About Escherichia

General information:
E. coli strains that cause human diarrhea of varying severity have been divided into six major categories: enterotoxigenic E. coli (ETEC), enteroinvasive E. coli (EIEC), enteropathogenic E. coli (EPEC), enterohemorrhagic E. coli (EHEC), enteroaggregative E. coli (EAEC), and diffusely adherent E. coli (DAEC).
Urinary tract infections (UTIs) are the most common extraintestinal E.coli infections and are caused by uropathogenic E.coli (UPEC). In addition, E. coli is the most common Gram-negative bacterium that causes meningitis, particularly during the neonatal period. The pathotype responsible for meningitis and sepsis is called neonatal meningitis-associated E.coli (NMEC).
Pathogenic E. coli cause various diseases in humans, including several types of diarrhea, urinary tract infections, sepsis, and meningitis.
Selected genomes:comparative pathogenomics
E. coli ED1a, 5209548 bp, NC_011745
E. coli SMS-3-5, 5068389 bp, NC_010498
E. coli str. K-12 substr. MG1655, 4639675 bp, NC_000913
AIEC O83:H1 str. LF82, 4773108 bp, NC_011993
AIEC O83:H1 str. NRG 857C, 4747819 bp, NC_017634
AIEC UM146, 4993013 bp, NC_017632
APEC APEC O1, 5082025 bp, NC_008563
APEC O78:H18 str. WS3294A, 4798435 bp, NC_020163
EAEC 55989, 5154862 bp, NC_011748
EAEC O44:H18 042, 5241977 bp, NC_017626
EHEC O103:H2 str. 12009, 5449314 bp, NC_013353
EHEC O111:H- str. 11128, 5371077 bp, NC_013364
EHEC O157:H7 str. EC4115, 5572075 bp, NC_011353
EHEC O157:H7 str. EDL933, 5528445 bp, NC_002655
EHEC O157:H7 str. Sakai, 5498450 bp, NC_002695
EHEC O157:H7 str. TW14359, 5528136 bp, NC_013008
EHEC O157:H7 str. Xuzhou21, 5386223 bp, NC_017906
EHEC O26:H11 str. 11368, 5697240 bp, NC_013361
EPEC O127:H6 str. E2348/69, 4965553 bp, NC_011601
EPEC O55:H7 str. CB9615, 5386352 bp, NC_013941
EPEC O55:H7 str. RM12579, 5263980 bp, NC_017656
ETEC E24377A, 4979619 bp, NC_009801
ETEC O78:H11:K80 str. H10407, 5153435 bp, NC_017633
ETEC UMNK88, 5186416 bp, NC_017641
NMEC O18:K1:H7 str. IHE3034, 5108383 bp, NC_017628
NMEC O45:K1:H7 str. S88, 5032268 bp, NC_011742
NMEC O7:K1 str. CE10, 5313531 bp, NC_017646
StxEAEC O104:H4 str. 2009EL-2050, 5253138 bp, NC_018650
StxEAEC O104:H4 str. 2009EL-2071, 5312586 bp, NC_018661
StxEAEC O104:H4 str. 2011C-3493, 5273097 bp, NC_018658
UPEC 536, 4938920 bp, NC_008253
UPEC ABU 83972, 5131397 bp, NC_017631
UPEC CFT073, 5231428 bp, NC_004431
UPEC NA114, 4971461 bp, NC_017644
UPEC O17:K52:H18 str. UMN026, 5202090 bp, NC_011751
UPEC O25b:H4-ST131, 5109767 bp, NZ_HG941718
UPEC O7:K1 str. IAI39, 5132068 bp, NC_011750
UPEC UTI89, 5065741 bp, NC_007946
UPEC VR50, 5000386 bp, NZ_CP011134
UPEC str. clone D i2, 5038386 bp, NC_017651
E. coli ColA, 6720 bp, NC_001373
E. coli SMS-3-5 pSMS35_8, 8909 bp, NC_010485
E. coli pCol-let, 5847 bp, AF197335
AIEC O83:H1 str. NRG 857C pO83_CORR, 147060 bp, NC_017659
AIEC UM146 plamsid pUM146, 114550 bp, NC_017630
APEC APEC O1 pAPEC-O1-ColBM, 174241 bp, NC_009837
EAEC 55989 55989p, 72482 bp, NC_011752
EAEC O44:H18 042 pAA, 113346 bp, NC_017627
EHEC O103:H2 str. 12009 pO103, 75546 bp, NC_013354
EHEC O157:H- str. 3072/96 pSFO157, 121239 bp, NC_009602
EHEC O157:H7 str. EC4115 pO157, 94644 bp, NC_011350
EHEC O157:H7 str. EDL933 pO157, 92077 bp, NC_007414
EHEC O157:H7 str. Sakai pO157, 92721 bp, NC_002128
EHEC O157:H7 str. TW14359 pO157, 94601 bp, NC_013010
EHEC O157:H7 str. Xuzhou21 pO157, 92728 bp, NC_017907
EHEC O26:H11 str. 11368 pO26_1, 85167 bp, NC_013369
EPEC B171 pB171, 68817 bp, AB024946
EPEC O127:H6 str. E2348/69 pMAR2, 97978 bp, NC_011603
EPEC O55:H7 str. CB9615 pO55, 66001 bp, NC_013942
EPEC O55:H7 str. RM12579 p12579_2, 66078 bp, NC_017657
ETEC E24377A pETEC_74, 74224 bp, NC_009790
ETEC E24377A pETEC_80, 79237 bp, NC_009786
ETEC O78:H11:K80 str. H10407 p666, 66681 bp, NC_017722
ETEC O78:H11:K80 str. H10407 p948, 94797 bp, NC_017724
ETEC O78:H11:K80 str. H10407 pEntH10407, 67094 bp, NC_013507
ETEC SE11 pSE11-3, 60555 bp, NC_011416
ETEC UMNK88 pUMNK88_Ent, 81475 bp, NC_017640
ETEC UMNK88 pUMNK88_Hly, 65549 bp, NC_017643
ETEC UMNK88 pUMNK88_K88, 81883 bp, NC_017639
NMEC O45:K1:H7 str. S88 pECOS88, 133853 bp, NC_011747
STEC O113:H21 str. EH41 pO113, 165548 bp, NC_007365
StxEAEC O104:H4 str. 2009EL-2050 pAA-09EL50, 74213 bp, NC_018654
StxEAEC O104:H4 str. 2009EL-2071 pAA-09EL71, 75573 bp, NC_018662
StxEAEC O104:H4 str. 2011C-3493 pAA-EA11, 74217 bp, NC_018666
UPEC UTI89 pUTI89, 114230 bp, NC_007941
UPEC VR50 pVR50B, 97864 bp, NZ_CP011136
Related publications:
Blattner FR, et al., 1997. The complete genome sequence of Escherichia coli K-12. Science 277(5331):1453-1474.
Makino K, et al., 1998. Complete nucleotide sequences of 93-kb and 3.3-kb plasmids of an enterohemorrhagic Escherichia coli O157:H7 derived from Sakai outbreak. DNA Res 5(1):1-9.
Burland V, et al., 1998. The complete DNA sequence and analysis of the large virulence plasmid of Escherichia coli O157:H7. Nucleic Acids Res. 26(18):4196-4204.
Tobe T, et al., 1999. Complete DNA sequence and structural analysis of the enteropathogenic Escherichia coli adherence factor plasmid. Infect. Immun. 67(10):5455-5462.
Perna NT, et al., 2001. Genome sequence of enterohaemorrhagic Escherichia coli O157:H7. Nature. 409(6819):529-533.
Hayashi T, et al., 2001. Complete genome sequence of enterohemorrhagic Escherichia coli O157:H7 and genomic comparison with a laboratory strain K-12. DNA Res. 8(1):11-22.
Welch RA, et al., 2002. Extensive mosaic structure revealed by the complete genome sequence of uropathogenic Escherichia coli Proc. Natl. Acad. Sci. USA. 99(26):17020-17024.
Chen SL, et al., 2006. Identification of genes subject to positive selection in uropathogenic strains of Escherichia coli: a comparative genomics approach. Proc Natl Acad Sci USA 103(15):5977-5982.
Johnson TJ, et al., 2006. Complete DNA sequence of a ColBM plasmid from avian pathogenic Escherichia coli suggests that it evolved from closely related ColV virulence plasmids. J Bacteriol 188(16):5975-5983.
Brzuszkiewicz E, et al., 2006. How to become a uropathogen: comparative genomic analysis of extraintestinal pathogenic Escherichia coli strains. Proc. Natl. Acad. Sci. USA. 103(34):12879-12884.
Johnson TJ, et al., 2007. The genome sequence of avian pathogenic Escherichia coli strain O1:K1:H7 shares strong similarities with human extraintestinal pathogenic E. coli genomes. J Bacteriol 189(8):3228-3236.
Rasko DA, et al., 2008. The pangenome structure of Escherichia coli: comparative genomic analysis of E. coli commensal and pathogenic isolates. J Bacteriol 190(20):6881-93.
Fricke WF, et al., 2008. Insights into the environmental resistance gene pool from the genome sequence of the multidrug-resistant environmental isolate Escherichia coli SMS-3-5. J Bacteriol 190(20):6779-94.
Iguchi A, et al., 2009. Complete genome sequence and comparative genome analysis of enteropathogenic Escherichia coli O127:H6 strain E2348/69. J Bacteriol 191(1):347-54.
Touchon M, et al., 2009. Organised genome dynamics in the Escherichia coli species results in highly diverse adaptive paths. PLoS Genet 5(1):e1000344.
Peigne C, et al., 2009. 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 77(6):2272-84.
Kulasekara BR, et al., 2009. Analysis of the genome of the Escherichia coli O157:H7 2006 spinach-associated outbreak isolate indicates candidate genes that may enhance virulence. Infect Immun 77(9):3713-21.
Ogura Y, et al., 2009. Comparative genomics reveal the mechanism of the parallel evolution of O157 and non-O157 enterohemorrhagic Escherichia coli. Proc Natl Acad Sci U S A 106(42):17939-44.
Zhou Z, et al., 2010. Derivation of Escherichia coli O157:H7 from its O55:H7 precursor. PLoS One 5(1):e8700.
Chaudhuri RR, et al., 2010. Complete genome sequence and comparative metabolic profiling of the prototypical enteroaggregative Escherichia coli strain 042. PLoS One 5(1):e8801.
Moriel DG, et al., 2010. Identification of protective and broadly conserved vaccine antigens from the genome of extraintestinal pathogenic Escherichia coli. Proc Natl Acad Sci U S A 107(20):9072-7.
Crossman LC, et al., 2010. A commensal gone bad: complete genome sequence of the prototypical enterotoxigenic Escherichia coli strain H10407. J Bacteriol 192(21):5822-31.
Zdziarski J, et al., 2010. Host imprints on bacterial genomes--rapid, divergent evolution in individual patients. PLoS Pathog 6(8):e1001078.
Krause DO, et al., 2011. Complete genome sequence of adherent invasive Escherichia coli UM146 isolated from Ileal Crohn's disease biopsy tissue. J Bacteriol 193(2):583.
Nash JH, et al., 2010. Genome sequence of adherent-invasive Escherichia coli and comparative genomic analysis with other E. coli pathotypes. BMC Genomics 11:667.
Avasthi TS, et al., 2011. Genome of multidrug-resistant uropathogenic Escherichia coli strain NA114 from India. J Bacteriol 193(16):4272-3.
Reeves PR, et al., 2011. Rates of mutation and host transmission for an Escherichia coli clone over 3 years. PLoS One 6(10):e26907.
Shepard SM, et al., 2012. Genome sequences and phylogenetic analysis of K88- and F18-positive porcine enterotoxigenic Escherichia coli. J Bacteriol 194(2):395-405.
Lu S, et al., 2011. Complete genome sequence of the neonatal-meningitis-associated Escherichia coli strain CE10. J Bacteriol 193(24):7005.
Eppinger M, et al., 2011. Genomic anatomy of Escherichia coli O157:H7 outbreaks. Proc Natl Acad Sci U S A 108(50):20142-7.
Kyle JL, et al., 2012. Escherichia coli serotype O55:H7 diversity supports parallel acquisition of bacteriophage at Shiga toxin phage insertion sites during evolution of the O157:H7 lineage. J Bacteriol 194(8):1885-96.
Xiong Y, et al., 2012. A novel Escherichia coli O157:H7 clone causing a major hemolytic uremic syndrome outbreak in China. PLoS One 7(4):e36144.
Ahmed SA, et al., 2012. Genomic comparison of Escherichia coli O104:H4 isolates from 2009 and 2011 reveals plasmid, and prophage heterogeneity, including shiga toxin encoding phage stx2. PLoS One 7(11):e48228.
Forde BM, et al., 2014. The complete genome sequence of Escherichia coli EC958: a high quality reference sequence for the globally disseminated multidrug resistant E. coli O25b:H4-ST131 clone. PLoS One 9(8):e104400.
Beatson SA, et al., 2015. Molecular analysis of asymptomatic bacteriuria Escherichia coli strain VR50 reveals adaptation to the urinary tract by gene acquisition. Infect Immun 83(5):1749-64.

Defined by the presence of a characteristic, diffuse pattern of adherence to HEp-2 cell monolayers.
Two subclasses of DAEC strains: diffusely adhering enteropathogenic E. coli (DA-EPEC) harbouring a LEE island and DAECs expressing adhesins of Afa/Dr family.
Pathogenic schema of DAEC

Major virulence factors in DAEC:
Afa/Dr family

Do not secrete the enterotoxigenic E. coli heat-liable or heat-stable enterotoxins and which adhere to HEp-2 cells in an aggregative (AA) pattern.
The AA pattern is recognized by the distinctive 'stacked brick' autoagglutination of the bacteria either on the surface of the HEp-2 cells or on the glass substratum.
EAEC strains are heterogeneous but the majority harbor a member of conserved family of virulence plasmids.
Pathogenic schema of EAEC

Major virulence factors in EAEC:
AAFs (Aggregative adherence fimbriae)
Effector delivery system
Pet (Plasmid-encoded enterotoxin)
EAST1 (EAEC heat-stable enterotoxin 1)
Dispersin (Anti-aggregation protein)

Genomic location of virulence-related genes in EAEC:

Have a locus for enterocyte effacement (LEE).
The ability to produce Shiga toxins.
Major virulence factors in EHEC:
ECP (E. coli common pilus)
Paa (Porcine attaching-effacing associated protein)
Effector delivery system
Efa-1/LifA (EHEC factor for adherence/lymphocyte inhibitory factor)
TTSS (Type III secretion system)
TTSS secreted effectors
Stx (Shiga toxin)
StcE (Secreted protease of C1 esterase inhibitor from EHEC)
Nutritional/Metabolic factor
Chu (E. coli heme uptake)
Ler (LEE encoded regulator)

Genomic location of virulence-related genes in EHEC:

Most of the pathogenic E.coli strains remain extracellular, but EIEC is an intracellular pathogen.
The virulence factors in EIEC are virually identical to those in Shigella species.
Dysentery caused by EIEC is clinically indistinguishable from that caused by members of the Shigella species.
EIEC possesses the biochemical profile of E. coli, yet with the genotypic or phenotypic characteristics of Shigella spp..
EIEC contains large plasmids that are functionally interchangeable and share significant degrees of DNA homology with the plasmid described in S. flexneri.
An important aspect of Shigella pathogenesis is the extremely low ID50. The ID50 for S. flexneri, S. sonnei, and S. dysenteriae is approximately 5000 organisms. In contrast, at least 108 EIEC must be ingested to produce disease. The reason for the significantly higher infectious dose for EIEC is unknown.
Major virulence factors in EIEC:
(Please see Shigella.)

Producing a histopathology on the intestinal epithelium known as the attaching and effacing (A/E) lesion.
Inability to produce Shiga toxins.
Typical EPEC strains carry a large virulence plasmid (the EPEC adhesion factor (EAF) plasmid) that allows them to produce bundle-forming pili and attach to epithelial cells in a characteristic pattern termed localized adherence (LA), denoting the presence of clusters or microcolonies on the surface of host cells. The LA pattern is characteristic only of EPEC strains of E. coli and therefore has been used widely as a diagnostic tool.
Pathogenic schema of EPEC

Major virulence factors in EPEC:
BFP (Bundle-forming Pili)
Paa (Porcine attaching-effacing associated protein)
Effector delivery system
TTSS (Type III secretion system)
TTSS secreted effectors
CDT (Cytolethal distending toxin)
Ler (LEE encoded regulator)
Per (Plasmid-encoded regulator)

Genomic location of virulence-related genes in EPEC:

Distinguished from other E. coli pathotypes their by production of enterotoxins LT (heat-labile enterotoxin) and ST (heat-stable enterotoxin). ETEC strains might express only an LT, only an ST, or both LTs and STs.
Pruducing one or more colonization factors (CFs) that mediate attachment to intestinal mucosal surfaces, a central step in ETEC virulence.
Pathogenic schema of ETEC

Major virulence factors in ETEC:
Adhesive fimbriae
Heat-labile toxin (LT)
Heat-stable toxin (ST)

Genomic location of virulence-related genes in ETEC:

E. coli strains possessing the K1 capsular polysaccharide are predominant (approximately 80%) among isolates from neonatal E. coli meningitis and that most of these K1 isolates are associated with a limited number of O types (e.g., O-18, O-7, O-1).
A natural route of infection (e.g., oral), gut colonization and translocation, dissemination to deeper tissues, and a level of bacteremia necessary prior to penetration of the blood-brain barrier.
E. coli K1 invades brain microvascular endothelial cells (BMECs) via a zipper mechanism and transmigrates through BMECs in an enclosed vacuole without intracellular multiplication.
Major virulence factors in NMEC:
FdeC (Factor adherence E. coli)
S fimbriae
Ibes (Invasion of brain endothelial cells)
K1 capsule
OmpA (Outer membrane protein A)
CNF-1 (Cytotoxic necrotizing factor 1)

Genomic location of virulence-related genes in NMEC:

A subgroup of extraintestinal pathogenic E. coli (ExPEC).
Typically carry large blocks of genes, called pathogenicity islands, not found in fecal isolates.
UPEC can invade and replicate within uroepithelial cells.
Major virulence factors in UPEC:
Curli fibers
Dr adhesins
F1C fimbriae
P fimbriae
S fimbriae
Type 1 fimbriae
Effector delivery system
Sat (Secreted autotransporter toxin)
Tsh (Temperature sensitive hemagglutinin)
CNF-1 (Cytotoxic necrotizing factor 1)
Immune modulation
TcpC (TIR domain containing protein)
Nutritional/Metabolic factor
Chu (E. coli heme uptake)
Salmochelin siderophore

Genomic location of virulence-related genes in UPEC:

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