The Development of "Air Sac Disease"

Gross, W. B.

doi:10.2307/1587774

Cited by 93 publications

(44 citation statements)

References 6 publications

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“…Early work established the respiratory tract to be a significant route of entry into the host (Gross, 1961), whilst the intestinal tract has been reported to be a reservoir for both pathogenic and non-pathogenic strains (Harry & Hemsley, 1965). Colonization of multiple internal organs occurs in birds that survive initial septicaemia.…”

Section: Progress Towards Unravelling Apec Virulence Factorsmentioning

confidence: 99%

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

Dziva¹,

Stevens²

2008

Avian Pathology

305

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: Progress Towards Unravelling Apec Virulence Factorsmentioning

confidence: 99%

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

Dziva¹,

Stevens²

2008

Avian Pathology

305

222

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“…These strains are designated avian pathogenic E. coli (APEC) (Dho-Moulin & Fairbrother 1999) and the diseases they cause are mainly septicemia, swollen head syndrome, omphalitis, cellulitis, yolk-sac infection and respiratory tract infections (Sojka & Carnaghan 1961, Morley & Thomson 1984, Randall et al 1984. It has been proposed that some of the above mentioned diseases such as septicemia and swollen head syndrome start as secondary infections triggered by an initial Mycoplasma or viral infection followed by an invasive phase (Gross 1961, Aycard & Lafont 1969, Dho & Lafont 1982, Morley & Thomson 1984). Omphalitis appears to be initiated by the bacterium actively crossing the egg barriers during the laying process or during incubation (Gross 1994) and in this case such types of bacteria would act just as opportunistic agents (Silveira et al 2002a).…”

Section: Introduction Introduction Introduction Introduction Introducmentioning

confidence: 99%

Typing of avian pathogenic Escherichia coli strains by REP-PCR

et al. 2006

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In the present study the repetitive extragenic palindromic (REP) polymerase chain reaction (PCR) technique was used to establish the clonal variability of 49 avian Escherichia coli (APEC) strains isolated from different outbreak cases of septicemia (n=24), swollen head syndrome (n=14) and omphalitis (n=11). Thirty commensal strains isolated from poultry with no signs of these illnesses were used as control strains. The purified DNA of these strains produced electrophoretic profiles ranging from 0 to 15 bands with molecular sizes varying from 100 bp to 6.1 kb, allowing the grouping of the 79 strains into a dendrogram containing 49 REP-types. Although REP-PCR showed good discriminating power it was not able to group the strains either into specific pathogenic classes or to differentiate between pathogenic and non-pathogenic strains. On the contrary, we recently demonstrated that other techniques such as ERIC-PCR and isoenzyme profiles are appropriate to discriminate between commensal and APEC strains and also to group these strains into specific pathogenic classes. In conclusion, REP-PCR seems to be a technique neither efficient nor universal for APEC strains discrimination. However, the population clonal structure obtained with the use of REP-PCR must not be ignored particularly if one takes into account that the APEC pathogenic mechanisms are not completely understood yet.

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“…In our experiment, only two infectious agents were used and it is possible that, with a third agent such as pathogenic strains of E. coli, Mim could produce more severe disease in the manner that has been suggested for Mg (Gross, 1961(Gross, , 1962Nakamura et al, 1994). There have also been reports that Mg may cause disease in chickens in circumstances other than mixed infection, such as nutritional de® ciencies (Jordan, 1985a), mechanical trauma to the trachea (Corsvet & Sadler, 1966), excessive dust or ammonia (Sato et al, 1973;Kempf et al, 1988) or even social stress (Freeman, 1976).…”

Section: Discussionmentioning

confidence: 99%

“…For example, Gross (1961) found that chickens inoculated at 1 day old with Mg followed by IBV or NDV or both viruses, at different intervals, showed increased spread and severity of infection. Adler et al (1962) reported that adult chickens infected with Mg followed by IBV at different intervals produced coryza, tracheitis and airsacculitis, whereas no such signs were seen in chickens infected with either agent alone.…”

Section: Serologymentioning

confidence: 99%