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Volume 30, Number 1—January 2024
CME ACTIVITY - Research

Early-Onset Infection Caused by Escherichia coli Sequence Type 1193 in Late Preterm and Full-Term Neonates

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Discussion
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Author affiliations: Escherichia coli National Reference Center, Robert-Debré University Hospital, Assistance Publique–Hôpitaux de Paris, Paris, France (C. Malaure, A. Birgy, P. Bidet, S. Bonacorsi); Paediatric Intensive Care Unit, Robert-Debré University Hospital, Assistance Publique–Hôpitaux de Paris, Paris (G. Geslain); Paris Cité University, Paris (G. Geslain, A. Birgy, P. Bidet, S. Bonacorsi); Avicenne University Hospital, Assistance Publique–Hôpitaux de Paris, Bobigny, France (I. Poilane); Louis Mourier University Hospital, Assistance Publique–Hôpitaux de Paris, Colombes, France (M. Allain); Saint Louis University Hospital, Assistance Publique–Hôpitaux de Paris, Paris (M. Liberge); Neonatal Care Unit, Robert-Debré University Hospital, Assistance Publique–Hôpitaux de Paris, Paris (N. Khattat); Hôpital Privé d'Antony, Ramsay Santé, Antony, France (P. Sikias)

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Introduction

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Release date: December 21, 2023; Expiration date: December 21, 2024
Learning Objectives

Upon completion of this activity, participants will be able to:

  • Assess the prevalence and complications of early-onset neonatal sepsis (EOS)

  • Compare characteristics of Escherichia coli isolates from EOS and healthy vaginal carriage in the current study

  • Analyze characteristics of sequence type 1193 EOS in the current study

  • Evaluate similarities and differences in E. coli EOS among preterm and term infants in the current study

CME Editor

Tony Pearson-Clarke, MS, Technical Writer/Editor, Emerging Infectious Diseases. Disclosure: Tony Pearson-Clarke, MS, has no relevant financial relationships.

CME Author

Charles P. Vega, MD, Health Sciences Clinical Professor of Family Medicine, University of California, Irvine School of Medicine, Irvine, California. Disclosure: Charles P. Vega, MD, has the following relevant financial relationships: served as an advisor or consultant for Boehringer Ingelheim; GlaxoSmithKline; Johnson & Johnson Services, Inc.

Authors

Célie Malaure, PharmD; Guillaume Geslai, MD; André Birgy, PharmD, PhD; Philippe Bidet, MD, PhD; Isabelle Poilane, PharmD; Margaux Allain, PharmD; Mathilde Liberge, PharmD; Nizar Khattat, MD; Paola Sikias, MD; Stéphane Bonacorsi, MD, PhD.

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Abstract

Using whole-genome sequencing, we characterized Escherichia coli strains causing early-onset sepsis (EOS) in 32 neonatal cases from a 2019–2021 prospective multicenter study in France and compared them to E. coli strains collected from vaginal swab specimens from women in third-trimester gestation. We observed no major differences in phylogenetic groups or virulence profiles between the 2 collections. However, sequence type (ST) analysis showed the presence of 6/32 (19%) ST1193 strains causing EOS, the same frequency as in the highly virulent clonal group ST95. Three ST1193 strains caused meningitis, and 3 harbored extended-spectrum β-lactamase. No ST1193 strains were isolated from vaginal swab specimens. Emerging ST1193 appears to be highly prevalent, virulent, and antimicrobial resistant in neonates. However, the physiopathology of EOS caused by ST1193 has not yet been elucidated. Clinicians should be aware of the possible presence of E. coli ST1193 in prenatal and neonatal contexts and provide appropriate monitoring and treatment.

Extraintestinal pathogenic Escherichia coli and Streptococcus agalactiae are bacterial pathogens that commonly cause early-onset neonatal sepsis (EOS) in industrialized countries. EOS is confirmed by a blood or cerebrospinal fluid culture positive for the causative pathogen <72 hours after birth. EOS incidence is ≈1/1,000 live births (1,2); 10% of cases are complicated by meningitis, which can lead to neurologic sequelae in up to 50% and death in 10% of cases in industrialized countries (3).

EOS caused by S. agalactiae can be prevented by peripartum antimicrobial prophylaxis but not EOS caused by E. coli. E. coli strains that cause neonatal meningitis have been well characterized, but E. coli strains that cause EOS less so (4,5). Neonatal meningitis E. coli strains belong mainly to phylogenetic group B2/sequence type complex (STc) 95 (6) and are frequently O18:K1, O1:K1, O83:K1, or O45S88:K1 serotypes (7,8). Most STc95 strains are distributed worldwide and still largely susceptible to antimicrobials (9). However, other strains that can cause EOS, notably in preterm neonates, might be resistant to probabilistic antimicrobial therapy. In a recent study in Israel (10), maternal carriage rates of extended-spectrum β-lactamase (ESBL)–producing E. coli were 17.5% for mothers and 12.9% for preterm neonates; in China, ESBL accounted for up to 48% of E. coli infections in neonates (11).

Characterizing E. coli strains that cause EOS would constitute a critical first step towards better understanding the pathophysiology of this condition and developing potential preventive strategies. We conducted a prospective study covering a large area in France to estimate annual incidence and pathogen distribution of EOS in neonates born at ≥34 weeks of gestation during 2019–2021 (12). In total, we recorded 107 cases of bacteremia including 35 caused by E. coli, 15 (incidence 0.89/1,000 births) in late-preterm and 20 (0.06/1,000 births) in full-term infants. We prospectively recorded data on maternal and infant demographics, maternal antimicrobial therapy, peripartum antimicrobial prophylaxis, and outcomes (12). We aimed to use whole-genome sequencing (WGS) to characterize E. coli strains that caused EOS in cases from this prospective study and stratify results according to these data. In addition, we determined to compare those strains to E. coli strains obtained from cultures from vaginal swabs collected to screen for S. agalactiae carriage at 34–38 weeks of gestation from woman with newborns who had no history of EOS. The ethics committee institutional review board (Ramsay Santé Recherche & Enseignement, IRB00010835) authorized the study (12).

Methods

Bacterial Strains

We recorded 35 cases of EOS caused by E. coli during a prospective study in 81 maternity wards of the Ile de France area during 2019–2021 (12). Thirty-two E. coli isolates were sent to the National Reference Center in Robert-Debré Hospital to be further characterized. For comparison with the isolates from the Ile de France study, we included 50 E. coli isolates obtained from cultures from vaginal swabs collected from 4 maternity wards to screen pregnant woman for S. agalactiae carriage at 34–38 weeks of gestation. We found healthy vaginal carriage (HVC) among all; that is, none of the infants of the pregnant women from the S. agalactiae screening developed EOS caused by E. coli.

Antimicrobial Susceptibility Testing and Phenotypic Characterization

We determined antimicrobial susceptibility of the E. coli strains using disk diffusion on Mueller-Hinton agar plates (bioMérieux, https://www.biomerieux.com), as recommended by Comité de l’Antibiogramme de la Société Française de Microbiologie (https://www.sfm-microbiologie.org) guidelines. We defined ESBL production by synergy between clavulanic acid and >1 extended-spectrum cephalosporin or aztreonam.

Molecular Characterization

We performed WGS on 82 isolates, 32 described elsewhere (12) and 50 from the HVC/S. agalactiae screening. We extracted bacterial genomic DNA using the DNeasy UltraClean Microbial Kit (QIAGEN, https://www.qiagen.com) and prepared libraries using Nextera Flex/DNA Prep library kits (Illumina, https://www.illumina.com) as specified by the manufacturers. We performed sequencing using 2 × 150 bp MiniSeq technology (Illumina) and assembled models using SPAdes (https://github.com/ablab/spades). We estimated quality of sequencing data using standard metrics, including N50 and mean coverage (Appendix). We determined phylogenetic groups, serotypes, fimH type, sequence type (ST), and STcs (which regroup all STs of <1 allele difference), whole-genome multilocus sequence typing (MLST), and hierarchical clustering of core genome MLST using Enterobase (https://enterobase.warwick.ac.uk) (13). We used the Center for Genomic Epidemiology website (https://genomicepidemiology.org) to search for resistance and virulence genes. We also used a local BLAST with a collection of virulence genes as described elsewhere (14). We used Fisher exact analysis for statistical comparisons among groups.

Results

Bacterial Collection and Demographic and Clinical Features of Patients

We studied 82 E. coli isolates. Birth locations of the neonates within Ile de France were diverse (30 different locations among 32 EOS case-patients). Babies were delivered at full term (≥37 weeks of gestation) in 59% (19/32) and preterm (<37 weeks of gestation) in 41% (13/32) of cases. In 6 (31%) cases from the full-term group and 7 cases (54%) from the preterm group, mothers received antimicrobial treatment <3 days before labor. We observed 6 cases of meningitis, 3 each from the full-term and preterm neonate groups (Table 1).

Diversity and Phylogenetics of EOS and HVC E. coli Strain Collections

Five of 7 major E. coli phylogroups—A, B1, B2, D, and F, but not C or E—were represented in similar proportions in both the Ile de France study and vaginal swab collections (p>0.05). The exceptions to this trend were phylogroup A being more common in vaginal swab (22%) than EOS (9.4%) isolates and group B2 more common in EOS (65.6%) than vaginal swab (48%) isolates (Figure 1). Among the 3 most frequent ST/STc variants in our study, STc10 (phylogroup A) was present in more HVC strains, whereas ST95 and STc14 (phylogroup B2) were more common in EOS strains. The imbalance was striking for STc14, which was present in 25% of EOS strains but only 4% of HVC strains (p = 0.01) (Figure 2). STc14 isolates included 6 ST1193, 2 ST14, and 2 ST404. Of note, the 6 ST1193 isolates were found exclusively in the EOS collection.

Virulence and Antimicrobial Resistance

We observed no significant difference in distribution of virulence factors between the EOS and HVC strain collections, except for genes encoding the K1 capsule, which were present significantly more in the EOS collection (Appendix Table 1). In contrast, antimicrobial resistance differed markedly between collections (Figure 3). Aminopenicillin resistance was ≈2 times higher among EOS (65.6%) than HVC (34%) collection strains (p = 0.007); ESBL was present in 12.5% of EOS and 8% of HVC strains (p>0.05). Resistance to fluoroquinolone and gentamicin were also more common among EOS strains (Figure 3).

We examined the distribution of phylogenetic groups and ST/STc frequency among EOS strains stratified by gestational term of newborns. Differences in rates of B2 phylogroup strains in the 2 subpopulations (69% in preterm, 63% in full-term neonates) were not statistically significant (Figure 4). STc14 (ST14/ST1193) was >2 times as frequent in the preterm (38.5%) as the full-term subpopulation (15.8%), but the difference was not statistically significant (p>0.05). Distribution of ST95, the second most frequent ST, was similar between preterm (15.4%) and full-term (21.1%) subpopulations (Figure 5). There were more mothers with STc14 E. coli isolates (5/13 [38.5%]) among those who received antimicrobial therapy <3 days before delivery than those who did not (3/19 [15.8%]) (p>0.05) (Figure 6). In contrast, there were fewer ST95 isolates among mothers receiving prenatal antimicrobial therapy (1/13 [7.69%]) than those receiving no therapy (5/19 [26.32%]) (p>0.05).

Main Features of EOS Caused by ST1193 E. coli and Characterization of Isolates

All 6 ST1193 EOS strains were isolated from different maternity hospitals. Half (3/6) of neonates with ST1193 EOS were born at full term. Three neonates had meningitis, 2 full-term and 1 preterm. Four (67%) mothers with ST1193 strains received prenatal antimicrobial therapy compared with 9 (35%) for the non-ST1193 strains (p>0.05) (Table 1; Figure 6). All strains were resistant to fluoroquinolones, 3 were resistant to azithromycin, and 3 others harbored an ESBL phenotype (Table 2). All strains were lactose nonfermenters (data not shown).

We assessed presence of putative virulence factors among the 6 ST1193 isolates (Table 2; Appendix Table 2) and identified presence of factors with a significant difference (p<0.05) among ST1193 compared with non-ST1193 strains: adherence protein Iha, colicin Ia immunity protein Imm, major pilin subunit PapA_F43, plasmid-encoded enterotoxin SenB, serine protease Sat, vacuolating autotransporter toxin Vat, and Type 1 fimbrin D-mannose specific adhesion 64.

Three strains harbored ESBL phenotypes contained the β-lactamase–encoding genes blaCTX-M-15 and blaOXA-1 associated with the aac(6')-Ib-cr genes, and 3/6 strains harbored the mph(A) gene (macrolide 2′-phosphotransferase), which inactivates macrolides, reinforcing observed phenotypic resistance to azithromycin. None of the non-ST1193 strains carried that gene. One strain was resistant only to fluoroquinolones (Table 2). All strains had different hierarchical cluster 10 (HC10) but the same HC20 (571), whereas ribosomal MLST (rMLST) split the strains into 2 main populations: rMLST 33503, which regroups the 3 ESBL-producing strains, and rMLST 1674, which contains 2 less-resistant isolates.

Discussion

In our study, we used WGS to characterize E. coli strains causing EOS from a prospective multicenter study in France (12) and compared them to E. coli strains obtained from vaginal samples from pregnant women at 34–38 weeks of gestation. Although we observed no major differences between the EOS study and vaginal sample collections in distribution of phylogroups or virulence factors except the K1 antigen, we identified emerging ST1193 strains as major causes of EOS. Three isolates of the ST1193 clonal group caused meningitis, and half harbored an ESBL. E. coli ST1193 thus appears to be the most virulent and antimicrobial-resistant E. coli group that causes EOS.

Among major phylogroups, B2 and, to a lesser extent, D are associated with extraintestinal infections, whereas A and B1 are most associated with commensal strains or intestinal infections (15). We also observed predominance of B2 strains in our EOS population, regardless of the term of birth of the newborns. Although the proportion of phylogroup A strains was higher in the HVC than the EOS population, B2 strains largely predominated in the HVC collection, as reported in previous studies (16,17). However, sequence typing enabled a finer comparison between the 2 collections. Among the HVC strains, phylogroup A/STc10 (ST10, ST13795, ST6826, and ST13957) was predominant but was rarely observed among the EOS patients, in which ST95 and STc14 (notably ST14 and ST1193) were largely predominant. The high frequency of ST95 was expected because of its virulence in neonates, notably those with neonatal meningitis, which is well known worldwide (6,18). Of note, ST95 was second most common among HVC strains, suggesting its capacity to colonize the vagina, at least temporarily. Five of 6 mothers with EOS caused by ST95 received no prepartum antimicrobials. In contrast, ST14 and ST1193 strains were frequently associated with women receiving prepartum antimicrobials (5/8), and those strains were not present among HVC patients, suggesting the vaginal environment might inhibit the presence of ST14 and ST1193 strains. Of note, that STc14 but not ST95 was more prevalent among preterm neonates with EOS and 3/6 infections caused by ST1193 strains occurred in preterm newborns. It might be that ST1193 strains are less virulent than ST95 strains commonly found in full-term neonates. However, almost all women with preterm newborns received antimicrobial drugs, which might favor the selection of resistant strains, such as ST1193.

ST1193 was identified within STc14 approximately 25 years ago; its prevalence in extraintestinal infections could become a public health burden (19–21). One study observed an increased rate of ST1193 causing bloodstream infections, mostly in elderly patients in Canada during 2016–2018 (22). In an analysis of the population structure of 218 ESBL–producing E. coli in urinary tract infections in febrile children in France during 2014–2017, we noted prevalence of ST1193 rose from 0% to 9% (23). Large epidemiologic studies of ST1193 prevalence in neonatal infection have only recently been conducted. In 2 studies, ST1193 was shown to be a major cause of neonatal sepsis; however, because the definition of EOS in those studies differed from ours, data are difficult to compare (11,24). The finding of a worrying percentage of ST1193 among EOS patients (19%) in our study population indicates that in the future that ST should be closely monitored using microbiologic detection.

One epidemiologic study of intracranial infections in neonates caused by E. coli (25) found ST1193 to be the most prevalent ST (28%). All 8 ST1193 isolates caused late-onset infections, although none caused EOS. Only 1 recent case of early-onset meningitis caused by E. coli ST1193 has been reported, but cases of meningitis caused by ST1193 occurring >72 hours after birth were described in another study (24,26). The recent case occurred in a late-preterm neonate with a history of prolonged rupture of the membrane with prepartum and peripartum antimicrobial drugs administered, as in most of our cases.

Given that 3/6 ST1193 strains caused neonatal meningitis, such strains were shown to have high invasive disease potential in newborns. Several virulence factors and genetic determinants have been shown to be involved in the pathophysiology of neonatal meningitis, such as capsule K1, siderophore salmochelin, plasmid pS88, and invasin IbeA (27). Of note, among these determinants, only the K1 capsule was present in the ST1193 strains. Several virulence factors (Iha, Imm, plasmid-encoded enterotoxin SenB, Sat) were present in all ST1193 strains, with a significant p value (p<0.05) compared with non-ST1193 (Appendix Table 2) strains, and were present in >85% of ST1193 strains in the large collection of 1 study (28). Therefore, without in vivo study, it is difficult to determine the specific roles of these key factors in the invasiveness of ST1193 in cerebrospinal fluid.

Except for consistency of fluoroquinolone resistance and carrying the fimH64 allele, which characterized all ST1193 E. coli strains described in previous studies, multiple plasmid-borne resistance genes have been reported but are inconsistently associated with ST1193 (19,28,29). No isolates harbored the same phenotypic antimicrobial resistance pattern, highlighting their diversity. The co-occurrence of blaCTX-M-15/blaOXA-1/aac(6′)-Ib-cr, which we observed in 3/6 of EOS strains, has been frequently described, initially in ST131 but also more recently in emerging lineages of ST1193 (30). Half of our strains, similar to findings from other studies (28), carried the mphA resistance gene and had a high azithromycin MIC (>32 mg/L) (data not shown), which might have contributed to the emergence of ST1193 given that azithromycin is among the most-prescribed antimicrobial drugs worldwide among adult outpatients (31).

As of May 2023, sequences of 2,031 E. coli ST1193 strains from all over the world are available in Enterobase (13). Of those, 80% belong to HC20 571, as did our strains, and most (82%) harbor rMLST 1674, whereas rMLST 33503 is found in only 8%. Hierarchical clustering analysis did not suggest the presence of a particular clone in our collection. Distribution of rMLSTs was notably different: half of our ST1193 strains belonged to rMLST 33503. Whether this subgroup is emerging or has specific invasive disease potential in neonates has yet to be determined.

Among its strengths, our prospective epidemiologic study, conducted in a large area of France, estimated annual incidence and pathogen distribution in EOS patients (12) and documented the unique molecular and phenotypic characteristics of the strains in our study. We were limited by the small number of patients; results, especially implication of ST1193 in infections in very preterm neonates, need to be confirmed in larger study populations.

In conclusion, our findings suggest that ST1193 is emerging as a major E. coli pathogen that can cause EOS and early-onset neonatal meningitis in full-term and late-preterm newborns and might surpass ST95 in incidence and causing illness because of its potential virulence combined with its resistance to multiple antimicrobials. Pediatricians and microbiologists should be aware of the public health threat from E. coli ST1193 and the benefits of prepartum/peripartum EOS treatment with effective antimicrobials. Isolating ST1193 E. coli strains in the neonatal context (from mother, newborn, or both) will require careful, sustained clinical monitoring of newborns. It might also require implementing measures to limit spread, especially in neonatal wards. On the basis of microbiologic evidence, ST1193 should be suspected when 3 properties are all present: high resistance to ciprofloxacin, K1 capsule, and non–lactose-fermenting colonies, each of which can easily be tested for in a microbiology laboratory. Further studies should help to define the genetic determinants of ST1193 virulence in neonates and confirm and subsequently explain its inability or weak ability to colonize the vagina. Clinicians need to be aware of the possible presence of E. coli ST1193 in prenatal and neonatal contexts and provide appropriate monitoring and treatment.

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Acknowledgments

This work was funded in part by l’Agence Nationale de la Recherche (project ANR-Seq-N-Vac).

C.M., G.G., and S.B. contributed conceptualization, methodology, and writing of the original draft; P.B., C.M., and G.G., formal analysis; P.S. and S.B., investigation; P.S., I.P., M.A., K.N., and M.L., resources; S.B., supervision; and all authors, writing, review, and editing.

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References

  1. Shane  AL, Sánchez  PJ, Stoll  BJ. Neonatal sepsis. Lancet. 2017;390:1770–80. DOIPubMedGoogle Scholar
  2. Stoll  BJ, Puopolo  KM, Hansen  NI, Sánchez  PJ, Bell  EF, Carlo  WA, et al.; Eunice Kennedy Shriver National Institute of Child Health and Human Development Neonatal Research Network. Early-onset neonatal sepsis 2015 to 2017, the rise of Escherichia coli, and the need for novel prevention strategies. JAMA Pediatr. 2020;174:e200593. DOIPubMedGoogle Scholar
  3. Gaschignard  J, Levy  C, Romain  O, Cohen  R, Bingen  E, Aujard  Y, et al. Neonatal bacterial meningitis: 444 cases in 7 years. Pediatr Infect Dis J. 2011;30:212–7. DOIPubMedGoogle Scholar
  4. Joshi  NS, Huynh  K, Lu  T, Lee  HC, Frymoyer  A. Epidemiology and trends in neonatal early onset sepsis in California, 2010-2017. J Perinatol. 2022;42:940–6. DOIPubMedGoogle Scholar
  5. Miselli  F, Cuoghi Costantini  R, Creti  R, Sforza  F, Fanaro  S, Ciccia  M, et al. Escherichia coli is overtaking group B Streptococcus in early-onset neonatal sepsis. Microorganisms. 2022;10:10. DOIPubMedGoogle Scholar
  6. Basmaci  R, Bonacorsi  S, Bidet  P, Biran  V, Aujard  Y, Bingen  E, et al. Escherichia coli meningitis features in 325 children from 2001 to 2013 in France. Clin Infect Dis. 2015;61:779–86. DOIPubMedGoogle Scholar
  7. Bonacorsi  S, Clermont  O, Houdouin  V, Cordevant  C, Brahimi  N, Marecat  A, et al. Molecular analysis and experimental virulence of French and North American Escherichia coli neonatal meningitis isolates: identification of a new virulent clone. J Infect Dis. 2003;187:1895–906. DOIPubMedGoogle Scholar
  8. Peigne  C, Bidet  P, Mahjoub-Messai  F, Plainvert  C, Barbe  V, Médigue  C, et al. The plasmid of Escherichia coli strain S88 (O45:K1:H7) that causes neonatal meningitis is closely related to avian pathogenic E. coli plasmids and is associated with high-level bacteremia in a neonatal rat meningitis model. Infect Immun. 2009;77:2272–84. DOIPubMedGoogle Scholar
  9. Riley  LW. Pandemic lineages of extraintestinal pathogenic Escherichia coli. Clin Microbiol Infect. 2014;20:380–90. DOIPubMedGoogle Scholar
  10. Frank Wolf  M, Abu Shqara  R, Naskovica  K, Zilberfarb  IA, Sgayer  I, Glikman  D, et al. Vertical transmission of extended-spectrum, beta-lactamase-producing Enterobacteriaceae during preterm delivery: a prospective study. Microorganisms. 2021;9:506. DOIPubMedGoogle Scholar
  11. Gu  S, Lai  J, Kang  W, Li  Y, Zhu  X, Ji  T, et al. Drug resistance characteristics and molecular typing of Escherichia coli isolates from neonates in class A tertiary hospitals: A multicentre study across China. J Infect. 2022;85:499–506. DOIPubMedGoogle Scholar
  12. Sikias  P, Biran  V, Foix-L’Hélias  L, Plainvert  C, Boileau  P, Bonacorsi  S; EOS study group. Early-onset neonatal sepsis in the Paris area: a population-based surveillance study from 2019 to 2021. Arch Dis Child Fetal Neonatal Ed. 2023;108:114–20. DOIPubMedGoogle Scholar
  13. Zhou  Z, Alikhan  N-F, Mohamed  K, Fan  Y, Achtman  M; Agama Study Group. The EnteroBase user’s guide, with case studies on Salmonella transmissions, Yersinia pestis phylogeny, and Escherichia core genomic diversity. Genome Res. 2020;30:138–52. DOIPubMedGoogle Scholar
  14. Cointe  A, Birgy  A, Mariani-Kurkdjian  P, Liguori  S, Courroux  C, Blanco  J, et al. Emerging multidrug-resistant hybrid pathotype Shiga toxin–producing Escherichia coli O80 and related strains of clonal complex 165, Europe. Emerg Infect Dis. 2018;24:2262–9. DOIPubMedGoogle Scholar
  15. Denamur  E, Clermont  O, Bonacorsi  S, Gordon  D. The population genetics of pathogenic Escherichia coli. Nat Rev Microbiol. 2021;19:37–54. DOIPubMedGoogle Scholar
  16. Sáez-López  E, Cossa  A, Benmessaoud  R, Madrid  L, Moraleda  C, Villanueva  S, et al. Characterization of vaginal Escherichia coli isolated from pregnant women in two different African sites. PLoS One. 2016;11:e0158695. DOIPubMedGoogle Scholar
  17. Watt  S, Lanotte  P, Mereghetti  L, Moulin-Schouleur  M, Picard  B, Quentin  R. Escherichia coli strains from pregnant women and neonates: intraspecies genetic distribution and prevalence of virulence factors. J Clin Microbiol. 2003;41:1929–35. DOIPubMedGoogle Scholar
  18. Johnson  TJ, Wannemuehler  Y, Johnson  SJ, Stell  AL, Doetkott  C, Johnson  JR, et al. Comparison of extraintestinal pathogenic Escherichia coli strains from human and avian sources reveals a mixed subset representing potential zoonotic pathogens. Appl Environ Microbiol. 2008;74:7043–50. DOIPubMedGoogle Scholar
  19. Pitout  JDD, Peirano  G, Chen  L, DeVinney  R, Matsumura  Y. Escherichia coli ST1193: Following in the Footsteps of E. coli ST131. Antimicrob Agents Chemother. 2022;66:e0051122. DOIPubMedGoogle Scholar
  20. Crémet  L, Caroff  N, Giraudeau  C, Reynaud  A, Caillon  J, Corvec  S. Detection of clonally related Escherichia coli isolates producing different CMY β-lactamases from a cystic fibrosis patient. J Antimicrob Chemother. 2013;68:1032–5. DOIPubMedGoogle Scholar
  21. Platell  JL, Trott  DJ, Johnson  JR, Heisig  P, Heisig  A, Clabots  CR, et al. Prominence of an O75 clonal group (clonal complex 14) among non-ST131 fluoroquinolone-resistant Escherichia coli causing extraintestinal infections in humans and dogs in Australia. Antimicrob Agents Chemother. 2012;56:3898–904. DOIPubMedGoogle Scholar
  22. Peirano  G, Matsumara  Y, Nobrega  D, DeVinney  R, Pitout  J. Population-based epidemiology of Escherichia coli ST1193 causing blood stream infections in a centralized Canadian region. Eur J Clin Microbiol Infect Dis. 2021. Online ahead of print.
  23. Birgy  A, Madhi  F, Jung  C, Levy  C, Cointe  A, Bidet  P, et al.; Group of the National Observatory of Urinary tract Infection due to ESBL-producing Enterobacteriaceae in children. Diversity and trends in population structure of ESBL-producing Enterobacteriaceae in febrile urinary tract infections in children in France from 2014 to 2017. J Antimicrob Chemother. 2020;75:96–105.PubMedGoogle Scholar
  24. Ding  Y, Zhang  J, Yao  K, Gao  W, Wang  Y. Molecular characteristics of the new emerging global clone ST1193 among clinical isolates of Escherichia coli from neonatal invasive infections in China. Eur J Clin Microbiol Infect Dis. 2021;40:833–40. DOIPubMedGoogle Scholar
  25. Zhong  Y-M, Zhang  X-H, Ma  Z, Liu  W-E. Prevalence of Escherichia coli ST1193 causing intracranial infection in Changsha, China. Trop Med Infect Dis. 2022;7:217. DOIPubMedGoogle Scholar
  26. Oldendorff  F, Linnér  A, Finder  M, Eisenlauer  P, Kjellberg  M, Giske  CG, et al. Case report: fatal outcome for a preterm newborn with meningitis caused by extended-spectrum β-lactamase-producing Escherichia coli sequence type 1193. Front Pediatr. 2022;10:866762. DOIPubMedGoogle Scholar
  27. De Francesco  MA, Bertelli  A, Corbellini  S, Scaltriti  E, Risso  F, Allegri  R, et al. Emergence of pandemic clonal lineage sequence types 131 and 69 of extraintestinal Escherichia coli as a cause of meningitis: is it time to revise molecular assays? Microbiol Spectr. 2023;11:e0327422. DOIPubMedGoogle Scholar
  28. Wyrsch  ER, Bushell  RN, Marenda  MS, Browning  GF, Djordjevic  SP. Global phylogeny and f virulence plasmid carriage in pandemic Escherichia coli ST1193. Microbiol Spectr. 2022;10:e0255422. DOIPubMedGoogle Scholar
  29. Johnson  TJ, Elnekave  E, Miller  EA, Munoz-Aguayo  J, Flores Figueroa  C, Johnston  B, et al. Phylogenomic analysis of extraintestinal pathogenic Escherichia coli sequence type 1193, an emerging multidrug-resistant clonal group. Antimicrob Agents Chemother. 2018;63:e0191318. DOIPubMedGoogle Scholar
  30. Jackson  N, Belmont  CR, Tarlton  NJ, Allegretti  YH, Adams-Sapper  S, Huang  YY, et al. Genetic predictive factors for nonsusceptible phenotypes and multidrug resistance in expanded-spectrum cephalosporin-resistant uropathogenic Escherichia coli from a multicenter cohort: insights into the phenotypic and genetic basis of coresistance. MSphere. 2022;7:e0047122. DOIPubMedGoogle Scholar
  31. Hicks  LA, Taylor  TH Jr, Hunkler  RJUS. U.S. outpatient antibiotic prescribing, 2010. N Engl J Med. 2013;368:1461–2. DOIPubMedGoogle Scholar

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Earning CME Credit

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Article Title: 
Early-Onset Infection Caused by Escherichia coli ST1193 in Late Preterm and Full-Term Neonates
CME Questions

  • Which of the following statements regarding early-onset neonatal sepsis (EOS) is most accurate?

    • EOS is defined by a positive blood or cerebrospinal fluid culture within 36 hours after birth

    • EOS affects approximately 1 in 1000 live births

    • Meningitis complicates nearly 50% of cases of EOS

    • EOS due to either Streptococcus agalactiae or E coli can be prevented through peripartum prophylaxis with antibiotics

  • Which of the following statements regarding virulence factors and antibiotic resistance among E coli isolates in the current study is most accurate?

    • Virulence factors and antibiotic resistance were more common in EOS vs healthy vaginal carriage (HVC) isolates

    • Virulence factors, but not antibiotic resistance, were more common in EOS vs HVC isolates

    • Antibiotic resistance, but not virulence factors, was more common in EOS vs HVC isolates

    • Virulence factors and antibiotic resistance were more common in HVC vs EOS isolates

  • Which of the following statements regarding sequence type (ST)1193 E coli EOS isolates in the current study is most accurate?

    • All cases were diagnosed in a single hospital

    • All cases had a preterm delivery

    • None of the mothers had received peripartum antibiotics

    • All strains were resistant to fluoroquinolones

  • Which of the following statements regarding EOS among term vs preterm infants in the current study is most accurate?

    • Type A was found significantly more frequently among preterm infants

    • Type F was found significantly more frequently among term infants

    • ST95 was found significantly more frequently among preterm infants

    • Generally, phylogenetic groups and ST/sequence type complex (STc) were similar in term and preterm infants

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Cite This Article

DOI: 10.3201/eid3001.230851

Original Publication Date: December 21, 2023

1These authors contributed equally to this manuscript.

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Table of Contents – Volume 30, Number 1—January 2024

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Comments

Please use the form below to submit correspondence to the authors or contact them at the following address:

Stéphane Bonacorsi, Service de Microbiologie, Hôpital Universitaire Robert-Debré, AP-HP, 48 Boulevard Sérurier 75019 Paris, France

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Page created: November 08, 2023
Page updated: December 21, 2023
Page reviewed: December 21, 2023
The conclusions, findings, and opinions expressed by authors contributing to this journal do not necessarily reflect the official position of the U.S. Department of Health and Human Services, the Public Health Service, the Centers for Disease Control and Prevention, or the authors' affiliated institutions. Use of trade names is for identification only and does not imply endorsement by any of the groups named above.
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