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To disclose the mechanism of cellular injury following porcine circovirus (PCV) infection, 12 pigs were examined by the terminal deoxynucleotidyl transferase-mediated dUTP-nick end labeling (TUNEL) method and immunohistochemistry. Histologically, the lymphoid tissues were characterized by marked apoptosis of lymphocytes, lymphocyte depletion, and macrophages and giant cells containing numerous inclusion bodies with or without apoptotic bodies. Immunohistochemically, there were many lysozyme-positive macrophages in the lymphoid follicles, while the number of CD79a-positive B lymphocytes was scanty. Apoptotic cells, which were proved to be TUNEL positive, revealed CD79a positivity. Although detectable mainly in the cytoplasm of macrophages, PCV antigens were found also in the nuclei of macrophages and apoptotic lymphocytes. Ultrastructurally, the presence of PCV virions was confirmed in apoptotic bodies phagocytosed by macrophages. These findings suggested that lymphocyte depletion with apoptotic death of B lymphocytes was caused by PCV, and that some of the inclusion bodies were phagolysosomes derived from the apoptosis. Thus, PCV may trigger the development of wasting disease syndrome by producing an immunocompromised state in pigs.

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The mortality and pathology caused by serotype 4 adenovirus, isolated from chickens with hydropericardium syndrome (HPS) in Japan, was investigated in specific-pathogen-free (SPF) chickens. One-day-old to 15-mo-old SPF chickens were inoculated intramuscularly, orally, and intranasally with liver homogenates from HPS chickens or isolated serotype 4 adenovirus. There were no clinical signs before death. The mortality rate in all groups of 1-day-old chicks was 100%, irrespective of the inoculum or inoculation route. Four-week-old chickens inoculated with liver homogenate also had a 100% mortality rate. Five-week-old chickens inoculated with cell culture of HPS adenovirus had a 40% mortality rate. The mortality rates of 7-mo-old hens inoculated with liver homogenates intramuscularly and orally were 75% and 25%, respectively. In 15-mo-old hens inoculated with liver homogenates intramuscularly, the mortality rate was 70%. Gross lesions were hydropericardium and swelling and congestion of the liver with occasional petechial hemorrhages. Histologically, the liver had diffuse or multifocal hepatic necrosis and hemorrhage with intranuclear inclusion bodies noted within hepatocytes. In the spleen, macrophages containing erythrocytes and yellow pigment were prominent in the red pulp. In the lung, a moderate diffuse macrophage infiltration was noted throughout the lung parenchyma, and these macrophages contained yellow pigment. In the pancreas of the chicks inoculated at 1 day old, there was multifocal necrosis of glands with intranuclear inclusion bodies. Intranuclear inclusion bodies were seen also in the gizzard, proventriculus, duodenum, cecum, kidney, and lung of the chicks inoculated at 1 day old. Immunohistochemically, the intranuclear inclusion bodies of various organs showed positive reactions against group I avian adenovirus. Adenovirus was recovered from the liver of chickens with HPS. This study indicates that HPS adenovirus is able to reproduce HPS lesions and mortality in SPF chicks and even adult chickens and that it is a highly pathogenic strain.

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Porcine deltacoronavirus (PDCoV) have recently emerged in several swine producing countries. Our survey found that in addition to porcine epidemic diarrhoea virus (PEDV), PDCoV has also been a causative enteric pathogen of diarrhoeic outbreaks occurring at swine farms around Japan since late 2013. Phylogenetic analysis using the complete genomes of PDCoVs detected in Japan in 2014 demonstrated that the PDCoVs from Japan may be closely related to the PDCoVs from the U.S. and Korea during 2013 to 2014 but not the PDCoVs from China and Hong Kong during 2004 to 2016 and from Thailand, Vietnam and Laos during 2015 to 2016. To investigate the pathogenicity of a representative Japanese PDCoV, we performed an experimental infection using hysterectomy-produced colostrum-deprived piglets. The PDCoV-inoculated piglets showed acute, watery diarrhoea, but all recovered and survived. In addition, all piglets inoculated with the Japanese PDCoV exhibited virus shedding at high level in faeces and viremia corresponding to their clinical symptoms. In the PDCoV-inoculated group, viruses were mainly detected from jejunums to colons by a quantitative PDCoV-specific PCR and microscopic observation. These findings would provide useful information for establishing a diagnostic methodology for distinguishing diarrhoea caused by PDCoV from that caused by other enteric pathogens, such as PEDV.

ABSTRACT. In this study, we investigated the expression of immunoglobulin A (IgA) in porcine salivary gland and its relationship with restraint stress in pigs. IgA was expressed in plasma cells in pig salivary gland, as confirmed by immunohistochemical staining. IgA was also detected in pig saliva itself by ELISA, and salivary IgA levels were increased by a restraint stress. Moreover, there was a circadian rhythm of IgA over the course of a day. These results are the first evidence of IgA expression related to stress in the pig saliva and may make IgA useful as a non-invasive biological marker to evaluate acute stress condition in the pigs.KEY WORDS: IgA, non-invasive biomarker, restraint stress, saliva, salivary glands.

Ten 250-day-old broiler breeders, seven 16-day-old broiler chicks, and three 25-day-old broiler chicks suffering from hydropericardium syndrome (HPS) in Japan were examined histologically, immunohistochemically, and ultrastructurally. Clinically, the chickens died suddenly without apparent signs. The mortality rates were 6.4%, 20.2%, and 26.1%, respectively. The common characteristic histologic lesion was necrosis of hepatocytes, accompanied by intranuclear inclusions of hepatocytes and hemorrhages. In the spleen, there were activation of macrophages in splenic sinus and ellipsoids and erythrophagocytosis in the splenic sinus. The interlobular interstitium of the lung showed marked edema. The air and blood capillary areas of parabronchi included many macrophages with yellow pigments. With immunoperoxidase staining, intranuclear inclusion bodies within degenerating hepatocytes stained positively for group I adenovirus antigen. Ultrastructurally, numerous viral particles (65-70 nm in diameter) were demonstrated in the intranuclear inclusions of hepatocytes. Group I adenovirus (serotype 4) was isolated from liver samples of adult broiler breeders and broiler chicks with HPS. This study suggests that HPS may be caused by group I adenovirus.