The relationship between the changes of erythrocyte lipids concentration and the osmotic fragility of erythrocytes was examined in cats infected with Haemobartonella felis. In these cats the cholesterol and phospholipid concentration of erythrocytes decreased markedly as anemia induced. by H. felis became severe, while both lipids of the plasma showed no significant change in concentration. The osmotic fragility of erythlocytes increased progressively in proportion to the decrease of erythrocyte lipids concentration. The phospholipid composition of erythrocytes was not changed by infection of H. felis. The mean size of erythrocytes was reduced in the infected cats as the anemia progressed, while it increased in the remission of the anemia. Discussion was made on the cause of lipids loss in erythrocytes of cats infected with H. felis.

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Serum lactate dehydrogenase (S-LDH) activity was determined four times over a time course in 178 Japanese Black cattle of two groups which were positive and negative, respectively, for antibody against bovine leukemia virus. As a result, no significant difference in S-LDH activity was evidenced by the two groups at any time of testing. Seven to 12 months later, some cattle of the negative group were antiobdy-positive when examined by the immunodiffusion or complement fixation test. They failed to indicate any significant change in S-LDH activity, as compared with this activity shown when they were antibody-negative. A comparison was made between the zymograms of 19 antibody-positive cattle and antibody-negative cattle, both of which groups were randomly selected. They revealed significantly high LDH₂ and LDH₃ activity and markedly low LDH₁ activity in the positive cattle. The mean S-LDH activity was significantly higher in 8 leukemic cattle than in both positive and negative groups, although no increase was found in 2 leukemic cattle. Moreover, the isoenzyme activity showed a significant increase in LDH₂ and LDH₃ even in cattle exhibiting no increase in total S-LDH activity.

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Eleven (11.7%) of 94 cows affected with the adult type of bovine leukosis were diagnosed as aleukemic cases by the hematological diagnostic key of the European Community (EC). Atypical mononuclear cells (AtMC) amounted to only 143-450/cmm (1.5-3.6%) in the peripheral blood of three of the 11 cows. These findings were indistinguishable from those of healthy cattle. Although no persistent lymphocytosis was observed in the other 8 cows, AtMC amounted to 891-2, 912/cmm (9.5-28.0%). Histopathological and ultrastructural studies on tumorous lesions and cells in the aleukemic cows revealed no essential differences from those on leukemic leukosis. A common finding of aleukemic leukosis obtained was practically no proliferative lesions of neoplastic cells in the spleen. One of the 3 cows without showing an increase in AtMC in the peripheral blood was considered to be in the early stage of disease. In it tumorous lesions were detected only in some of the lymph and hemolymph nodes. On the other hand, fairly marked tumorous lesions were found in the visceral organs of the other 2 cows. Neoplastic cells were located dispersedly in the dilated sinus of most of the lymph nodes in the 3 cows. This findings seemed to indicate that there might be enough room in the sinus for neoplastic cells to proliferate in the lymph nodes and to obstruct the AtMC flow into the peripheral circulation. From the results obtained, discussion was made on the necessity of careful observation of the blood smear for an accurate diagnosis of aleukemic bovine leukosis by the hematological diagnostic key of EC.

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A necrotizing encephalopathy with massive cerebral cortical necrosis was produced in suckling rats inoculated intracerebrally with MHV-A59 strain. After inoculation at 3 days of age most rats died on 6 to 13 days postinoculation showing a central nervous symptom. At autopsy the cornus ammonis was visible through the edematous leptomeninges owing to liquefactive necrosis of the cerebral cortex with increased cerebrospinal fluid in the lesion. By immunofluorescence viral antigen was detected in neurons of the cerebral cortex on day 2 or later postinoculation. Histopathologically degeneration or necrosis of neurons and glial cells were recognized in some liquefactive foci. After inoculation of the same virus at 7 days of age all suckling rats survived, while they had necrotic lesions in the brain, which tended to have repairing process consisting of gliamesenchymal scarring. There were little changes in the brain of rats inoculated at 2 weeks of age.

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A total of 64 canine cases of so-called mitral valvular fibrosis were studied morphologically and histologically. They were divided into three groups. Group I had small, discrete lesions with or without large nodules in the rough zone. Group II exhibited extensive thickening all over the rough zone. Group III had remarkably thickened leaflets and ruptured chordae tendineae. Morphologically, as the disease progressed in severity, the leaflets apparently became more and more redundant and the chordae tendineae gradually elongated. Chordal rupture was found in 8 of 12 cases of Group III. The Characteristic histological changes were the destruction of collagen bundles and the deposition of acid mucopolysaccharide in the spongiosa and the fibrosa. The destruction of chordal collagen bundles was especially severe in the case of chordal rupture. It is considered that these morphological changes closely resemble those found in the mitral valve prolapse syndrome in human beings.

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Sendai virus was first isolated from the tracheas and lungs of mice 1 to 2 days after cage-mating with infetctors, following by formation of lung consolidation in all mice examined 6 to 7 days. HI antibody was demonstrated in all mice 7 to 10 days, increasing in titers to 14 days. Isolation of the virus was negative from 12 days till 30 weeks when the experiments were terminated, except for some mice sacrificed 9 weeks which harbored the virus in their tracheas. HI antibody remained at high titers till the end of experiment and lung lesions persisted in more than a half of mice examined, although the affected area was localized around bronchioles in late stage of the infection. These findings were almost the same in both ddY and ICR strains of mice used, but a high mortality as 26.2 per cent was shown in ICR mice, being significantly different from 3.6 per cent in ddY mice. In offsprings from infected dams, maternal HI antibody of high titer was demonstrated at weaning, then it rapidly decreased to the lowest titer 7 to 14 weeks of age when the virus was isolated from the respiratory tracts of a few individuals. Thereafter the antibody titers increased again and isolation of the virus became negative. Detection rates of lung lesions were remarkably low in coraparison with those of their dams and neither death nor such clinical signs as ruffled fur and emaciation appeared.

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Leukocyte migration inhibition tests (LIT) with chicken peritoneal cells were carried out by the direct and the indirect techniques in chickens immunized with Eimeria tenella. In LIT by the direct technique, migration of peritoneal cells was inhibited by adding antigen prepared from the 2nd-generation merozoites. The activities of leukocyte migration inhibitory factor (LIF) were detected from 1 week after a single inoculation with 50, 000 oocysts of 3 weeks after the last of 3 repeated inoculations with 50, 000 oocysts. Spleen cells obtained from immunized chickens elaborated LIF into the medium when they were cultivated with antigen. In LIT by the indirect technique, supernatant of the cultures of spleen cells from immunized chickens inhibited migration of peritoneal cells collected from normal chickens. The LIF activities detectable by the indirect technique were demonstrated for 5 weeks after the last of 3 repeated inoculations with 50, 000 oocysts.

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Fourteen cases of swine porphyria were collected at a slaughter house in Tokyo, and investigated clinically and pathologically. All animals were born from a boar of Duroc race, indicating or suggesting occurrence by a Menderian recessive factor. All the cases had delay of growth, anemia and porphyrinulia. Chocolate-brown discoloration occurred markedly or moderately in the bones, bone-marrow, liver, spleen, lung, kidney, adrenal cortex, medullary cord of lymph node and anterior lobe of pituitary gland, which gave red fluorescence under ultraviolet light. Histopathologically, the deposition of porphyrin granules were mainly observed in reticuloendothelial cells of these discolored organs and epithelial cells as well as hyalin casts within renal tubules. Extramedullary hematopoiesis was present focally in the spleen, liver, kidney and adrenal gland, and degeneration was observed in liver cells and renal epithelial cells.

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Histopathological observation was conducted mainly on the laminar layers of 17 affected and 13 unaffected hoofs from 10 laminitis-affected horses and also on the branches of digital nerves and the vascular nerves of digital arteries and veins from laminitis-affected and 20 control laminitis-unaffected horses. The laminar layer in the laminitis-affected hoofs thickened and was 22.2±8.3 mm thick (A), while 6.6±4.1 mm in the laminitis-unaffected (B) and 3.7±0.9 mm in 43 control hoofs (C); there were significant differences between A and B, A and C, and B and C, respectively. Principal changes in the laminitis-affected hoofs were: (a) in the epidermal laminae, irregular striking growths of the epithelium, hydropic degeneration of ebithelial cells, nonformation, defective formation or degeneration of onychogenic fibrils, and formation of keratohyalin granules; (b) in the dermal laminae and laminar corium, edema, capillary and venular dilatation, and edema of the nerve bundles. The peripheral nerves, including the vascular nerves, showed frequent edema and/or multifocal loss of nerve fibers in the nerve bundles. The morphological entity of the thickening of the laminar layer was regenerative growths of the epidermal laminae in the line of defective onychogenic process (squamous metaplasia). The changes in the laminar layer may have been effected by circulatory disturbances and such a disorder of vascular movement as is inferred from the organic disturbances in the peripheral nerves may have played an important role as the origin of the circulatory disturbances.

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[in Japanese]

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[in Japanese]

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[in Japanese]

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