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Sinks and Bacterial Healthcare-Associated Infections in ICU: Comparison
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Please note this is a comparison between Version 2 by Lindsay Dong and Version 1 by Catherine Mullié.

Sink drains in hospitals have long been known to harbor an abundant microbiota comprising up to 103–105 CFU/mL Gram-negative rods, especially waterborne bacteria. intensive care unit (ICU) sink/sink drains can be contaminated by MDR bacteria originating from patients. These reservoirs can in turn be a source of contamination of other ICU patients. Studies have used molecular biology techniques to ascertain whether bacterial clones causing such heathcare-associated infections can indeed come from contaminated sinks.

  • sink
  • sink drain
  • bacterial dissemination
  • hospital acquired infection
  • intensive care unit
  • molecular biology typing

1. Introduction

Patients hospitalized in intensive care units (ICUs) are acknowledged as having a higher risk of healthcare-associated infections (HAIs) than other patients[1][2]. This higher risk has been linked with multiple risk factors such as length of stay, inadequate and/or long-term antibiotic administration, assisted-ventilation or catheters[3][4]. Moreover, those HAIs are often caused by multidrug resistant (MDR) bacteria, leading to struggles in efficiently tackling those infections in already critically ill patients and even sometimes to therapeutic dead-ends [1][5]. Two main routes of contamination are classically described: (i) autoinfection where patients are contaminated by bacteria they themselves brought in the healthcare facility (in their intestinal or nasal microbiota, for example) and (ii) cross-contamination where bacteria are acquired directly or indirectly from other patients, healthcare workers, the environment, and/or medical devices [6]. Regarding cross-contaminations, recommendations and guidelines have been published worldwide to mitigate this known route of transmission, especially through hand hygiene good practices [6][7]. However, direct or indirect cross-contamination via the environment (e.g., through water, air, or high-touch surfaces) is not so readily recognized as an important transmission route [8]. Amongst possible environmental sources of contamination, sinks and more specifically sink drains have been pointed out but their role is still debated [9][10]. One of the major hurdles in assessing the importance of this contamination source is the ability to assign bacteria isolated from patients and the presumed environmental source to a same bacterial clone and, taking into account the chronology, establish a cause-effect link. Phenotypic characters, including antibiotic resistance profiles, are not discriminatory enough to ascertain that isolates belong to a same clone, as previously demonstrated [11]. Therefore, molecular biology techniques such as Pulsed-Field Gel Electrophoresis (PFGE) or Whole Genome Sequencing (WGS) have been used to try and establish a link between sink and clinical bacterial isolates.

2. Sinks and Bacterial Healthcare-Associated Infections in ICU 

Protracted and discontinuous outbreaks of MDR bacteria in absence of a temporal overlap of clinical cases point to an environment-to-patient transmission rather than a person-to-person contamination. Environmental investigations are therefore often performed in such contexts. Sinks, sink drains and sink-associated surfaces are frequently sampled in such investigations due to the propensity of some known bacterial species such as P. aeruginosa and enterobacteria to persist in these wet environments [12][13][14][15]. Indeed, sink drains in hospitals have long been known to harbor an abundant microbiota comprising up to 103–105 CFU/mL Gram-negative rods, especially waterborne bacteria [16][17].
Getting rid of a bacterial colonization in sink drains, especially if the colonizing species is prone to develop biofilms, has been described as extremely difficult [18][19][20][15][21]. Nevertheless, the debate on the role of such reservoirs in the dissemination of MDR bacteria in healthcare settings and their implication in HAIs is still on-going, especially in patients with multiple risk factors such as those housed in ICUs.
Molecular biology techniques have been used to try and establish a link between sink and clinical bacterial isolates. Among those, PFGE was referred to as the gold standard for clone discrimination from 2000 until the second part of the 2010s. After a brief incursion into partial genome sequencing through the use of MultiLocus Sequence Typing (MLST), WGS is currently taking the front place. This evolution is driven by the now lower cost of sequencing provided by next generation sequencing techniques and the need for more discriminatory methods. Apart from MLST, which relies on libraries/schemes available online to attribute an isolate to a previously described Sequence Type (ST) or a new one, most of these techniques rely on direct comparison between strains electrophoretic DNA patterns or DNA sequences. From an epidemiological point of view, this raises the recurring question of cut-off values to assign isolates to a same cluster for each of these techniques. This parameter is critical and should be described in every study dealing with the problematic at hands to allow readers to compare study results and make their own opinion on the relatedness of isolates. Ideally, for a given technique, a consensus cut-off should be reached and used by all works employing this method. This was partly the case for PFGE in the 2000s–2010s era with the criteria proposed by Tenover et al. [22], which were quite readily used by most investigators even though they were found too discriminatory by others [23]. The issue of cut-off values remains topical with WGS. The number of Single Nucleotide polymorphisms (SNPs) indicative of distinct bacterial clones can vary from one species to another, depending on the estimated genome mutation rate for each species. This piece of information is therefore crucial for the reader. A systematic review revealed that only 57.8% on the papers actually mentioned (directly or indirectly) a cut-off value [24].  As for MLST, the cut-off value might not be the most suitable criterion but rather the precise identification of the scheme used to attribute an isolate to a given ST. Indeed, previous reports have shown discrepancies between MLST schemes available for a same bacterial species [25], which could lead to errors when comparing results obtained in papers using different MLST schemes.
Most of the time, the sink-to-patient transmission is indirectly advocated for by the success of mitigation strategies such as (i) tap water-free or waterless care [26][27], (ii) sink drain decontamination with acetic acid or bleach [23][26][28], (iii) replacement of contaminated sinks/sink drains[26][28][29][30], (iv) implementation of self-disinfecting sink drains to get rid of bacterial contaminations [31][32], and (v) removal of sinks from ICUs [33].
Finally, the use of more discriminatory molecular biology techniques could remodel the landscape of evidence gathered for sink/sink drains as a possible reservoir for outbreaks of MDR bacteria in ICU. The percentage of studies successfully linking environmental isolates with clinical ones has indeed been reduced from 80% using PFGE to 50% using WGS [24]. This decrease is not statistically significant (p = 0.1155, Fisher’s exact test) as is but could become so with the addition of results from future studies using WGS to discriminate bacterial clones.

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