.
We conducted a retrospective study comparing frequency and rates of community respiratory viruses detected in NIHCC patients between January 2015 and March 2021. Test results from nasopharyngeal swabs and washes, bronchoalveolar lavages, and bronchial washes were included in this study. Results from viral-challenge studies and repeated positives were excluded. A quantitative data analysis was completed using cross tabulations. Comparisons were performed using mixed models, applying the Dunnett correction for multiplicity.
Frequency of all respiratory pathogens declined from an annual range of 0.88%–1.97% between January 2015 and March 2020 to 0.29% between April 2020 and March 2021. Individual viral pathogens declined sharply in frequency during the same period, with no cases of influenza A/B orparainfluenza and 1 case of respiratory syncytial virus (RSV). Rhino/enterovirusdetection continued, but with a substantially lower frequency of 4.27% between April 2020 and March 2021, compared with an annual range of 8.65%–18.28% between January 2015 and March 2020.
The decrease in viral respiratory infections detected in NIHCC patients during the pandemic was likely due to the layered COVID-19 prevention and mitigation measures implemented in the community and the hospital. Hospitals should consider continuing the use of nonpharmaceutical interventions in the future to prevent nosocomial transmission of respiratory viruses during times of high community viral load.
Voluntary asymptomatic severe acute respiratory coronavirus virus 2 (SARS-CoV-2) testing was provided by the NIH Clinical Center over 1 year. Among 105,927 tests, 0.2% were positive. Among eligible staff, 79% participated with variable frequency and 61% of positive individuals had symptoms at the time of testing. Saliva specimen collection was chosen as an option less frequently than midturbinate collection.
In the National Institutes of Health (NIH) Clinical Center, patients colonized or infected with vancomycin-resistant Enterococcus (VRE) are placed in contact isolation until they are deemed “decolonized,” defined as having 3 consecutive perirectal swabs negative for VRE. Some decolonized patients later develop recurrent growth of VRE from surveillance or clinical cultures (ie, “recolonized”), although that finding may represent recrudescence or new acquisition of VRE. We describe the dynamics of VRE colonization and infection and their relationship to receipt of antibiotics.
In this retrospective cohort study of patients at the National Institutes of Health Clinical Center, baseline characteristics were collected via chart review. Antibiotic exposure and hospital days were calculated as proportions of VRE decolonized days. Using survival analysis, we assessed the relationship between antibiotic exposure and time to VRE recolonization in a subcohort analysis of 72 decolonized patients.
In total, 350 patients were either colonized or infected with VRE. Among polymerase chain reaction (PCR)-positive, culture (Cx)-negative (PCR+/Cx−) patients, PCR had a 39% positive predictive value for colonization. Colonization with VRE was significantly associated with VRE infection. Among 72 patients who met decolonization criteria, 21 (29%) subsequently became recolonized. VRE recolonization was 4.3 (P = .001) and 2.0 (P = .22) times higher in patients with proportions of antibiotic days and antianaerobic antibiotic days above the median, respectively.
Colonization is associated with clinical VRE infection and increased mortality. Despite negative perirectal cultures, re-exposure to antibiotics increases the risk of VRE recolonization.
Multidrug-resistant Acinetobacter baumannii (MDRAB) is difficult to treat and eradicate. Several reports describe isolation and environmental cleaning strategies that controlled hospital MDRAB outbreaks. Such interventions were insufficient to interrupt MDRAB transmission in 2 intensive care unit-based outbreaks in our hospital. We describe strategies that were associated with termination of MDRAB outbreaks at the National Institutes of Health Clinical Center.
In response to MDRAB outbreaks in 2007 and 2009, we implemented multiple interventions, including stakeholder meetings, enhanced isolation precautions, active microbial surveillance, cohorting, and extensive environmental cleaning. We conducted a case-control study to analyze risk factors for acquiring MDRAB. In each outbreak, infection control adherence monitors were placed in MDRAB cohort areas to observe and correct staff infection control behavior.
Between May 2007 and December 2009, 63 patients acquired nosocomial MDRAB; 57 (90%) acquired 1 or more of 4 outbreak strains. Of 347 environmental cultures, only 2 grew outbreak strains of MDRAB from areas other than MDRAB patient rooms. Adherence monitors recorded 1,330 isolation room entries in 2007, of which 8% required interventions. In 2009, around-the-clock monitors recorded 4,892 staff observations, including 127 (2.6%) instances of nonadherence with precautions, requiring 68 interventions (1.4%). Physicians were responsible for more violations than other staff (58% of hand hygiene violations and 37% of violations relating to gown and glove use). Each outbreak terminated in temporal association with initiation of adherence monitoring.
Although labor intensive, adherence monitoring may be useful as part of a multifaceted strategy to limit nosocomial transmission of MDRAB.
The past decade has witnessed an intense interest in healthcare-associated infections as well as increases in legislation and reporting requirements aimed at decreasing the number of these costly infections. In the next decade, healthcare epidemiology must address major gaps in understanding of the epidemiology and pathogenesis of healthcare-associated infections and in knowledge of the efficacy of interventions for healthcare-associated infections and the efficacy in implementing such interventions.
This guideline provides the updated recommendations of the Society for Healthcare Epidemiology of America (SHEA) regarding the management of healthcare providers who are infected with hepatitis B virus (HBV), hepatitis C virus (HCV), and/or the human immunodeficiency virus (HIV). For the reasons cited in the guideline, SHEA continues to recommend that, although some aspects of the approach to and administrative management of each of these infectious syndromes in healthcare providers are similar, separate management strategies for healthcare workers who are infected with these unrelated viruses remain appropriate. As we did in both prior iterations of this document, SHEA emphasizes the use of appropriate infection control procedures to minimize exposure of patients or providers to blood, emphasizes that transfers of blood from patients to providers and from providers to patients should be avoided, and recommends that infected healthcare providers should not be totally prohibited from participating in patient-care activities solely on the basis of a bloodborne pathogen infection. The types of procedures assessed by the panel as associated with an increased risk for provider-to-patient transmission of these pathogens are discussed in detail. For each pathogen, recommendations are graduated according to the relative viral load level of the infected provider (Tables 1 and 2). However, SHEA emphasizes that, because of the complexity of these cases, each such case will be slightly different from the next, and each should be independently considered in context.
Although influenza vaccination of healthcare workers reduces influenza-like illness and overall mortality among patients, national rates of vaccination for healthcare providers are unacceptably low. We report the implementation of a new mandatory vaccination policy by means of a streamlined electronic enrollment and vaccination tracking system at the National Institutes of Health (NIH) Clinical Center.
To evaluate the outcome of a new mandatory staff influenza vaccination program.
A new hospital policy endorsed by all the component NIH institutes and the Clinical Center departments mandated that employees who have patient contact either be vaccinated annually against influenza or sign a declination specifying the reason(s) for refusal. Those who fail to comply would be required to appear before the Medical Executive Committee to explain their rationale. We collected in a database the names of all physician and nonphysician staff who had patient contact. When a staff member either was vaccinated or declined vaccination, a simple system of badge scanning and bar-coded data entry captured essential data. The database was continuously updated, and it provided a list of noncompliant employees with whom to follow up.
By February 12, 2009, all 2,754 identified patient-care employees either were vaccinated or formally declined vaccination. Among those, 2,424 (88%) were vaccinated either at the NIH or elsewhere, 36 (1.3%) reported medical contraindications, and 294 (10.7%) declined vaccination for other reasons. Among the 294 employees without medical contraindications who declined, the most frequent reason given for declination was concern about side effects.
Implementation of a novel vaccination tracking process and a hospital policy requiring influenza vaccination or declination yielded dramatic improvement in healthcare worker vaccination rates and likely will result in increased patient safety in our hospital.
Nosocomial outbreaks of Legionnaires disease have been linked to contaminated water in hospitals. Immunocompromised patients are particularly vulnerable and, when infected, have a high mortality rate. We report the investigation of a cluster of cases of nosocomial pneumonia attributable to Legionella pneumophila serogroup 1 that occurred among patients on our stem cell transplantation unit.
We conducted a record review to identify common points of potential exposure, followed by environmental and water sampling for Legionella species from those sources. We used an air sampler to in an attempt to detect aerosolized Legionella and pulsed-field gel electrophoresis to compare clinical and environmental isolates.
The most likely sources identified were the water supply in the patients' rooms and a decorative fountain in the radiation oncology suite. Samples from the patients' rooms did not grow Legionella species. Cultures of the fountain, which had been restarted 4 months earlier after being shut off for 5 months, yielded L. pneumophila serogroup 1. The isolates from both patients and the fountain were identical by pulsed-field gel electrophoresis. Both patients developed pneumonia within 10 days of completing radiation therapy, and each reported having observed the fountain at close range. Both patients' infections were identified early and treated promptly, and both recovered.
This cluster was caused by contamination of a decorative fountain despite its being equipped with a filter and ozone generator. Fountains are a potential source of nosocomial Legionnaires disease despite standard maintenance and sanitizing measures. In our opinion, fountains present unacceptable risk in hospitals serving immunocompromised patients.
Clostridium difficile-associated diarrhea (CDAD) is an important infection in hospital settings. Its impact on outpatient care has not been well defined.
To examine risk factors of ambulatory cancer patients with CDAD.
Memorial Sloan-Kettering Cancer Center, a tertiary-care hospital.
Cases of CDAD among oncology outpatients from January 1999 through December 2000 were identified via positive C. difficile toxin assay results on stool specimens sent from clinics or the emergency department. A 1:3 matched case-control study examined exposures associated with CDAD.
Forty-eight episodes of CDAD were identified in cancer outpatients. The mean age was 51 years; 44% were female. Forty-one (85%) had received antibiotics within 60 days of diagnosis, completing courses a median of 16.5 days prior to diagnosis. Case-patients received longer courses of first-generation cephalosporins (4.8 vs 3.2 days; P = .03) and fluoroquinolones (23.6 vs 8 days; P < .01) than did control-patients. Those receiving clindamycin were 3.9-fold more likely to develop CDAD (P < .01). For each additional day of clindamycin or third-generation cephalosporin exposure, patients were 1.29- and 1.26-fold more likely to develop CDAD (P < .01 and .04, respectively). The 38 CDAD patients hospitalized during the risk period (79.2%) spent more time as inpatients than did control-patients (19.3 vs 9.7 days; P <. 001).
Antibiotic use, especially with cephalosporins and clindamycin, and prolonged hospitalization contributed to the development of CDAD. Outpatient CDAD appears to be most strongly related to inpatient exposures; reasons for the delayed development of symptoms are unknown.
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