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To describe the cumulative seroprevalence of severe acute respiratory coronavirus virus 2 (SARS-CoV-2) antibodies during the coronavirus disease 2019 (COVID-19) pandemic among employees of a large pediatric healthcare system.
Design, setting, and participants:
Prospective observational cohort study open to adult employees at the Children’s Hospital of Philadelphia, conducted April 20–December 17, 2020.
Methods:
Employees were recruited starting with high-risk exposure groups, utilizing e-mails, flyers, and announcements at virtual town hall meetings. At baseline, 1 month, 2 months, and 6 months, participants reported occupational and community exposures and gave a blood sample for SARS-CoV-2 antibody measurement by enzyme-linked immunosorbent assays (ELISAs). A post hoc Cox proportional hazards regression model was performed to identify factors associated with increased risk for seropositivity.
Results:
In total, 1,740 employees were enrolled. At 6 months, the cumulative seroprevalence was 5.3%, which was below estimated community point seroprevalence. Seroprevalence was 5.8% among employees who provided direct care and was 3.4% among employees who did not perform direct patient care. Most participants who were seropositive at baseline remained positive at follow-up assessments. In a post hoc analysis, direct patient care (hazard ratio [HR], 1.95; 95% confidence interval [CI], 1.03–3.68), Black race (HR, 2.70; 95% CI, 1.24–5.87), and exposure to a confirmed case in a nonhealthcare setting (HR, 4.32; 95% CI, 2.71–6.88) were associated with statistically significant increased risk for seropositivity.
Conclusions:
Employee SARS-CoV-2 seroprevalence rates remained below the point-prevalence rates of the surrounding community. Provision of direct patient care, Black race, and exposure to a confirmed case in a nonhealthcare setting conferred increased risk. These data can inform occupational protection measures to maximize protection of employees within the workplace during future COVID-19 waves or other epidemics.
Of the 13 US vancomycin-resistant Staphylococcus aureus (VRSA) cases, 8 were identified in southeastern Michigan, primarily in patients with chronic lower-extremity wounds. VRSA infections develop when the vanA gene from vancomycin-resistant enterococcus (VRE) transfers to S. aureus. Incl8-like plasmids in VRE and pSK41-like plasmids in S. aureus appear to be important precursors to this transfer.
Objective.
Identify the prevalence of VRSA precursor organisms.
Design.
Prospective cohort with embedded case-control study.
Participants.
Southeastern Michigan adults with chronic lower-extremity wounds.
Methods.
Adults presenting to 3 southeastern Michigan medical centers during the period February 15 through March 4, 2011, with chronic lower-extremity wounds had wound, nares, and perirectal swab specimens cultured for S. aureus and VRE, which were tested for pSK41-like and Incl8-like plasmids by polymerase chain reaction. We interviewed participants and reviewed clinical records. Risk factors for pSK41-positive S. aureus were assessed among all study participants (cohort analysis) and among only S. aureus-colonized participants (case-control analysis).
Results.
Of 179 participants with wound cultures, 26% were colonized with methicillin-susceptible S. aureus, 27% were colonized with methicillin-resistant S. aureus, and 4% were colonized with VRE, although only 17% consented to perirectal culture. Six participants (3%) had pSK41-positive S. aureus, and none had Incl8-positive VRE. Having chronic wounds for over 2 years was associated with pSK41-positive S. aureus colonization in both analyses.
Conclusions.
Colonization with VRSA precursor organisms was rare. Having long-standing chronic wounds was a risk factor for pSK41-positive S. aureus colonization. Additional investigation into the prevalence of VRSA precursors among a larger cohort of patients is warranted.
To determine the degree to which species identification or strain relatedness assessment of successive blood culture isolates of coagulase-negative staphylococci (CNS) may improve the clinical diagnosis of bloodstream infection (BSI).
Setting:
400-bed community hospital.
Design:
Prospective laboratory survey during which all CNS blood culture isolates obtained between mid-August 1996 and mid-February 1997 (study period) were saved and later identified to the species level; selected isolates were genotyped using pulsed-field gel electrophoresis at the Centers for Disease Control and Prevention (CDC). Retrospective review of medical records of 37 patients with multiple cultures positive for CNS.
Results:
During the study period, 171 patients had blood cultures positive for CNS; 130 had single positive cultures and 41 had ≥2 positive cultures. Of these 41, 23 (62%) were from patients with signs and symptoms of BSI according to CDC surveillance definitions. Species identification and strain clonality of CNS isolates from patients with ≥2 positives revealed 3 (13%) of the 23 patients did not have a consistent CNS species, and another 3 (13%) did not have a consistent genotype in the ≥2 positive cultures, suggesting that CNS from these patients probably were contaminants. Thus, species identification and strain clonality assessment reduced by 27% the number of patients with BSI diagnosed based on the presence of symptoms and ≥2 positive blood cultures.
Conclusions:
Routine species identification and selected strain genotyping of CNS may reduce the misinterpretation of probable contaminants among patients with ≥2 positive blood cultures.
Coagulase-negative staphylococci (CNS) are the major cause of nosocomial bloodstream infection. Emergence of vancomycin resistance among CNS is a serious public health concern, because CNS usually are multidrug-resistant, and glycopeptide antibiotics, among which only vancomycin is available in the United States, are the only remaining effective therapy. In this report, we describe the first bloodstream infection in the United States associated with a Staphylococcus epidermidis strain with decreased susceptibility to vancomycin.
Methods:
We reviewed the hospital's microbiology records for all CNS strains, reviewed the patient's medical and laboratory records, and obtained all available CNS isolates with decreased susceptibility to vancomycin. Blood cultures were processed and CNS isolates identified by using standard methods; antimicrobial susceptibility was determined by using minimum inhibitory concentration (MIC) and disk-diffusion methods. Nares cultures were obtained from exposed healthcare workers (HCWs) to identify possible colonization by CNS with decreased susceptibility to vancomycin.
Results:
The bloodstream infection by an S epidermidis strain with decreased susceptibility to vancomycin occurred in a 49-year-old woman with carcinoma. She had two blood cultures positive for CNS; both isolates were S epidermidis. Although susceptible to vancomycin by the disk-diffusion method (16-17 mm), the isolates were intermediate by MIC (8-6 μg/mL). The patient had received an extended course of vancomycin therapy; she died of her underlying disease. No HCW was colonized by CNS with decreased susceptibility to vancomycin.
Conclusions:
This is the first report in the United States of bloodstream infection due to S epidermidis with decreased susceptibility to vancomycin. Contact precautions likely played a role in preventing nosocomial transmission of this strain, and disk-diffusion methods may be inadequate to detect CNS with decreased susceptibility to vancomycin.
In this study, we measured microbial growth and endotoxin production in the intravenous anesthetic propofol using 10 different microbial strains; 6 isolated from outbreak cases and 4 from laboratory stock cultures.
Design:
In each trial, endotoxin-free glass tubes containing 10 ml propofol were inoculated with 10°-103 CFU/ml of the test organism and incubated at 30°C for 72 hours.
Setting:
In May and June 1990, the Centers for Disease Control received reports of 5 outbreaks in 5 states of postsurgical patient infections and/or pyrogenic reactions. Epidemiologic and laboratory investigations implicated extrinsic contamination of an intravenous anesthetic, propofol, as the probable source of these outbreaks.
Results:
After 24 hours, 9 of the 10 cultures increased in viable counts by 3 to 6 logs. At least 1 ng/ml of endotoxin was produced within 24 hours by Escherichia coli, Enterobacter cloacae, and Acinetobacter calcoaceticus subspecies anitratus.
Conclusions:
Propofol can support rapid microbial growth and endotoxin production. To avoid infectious complications, scrupulous aseptic technique should be used when preparing or administering this anesthetic.
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