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.

Avian polyomavirus (APV) and psittacine beak and feather disease virus (PBFDV) induce contagious and persistent diseases that affect the beaks, feathers, and immune systems of companion birds. APV causes hepatitis, ascites, hydropericardium, depression, feather disorders, abdominal distension, and potentially death. PBFDV can induce progressive beak deformity, feather dystrophy, and plumage loss. We conducted the first prevalence survey of both APV and PBFDV infections in companion birds in eastern Turkey. A total of 113 fresh dropping samples from apparently healthy companion birds were collected in a random selection. The dropping samples were analysed for PBFDV and APV by PCR. Positive samples were sequenced with the Sanger method. The sequence was confirmed through alignment and the phylogenetic tree generated through the maximum likelihood method computationally. PBFDV and APV were detected in a respective 48.7% and 23.0% of samples. Coinfection was found in 12.4% of the samples, these all being from budgerigars (Melopsittacus undulatus). APV and PBFDV were detected in budgerigar and cockatiel (Nymphicus hollandicus) samples. This report provides a foundation for future studies on the influence of these viruses on the health of companion birds. These high positive rates for both pathogens emphasise that healthy M. undulatus and N. hollandicus in eastern Turkey may be prone to the emergence and spread of APV and PBFDV with subclinical potential.

The objective of this study was to identify the causative agents of hepatitis observed in broiler chickens at processing. Livers of chickens from 16 broiler farms in Saskatchewan with gross lesions of hepatitis were collected at processing. In addition to routine bacterial isolation and histopathological examination, serologic studies for infectious bursal disease virus (IBDV) and Chicken anaemia virus (CAV), calculation of the ratio of the weight of the bursa of Fabricius (BF) to body weight (BBW), and histopathological examination of the BF were done. Of the 264 livers with gross lesions, 83% had multifocal to coalescing necrotizing hepatitis, 16% had perihepatitis, and 1% had hemorrhages. No definitive causative microorganisms were isolated from the hepatic lesions; however, no significant bacterial isolations were made. Bursal atrophy, low BBW ratio, and high titer of antibody against IBDV each correlated with the rate of total condemnations (P = 0.0188, P = 0.0001, and P = 0.0073, respectively). Nucleotide sequencing of IBDV isolated from the BF identified the variant strains Delaware-E and 586. Condemnation because of hepatic lesions was correlated with titer of antibody against IBDV and BBW (P = 0.016 and P = 0.027). The results of this study demonstrate that hepatic lesions in Saskatchewan chickens are not currently caused by a primary bacterial pathogen but are associated with indicators of immunosuppression that is likely due to variant IBDV.

The helicase genes and hypervariable regions (HVRs) of three avian hepatitis E viruses (HEVs) detected at three different farms were sequenced and characterized. Two isolates (DW-L and GI-B2) were classified as genotype 2 and one isolate (GR-B) was classified as genotype 1. A phylogenetic tree, based on the helicase gene and HVR nucleotide sequences, revealed the newly detected viruses and other avian HEVs were classified similarly. Unlike previously reported avian HEVs, the DW-L isolate detected in broiler breeders with characteristic lesions of avian HEV had no prolinerich motif in its HVR, suggesting that the proline-rich motif is non-essential for viral replication and infection.

Inclusion body hepatitis (IBH) has been reported in many countriesin the world. The IBH characterized presence of intra-nuclear inclusion bodies in hepatocytes in chickens. On December 2015, an onset of high acute mortality in a flock of 12, 18 and 23- day-old broiler chickens in Malacca and Johore was reported to the RegionalVeterinary Laboratory, Johor Bahru, Peninsular Malaysia. The birds showed lethargy, huddling, ruffled feathers, and inappetence. At necropsy, the livers were enlarged, pale yellow, friable andwith multiple petechial hemorrhages, the kidney were congested and enlarged, with hydropericardium and gizzard erosion. Large eosinophilic intranuclear inclusion bodies were seen in hepatocytes. PCR revealed liver were positive of FAdV at expected band of 1219 bp and the nucleotide sequence share 95-99% identity with the fowl adenovirus species E, serotype 8b. Based on the acute high mortality, age of the broilers, gross and microscopic lesions (especially intranuclear inclusion bodies) and molecular finding, the condition was diagnosed as adenovirus inclusion body hepatitis.

To determine the effect of swine hepatitis E virus (HEV) infection on pregnant gilts, their fetuses, and offspring, 12 gilts were intravenously inoculated with swine HEV. Six gilts, who were not inoculated, served as controls. All inoculated gilts became actively infected and shed HEV in feces, but vertical transmission was not detected in the fetuses. There was no evidence of clinical disease in the gilts or their offspring. Mild multifocal lymphohistiocytic hepatitis was observed in 4 of 12 inoculated gilts. There was no significant effect of swine HEV on fetal size, fetal viability, or offspring birth weight or weight gain. The offspring acquired anti-HEV colostral antibodies but remained seronegative after the antibodies waned by 71 days of age. Swine HEV infection induced subclinical hepatitis in pregnant gilts, but had no effect on the gilts' reproductive performance, or the fetuses or offspring. Fulminant hepatitis associated with HEV infection was not reproduced in gilts.

The purposes of this study were to set up the method of the natural killer(NK) cell activity assay using the flow cytometer and to examine the characteristics and distribution of the NK cell during rat hepatocarcinogenesis. Forty five male 6 week-old specific pathogen free(SPF) Sprague-Dawley rats were randomly divided into three groups. Group I was the non-treated control and given normal diet and water. Group II was treated with diethylnitrosamine(DEN, 200mg/kg, i.p.) and partial hepatectomy. Group III was treated with DEN, partial hepatectomy and 0.05% phenobarbital sodium in water from 3 to 16 weeks. All animals were examined the morphology of the large granular lymphocyte(LGL), the LGL percent of the total lymphocytes and the LGL conjugation rate with YAC-1 cell in peripheral blood, spleen and liver. Moreover, activity of the LGL isolated from peripheral blood lymphocytes was determined using the flow cytometer. As results, LGL were observed in the peripheral blood, spleen and liver. LGL were observed the relatively faintly staining basophilic cytoplasm with granules, and eccentric, often kidney-shpaed nuclei in Giemsa stain. Its size was 11~13 micro meter. LGL percentage of the isolated lymphocytes in peripheral blood, spleen and liver were 1.8~2.3%, 1.3~1.4% and 0.87~0.99%, respectively. LGL conjugation rate with YAC-1 cell was shown to be peripheral blood(9.3~10.3%) spleen(7.7%~8.7%)liver(5.6~7.0%). The activity of the LGL isolated from peripheral blood lymphocytes in Group I, II and III was 33.7%, 30.5% and 35.4%, respectively. However, all values were not sighificantly between groups.

The aim of this study was to establish selective hepatic artery catheterization technique through percutaneous femoral artery puncture and to offer digital subtraction angiography(DSA) of hepatic artery in beagle dogs. Percutaneous femoral artery puncture was performed with Sheldinger's method. Microferret TM- 18 Infusion catheter(William, Cook, Europe) was introduced into abdominal aorta. Then, under fluoroscopy, iopamidol 370(Bracco, Italy) was injected to identify celiac artery and `J' shpaed guide wire was introduced into celiac artery. Catheter could be introduced into celiac artery through guide wire. In this manner, catheter was located at the insertion of hepatic artery and DSA was performed. In DSA of beagle dogs, hepatic artery which was divided into lateral branch, right-medial branch, right-lateral branch of hepatic artery, cystic artery and gastroduodenal artery was opacified without superimposition of any other body structure and so was the parenchyme of liver afterward. In autopsy angiographic finding of resected liver, cystic artery, caudate branch, lateral branch, right-medial branch, right-lateral branch and quadrate branch of hepatic artery were identifed. It was concluded that selective hepatic artery catheterization technique was a minimally invasive method that facillitated the approach of hepatic artery and DSA was an excellent tool to visualize the vessle of liver in dogs.

The present study was aimed to know the chronic hepatitis with abdominal effusion in a beagle dog and its therapeutic management. A 2.5 year old male beagle was presented to Madras Veterinary College teaching Hospital, madras veterinary college, Chennai with the history of inappetence, abdominal distension for past 10 days and the clinical signs of inappetence, fever and palpablelymph node and congested mucous membrane. On Physical examination, dog showed respiratory distress and dull. Dog was subjected for radiography examination, haematology, biochemistry parameters and ultrasound examination. On first day of examination, dog was treated with Lasix at the dose rate of 3 mg/kg body weight, antibiotics and Tribivet injection. Hematology and biochemical values revealed neutrophilia, elevated alkaline phosphatase, total bilirubin, direct bilirubin, and decreased total protein and albumin. The lateral view radiography of abdomen revealed fluid shadow and ultrasound examination revealed that chronic hepatitis with moderate abdominal effusion. In case of clinical suspicion of hepatitis an ultrasonographic liver scan can be of diagnostic aid and the finding of an altered structure can be indicative of a liver problem. In many cases of chronic hepatitis may not be associated with ultrasound abnormalities but ascites can be easily identified. Dog was treated with antibiotic cefotaxime at the dose rate of 25 mg/Kg body weight and Lasix at the dose rate of 3 mg/Kg body weight with liver supplement of Lysibin which contain silymarin and supplement with Astymin syrup for 3 weeks. The animal was reviewed after three weeks of treatment which was subjected for haeamtology, biochemistry and ultrasound examination which revealed there was improvement in the blood parameters with decreased total protein and normal level of Alkaline phosphatase and bilirubin level and ultrasound examination revealed normal study of abdominal effusion and liver echogenicity and dog had normal  appetite and normal  vital parameters. In this case hepatitis may be due to any viral etiology like adenovirus that may cause hepatitis with effusion that may be respond to treatment and diuretics and brought normal parameters of vital in dog. Chronic hepatitis with effusion may be further confirmed by Liver biopsy and molecular diagnosis.