Escherichia coli Serotypes Isolated from Salpingitis and Chronic Respiratory Disease of Poultry

Glantz, Paul J.; Narotsky, Saul.; Bubash, G. R.

doi:10.2307/1587902

Cited by 31 publications

(12 citation statements)

References 4 publications

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“…In the other patients (23,27,30) with non-typable strains, the other markers were too dissimilar (Table 4) to warrant preparing further sera. DISCUSSION 0 serotyping has been extensively used in the study of the spread of Escherichia coli in man (Linzenmeier, Freislederer, Apak & Metz, 1961;Linzenmeier, 1962;Ewing, 1962;Turck, Petersdorf & Fournier, 1962;Nejedla, Srajbr & Lanc, 1967; (Sojka & Carnagham, 1961;Glantz, Narotsky & Bubash, 1962;Soderlind, 1965;Gossling & Rhoades, 1966;Hemsley, Barnum & Ingram, 1967;Shooter, Cooke, Rousseau & Breaden, 1970) and the environment (Muller, 1967;Cooke et al 1970). At first only a limited number of 0 antisera were available but nevertheless this initiated these studies.…”

Section: Resultsmentioning

confidence: 99%

Further studies of Escherichia coli in babies after normal delivery

Bettelheim

Teoh-Chan

Chandler

et al. 1974

J. Hyg.

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SUlMMARYPrevious work showed that on the basis of 0 serotyping alone of Escherichia coli, the majority of babies acquired the same 0 serotype as was found in the stools of their respective mothers. Further characterization of the E. coli by H serotyping, determination of their antibiotic resistance and ability to ferment six carbohydrates showed that in the majority of cases the previous results were confirmed. In a minority of cases this further testing showed that the strains were not identical. In some instances a number of strains isolated from the same pair showed different combinations of the markers used.

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Section: Resultsmentioning

confidence: 99%

Further studies of Escherichia coli in babies after normal delivery

Bettelheim

Teoh-Chan

Chandler

et al. 1974

J. Hyg.

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“…Sometimes E. coli is the primary cause of disease, particularly in young birds (Cheville & Arp, 1978), but also in adults (Dhillon & Jack, 1996). Many serotypes of E. coli have been isolated throughout the world (Sojka & Carnaghan, 1961;Glanz et al, 1962;Hemsley et al, 1967;Rosenberger & Chand, 1981;Cloud et al, 1985).…”

Section: Introductionmentioning

confidence: 99%

SevereEscherichia coliO111 septicaemia and polyserositis in hens at the start of lay

et al. 2000

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Three very severe episodes of Escherichia coli infection in hens from the same farm, at the beginning of laying, are reported. They were characterized by no clinical signs, but sudden mortality, from 5 to 10%, with severe lesions of septicaemia and fibrinous polyserositis. A Gram-negative bacterium was consistently isolated in pure culture from tissues. Isolates were typed biochemically as E. coli, but they were lactose negative and non-motile. The serotyping tests typed the isolates as somatic group O111. The isolates were sensitive to enrofloxacin, amoxycil and colimycin, and partially sensitive to flumequine, all of which were used for therapy. The disease was reproduced experimentally in both specific pathogen free chickens and commercial layers by intramuscular inoculation of the E. coli, but only in some layers when inoculated by the oro-nasal route. The stress of the onset of lay seemed to be the most probable precipitating cause of the disease.

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“…While most strains are commensal, certain strains designated avian pathogenic E. coli (APEC) have the ability to cause severe disease. Predominant serotypes of APEC are O1:K1, O2:K1, and O78:K80 (7,13,18,26). APECs most likely enter and colonize the avian respiratory tract by inhalation of fecal dust, leading to localized infections such as airsacculitis and pneumonia.…”

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Identification of Genes Required for Avian Escherichia coli Septicemia by Signature-Tagged Mutagenesis

et al. 2005

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Infections with avian pathogenic Escherichia coli (APEC) cause colibacillosis, an acute and largely systemic disease resulting in significant economic losses in poultry industry worldwide. Although various virulenceassociated genes have been identified in APEC, their actual role in pathogenesis is still not fully understood, and, furthermore, certain steps of the infection process have not been related to previously identified factors. Here we describe the application of a signature-tagged transposon mutagenesis (STM) approach to identify critical genes required for APEC infections in vivo. Twenty pools of about 1,800 IMT5155 (O2:H5) mutants were screened in an infection model using 5-week-old chickens, and potentially attenuated mutants were subjected to a secondary screen and in vivo competition assays to confirm their attenuation. A total of 28 genes required for E. coli septicemia in chickens were identified as candidates for further characterization. Among these disrupted genes, six encode proteins involved in biosynthesis of extracellular polysaccharides and lipopolysaccharides; two encode iron transporters that have not been previously characterized in APEC in in vivo studies, and four showed similarity to membrane or periplasmic proteins. In addition, several metabolic enzymes, putative proteins with unknown function, and open reading frames with no similarity to other database entries were identified. This genome-wide analysis has identified both novel and previously known factors potentially involved in pathogenesis of APEC infection.Escherichia coli typically colonizes the avian gastrointestinal tract and other mucosal surfaces. While most strains are commensal, certain strains designated avian pathogenic E. coli (APEC) have the ability to cause severe disease. Predominant serotypes of APEC are O1:K1, O2:K1, and O78:K80 (7,13,18,26). APECs most likely enter and colonize the avian respiratory tract by inhalation of fecal dust, leading to localized infections such as airsacculitis and pneumonia. In certain cases, they spread into various internal organs and typically cause pericarditis, perihepatitis, peritonitis, salpingitis, and other extraintestinal diseases. Colibacillosis of poultry is characterized in its acute form by septicemia, commonly resulting in sudden death (6).Several bacterial factors have been associated with the virulence of APEC, including adhesins, toxins, iron acquisition systems, colicin V plasmid, serum resistance proteins, and capsule as well as lipopolysaccharide complexes (15,21,37). However, the mechanisms underlying pathogenicity are still not fully understood, and only certain steps of the infection process can be accounted for by these known virulence factors. In recent years, genome-wide analyses have led to a better understanding of the molecular mechanisms of pathogenicity. New molecular approaches have also aided in the identification of genes involved in pathogenesis, including in vivo expression technology, selective capture of transcribed sequences (SCOTS), different...

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Escherichia coli Serotypes Isolated from Salpingitis and Chronic Respiratory Disease of Poultry

Cited by 31 publications

References 4 publications

Further studies of Escherichia coli in babies after normal delivery

Further studies of Escherichia coli in babies after normal delivery

SevereEscherichia coliO111 septicaemia and polyserositis in hens at the start of lay

Identification of Genes Required for Avian Escherichia coli Septicemia by Signature-Tagged Mutagenesis

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