In 2016, Overdevest et al. evaluated the colonisation durations of ESBL-EC in nursing home A for the period 2013–2014 (14 months), and found a prolonged colonisation duration of residents with ESBL-ST131, with a median of 13 months compared to two to three months for other ESBL-producing E. coli (ESBL-non-ST131) (p < 0.001)(8). In this study, we evaluated the duration of rectal ESBL- producing E. coli colonisation in residents of nursing home A for a study period of six years (2013–2019) and included a second Dutch nursing home (nursing home B) with a study period of two years. (2017–2019). In concordance with Overdevest et al. we found a prolonged colonisation of residents with ESBL-ST131, with a median of 13 months compared to eight months for ESBL-non-ST131 (p = 0,028). Remarkably, in the subgroup ST131 the median colonisation length was significantly longer in female than in males: 25,6 months versus 8,1 months (p = 0,013).
On a resident level, prolonged colonisation is a risk for the reason that colonisation can proceed to (extraintestinal) infections (16) for an extended time, and extraintestinal infections due to Escherichia coli cause considerable morbidity, mortality, and increased health care costs (17).
At the institutional level, prolonged colonisation is a risk as colonised residents can contribute to transmission for an extended times. And once ESBL-ST131 is introduced and spread in a nursing home, it will take a lot of effort and time for ESBL-ST131 to disappear from a nursing home setting partly because of the prolonged duration of colonisation (8).
There are a few other studies that investigated duration of colonisation for ESBL-ST131 versus other ESBL-EC. Van Duijkeren et al. found that ESBL-EC colonisation persisted for > 8 months in one-third of the ESBL-positive persons and found that prolonged colonisation was statistically significantly associated with the detection of phylogenetic group B2 and ST131, among others (18). Titelman et al. showed that colonisation with E. coli was still apparent after 12 months in 64% (n = 26), and 40% (n = 14) of carrying E. coli ST131 or other STs, respectively (p = 0.12) (19). Ismail et al. investigated the incidence and duration of colonisation of ciprofloxacin-resistant E. coli in nursing homes in Michigan. The study showed that ST131 strains in residents were carried for significantly longer duration when compared to non-ST131 strains (10 months versus 3 months) (20).
The exact reason for the prolonged ESBL-ST131 colonisation is still unclear, but several studies have demonstrated that ESBL-ST131 has enhanced intestinal colonisation capabilities over other E. coli, which are mediated by type-1 fimbriae. Type-1 fimbriae are adhesion organelles that facilitate adherence to mucosal surfaces (21) via interaction with mannosylated receptors (22). Sarkar et al. investigated clinical ESBL-ST131 isolates and type 1 fimbriae null mutants for colonisation of human intestinal epithelia and in mouse intestinal colonisation (22). The study demonstrated that ST131 strains adhered and invaded human intestinal epithelial cells more than commensal E. coli strains. Moreover, they showed that ST131 strains can overcome host colonisation resistance to establish persistence within the intestines, and that type-1 fimbriae enhanced long term colonisation. Type-1 fimbriae also have critical role in biofilm formation by ST131 strains. In vitro studies of Sarkar et al. (23) and of Kudinha et al. (24) suggested that ST131 strains are more capable at biofilm production than other E. coli strains. Gibreel et al. investigated the metabolic profiles of 300 E. coli strains using Vitek2 Advanced Expert System and showed that ST131 strains were significantly more likely to have a higher metabolic potential than strains of other sequence types (25). These traits (improved biofilm production and high metabolic potential) probably enhance the ability of ST131 to establish and maintain intestinal colonisation (3,26).
The large difference of median colonisation length between female and male (25,6 months versus 8,1 months) in the subgroup ST131 was an unexpected finding. This finding could not explained by differences in age distribution with in the subgroup, nor by the number of residents who died during the study period. (S3). A possible explanation could be a difference in the presence of known risk factors for (prolonged) ESBL colonisation between the sexes, such as antibiotic use, proton pump inhibitor use or variables associated with higher need for care (18,27). Unfortunately, such clinical information was not acquired in this study. Further studies into this observed difference are warranted.
Another limitation of this study is the setting. The study was performed in two Dutch nursing homes in an outbreak situation, which may reduce generalizability for other settings and/or patient populations. The major strength of our study includes the standardised cultures taken at defined intervals and most important the long follow-up period up to six years in nursing home A and 2 years in nursing home B.