Infection Control & Hospital Epidemiology
opportunities (93.4%) versus 39 of 91 opportunities (42.9%) for stool sampling. For weekly surveillance, compliance with peri- rectal swabbing was 85.9% (116 of 135) versus 65.2% (88 of 135) for stool sampling.
Sensitivity of VRE colonization by collection method
In 67 collections, both a stool sample and a perirectal swab were collected from the same patient at the same time and 1 or both of the samples were positive for VRE. Some of these samples were collected from patients previously identified as VRE colonized. Perirectal swabs were sensitive for VRE in 64 of 67 of those collections (95.5%). Stool samples were sensitive for VRE in 56 of 67 of those collections (83.6%; P=.023). If each patient con- tributed only 1 collection, and the first VRE-positive collection from the patient was used, 30 of 32 perirectal swabs (93.8%) were sensitive for VRE versus 27 of 32 stool samples (84.4%).
VRE colonization versus bloodstream infections
During the study period, we detected 10 VRE BSIs among the study population. VRE BSIs were more common among VRE- colonized patients (8 of 43) than non–VRE-colonized patients (2 of 48; P=.028). The 30-day mortality rate for those with VRE BSIs was 30.0%. For the 2 patients who developed a VRE BSI without VRE colonization on surveillance, 1 patient had 1 negative swab on surveillance 2 days before developing VRE BSI. The other patient transferred out of the unit, and 48 days had elapsed since the last surveillance. Another 3 patients had other VRE infections: an abscess, a positive omental fluid sample, and a urinary tract infection (UTI).
VRE strain typing
Of 10 patients with VRE BSI, 3 had both a blood-culture isolate and a surveillance isolate available for strain typing analyses. The bloodstream isolates were distinct and unrelated. All 3 colonizing isolates were >90% similar to the patient’s infecting strain, with 2 colonization–infection pairs being >95% similar (Fig. 2).
Discussion
Vancomycin-resistant enterococcal infections disproportionately affect high-risk patient populations, including liver and HSC
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transplant recipients.2,3 In our study, those on immunosuppres- sive regimens were at statistically significant higher risk of VRE colonization. Screening programs in high-risk units within a hospital have the potential to improve infection control6–8 and may identify patients who would benefit from early empiric therapy for VRE.6,9–11 The prior literature suggests that stool collection is the most reliable means of VRE surveillance, but it can be time-consuming and unpleasant, which can lead to low compliance.6 Our hypothesis that obtaining perirectal swabs is more convenient was correct: compliance with perirectal swab- bing was significantly higher than compliance with stool sampling (89% vs 56%; P≤0.001). Our finding that perirectal swabs were more sensitive than
stool samples in detecting VRE (96% vs 84%; P=.023) was unexpected. Prior studies have repeatedly shown that perirectal swabs are less sensitive than stool samples for other patho- gens.17,18 Moreover, prior work by D’agata et al12 found that rectal swabs had a sensitivity of 58% in detecting VRE compared with stool samples. The D’agata study also reported that swabs detected VRE with high-density colonization but not low-density colonization (100% vs 0%, respectively). Possibly, patients from our liver transplant SICU were more commonly VRE colonized at a high density, but this would not explain why stool sampling performed relatively poorly. Alternatively, it is possible that the Spectra VRE media chosen for the study favored growth from perirectal swabs instead of stool samples. Spectra VRE media was chosen because it is FDA-approved for use with both stool sample and rectal swabs. The availability of commercial chromogenic agar allows for better recovery of VRE from stool samples and rectal swabs when compared with bile esculin azide agar sup- plemented with vancomycin, with reported sensitivities of >95%.19–21 However, we hesitate to draw premature conclusions, and further investigation is warranted. Weekly surveillance identified that 25% of patients developed
incident VRE colonization. Similar research conducted at the University of Alabama at Birmingham demonstrated that 22% of patients developed incident VRE colonization during their ICU stay.13 Widespread genotypic testing was not performed, so we could not determine whether the incident VRE cases represent VRE transmission or VRE “emerged,” that is, some patients had undetectable levels of VRE on admission that increased to the level of detection during their ICU stay, which is known as the “intestinal domination” effect.22 VRE colonization pressure was high in the unit, which could have contributed to increased risk for transmission. But neither UCLA nor the University of Alabama at Birmingham ICU units had significant burden of other trans- missible pathogens like Clostridium difficile; thus, we favor a conclusion that includes some proportion of VRE emergence. Regardless, our study data indicate that a significant burden of VRE is missed by admission-only surveillance. Given the high burden of infection, RRMC started active daily management for central lines, which decreased central-line–associated BSIs from 4.08 per 1,000 patient days in 2015 to 1.58 per 1,000 patient days in 2016. Ongoing monitoring of VRE clinical infections, relative to other MDROs, will be used to determine the role of active VRE surveillance as part of a comprehensive infection control program. Multiple investigations have demonstrated that VRE-colonized
Fig. 2. DNA fingerprints of VRE surveillance and bloodstream infection isolates. The diagram shows the matching strain types for patients with both a blood culture isolate and surveillance isolate available. Note. DNA, deoxyribonucleic acid; VRE, vancomycin-resistant enterococci; L, ladder; A, surveillance isolate; B, blood isolate.
patients are at higher risk for VRE infection, and our data con- firmed that outcome.9 Our limited genotypic analysis provided linkage between the VRE bloodstream isolate and the colonizing isolate. The similarity between isolates, instead of identicalness, is a limitation of the repPCR typing method. Further research is
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