Fowl adenovirus can cause important diseases in chickens such as inclusion body hepatitis, hepatitis hydropericardium syndrome, and gizzard erosion and ulceration. Inclusion body hepatitis has been regularly reported from many countries. This is the first case report from Turkey, describing an outbreak of inclusion body hepatitis in broiler farms due to fowl adenovirus-8b (FAdV-8b). Broiler flocks with mortality about 10% were visited in Turkey, and necropsy was performed on dead birds. Samples were subjected to PCR assay to detect FAdV and other viral pathogens. After sequencing, phylogenetic analysis was performed and the nucleotide sequences of hexon genes were compared with the FAdV sequences data available in GenBank. Clinical signs such as anorexia, depression, ruffled feathers, huddling, and greenish diarrhoea were observed. Mortality started at the 8ᵗʰ day of age and ranged from 10% to 14%. Necropsy showed severe hepatitis, jaundice, and pancreatitis. The main necropsy findings included a pale, enlarged, haemorrhagic, and friable liver along with swollen and haemorrhagic kidneys and spleen. PCR and sequence analysis revealed the presence of fowl adenovirus serotype 8b (FAdV-E). This is the first report on characterisation and the pathological lesions associated with FAdV in broilers in Turkey. Our findings suggest that FAdV strains could be an emerging pathogen in Turkish broilers and could actively contribute to hepatitis and immunosuppression.

Objective—To evaluate the specificity of a canine pancreas-specific lipase (cPSL) assay for diagnosing pancreatitis in dogs without clinical or histologic evidence of the disease. Animals—20 dogs from another study with macroscopic evidence of pancreatitis and 44 dogs surrendered for euthanasia or expected to die. Procedures—Prior to death, physical examination of each dog was performed and blood samples were collected for serum biochemical, serum cPSL, and hematologic analyses. After death, the pancreas was removed, sectioned in 1- to 2-cm slices, and evaluated by a pathologist. Dogs were classified by whether they had clinical or macroscopic pancreatitis. Each pancreatic section was histologically examined, and mean cumulative scores (MCSs) were assigned for 8 histologic characteristics. For each characteristic, comparisons were made between dogs with and without pancreatitis to establish histologic criteria for lack of evidence of pancreatitis. Results—For all histologic characteristics except lymphocytic infiltration, the median MCS differed significantly between dogs with and without pancreatitis. Dogs were categorized as having no histologic evidence of pancreatitis when the MCSs for neutrophilic infiltration, pancreatic necrosis, peripancreatic fat necrosis, and edema were 0.0. On the basis of these criteria, 40 dogs were classified as having no evidence of pancreatitis. The cPSL concentration was within reference limits in 38 of these 40 dogs and was less than the cutoff value for diagnosing pancreatitis (400 μg/L) in 39 of the 40 dogs, resulting in a specificity of 97.5% (95% confidence interval, 86.8% to 99.9%). Conclusions and Clinical Relevance—The cutoff cPSL value used in this study may be useful for diagnosing pancreatitis in dogs with a lack of histologic lesions consistent with pancreatitis and for which pancreatitis is not considered a major differential diagnosis.

The quantification of serum proteins is a useful tool for diagnosing and monitoring various diseases that involve changes in the concentrations of these proteins. As canine acute pancreatitis (AP) accompanies the systemic inflammatory response syndrome, serum proteins such as C-reactive protein (CRP) have been used as inflammatory markers for dogs with AP. The goal of this study was to investigate the overall profiles of serum proteins by serum protein electrophoresis (SPE) and to determine the concentration of acute phase proteins (APPs) in dogs with AP in order to better understand serum protein profiles as diagnostic markers in these dogs. Decreased levels of albumin and increased levels of alpha-2 globulin were observed in dogs with AP by SPE. Among APPs, elevated concentrations of CRP, serum amyloid A (SAA), and haptoglobin were detected. The concentration of SAA was positively correlated with that of CRP, which suggests that SAA could be a sensitive marker of inflammation in dogs with AP, similar to CRP.

The objective of this study was to examine the effects of immunosuppressive prednisolone therapy on pancreatic tissue and the concentration of serum canine pancreatic lipase immunoreactivity (cPLI) in healthy dogs. Six healthy beagle dogs were subcutaneously administered an immunosuppressive dose of prednisolone [4 mg/kg body weight (BW)] once daily for either 2 or 3 weeks. Serum cPLI concentration was measured before and after treatment. Ultrasonographic examination of the pancreas and laparoscopic biopsy and histopathological examination of the right pancreatic lobe and the liver were also conducted before and after treatment. The expression of pancreatic lipase messenger ribonucleic acid (mRNA) in the pancreas and liver was examined by polymerase chain reaction (PCR). Although the serum cPLI concentration was significantly higher on day 14 and on the day of the second laparoscopy than before treatment, it was classified as normal (≤ 200 μg/L) in 5 dogs and as abnormal (≥ 400 μg/L) in only 1 dog. None of the 6 dogs showed clinical signs of pancreatitis during the study period. After treatment, ultrasonographic examination of the pancreas showed no changes except for a hypoechoic pancreas in 1 dog. Histopathological examination of the right pancreatic lobe in all dogs showed no evidence of pancreatitis after treatment. Pancreatic lipase mRNA expression was detected in the pancreas, but not in the liver, before and after treatment. The administration of 4 mg/kg BW per day of prednisolone for 2 or 3 weeks increased the serum cPLI concentration without clinical signs of pancreatitis, although an abnormal cPLI concentration (≥ 400 μg/L) was observed in only 1 dog. No ultrasonographic or histological evidence of pancreatitis was observed in any of the dogs.

While pancreatitis is now recognized as a common ailment in cats, the diagnosis remains challenging due to discordant results and suboptimal sensitivity of ultrasound and specific feline pancreatic lipase (Spec fPL) assay. Pancreatitis also shares similar clinical features with pancreatic carcinoma, a rare but aggressive disease with a grave prognosis. The objective of this pilot study was to compare the plasma proteomes of normal healthy cats (n = 6), cats with pancreatitis (n = 6), and cats with pancreatic carcinoma (n = 6) in order to identify potential new biomarkers of feline pancreatic disease. After plasma protein separation by 2-dimensional gel electrophoresis, protein spots were detected by Coomassie Brilliant Blue G-250 staining and identified by mass spectrometry. Alpha-1-acid glycoprotein (AGP), apolipoprotein-A1 (Apo-A1), and apolipoprotein-A1 precursor (Pre Apo-A1) appeared to be differentially expressed, which suggests the presence of a systemic acute-phase response and alteration of lipid metabolism in cats with pancreatic disease. Future studies involving greater case numbers are needed in order to assess the utility of these proteins as potential biomarkers. More sensitive proteomic techniques may also be helpful in detecting significant but low-abundance proteins.

Objective: To obtain ultrasonographic reference values for the thickness of the pancreas and the diameter of the pancreatic duct in clinically normal dogs. Animals: 242 adult dogs with no clinical signs of gastrointestinal tract disease. Procedures: The maximum pancreatic thickness and the diameter of the pancreatic duct were recorded ultrasonographically at the level of the left lobe, body, and right lobe of the pancreas. Results: Mean ± SD pancreatic thickness measurements were as follows: left lobe, 6.5 ± 1.7 mm (n = 214); body, 6.3 ± 1.6 mm (155); and right lobe, 8.1 ± 1.8 mm (239). The mean pancreatic duct diameter was 0.6 ± 0.2 mm (n = 42) in the left lobe and 0.7 ± 0.2 mm (213) in the right lobe. The right pancreatic duct was visible in 213/242 (88.0%) dogs, and the left pancreatic duct was visible in 41/242 (16.9%) dogs. However, the body was visible in only 16/242 (6.6%) dogs. Pancreatic thickness and diameter of the pancreatic duct significantly increased with body weight in all lobes, but age was not correlated with the measurements. Conclusions and Clinical Relevance: Ultrasonographic reference values for the pancreas and pancreatic duct of dogs were determined. Results of this study indicated that the pancreatic duct was visible, especially in the right lobe of the pancreas. These values may be useful for the assessment of pancreatic abnormalities, such as chronic pancreatitis and exocrine pancreatic insufficiency.