Quantity of virulent fowl adenovirus serotype 1 correlates with clinical signs, macroscopical and pathohistological lesions in gizzards following experimental induction of gizzard erosion in broilers

Abstract

In the present study day-old specific-pathogen-free (SPF) and commercial broilers with maternally derived fowl adenovirus serotype 1 (FAdV-1) antibodies were orally infected with a European “pathogenic” FAdV-1, isolated from broilers showing signs of gizzard erosion. During the experiment, broilers were observed and weighed daily up to 17 days post infection (dpi). Clinically, both infected groups showed significant decrease of weight compared to respective negative control groups. Birds were examined by necropsy at 3, 7, 10, 14 and 17 dpi. Pathological changes in the gizzards were noticed in both experimentally infected groups from 7 dpi onwards. Macroscopically, erosion of the koilin layer and inflammation or ulceration of the gizzard mucosa were observed. Histologically, presence of FAdV-1 in intranuclear inclusion bodies of degenerated glandular epithelial cells was demonstrated by in-situ hybridization and inflammatory cell infiltration of the lamina propria, submucosa and muscle layer was detected. Tissue samples were investigated by a recently developed real-time PCR and the viral DNA load was calculated from gizzard, liver, spleen and cloacal swabs with the highest amounts of FAdV-1 DNA found in the gizzard. For the first time, successful reproduction of clinical signs in broilers as well as pathological lesions in the gizzard were achieved with a European FAdV-1 isolate displaying some genetic differences to so far reported virulent FAdV-1 from Japan. Furthermore, highest viral load in gizzards could be linked with macroscopical and histological lesions. Therefore, the conducted analyses provide important insights into the pathogenesis of adenoviral gizzard erosion.

A comparative pathogenicity analysis of two adenovirus strains, 1/A and 8a/E, isolated from poultry in Poland

“…Cook et al [3] indicated that the replication rate of adenovirus strains reached a peak in the first three weeks postinfection and that those strains had a higher degree of tropism for the digestive tract than for other internal organs. Similar results were obtained by other authors [9,10,30], also showing that the rate of replication of strain FAdV-1/A is highest in the gizzard, liver, spleen, and intestine.…”

Chronological analysis of gross and histological lesions induced by field strains of fowl adenovirus serotypes 1, 8b and 11 in one-day-old chickens

“…These findings, together with the fact that FAdV-1 was detectable in the gizzard, but not in the liver (with the exception of one bird during the incubation stage), suggests that the epithelial lining of the gizzard, and perhaps also of the remaining sections of the alimentary tract, may serve as a reservoir of FAdV and play a role in transmission by shedding it long after typical liver lesions have resolved. Interestingly, this is consistent with pathogenic FAdV-1 strains that can induce gizzard erosions in chickens (Grafl et al, 2013), as well as some human adenoviruses that specifically attach to and infect epithelial cells of the alimentary system (Favier et al, 2004). In a previous study, following ocular inoculation with FAdV-8 at a similar age but with a higher dose of virus than that used in this study, viral antigens were detected in the epithelial cells of the intestine up to 13 days PI, but only low levels of antigen were detected in the proventriculus in a small proportion of birds between 2 and 5 days PI (Saifuddin & Wilks, 1991).…”

“…The FAdV-1 isolate used in our study was included since it was the only contemporary FAdV-1 isolate available in Australia and its pathogenicity and role in IBH outbreaks in Australia were unknown. The contrast in pathogenicity of the FAdV-1 isolate used here and that of the ones examined by other workers (Okuda et al, 2001;Domanska-Blicharz et al, 2011;Lim et al, 2012;Grafl et al, 2013) was highlighted in our study. Interestingly, some strains of FAdV-8 have been implicated in cases with both gizzard erosions and IBH (Okuda et al, 2004).…”

“…Although the tissue tropism differed, similar findings were reported for experimentally induced gizzard erosions by inoculation with FAdV-1 (Grafl et al, 2013). Noteworthy is the relationship between histopathology and virus detection in the bursa during the degenerative stage, indicating the involvement of this primary lymphoid organ in the pathology of FAdV infection.…”

Clinical signs and progression of lesions in the gizzard are not influenced by inclusion of ground oats or whole wheat in the diet following experimental infection with pathogenic fowl adenovirus serotype 1

“…A presumptive diagnosis is confirmed by virological and/or histological investigations. Experimental infection of specific pathogen-free (SPF) chickens with Asian and European FAdV-1 field isolates was successful in reproducing AGE (Okuda et al, 2001a, b;Nakamura et al, 2002;Domanska-Blicharz et al, 2011;Grafl et al, 2013). Furthermore, studies have investigated a number of factors that may influence the development of AGE, such as type or age of birds, and their immune status (Okuda et al, 2001a, b;Muroga et al, 2006;Grafl et al, 2014).…”