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Background Infections following tissue expander (TE) placement are frequent complications in breast reconstruction. While breast surgery is a clean case, implant‐based breast reconstruction has rates of infection up to 31%, decidedly higher than the typical 1% to 2% rate of surgical site infections (SSI). Few authors use the Center for Disease Control's (CDC) SSI definition for TE infections. We highlight how adoption of a consistent definition of TE infection may change how infections are researched, categorized, and ultimately managed. Methods Two researchers with definitional discrepancies of infection performed an independent analysis of all postmastectomy patients receiving TEs (n = 175) in 2017. Results Researcher One, using a clinical definition, delineated an infection rate of 19.4%. Antibiotics alone successfully treated 50% of cases. Researcher Two found an infection rate of 13.7% using CDC criteria. These infections were further delineated by a SSI rate of 6.3% and a TE infection rate post port access of 7.4%. Only 45.5% SSI's and 15.4% of TE infections were salvaged with antibiotics alone. Conclusions Rigorous adoption of CDC criteria for infection characterization in published research will help standardize the definition of infection and allow surgeons to create evidence‐based infection prevention regimens.

Summary Antigen presentation by enterocytes isolated from the rat small bowel was studied by using T cell proliferation, and immunorcgulatory function in an antigen-driven culture system, as indicator systems. Lymph node T cells obtained from rats immunized with ovalbumin (OA) failed to divide when cultured for 4 days in the presence of freshly isolated la+ enterocytes and OA. However, cell division was noted when enterocytes were removed after 18 h by Percoll gradient centrifugation, followed by culture ofT cells for a further 4 days in the absence of antigen. The failure to divide in the primary culture was due to the secretion by enterocytes ofa dialysable non-specific inhibitor. Antigen presentation by enterocytes was specific and was inhibited by monoclonal mouse anti-rat la antibody, 0X6. An epithelial cell line (REC-2) was established from normal rat small intestine. These cells expressed la molecules following incubation with Concanavalin-A stimulated spleen cell supernatant, and were capable of both presenting antigen, and inducing interieukin-2 (lL-2) production, when cultured with primed T cells. Furthermore. la' REC-2 cells functioned as stimulators in a primary mixed lymphocyte reaction (MLR). Both OA-primed T cells activated by enterocytes and antigen, and allogeneic MLR-activated T cells, mediated suppression which was not specific for the initiating antigen. These experiments indicated two mechanisms mediate suppression of cell division in gut mucosa. The contribution of these mechanisms to the control of inflammation at mucosal sites requires investigation.

Background: In June 2019, the Maryland Department of Health (MDH) was notified of a hospitalized patient with Candida auris bloodstream infection. The MDH initiated a contact investigation to identify additional patients with C. auris colonization. Many of the contacts had been discharged home from the hospital and were therefore not available for screening. Healthcare facilities in Maryland, Virginia, and Washington, DC, submit patient data to a regional health information exchange (HIE) called the Chesapeake Regional Information System for our Patients (CRISP). CRISP includes a notification system that alerts providers when flagged patients have healthcare encounters. We aimed to use this system to identify discharged C. auris contacts on their next inpatient encounter to rapidly screen them and to detect new cases. Methods:C. auris contacts were defined as patients located on an inpatient unit on the same day, receiving wound care from the same team, or having a procedure in the same operating room on the same day as the index patient or any patients subsequently identified as having C. auris infection or colonization detected either during the normal course of clinical care or through screening. Contacts who remained hospitalized were screened during inpatient point prevalence surveys (PPSs). Contacts discharged to postacute-care facilities were screened by facility staff. Contacts who had been discharged home were flagged in CRISP, and MDH staff received CRISP encounter alerts when these patients were readmitted. MDH staff then contacted the admitting facilities to recommend screening for C. auris. Axilla and groin swabs were collected and tested by rt-PCR at the Mid-Atlantic Regional Antibiotic Resistance Laboratory Network laboratory. Results: As of October 8, 2019, 4,017 contacts were identified. Among these, 936 (23%) contacts at 56 healthcare facilities (33 acute-care hospitals and 23 postacute-care facilities) were screened for C. auris, and 10 patients with C. auris colonization were identified (1.1% of contacts who underwent C. auris screening). Of these, 6 (60%) were identified through CRISP notification and 4 (40%) were identified by PPSs conducted in acute-care hospitals. Conclusions: In this ongoing C. auris outbreak, a large proportion of colonized patients was identified using an electronic encounter notification system within a regional HIE. This approach was effective for identifying opportunities to screen contacts at their next healthcare encounter and can augment other means of case detection, like PPSs. HIEs should incorporate mechanisms to facilitate contact tracing for public health investigations.Funding: NoneDisclosures: None

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