Prevalence of amyloid deposition in mature healthy chickens in the flock that previously had outbreaks of vaccine-associated amyloidosis

Abstract

Avian amyloid A (AA) amyloidosis is commonly observed in adult birds with chronic inflammation, such as that caused by bacterial infection. We previously described vaccine-associated AA amyloidosis in juvenile chickens. In this study, the prevalence of amyloid deposition was measured in mature healthy chickens that survived a previous outbreak of avian AA amyloidosis while they were juveniles. Herein, we analyzed the amyloid deposition in mature chickens and compared the prevalence of amyloid deposition with juvenile chickens obtained in our previous study (Murakami et al., 2013). We found that: 1) amyloid deposition in the liver was absent in mature chickens, while juvenile chickens had a rate of 24%; 2) amyloid deposition in the spleen was observed in 36% of juvenile chickens and in 40% of mature chickens; 3) amyloid deposition in the pectoral muscle of mature chickens (43.75%) was approximately half that of juvenile chickens (88%). These results suggest that additional amyloid deposition in chickens previously exposed to AA amyloidosis may not worsen with age. Further, amyloid deposition in chickens may tend to regress when causative factors, such as vaccinations and/or chronic inflammation, are absent.

Experimental induction of chicken amyloid A amyloidosis in white layer chickens by inoculation with inactivated vaccines

“…Transmission of amyloidosis from animals to humans may be possible as it has been shown previously that AA-amyloidosis can be transmitted orally within and between species (Murakami et al, 2013a(Murakami et al, , 2013b or similar to prion diseases, through a seeding-nucleation process . Transmission of amyloidosis from animals to humans has been a concern in recent years and although it has not yet been confirmed, it should be considered a public health issue (Benditt & Eriksen, 1977;Higuchi, 2013;Murakami et al, 2013a;Murakami et al, 2013b;Ibi et al, 2015). Amyloid fibril deposition was detected in the liver, spleen, duodenum, and at the injection sites as reported previously (Murakami et al, 2013a(Murakami et al, , 2013b.…”

“…In spontaneous outbreaks of AA amyloidosis in flocks, the morbidity rate is between 1 and 4% but may increase to 20% (Landman et al, 1994). Other researchers have reported that the mortality rate in flocks can be up to 2% (Murakami et al, 2013a;Ibi et al, 2015). Bacterial oil-emulsion vaccines have been associated with systemic amyloidosis in chickens, and they are strongly suspected as a cause of outbreaks in flocks but this has not yet been confirmed experimentally (Von Rampin et al, 1989).…”

“…AA amyloidosis can be induced experimentally by repeated inflammatory stimulations such as a mixture of killed malaria parasites and Freund's adjuvant (Thompson et al, 1947), Staphylococcus aureus (Mac-Donald & Carlson, 1969), Mycoplasma synoviae (Maestrini & Pascucci, 1970), Escherichia coli and crude endotoxin (Ling et al, 1991), crude extracts of E. coli and Salmonella Typhimurium (Ling, 1992), Salmonella Pullorum (Wang & Di, 1992), E. faecalis (Landman et al, 1997), methylcholanthrene (Rigdon, 1960), and azo-casein (Druet & Janigan, 1966). Recent research has shown that chickens can develop AA amyloidosis at any age (Ibi et al, 2015).…”

“…The main organs involved in amyloid deposition in chickens are liver and spleen, but depositions have also been reported in the intestines, kidney, heart, gonads, endocrine organs, brain, lungs, and skin (Landman et al, 1998). Deposition of amyloid fibrils at the injection site in vaccinated chickens has also been reported (Murakami et al, 2013a;Murakami et al, 2013b;Ibi et al, 2015).…”

Hepatic changes in Gallus gallus domesticus in Brazil

“…The avian liver can be affected by multiple conditions or etiologies. Among the non-infectious causes, there are degenerative changes, such as hydropic, glycogenic and fatty degeneration; metabolic disorders such as hemosiderosis (Abdul-Aziz & Fletcher 2016), amyloidosis (Murakami et al 2013b, Ibi et al 2015, Carnaccini et al 2016, urate deposition (Crespo & Shivaprasad 2013), fatty liver and hemorrhagic liver syndrome (Mete et al 2013, Trott et al 2014, as well as circulatory disorders (Abdul-Aziz & Fletcher 2016), and primary neoplasms such as hepatocellular adenoma, hepatocellular carcinoma, cholangioma and cholangiocarcinoma (Abdul-Aziz & Fletcher 2016, Williams et al 2020. In addition to these, the liver is also affected by neoplasms of infectious etiology, such as in Marek's disease (MD), lymphoid leukosis and reticuloendotheliosis viruses (Abdul-Aziz & Fletcher 2016).…”