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EcoSal Plus

Domain 8:

Pathogenesis

Molecular Epidemiology of Extraintestinal Pathogenic

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  • Authors: James R. Johnson1, and Thomas A. Russo2
  • Editor: Michael S. Donnenberg3
  • VIEW AFFILIATIONS HIDE AFFILIATIONS
    Affiliations: 1: Mucosal and Vaccine Research Center, VA Medical Center, Minneapolis, MN 55417, and Department of Medicine, University of Minnesota, Minneapolis, MN 55455; 2: VA Medical Center, Department of Medicine, Department of Microbiology, and The Witebsky Center for Microbial Pathogenesis and Immunology, University of Buffalo, Buffalo, NY 14214; 3: University of Maryland, School of Medicine, Baltimore, MD
  • Received 29 April 2004 Accepted 04 August 2004 Published 15 November 2004
  • Address correspondence to James R. Johnson johns007@umn.edu
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  • Abstract:

    Extraintestinal pathogenic (ExPEC), the specialized strains that possess the ability to overcome or subvert host defenses and cause extraintestinal disease, are important pathogens in humans and certain animals. Molecular epidemiological analysis has led to an appreciation of ExPEC as being distinct from other (including intestinal pathogenic and commensal variants) and has offered insights into the ecology, evolution, reservoirs, transmission pathways, host-pathogen interactions, and pathogenetic mechanisms of ExPEC. Molecular epidemiological analysis also provides an essential complement to experimental assessment of virulence mechanisms. This chapter first reviews the basic conceptual and methodological underpinnings of the molecular epidemiological approach and then summarizes the main aspects of ExPEC that have been investigated using this approach.

  • Citation: Johnson J, Russo T. 2004. Molecular Epidemiology of Extraintestinal Pathogenic , EcoSal Plus 2004; doi:10.1128/ecosalplus.8.6.1.4

Key Concept Ranking

Random Amplified Polymorphic DNA
0.44747096
Restriction Fragment Length Polymorphism
0.44747096
Random Amplified Polymorphic DNA
0.44747096
Restriction Fragment Length Polymorphism
0.44747096
Outer Membrane Protein A
0.43003705
Type 1 Fimbriae
0.414482
0.44747096

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ecosalplus.8.6.1.4.citations
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/content/journal/ecosalplus/10.1128/ecosalplus.8.6.1.4
2004-11-15
2017-11-21

Abstract:

Extraintestinal pathogenic (ExPEC), the specialized strains that possess the ability to overcome or subvert host defenses and cause extraintestinal disease, are important pathogens in humans and certain animals. Molecular epidemiological analysis has led to an appreciation of ExPEC as being distinct from other (including intestinal pathogenic and commensal variants) and has offered insights into the ecology, evolution, reservoirs, transmission pathways, host-pathogen interactions, and pathogenetic mechanisms of ExPEC. Molecular epidemiological analysis also provides an essential complement to experimental assessment of virulence mechanisms. This chapter first reviews the basic conceptual and methodological underpinnings of the molecular epidemiological approach and then summarizes the main aspects of ExPEC that have been investigated using this approach.

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Figures

Image of Figure 1
Figure 1

Open boxes represent genes within the operon (including , structural subunit; , usher; , minor tip pilins; and , adhesin). Forward and reverse primers (right- and left-pointing black triangles, respectively, above and below the operon) are used in combinations as shown to yield the indicated PCR products (thin rectangles, below operon). Heavily striped rectangles, and allele PCR products. Solid black rectangles, gene PCR products. Finely striped rectangles, long PCR operon fragments (as generated using either flanking or internal allele-specific reverse primers, as illustrated for allele I-I′).

Reprinted from reference ( 35 ), with permission.

Citation: Johnson J, Russo T. 2004. Molecular Epidemiology of Extraintestinal Pathogenic , EcoSal Plus 2004; doi:10.1128/ecosalplus.8.6.1.4
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Figure 2

Shown are I PFGE profiles for eight CGA pyelonephritis isolates (lanes 1–5 and 8–10; “Py” strain designations, bold) and for two comparison CGA cystitis isolates (lanes 6 and 7: UMN 26, from Minnesota, and UCB 102, from California) ( 43 , 45 ). Geographical source for the pyelonephritis isolates is indicated above the strain designations.

Citation: Johnson J, Russo T. 2004. Molecular Epidemiology of Extraintestinal Pathogenic , EcoSal Plus 2004; doi:10.1128/ecosalplus.8.6.1.4
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Figure 3

RAPD profiles generated by using primer 1247 ( 47 ) show O18:K1:H7 strains NU14 (cystitis: lane 3) and RS218 (neonatal meningitis: lane 4) to be indistinguishable from one another but distinct from strain 536 (O6:K15:H31, pyelonephritis: lane 2). M (lanes 1 and 5), 100-bp marker.

Reprinted from reference ( 55 ), with permission.

Citation: Johnson J, Russo T. 2004. Molecular Epidemiology of Extraintestinal Pathogenic , EcoSal Plus 2004; doi:10.1128/ecosalplus.8.6.1.4
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Figure 4

Genomic profiles (shown in computer reconstruction), as generated for each isolate by using RAPD primers 1247, 1254, 1281, and 1283, were concatenated for cluster analysis. Pyelonephritis isolates ( = 10; “Py” strain designations) are labeled in bold if from clonal group A (CGA) ( = 5) and in lightface italic if non-CGA ( = 5). CGA isolates (bold) are bracketed and labeled as to syndrome (CY, cystitis; PY, pyelonephritis) and serogroup (O11/O17/O77) (right), with the corresponding cluster shown in bold (left). The two O15:K52:H1 control strains are bracketed and labeled by serotype. Reference strains from the Reference (ECOR) collection (bold) are identified as to phylogenetic group (right). The depth of the molecular weight ladder cluster (brackets; MW) reflects the intrinsic variability inherent in gel electrophoresis and image analysis, independent of amplification.

Reprinted from reference ( 45 ), with permission.

Citation: Johnson J, Russo T. 2004. Molecular Epidemiology of Extraintestinal Pathogenic , EcoSal Plus 2004; doi:10.1128/ecosalplus.8.6.1.4
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Figure 5

Dendrogram at left depicts phylogenetic relationships for the 72 members of the Reference (ECOR) collection, as inferred based on multilocus enzyme electrophoresis ( 51 ). The four major phylogenetic groups (A, B1, B2, and D) and the nonaligned strains (“non”) are bracketed and labeled. Bullets at right indicate presence of putative virulence genes ( , P fimbriae; , group II capsule synthesis; , S and F1C fimbriae; , aerobactin system; , serum resistance; and , type 1 fimbriae). Horizontal bars at right indicate the 10 ECOR strains isolated from humans with symptomatic UTI. The remaining strains, except for one asymptomatic bacteriuria isolate, are fecal isolates from healthy human or animal hosts. Note the concentration of (chromosomal) virulence genes , , and within phylogenetic groups B2 and D, but their occasional joint appearance also in distant lineages, consistent with coordinate horizontal transfer. The more scattered phylogenetic distribution of is consistent with this gene's typically plasmid location, whereas is nearly universally prevalent, consistent with its presence in other species of , presumably reflecting an origin in a shared enterobacterial ancestor. Note the concentration of UTI isolates within phylogenetic groups B2 and D and the association of virulence genes with UTI isolates.

Reprinted from reference ( 77 ), with permission.

Citation: Johnson J, Russo T. 2004. Molecular Epidemiology of Extraintestinal Pathogenic , EcoSal Plus 2004; doi:10.1128/ecosalplus.8.6.1.4
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Figure 6

The map is based on the chromosome of MG1655 (K-12). PAIs are indicated according to their chromosomal insertion sites next to tRNA-encoding genes. Contents, by PAI, include: PAI I (α-hemolysin, F17-like fimbriae, CS12-like fimbriae); PAI II (α-hemolysin, P fimbriae with III); PAI III (S fimbriae, siderophore system, Tsh-like hemoglobin protease); PAI IV (yersiniabactin system). Many additional smaller DNA insertions compared to K-12 are present (not shown).

Reprinted from reference ( 135 ), with permission.

Citation: Johnson J, Russo T. 2004. Molecular Epidemiology of Extraintestinal Pathogenic , EcoSal Plus 2004; doi:10.1128/ecosalplus.8.6.1.4
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Figure 7

Known or putative open reading frames (ORFs) are grouped according to the following characteristics: blue, functional, known ORFs; green, truncated ORFs with a start codon and a stop codon; gray, as yet unidentified ORFs without homologues on the DNA level. Nonfunctional ORFs (e.g., due to internal stop codons or frameshifts) are indicated by hatched symbols. ORF numbers are indicated below the corresponding ORF symbols. Functional or truncated tRNA-encoding genes are marked in red. Direct repeat (DR) structures flanking PAIs are indicated. Thick black lines below the PAIs represent regions that were detected by PCR. Several PAI-specific PCRs were grouped into PAI regions.

Reprinted from reference ( 135 ), with permission.

Citation: Johnson J, Russo T. 2004. Molecular Epidemiology of Extraintestinal Pathogenic , EcoSal Plus 2004; doi:10.1128/ecosalplus.8.6.1.4
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Figure 8

In vitro binding of isogenic recombinant strains expressing the Ala-62 or Ser-62 FimH variants (from strains NU14 and 536, respectively) to (A) a trimannose substrate (bovine RNAse B), (B) human collagen type IV, and (C) a monomannose substrate (yeast mannan). Both variants bind equally well to trimannose, but the Ala-62 variant exhibits stronger type IV collagen and monomannose binding than does the Ser-62 variant. (Commensal-associated FimH variants exhibit equally strong trimannose binding but minimal binding to type IV collagen or monomannose [not shown].) Open columns, bacteria incubated without α-methyl mannoside (αmM); solid columns, bacteria incubated with 50 mM αmM. Data are mean + SEM ( = 4) of number of bacteria bound per well.

Reprinted from reference ( 55 ), with permission.

Citation: Johnson J, Russo T. 2004. Molecular Epidemiology of Extraintestinal Pathogenic , EcoSal Plus 2004; doi:10.1128/ecosalplus.8.6.1.4
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Figure 9

(A) PFGE profiles. Lane numbers are shown below gel images. Lanes 1 through 10, profiles of nine of the unique strains, with strain designations shown above gel lanes, plus subtype 1″ (lane 9). Lanes 11 through 16, profiles of independent isolates of strain 1, as recovered from various anatomical sites from the woman (lanes 11–13), man (lanes 14 and 15), and cat (lane 16). (B) Distribution of 14 unique strains over time (week of sampling shown below grid), as recovered from various anatomical sites from the three household members. Female symbol, woman; male symbol, man; NG, no growth; •, no sample. Strains isolated more than once appear in colored boxes, with a unique color for each strain. Strains isolated only once appear in colorless boxes. Week 12, which coincided with symptoms of acute UTI in the woman, yielded strain 1 from the woman's urine specimen (boldface box). There is no strain 7.

Reprinted from reference ( 233 ), with permission.

Citation: Johnson J, Russo T. 2004. Molecular Epidemiology of Extraintestinal Pathogenic , EcoSal Plus 2004; doi:10.1128/ecosalplus.8.6.1.4
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Tables

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Table 1

Virulence-associated traits of ExPEC, by functional category

Citation: Johnson J, Russo T. 2004. Molecular Epidemiology of Extraintestinal Pathogenic , EcoSal Plus 2004; doi:10.1128/ecosalplus.8.6.1.4

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