Please note, due to essential maintenance online transactions will not be possible between 02:30 and 04:00 BST, on Tuesday 17th September 2019 (22:30-00:00 EDT, 17 Sep, 2019). We apologise for any inconvenience.
To send content items to your account,
please confirm that you agree to abide by our usage policies.
If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account.
Find out more about sending content to .
To send content items to your Kindle, first ensure firstname.lastname@example.org
is added to your Approved Personal Document E-mail List under your Personal Document Settings
on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part
of your Kindle email address below.
Find out more about sending to your Kindle.
Note you can select to send to either the @free.kindle.com or @kindle.com variations.
‘@free.kindle.com’ emails are free but can only be sent to your device when it is connected to wi-fi.
‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.
The immune system of high-order organisms is a highly specialized compartment that eliminates transformed cells and cells infected with viruses or bacteria through a controlled process of cell-mediated cytotoxicity. The immune cells responsible for mediating cell death are collectively called cytotoxic lymphocytes (CLs) and are made up of natural killer (NK) cells and cytotoxic T lymphocytes (CTL). CLs are distinguished primarily by their respective mechanism of antigen recognition. NK cells form part of the innate immune response, a generalized first line of defense. NK cells are generally CD3–CD56+ lymphocytes that recognize and respond to abnormal cells through an imbalance of facilitatory and inhibitory receptors (Bottino et al., 2004;Moretta et al., 2004). CTLs formpart of the adaptive immune response, a more specific response that is generated subsequent to and as a consequence of the innate response. These cells use their clonotypic T-cell receptors (TcRs) to recognize a peptide antigen presented on the major histocompatability complex (MHC) proteins on the surface of the target cell. CTLs can be identified on the basis of expression of CD3 and CD8 (CD3+CD8+) on their cell surface. In addition, some CD4+ T cells (typically T-helper cells) can have limited cytotoxic capacity
Surgical-site infection (SSI) is a serious and costly complication following coronary artery bypass graft (CABG). We analyzed surgical factors, microbiology, and complications at a 608-bed community teaching hospital to identify opportunities for prevention.
All patients undergoing CABG procedures from June 1997 through December 2000 were analyzed. Hospital records and postdischarge surveillance data were reviewed for demographics, surgical information, timing and classification of infection, microbiology, and bacteremic events.
Of 3,443 patients undergoing CABG, sternal SSI developed in 122 (3.5%); 71 (58.2%) were classified as superficial SSI and 51 (41.8%) as deep SSI. Surgical antimicrobial prophylaxis was employed in all cases. On average, infection occurred 21.5 days (range, 4 to 315) after CABG. Most cases were diagnosed on readmission (59%); 20 cases (16%) were identified by postdischarge surveillance. Microbiological data were positive in 109 (89.3%), with a single pathogen implicated in most (86.2%). Gram-positive cocci were most frequently recovered (81%); gram-negative bacilli (17%), gram-positive bacilli (1%), and yeast (1%) were less common. Staphylococcus aureus was the most frequently isolated pathogen (49%). Bacteremia was noted in 22 instances (18%). It was significantly associated with deep SSI (P =. 002) and identified only in S. aureus cases.
SSI complicated 3.5% of the procedures. S. aureus was implicated in most of the cases and was significantly associated with deep SSI. It was the only pathogen associated with secondary bacteremia. In addition to standard guidelines, targeted methods against S. aureus should help reduce the overall rate of SSI.
To determine the prevalence of stool colonization with vancomycin-resistant enterococci (VRE) among healthcare workers (HCWs) and their families.
Prospective assessment of fecal colonization with VRE.
A 603-bed, tertiary-care teaching hospital.
Healthy volunteers recruited from hospital employees and their households were screened to exclude pregnancy, diabetes mellitus, immunosuppressive disorders, and recent use of antimicrobials.
Self-obtained stool swabs were used to obtain cultures. Isolated enterococci were screened for vancomycin resistance and species were identified. Intra-household isolates were genotyped using pulsed-field gel electrophoresis (PFGE).
The participants (n = 228; age range, 28 days to 80 years) were from 137 households with and 91 without employees who had contact with patients. Enterococcus species were isolated from 127 stool specimens (55.7%). VRE were detected in 12 individuals, representing 6 E. casseliflavus, 5 E. faecium, and 1 E. gallinarum. VRE were more commonly isolated in employees who had contact with patients (5 of 52 vs 0 of 40; relative risk [RR], 1.9; 95% confidence interval [CI95], 1.5 to 2.2; P = .07) and their household members (10 of 137 vs 2 of 91; RR, 3.3; CI95, 0.7 to 14.8; P = .13). In 2 households (2 adults in a physician's household and an adult plus a child in a nurse's household) PFGE analysis demonstrated identical intra-household strains of vancomycin-resistant E. faecium.
VRE colonization was found in 5.3% of screened stools and was more prevalent in HCWs who had contact with patients and their households. Identical PFGE patterns between 2 employees who had contact with patients and their household members demonstrated probable intra-household spread. Although the mode of acquisition was uncertain, the association with employees who had contact with patients suggests possible occupational sources. These findings demonstrate the spread of VRE within the household and implicate occupational risk for its acquisition.