Serotypes of Escherichia coli isolated from septicaemic chickens in Galicia (Northwest Spain)

Blanco, Jesús E.; Blanco, Miguel; Mora, Azucena; Jansen, Wim; Garcı́a, Vidal; Vázquez, María L. Gariboglio; Blanco, Jorge

doi:10.1016/s0378-1135(98)00182-5

Cited by 87 publications

(57 citation statements)

References 16 publications

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“…Consequently, representative strains from these serotypes provide the focus for unravelling APEC virulence mechanisms and for the development and evaluation of vaccine candidates. These predominant serogroups can also be recovered from faeces of apparently healthy birds (Blanco et al, 1998), reinforcing the notion that the intestinal tract may be an important natural reservoir for APEC and that predisposing factors may be required to produce disease. Significantly, several studies have reported shared characteristics including serogroups between commensal E. coli and APEC (Heller & Drabkin, 1977;Blanco et al, 1998;McPeake et al, 2005;Rodriguez-Siek et al, 2005a), implying that APEC could arise from commensal E. coli following acquisition of pathogenic traits.…”

Section: The Apec Pathotypesupporting

confidence: 57%

“…There are numerous other predisposing factors associated with APEC infections (Barnes & Gross, 1997), and these have led to the notion that this disease could result from opportunistic infection, thus underestimating the virulence of APEC. Consistent with this belief, many serotypes of E. coli including those believed to be harmlessly carried in the intestinal tract have been recovered from diseased birds (Blanco et al, 1998;McPeake et al, 2005;RodriguezSiek et al, 2005a). Indeed, earlier workers regarded systemic E. coli infection as an indicator of physiological stress in chickens (Kendler & Harry, 1967).…”

Section: Introductionmentioning

confidence: 84%

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Colibacillosis in poultry: unravelling the molecular basis of virulence of avian pathogenicEscherichia coliin their natural hosts

Dziva¹,

Stevens²

2008

Avian Pathology

303

222

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Avian colibacillosis is caused by a group of pathogens designated avian pathogenic Escherichia coli (APEC). Despite being known for over a century, avian colibacillosis remains one of the major endemic diseases afflicting the poultry industry worldwide. Autologous bacterins provide limited serotype-specific protection, yet multiple serogroups are associated with disease, especially O1, O2 and O78 among many others. Experimental infection models have facilitated the identification of some key APEC virulence genes and have allowed testing of vaccine candidates. Well-recognized virulence factors include Type 1 (F1) and P (Pap/ Prs) fimbriae for colonization, IbeA for invasion, iron acquisition systems, TraT and Iss for serum survival, K and O antigens for anti-phagocytic activity, and a temperature-sensitive haemagglutinin of imprecise function. Intriguingly, these factors do not occur universally among APEC, suggesting the presence of multiple alternative mechanisms mediating pathogenicity. The recent availability of the first complete APEC genome sequence can be expected to accelerate the identification of bacterial genes expressed during infection and required for virulence. High-throughput molecular approaches like signature-tagged transposon mutagenesis have already proved invaluable in revealing portfolios of genes expressed by pathogenic bacteria during infection, and this has enabled identification of APEC O2 factors required for septicaemia in the chicken model. Complimentary approaches, such as in vivo-induced antigen technology, exist to define the activities of APEC in vivo. In recent years, reverse vaccinology and immuno-proteomic approaches have also enabled identification of novel vaccine candidates in other bacterial pathogens. Collectively, such information provides the basis for the development or improvement of strategies to control APEC infections in the food-producing avian species.

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Section: The Apec Pathotypesupporting

confidence: 57%

Section: Introductionmentioning

confidence: 84%

Colibacillosis in poultry: unravelling the molecular basis of virulence of avian pathogenicEscherichia coliin their natural hosts

Dziva¹,

Stevens²

2008

Avian Pathology

303

222

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“…Ampicillin (100 mg ml 21 ), kanamycin (25 mg ml 21 ), nalidixic acid (30 mg ml 21 ) and tetracycline (10 mg ml 21 ) were used when required. The determination of O serogroups was carried out as previously described employing all available O (O1-O181) antisera (Blanco et al, 1998). All antisera were obtained and absorbed with the corresponding cross-reacting antigens to remove non-specific agglutinins.…”

Section: Methodsmentioning

confidence: 99%

ibeA, a virulence factor of avian pathogenic Escherichia coli

et al. 2005

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The presence of ibeA, a gene encoding a known virulence factor of Escherichia coli strains responsible for neonatal meningitis in humans, was investigated in the genome of 213 avian pathogenic E. coli (APEC) strains and 55 non-pathogenic E. coli strains of avian origin. Fifty-three strains were found to be ibeA + , all of which belonged to the APEC group. The ibeA gene is therefore positively linked to the pathogenicity of strains (P<0?0001). Analysis of the serogroup of strains revealed a positive association of ibeA with serogroups O18, O88 and O2. On the contrary, only 1/59 O78 strains are ibeA + , indicating a negative association of ibeA with this serogroup (P<0?0001). The role of ibeA in the virulence of the APEC strain BEN 2908 was investigated by constructing an ibeA mutant. Challenge assays on 3-week-old chickens showed a reduced virulence for the ibeA mutant. Furthermore, the APEC strain BEN 2908 was able to invade brain microvascular epithelial cells, this invasion being significantly reduced upon inactivation of ibeA. Altogether, these results suggest a role of ibeA in the pathogenicity of some APEC strains and confirm the close relationship between APEC and other human extraintestinal pathogenic E. coli isolates.

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“…APEC are restricted to a few important O-serogroups, with 15-61% of the total number of isolates belonging to serogroups O1, O2 and O78, but their specific virulence factors have not been completely identified (Babai et al, 1997;Blanco et al, 1998). The colonisation of the respiratory tract is most probably mediated by adhesins, such as the P fimbriae which are more frequently expressed by septicaemic APEC than by E. coli isolated from healthy chickens (Dozois et al, 1992).…”

Section: Introductionmentioning

confidence: 99%

Examination of Escherichia coli from poultry for selected adhesin genes important in disease caused by mammalian pathogenic E. coli

Stordeur

Marlier

Blanco

et al. 2002

Veterinary Microbiology

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A collection of 1601 extraintestinal and intestinal Escherichia coli isolated from chickens, turkeys and ducks, in Belgium, France and Spain, was hybridised with gene probes specific for fimbrial and afimbrial adhesins (F17, F18, S hSfa/F1Ci, Bfp, Afa, Cs31A, Intimin hEaei, Aida-1) of intestinal, urinary and invasive E. coli of mammals and with a probe specific for the P (Pap/Prs) fimbrial adhesin of urinary and invasive E. coli of mammals and birds. Three hundred and eightythree strains (23.9%) were P-positive, 76 strains (4.8%) were Afa-positive, 75 strains (4.7%) were F17-positive, 67 strains (4.2%) were S-positive, 23 (1.4%) were Intimin-positive, and all were F18-, Cs31A-, Aida1-and Bfp-negative. The 75 F17-positive strains harboured different major subunit A-encoding gene variants, but the f17Ac variant was the most frequent (52 strains, 69.3%) and seven strains (9.3%) were not typeable. The f17G gene variant coding for the GII adhesin was the most frequent (56 strains, 75.0%), whereas the f17GI gene variant was present in four strains (5%) and 15 strains (20.0%) were not typeable. All Afa-positive strains harboured the afa-8 variant. The 23 Intimin-positive E. coli tested positive for the b-variant (16 strains; 69.6%) or for the g-variant (seven strains; 30.4%) of the eae gene. Chicken and turkey E. coli were more frequently probe-positive (43.6 and 43.1%, respectively) than duck E. coli (31.5%) and extraintestinal E. coli were also more frequently probe-positive (48.4%) than intestinal strains (18.5%). Different combinations of probe positive hybridisation results were observed in 72 of the 540 probe-positive E. coli (13.3%). The most frequent combinations were between AfaE-8 and F17 probes (47 strains; 8.7%) and between P and S probes (13 strains; 2.4%). Although f17-and afa-8-related DNA sequences can be plasmid-located in mammalian E. coli, they were not in avian E. coli. Besides the P fimbrial adhesins, F17 and S fimbrial and Afa-VIII and Intimin afimbrial adhesins may thus represent colonisation factors of avian pathogenic E. coli. #

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Serotypes of Escherichia coli isolated from septicaemic chickens in Galicia (Northwest Spain)

Cited by 87 publications

References 16 publications

Colibacillosis in poultry: unravelling the molecular basis of virulence of avian pathogenicEscherichia coliin their natural hosts

Colibacillosis in poultry: unravelling the molecular basis of virulence of avian pathogenicEscherichia coliin their natural hosts

ibeA, a virulence factor of avian pathogenic Escherichia coli

Examination of Escherichia coli from poultry for selected adhesin genes important in disease caused by mammalian pathogenic E. coli

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