An unexpected finding in our study population was the extremely high prevalence of ST131 in our sample of sequentially collected ESBL-producing E. coli isolates (96%) during an early point in the rise of worldwide ESBL prevalence, which is much higher than rates reported in other studies. Data from the same time period (2010–2011) from France found that ST131 comprised 20% of ESBL-producing E. coli isolates, and data from Chicago found that ST131 comprised 49% of isolates in Chicago [12, 13]. In the current study, 80% of ST131 samples with fimH sequencing performed had an H allele type of H30, the ST131 subclone that has been most closely associated with fluoroquinolone resistance. This high proportion of ST131/H30 isolates is consistent with other studies from Detroit, which have reported high rates of resistant organisms and newly emergent strains [14,15,16]. Data utilizing whole-genome sequencing of almost 2000 clinical E. coli isolates from the US and Germany during the 2010–2011 period demonstrated that nearly all CTX-M ESBL-producing E. coli infections were due to the H30-Rx ST131 subclone, which was associated with higher rates of sepsis . The current data echo this finding of rapid clonal expansion.
We found no increase in the severity of infection or increased occurrence of adverse patient outcomes of patients with ST131 infections compared to those with non-ST131 infections. In fact, patients with ST131 infection were readmitted less often following discharge in both adjusted and unadjusted models, though numbers of non-ST131 infections were small. The lack of differences observed in clinical outcomes between ST131 and non-ST131 populations were possibly due to the small sample size of non-ST131isolates, limiting statistical power . Additionally, our patient population had higher rates of chronic illness (in both the ST131 and non-ST131 groups) than many prior studies of ESBL-producing E. coli infections, with 49% admitted from nursing home or long-term care facility residences, and the average Charlson score was 3.5.
Patients infected with ESBL-producing E. coli were generally elderly with multiple comorbidities and significant prior healthcare exposure, including prior LTCF stays and acute care hospitalizations. The current results suggest that elderly patients in skilled nursing facilities or with other recent healthcare exposures should be considered at increased risk for infection due to ST131 E. coli. Rates of 30-day readmission, and particularly readmission due to infection, were high. Given that the minority of readmissions were due to infection, the overall readmission rate may be driven by the high level of chronic disease in this population.
These data are limited by the narrowly defined patient group, i.e., hospitalized patients infected with ESBL-producing E. coli. However, this allowed for the comparison of patient outcomes within a very specifically characterized phenotypic group, lessening the potential for unmeasured bias between ST131 and non-ST131 groups. Additionally, our use of a multiplex PCR-based assay has potential to produce false-negative results and may miss non-025b subtypes of ST131. All negative results were tested in duplicate, and additional sequencing of the H30 allele in a selection of isolates was performed to reduce the likelihood of false-negative results. While these data are several years old, we believe that the lessons learned from this study are important and applicable to the current study of E. coli and other resistant bacteria.
This study identified ESBL production among several non-ST131 E. coli strain types. Therefore, the use of ST131 typing alone should not be used to definitively determine resistance patterns. Susceptibility and molecular resistance gene-based assays remain the most effective diagnostic tests in determining optimal antimicrobial therapy for extraintestinal E. coli infections. However, strain typing can be useful in helping to understand important epidemiologic characteristics of pathogen and resistance spread.