Currently, VRE has an uneven geographic distribution. Countries present unequal rates, being lately much more prevalent in areas of the Eastern Mediterranean and Southeast Asia [10]. In Spain, outbreaks have been described mainly in risk units with immunosuppressed patients [4]. At our center we had never isolated a VanB VRE strain before. In fact, it is one of the few extensive outbreaks described in our country in a conventional hospitalization ward [8].
Patients considered at high risk for VRE infections are those with prolonged admissions and/or with impaired immunity. According to CDC data, up to 70% of E. faecium bacteremia of vascular origin in solid organ transplant units present resistance to vancomycin in the United States [2]. Furthermore, VRE infections are associated with high morbidity and mortality and prolonged admissions [11].
These results do not correspond to what was observed in our study, where only one patient required antibiotic treatment with a favorable evolution. This low clinical impact coincides with what has been described in other outbreaks [4,7,12]. The fact that the outbreak happened in a conventional ward where there are no severely immunosuppressed patients could have contributed to this low impact.
It has been described that Enterococcus spp. can survive on fomites for a long time [13]. In our study, it was isolated in up to 28% of samples from material that does not enter the patient’s rooms or come into contact with them, since they are found in areas where only healthcare personnel enter. This fact, together with the observation of insufficient adherence to hand hygiene, strongly suggests that the staff's hands could have contributed to the spread of the microorganism and poor control of the outbreak, despite the measures implemented. The outbreak was likely perpetuated by repeated contamination of surfaces by staff. On the other hand, the results indicate the importance of intensifying the cleaning and disinfection of surfaces not only in the patient rooms and the material in contact with them, but also in the areas reserved for healthcare personnel.
Initially, training for professionals was carried out at the hospitalization ward affected by the outbreak. However, as soon as it was noticed the massive dissemination on other wards (Convalescence Unit), it was decided to extend the training to the remaining professionals. Despite the high positivity rate maintained over time, the clinical impact was low, so weekly screenings were stopped, prioritizing the implementation of more sensitive microbiological methods for the detection of VRE in clinical samples.
One of the limitations of the study is that the active search for colonized patients was stopped due to the low clinical impact. Therefore, we cannot really say the outbreak was controlled. Furthermore, the study and the measures were focused on a single ward, because there were no positive clinical samples in other areas of the hospital. The published series of VRE outbreaks show much longer follow-ups, in some cases even establishing quarantine rooms [12]. In our case, we chose to monitor clinical samples.
Another limitation of the study is that patients with a negative carrier study were not followed-up after they were discharged. In previous studies, it has been described that up to four rectal swabs on alternate days are needed to increase diagnostic sensitivity to > 90% of carriers [14]. In our case, we could have missed some carriers given that if a patient had a short admission and did not coincide with the screening day, he could have been discharged without a rectal study or with a single negative sample.
From the microbiological point of view, low levels of vancomycin resistance expression of the vanB genotype make its phenotypic detection complex. Sensitivity problems have been described for its detection if routine commercial antibiotic sensitivity methods are used, such as Vitek2 [15].
In our case, the clinical strains that were suspected to cause the outbreak provided sensitive MICs through automated microdilution, and it was not until the verification of the phenotype through manual sensitivity techniques (disco plate and epsilon test) that the finding was confirmed. This means modifying the usual work routine if the circulation of this resistance mechanism is not previously suspected in the healthcare facilities.
On the other hand, laboratories do not have rapid detection techniques for this resistance mechanism as it is not a common resistance mechanism in our environment. The process of acquiring and implementing new techniques requires more time than necessary for the proper and early control of an outbreak.
The epidemiological outbreak study allows us to confirm that it is a nosocomial outbreak with a clear environmental reservoir, in which a single clone colonizes different wards of the facility. This clone belongs to ST117, which has previously been shown to be involved in the hospital spread of vancomycin resistance in most European countries [16–20].