In the United States, the gold standard for malaria diagnosis is microscopic blood smear examination. Because malaria is not endemic in the United States, diagnostic capabilities may be limited, causing delays in diagnosis and increased morbidity and mortality. A survey of the malaria diagnostic practices of U.S. laboratories was conducted from June to July 2017; members of the American Society for Microbiology's listserv received a questionnaire inquiring about malaria diagnostic test availability, techniques, and reporting. Results were assessed using the Clinical and Laboratory Standards Institute (CLSI) guidelines for malaria diagnostics. After excluding incomplete and duplicate responses, responses representing 175 laboratories were included. Most labs (99%) received at least one specimen annually for malaria diagnosis, and 31% reported receiving only 1 to 10 specimens. The majority (74%) diagnosed five or fewer cases of malaria per year. Most (90%) performed blood smears on-site. Two-thirds (70%) provided initial blood smear results within 4 h. Although diagnostic testing for malaria was available 24/7 at 74% (141) of responding laboratories, only 12% (17) met criteria for analysis and reporting of malaria testing, significantly more than reported in a similar survey in 2010 (3%; < 0.05). The majority of laboratories surveyed had the capability for timely diagnosis of malaria; few comply with CLSI guidelines. Inexperience may factor into this noncompliance; many laboratories see few to no cases of malaria per year. Although reported adherence to CLSI guidelines was higher than in 2010, there is a need to further improve laboratory compliance with recommendations.
Background: Urinary tract infections (UTI) are the most common bacterial infections among infants and young children with fever without a source. Extended-spectrum β-lactamases (ESBLs) have emerged as emerging cause of UTI globally; however, data about risk factors and clinical features of children with ESBL-UTI have been scarce. Objective: To describe the predisposing risk factors, clinical and microbiologic features associated with pediatric UTIs caused by ESBL-producing bacteria (ESBL-PB). Methods: Our nested case-control study ran from January 1, 2012 to December 31, 2016. Pediatric patients with ESBL-PB UTI were compared with patients with non-ESBL-PB UTI matched for age and year of diagnosis. Results: A total of 720 children were enrolled (240 cases and 480 controls). Patients with ESBL-PB UTI were more likely to have a history of prior intensive care unit (ICU) admission (22.5% vs. 12.3%, P < 0.001), at least one underlying comorbidity (19.2% vs. 5.8%, P < 0.001), prior hospitalization (47.1% vs. 32.9%, P < 0.001), exposure to a cephalosporin antibiotic within 30 days before culture (7.5% vs. 4.2%, P = 0.035), and to have cystostomy (7.9% vs. 1.5%, P < 0.001) compared with those with non-ESBL-PB UTI. Patients with ESBL-PB UTI were more likely to present with hypothermia (48.8% vs. 38.5%, P = 0.009); had significantly longer average hospital stays {8.7 days [95% confidence interval (CI): 3.2–14.3] vs. 4.0 days (95% CI: 2.5–5.5)} and were more likely to be admitted to the ICU [odds ratio (OR) 1.8; 95% CI: 1.1-2.9). Multivariate analysis determined that only having cystostomy (OR 3.7; 95% CI: 1.4–9.4] and at least one underlying comorbidity (OR 2.4; 95% CI: 1.3–4.3) were the independent risk factors for ESBL-PB UTI. All ESBL-PB isolates tested against meropenem were susceptible, majority were resistant to multiple non-beta-lactam antibiotics. Conclusions: Children with underlying comorbidities and cystostomy are at higher risk for ESBL-PB UTI, but majority of ESBL cases were patients without any known risk factors. Clinical signs/symptoms and commonly used biochemical markers were unreliable to differentiate cases caused by ESBL-PB from those caused by non-ESBL-PB. Further research is needed to elucidate the conditions most associated with ESBL-PB UTIs among children to properly guide empirical therapy in patients at-risk for these infections, to improve the outcomes, and finally, to determine strategies for rational antimicrobial use.
BackgroundPatients in long-term acute care hospitals (LTACHs) and skilled nursing facilities with ventilator units (VSNFs) are at high risk for Candida auris colonization; among patients colonized with this emerging pathogen, 5%–10% develop invasive disease with >45% mortality. In September 2018, a California LTACH-affiliated laboratory began enhanced C. auris surveillance by classifying species of Candida isolated from routine urine specimens. In February 2019, the first known Southern California case was detected in an Orange County (OC) LTACH; the patient had not traveled outside the region, indicating local acquisition. We performed point prevalence surveys (PPS) and infection prevention (IP) assessments at all OC LTACHs and VSNF subacute units to identify patients colonized with C. auris and control transmission.MethodsDuring March–August 2019, we conducted PPS at facilities by collecting composite axilla and groin swabs for C. auris polymerase chain reaction testing and reflex culture from all patients who assented. Facilities with ≥1 C. auris-colonized patient repeated a PPS every 2 weeks to assess for new transmission. Isolate relatedness was assessed by whole-genome sequencing (WGS). We evaluated hand hygiene (HH) adherence, access to alcohol-based hand rubs (ABHR), and cleaning of high-touch surfaces to guide IP recommendations.ResultsThe first PPS at all OC LTACHs (n = 3) and adult VSNFs (n = 14) identified 45 C. auris-colonized patients in 3 (100%) LTACHs and 6 (43%) VSNFs; after repeated PPS, the total count reached 124. Most patients (70%) were at 2 facilities (Table 1). Three of 124 patients developed candidemia. To date, isolates from 48 patients have completed WGS; all were highly related (<11 single-nucleotide polymorphisms) in the African clade. Of 9 facilities with C. auris, 5 had HH adherence < 50%, 3 had limited ABHR, and at 2, <60% of assessed high-touch surfaces were clean. We recommended regular HH and cleaning audits, and increased ABHR.ConclusionOur investigation, prompted by enhanced surveillance, identified C. auris at 9 OC facilities. WGS indicated a single introduction and local transmission. Early detection, followed by rapid county-wide investigation and IP support, enabled containment efforts for C. auris in OC. Disclosures All authors: No reported disclosures.
Background: In 2015, an international outbreak of Mycobacterium chimaera infections among patients undergoing cardiothoracic surgeries was associated with exposure to contaminated LivaNova 3T heater-cooler devices (HCDs). From June 2017 to October 2020, the Centers for Disease Control and Prevention was notified of 18 patients with M. chimaera infections who had undergone cardiothoracic surgeries at 2 hospitals in Kansas (14 patients) and California (4 patients); 17 had exposure to 3T HCDs. Whole-genome sequencing of the clinical and environmental isolates matched the global outbreak strain identified in 2015. Methods: Investigations were conducted at each hospital to determine the cause of ongoing infections. Investigative methods included query of microbiologic records to identify additional cases, medical chart review, observations of operating room setup, HCD use and maintenance practices, and collection of HCD and environmental samples. Results: Onsite observations identified deviations in the positioning and maintenance of the 3T HCDs from the US Food and Drug Administration (FDA) recommendations and the manufacturer’s updated cleaning and disinfection protocols. Additionally, most 3T HCDs had not undergone the recommended vacuum and sealing upgrades by the manufacturer to decrease the dispersal of M. chimaera–containing aerosols into the operating room, despite hospital requests to the manufacturer. Conclusions: These findings highlight the need for continued awareness of the risk of M. chimaera infections associated with 3T HCDs, even if the devices are newly manufactured. Hospitals should maintain vigilance in adhering to FDA recommendations and the manufacturer’s protocols and in identifying patients with potential M. chimaera infections with exposure to these devices.
V erona-integron-encoded metallo-β-lactamaseproducing carbapenem-resistant Pseudomonas aeruginosa (VIM-CRPA) and other carbapenemaseproducing organisms (CPOs) are emerging public health threats. CPOs cause infections that are often extensively drug-resistant and associated with substantial rates of illness and death. By colonizing faucet aerators and wastewater plumbing systems, CPOs can spread rapidly within healthcare facilities, including to patients (1-9). VIM is a carbapenemase, a type of enzyme that inactivates carbapenems and other β-lactam antimicrobial drugs that are frequently encoded on mobile genetic elements, which in turn can lead to horizontal spread. VIM-CRPA is uncommon in the United States; <150 isolates are reported to CDC annually (10). During June 2017-November 2019, in a city of 250,000 residents in western Texas, USA (city A), 36 patients with VIM-CRPA were identified. Most were hospitalized for >1 night at an acute-care hospital (hospital A) in the 6 months before VIM-CRPA was isolated, but patients did not have overlapping hospital stays or common procedures. We assessed water sources and plumbing in hospital A to identify potential VIM-CRPA reservoirs.Beginning in June 2017, the Texas Department of State Health Services asked clinical laboratories to voluntarily submit clinical P. aeruginosa isolates resistant to imipenem, meropenem, or doripenem to the Texas Department of State Health Services Laboratory for mechanism testing through the Antibiotic Resistance Laboratory Network (https:// www.cdc.gov/drugresistance/ar-lab-networks/ domestic.html). The 2 clinical laboratories that served hospitals in city A began submitting all CRPA for mechanism testing in June 2017 (hospital A) and April 2018 (hospital B). During July 2017-January 2019, a total of 36 patients with VIM-CRPA isolated from clinical cultures were identified from city laboratories; 21 (58%) had been admitted to hospital A for >1 night in the 6 months before culture collection.We reviewed medical records from hospital A of patients with VIM-CRPA. Median patient age was 57 (range 9-84) years; 57% were male. VIM-CRPA was isolated from wounds in 9 (43%) patients, respiratory sources in 7 (33%), and urine in 5 (24%). Most patients primarily received care on
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