E. coli endocarditis remains a rare entity and represents approximately 0.51% of cases of infective endocarditis. It seems to be increasingly reported in older women [
1,
3]. In most of the reported cases, endocarditis originated from a urinary tract infection and in a recent retrospective analysis, of the published cases, 52% of patients had a preceding urinary tract infection [
1]. Additionally, it has been shown that some co-morbidities, such as diabetes, malignancy, excessive alcohol consumption, hemodialysis could predispose to
E. coli infective endocarditis [
1]. Several studies have reported, that among the four heart valves, the native mitral valve seems to be the most frequently affected endocarditis caused by
E. coli [
1,
4‐
10].. Here, we report a rare case of
E. coli O2:K7:H6, B2, ST141 associated with urinary tract infection (UTI) and endocarditis. O2:H6, B2, ST141 Shiga toxin-producing
E. coli (STEC) encoding Stx2b has been described as being closely related to adherent-invasive
E. coli (AIEC) [
11]. The heteropathogenic potential of these strains has been associated with their identification as diarrheagenic [
11,
12] and their ability to cause urinary tract infection (UTI) in an animal model [
11]. The serotype O2:H6 has been listed as isolated from UTI, bacteremia, ulcerative colitis, (bloody) diarrhea and meningitis in the IEC database, however, as of this case presentation, this is the only isolate with this particular serotype. Strains that have been fully O:K:H serotyped by the IEC are either O2:K1:H6 or O2:K7:H1 or O2:K7:H5. Our patient presented infective endocarditis of her native mitral valve, septic encephalopathy (with clinical signs of meningitis) and acute cholecystitis due to
E. coli bloodstream infection secondary to hydronephrosis and urinary tract infection. How E.coli affects native valves is not completely known [
1]. It is possible that specific virulence factors from extra-intestinal pathogenic
E.coli (ExPEC) from the urinary tract may be strongly associated with the development of
E. coli infective endocarditis. Studies have found that some
E. coli strains with a high prevalence of phylogenetic type B2 could increase the probability for the pathogens to invade cardiac endothelia [
13‐
15]. ExPEC are part of the gut microbiota of the healthy population but they are able also to produce disease after colonization of other non-intestinal niches. This pathogenesis has been related to their important genetic contents of virulence factors. Molecular epidemiological analyses have shown that ExPEC are distinct from commensal and diarrheagenic
E. coli (DEC) in terms of pathogenic potential, ecology, evolution, reservoirs, transmission, pathways, host–pathogen interactions, and virulence mechanisms [
16]. According to epidemiological and infection model data definitions the present isolate can be classified as both ExPEC
JJ [
17] and uropathogenic
E. coli (UPEC
HM) [
18]. Adhesins can play a key role in pathogenic process. As suggested by Nogueira et al. some of these factors could enable
E. coli to adhere to cardiac valves [
4]. The present isolate was positive for at least two adhesins, P fimbriae (
papA_F12 and
papC) and S fimbrial/F1C fimbriae (
focC, focI, sfaD, sfaE and
sfaS) that are frequent in uropathogenic human isolates and extraintestinal avian pathogenic
E. coli (APEC) isolates. The WGS analysis showed that C615–19 harbored an array of ExPEC virulence (Table
1) factors such as the
iss and
ompT genes. Interestingly, both genes play a role in the ability of the bacterium to resist the innate host defenses. OmpT is active in the degradation of cationic peptides (defensins) excreted by epithelial cells from the urinary tract [
19] and iss has been associated with increased serum survival [
20] and found in
E. coli isolated from female patients with bacteremia of urinary tract origin [
21]. Little is known about the virulence genotypes of
E. coli isolated from native valve endocarditis. However, one study [
3] screened five
E. coli strains for the presence of eight virulence genes,
papG, sfaS, ibeA, iucC, hly, cnf1, fyuA iroN; they found that the strains harbored between three and five of the genes. Notably, C615–19 harbored all eight genes, except
ibeA suggesting that it is a highly virulent strain which is also supported by our WGS analysis. Even though this
E. coli strain is of a unique serotype, it shares virulence traits with ExPEC causing bacteremia and belongs to the most prevalent phylogenetic group, B2. These strains harbor multiple virulence factors that enable them to adhere, invade, escape host defenses and acquire essential nutrients, such as iron. C615–19 harbors all these factors. In conclusion,
E. coli endocarditis is reported with increasing frequency, in particular among elderly patients, with high morbidity and mortality. The relationship between the virulent factors present in ExPEC strains and some serotypes of
E. coli that could facilitate the adherence to cardiac valves warrants further attention to the typing of
E. coli. It is possible, that
E. coli O2:K7:H6 harboring this particular set of virulence genes may be associated with increased morbidity due to native valve endocarditis.