• Korean Journal of Veterinary Research
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• v.32 no.2
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• pp.227-233
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• 1992

Out of twenty rabbits which died of rabbit hemorrhagic disease spontaneously occurring in Korea, five animals had a concurrent infection with Encephalitozoon cuniculi in the cerebrum. The lesions were composed of granulomas, leptomeningitis and perivascular cuffing with mononuclear cells. The granulomas consisted of a central necrotic focus surrounded by an infiltration with plasma cells, lymphocytes and macrophages. Gliosis was associated with the granulomas. Gram-positive organisms were detected in the cerebrum from two rabbits. They were oval to rod-shaped with blunt round ends. The distribution of the pathogens was investigated by the direct avidin-biotin peroxidase complex method. They were present in pseudocysts and macrophages. Pseudocysts were found in the granulomas as well as the neuropil without cellular reactions. Some organisms were present within reticulo-endothelial cells of blood capillaries and macrophages in the subarachnoid spaces. These organisms had ultrastructural characteristics consistent with Encephalitozoon cuniculi.

• Korean Journal of Veterinary Research
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• v.35 no.2
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• pp.369-374
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• 1995

Aujeszky's disease virus(ADV) was inoculated intranasally into the Korean native goats to investigate pathological findings and pathogenesis of ADV infection by using of histological and immunohistochemical methods and in situ hybridization(ISH). Clinical signs of salvation, pyrexia, pruritus and staggering were followed by death with five days after inoculation, Pathoanatomical findings were edema of the lung and the urinary bladder with hemorrhage and congestion, petechial hemorrhages on the endo-and epicardium, renal congestion, moderate splenomegaly and cystic edema. Main microsocpic lesions observed in all infected goats were confined to the CNS and charcterized by perivascular cuffing with lymphocytes and macrophages, focal gliosis, neuronal degeneration and necrosis, and intranuclear inclusion bodies in the neurons and glial cells. Positive reactions to ADV were detected more frequently in the nuclei than in the cytoplasms of infected nerve cells in the CNS by immunohistochemistry and ISH. Frequenctly localized sites of ADV in the CNS were olfactory bulb, prietal cortex, callosal sulcus and corpus callosum. Positive reactions were also detected in the tonsillar epithelium, and alveolar macrophage and sloughed epithelium of the lung.

• Korean Journal of Veterinary Service
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• v.13 no.1
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• pp.32-43
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• 1990

In order to investigate the clinico-pathological and immunohistochemical changes in the rats infected with Aujeszky’s disease virus(ADV), 100 heads of 4 weeks-old rats were inoculated intraperitoneally and intranasally, with the domestically isolated ADV, NYJ-1-87 strain, at $10^{3.0}$ or $10^{5.0}$$TCID_ {50}$/0.2ml. Results obtained through the experiments were summarized as follows : 1. Clinical signs such as dulness, anorexia, pruritus, fascial edema, dyspnea and ataxia were observed from the 2nd day and died at the 3rd to 5th day after ADV inoculation. By necropsy, congestion and hemorrhage were observed in the abdominal organs, while no specific changes were detected in the other organs. 2. In histopathological observation, degeneration and necrosis of the nervous cells, non-suppurative meningoencephalitis, microgliosis and perivascular cuffing were manifested in central nerve system but no specific changes were observed in the other organs. 3. By immunohistochemical staining using peroxidase antiperoxidase, the positive cells were detected in the tissues of kideny, spleen, urinary bladder and lung.

• Korean Journal of Veterinary Service
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• v.40 no.3
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• pp.161-168
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• 2017

Caprine arthritis encephalitis (CAE) virus is a causative agent of caprine arthritis-encephalitis. In our previous study we reported a prevalence of CAE. In this study, we described the further detailed pathological features of CAE and examined the detection of virus by in situ hybridization (ISH). Histopathologically, interstitial pneumonia and bronchopneumonia in lung, focal inflammation in mammary glands, perivascular cuffing in brain, arthritis, and focal necrosis, mild steatosis, inflammatory cell infiltration of liver were noted. CAEV proviral-DNA was identified by nested polymerase chain reaction (PCR) in blood cells, brain, synovial fluid, and lymph node. Confirmation by nested PCR involved amplification of a 296 bp ($1^{st}$ PCR) and 185 bp ($2^{nd}$ PCR) fragments corresponding to a conserved region on the gag gene of CAEV. Positive ISH signals were detected in the brain and liver. In conclusion, significant histopathological findings included parenchymal infection in various organs, including the lung, liver, brain, joint, and mammary gland were noted in the CAEV infected dairy goat. ISH can help confirm the diagnosis of CAE in formalin-fixed samples.

• Applied Microscopy
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• v.33 no.1
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• pp.1-16
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• 2003

As is well known that N-nitroso-N-methylurethane (NNNMU) causes acute lung injury (ALI) in experimental animals. And ALI caused by NNNMU is very similar to ARDS in human being in its pathology and progress. In its context, we investigated the pathogenetic mechanism of ARDS associated with oxidative stress by neutrophils in Sprague-Dawley rat model of NNNMU-induced ALI. NNNMU had increased lung weight/body weight ratio (L/B ratio), lung myeloperoxidase (MPO) activity, protein content and number of neutrophils in bronchoalveolar fluid (BALF) compared with those of control rat (p<0.001, respectively). In contrast, the amount of pulmonary surfactant in BALF was decreased by NNNMU (p<0.001). Morphologically, light microscopic examination denoted pathological findings such as formation of hyaline membrane, infiltration of neutrophils and perivascular cuffing in the lungs of NNNMU-treated rats. In addition, ultrastructural changes such as the necrosis of endothelial cells, swelling and vacuolization of lamellar bodies of alveolar type II cells, and the degeneration of pulmonary surfactant were identified after treatment of NNNMU. Very interestingly, cerium chloride electron microscopic cytochemistry showed that NNNMU had increased the production of cerrous-peroxide granules in the lung, which signified the increased production of hydrogen peroxide in the lung. Collectively, we conclude that NNNMU causes acute lung leak by the mechanism of neutrophilic oxidative stress of the lung.

• Parasites, Hosts and Diseases
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• v.55 no.3
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• pp.267-285
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• 2017

Angiostrongylus cantonensis invades the central nervous system (CNS) of humans to induce eosinophilic meningitis and meningoencephalitis and leads to persistent headache, cognitive dysfunction, and ataxic gait. Infected mice (nonpermissive host), admittedly, suffer more serious pathological injuries than rats (permissive host). However, the pathological basis of these manifestations is incompletely elucidated. In this study, the behavioral test, histological and immunohistochemical techniques, and analysis of apoptotic gene expression, especially caspase-3, were conducted. The movement and motor coordination were investigated at week 2 post infection (PI) and week 3 PI in mice and rats, respectively. The cognitive impairs could be found in mice at week 2 PI but not in rats. The plaque-like lesion, perivascular cuffing of inflammatory cells, and dilated vessels within the cerebral cortex and hippocampus were more serious in mice than in rats at week 3 PI. Transcriptomic analysis showed activated extrinsic apoptotic pathway through increased expression of TNFR1 and caspase-8 in mice CNS. Immunohistochemical and double-labeling for NeuN and caspase-3 indicated the dramatically increased expression of caspase-3 in neuron of the cerebral cortex and hippocampus in mice but not in rats. Furthermore, western-blotting results showed high expression of cleaved caspase-3 proteins in mice but relatively low expression in rats. Thus, extrinsic apoptotic pathway participated in neuronal apoptosis might be the pathological basis of distinct behavioral dysfunctions in rodents with A. cantonensis infection. It provides the evidences of a primary molecular mechanism for the behavioral dysfunction and paves the ways to clinical diagnosis and therapy for A. cantonensis infection.

• Korean Journal of Veterinary Research
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• v.30 no.4
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• pp.441-446
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• 1990

Encephalomyocarditis virus infection in pigs, characterized by severe reproductive failure in sows and sudden death in less than 7 day-old-piglets, a period of several months from October to December of 1989, in Korea was occurred. The most outstanding gross lesions at necropsy were found in the heart which were consisted of pale, yellow brown necrotic foci of varying size in myocardium. In some cases, pulmonary edema and liver congestion were observed. Histopathology of the heart revealed the interstitial myocarditis, endocarditis and epicarditis with lymphocytic, plasmacytic and macrophage cell infiltration and, in some cases, calcification of the necrotic myocardial muscle fibers. In some cases of brain, the perivascular cuffing and glial nodules were observed. In the liver and the lacrimal gland varying degrees of multifocal necrosis were seen. The virus was isolated from the heart and the brain in a stillborn piglet and a mummified fetus. This outbreak represents the first case of encephalomyocarditis virus infection of pigs in Korea.

• Korean Journal of Veterinary Pathology
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• v.2 no.2
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• pp.117-125
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• 1998

Pathological studies were performed on the five piglets experimentally infected with Aujeszky's disease virus(pseudorabies), NYJ isolate, isolated from the naturally infected pigs in Korea: two piglets were inoculated intramuscularly, two piglets intranasally, and one piglet subcutaneously at the dose of 1$m\ell$ per animal with the 105.5 $TCID_50$/0.1ml titer. Clinical signs included dyspnea, high fever(＞$41^{\circ}C$), anorexia, vomiting, diarrhea or constipation, ataxia, circling movement, posterior paralysis, intermittent convulsion, and coma followed by death although some variations by age and inoculated routes were observed. Gross features included multiple necrotic foci in the liver, congestion and hemorrhage in the lymph nodes and spleen, petechial hemorrhage in the kidney, hemorrhagic pneumonia, marked meningeal congestion, severe sub meningeal hemorrhage in the spinal cord, excessive cerebrospinal fluid retention, and muscular necrosis at the inoculated area. Microscopically, non suppurative meningoencephalitis with gliosis and perivascular cuffing in CNS, ganglioneuritis, necrohemorrhagic splenitis, necrotic hepatitis, tonsillitis and rhinitis, hemorrhagic or interstitial pneumonia, and non-suppurative myositis in the injected area were observed. Eosinophilic intranuclear inclusion bodies were found in a variety of tissues the including the liver, kidney, adrenal gland, spleen, lymph nodes, tonsil, and lung. Ultrastructurally, virus particles were confirmed in nucleus and cytoplasms of pneumocytes around the necrotic areas.

• Korean Journal of Veterinary Research
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• v.44 no.3
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• pp.349-355
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• 2004

The aim of this study was to evaluate the expression of galectin-3, one of beta-galactoside-binding proteins, in the experimental autoimmune encephalomyelitis(EAE) model of Lewis rats or non-obese diabetic (NOD) mice. Western blot analysis showed that galectin-3 was weakly expressed in the spinal cords of complete Freund's adjuvant(CFA) immunized control rats. In EAE, however, galectin-3 expression was significantly increased at the peak stage(days 14 post-immunization), while it was decreased slightly at the recovery stage(day 21 post-immunization). Immunohistochemical analysis showed that galectin-3 was detected in some macrophages in demyelinating lesions of NOD mice, while galectin-3 was immunoreacted in some inflammatory cells in the perivascular cuffing in rat EAE lesions. Collectively, it is postulated that the expression of galectin-3 is significantly increased in response to neuroimmunological stimulation in the central nervous system, whereas it is weak in normal rats and mice.

• Korean Journal of Veterinary Research
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• v.32 no.4
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• pp.605-608
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• 1992

This paper dealt with the clinical and pathological observations on the experimental rabbit viral hepatitis. Rabbits with 2-14 months of ages were intramuscularly inoculated with virus suspension. The results were summarized as follows. Ninety percents of experimental rabbits inoculated with virus died within 96 hours postinoculation. Common clinical signs were inappetence, increase in body temperature, depression, mild diarrhea and in three cases, bloody foam from nostrils was recognized. At necropsy, in most of the experimental cases, there were hyperemia or haemorrhages in many organs and pale liver. Intestinal catarrh and retention of turbid urine in urinary bladder were seen in some cases. Histopathologically, liver necrosis was found in all the cases died of this disease. However, there was a difference in the severity of hepatic necrosis. Haemorrhages were Iecognized in lungs, heart, liver, spleen, kidneys and thymus, in order. Liver necrosis was marked even in the cases with no haemorrhage. Perivascular cuffing in brain and catarrhal enteritis in small intestine were seen in many cases. From these results, consistent and primary lesion in this viral disease is hepatitis in susceptible rabbits. It was concluded that rabbit hepatitis virus might have the properties of hepatotropism and consequently induce peripheral necrosis in the liver leading to acute viremia with haemorrhages.