Severe<i>Escherichia coli</i>O111 septicaemia and polyserositis in hens at the start of lay

Zanella, A.; Alborali, G. L.; Bardotti, Massimiliano; Candotti, P.; Guadagnini, P. F.; Martino, Piera Anna; Stonfer, M.

doi:10.1080/03079450050118430

Cited by 59 publications

(53 citation statements)

References 11 publications

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“…The factors chosen for this study, included serogroup, since certain groups have been linked to the ability to cause disease [2,42]; the ability to ferment lactose, given that some recent outbreaks have involved lactose-negative strains of E. coli [44]; and the ability to cause hemolysis, since this trait has been linked to virulence in other E. coli pathotypes [27]. Additionally, the occurrence of several genes among these avian E. coli was determined.…”

Section: Introductionmentioning

confidence: 99%

Characterizing the APEC pathotype

et al. 2005

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-The purpose of this study was to compare avian pathogenic Escherichia coli (APEC) isolates to fecal isolates of apparently healthy poultry (avian fecal E. coli or AFEC) by their possession of various traits in order to ascertain whether APEC and AFEC are distinct and if the APEC strains constitute a distinct pathotype. Four hundred and fifty-one APEC and one hundred and four AFEC isolates were examined for possession of traits associated with the virulence of human extraintestinal pathogenic E. coli (ExPEC) as well as APEC. Several of the genes occurred in the majority of APEC and only infrequently in AFEC, including cvaC, iroN, iss, iutA, sitA, tsh, fyuA, irp2, and ompT. Of these genes, several have been found on large plasmids in APEC. Other genes occurred in significantly more APEC than AFEC but did not occur in the majority of APEC. Isolates were also evaluated by serogroup, lactose utilization, and hemolytic reaction. Twenty-nine and a half percent of the APEC and forty-two and three tenths percent of the AFEC were not serogrouped because they were not typeable with standard antisera, typed to multiple serogroups, were rough, autoagglutinated, or were not done. Around 65% of the typeable APEC (205 isolates) and AFEC (41 isolates) were classified into shared serogroups, and about a third of both fell into APEC-(113 isolates) or AFEC-(19 isolates) unique serogroups. Most were able to use lactose. No isolate was hemolytic. Overall, the majority of the APEC isolates surveyed shared a common set of putative virulence genes, many of which have been localized to an APEC plasmid known as pTJ100. This common set of genes may prove useful in defining an APEC pathotype. avian pathogenic Escherichia coli (APEC) / pathotype / virulence plasmid / ExPEC / pTJ100

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Section: Introductionmentioning

confidence: 99%

Characterizing the APEC pathotype

et al. 2005

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“…Traditionally, it was mostly associated with losses in broilers, but in Europe from the mid-1990s onwards it has been increasingly observed in layer hens (Zanella et al, 2000;Vandekerchove et al, 2004a). In our recent field study, we described a distinct syndrome associated with colibacillosis in laying hens, characterized by acute mortality without prior clinical signs of disease and without a significant impact on egg production or quality.…”

Section: Introductionmentioning

confidence: 99%

Risk factors associated with colibacillosis outbreaks in caged layer flocks

Vandekerchove

Herdt²,

Laevens

et al. 2004

Avian Pathology

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Colibacillosis appears to be of increasing significance in layer flocks, but there have been no studies of the risk factors associated with outbreaks. This study aimed to investigate the possible associations between risk factors of non-infectious nature and outbreaks of mortality due to colibacillosis in flocks of caged layer hens. Information on management, biosecurity measures and housing conditions was collected in 20 flocks suffering from the disease and in 20 clinically healthy control flocks. The data were processed using multiple logistic regression. The statistical analysis demonstrated that an increase in the distance to the nearest poultry farm by 1 km was associated with a six-fold decreased risk of an outbreak of colibacillosis (odds ratio/0.16). Furthermore, a 1 l increase in cage volume per hen was associated with a 33% decrease in the risk of an outbreak (odds ratio/0.75). It was concluded that the distance between poultry farms and the hen density in the cages are important risk factors for outbreaks of colibacillosis in flocks of layer hens.

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“…Colibacillosis is a disease of severe economic significance to all poultry producers worldwide and is characterized by a diverse array of lesions. Recent reports in Western Europe implicate a resurgence of this disease in the poultry industry, particularly in chicken layers (Zanella et al, 2000;Vandekerchove et al, 2004;Jordan et al, 2005). Depending on the virulence status of the strain, host status and presence and type of predisposing factors, the infection manifests as an initial septicaemia that is followed by either sudden death or localized inflammation in multiple organs.…”

Section: Introductionmentioning

confidence: 99%

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

Dziva¹,

Stevens²

2008

Avian Pathology

299

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

Cited by 59 publications

References 11 publications

Characterizing the APEC pathotype

Characterizing the APEC pathotype

Risk factors associated with colibacillosis outbreaks in caged layer flocks

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

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