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Biomedical subjects

C Itakura

Publications and source records attributed to C Itakura.

At least 73 records · Page 4Linked to original sources

Catarrhal proventriculitis associated with a filamentous organism in pet birds.

Catarrhal proventriculitis due to infection by an unidentified organism was diagnosed in 79 of 534 pet birds examined histologically. It was more prevalent in domestic birds (70 cases) than in imported ones (9 cases). A high incidence of the disease was encountered in budgerigars (Melopsittacus undulatus) and it was occasionally found in finches (Poephila gouldiae gouldiae), parakeets (Psittacula Krameri manillensis), Amazona parrots (Amazona aestiva aestiva) and cockatiels (Nymphicus hollandicus). The agent was a large filamentous rod, and was stained positively with Gram, GMS and PAS methods. Histologically, it induced a mild to moderate exudative or proliferative inflammation in the proventriculus. All the cases had an erosion in the gizzard. Ultrastructurally, the organism had a eukaryotic nucleus and three cell-wall layers. Concurrent infections were very common, including adenoviruses (37 cases), giardiasis (31 cases), candidiasis (13 cases), papovaviruses (11 cases) and knemidocoptic mites (11 cases).

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Histopathological survey of protozoa, helminths and acarids of imported and local psittacine and passerine birds in Japan.

A total of 534 psittacine and passerine birds consisting of 241 imported and 293 local birds were examined histologically. As a result, the following parasites were found: Giardia (86 cases), Knemido-coptes (26 cases), coccidia (10 cases), Ascaridia (6 cases), Cryptosporidium (5 cases), Sarcocystis (5 cases), tapeworm (4 cases), microfilaria (2 cases), Hexamita (1 case), and Spiroptera (1 case). High incidences of giardiasis and knemido-coptic infestation were detected in the local birds, but rarely in the imported birds. Giardial trophozoites were observed mainly in the duodenum of budgerigars (Melopsittacus undulatus). Knemidocoptic mites burrowed into the epidermis producing proliferative dermatitis in 25 budgerigars and 1 African Grey Parrot (Psittacus erithacus erithacus). This ectoparasite often infested the skin around the cloaca. Coccidiosis was seen only in the small intestines of the finch (Poephila gouldiae gouldiae), African Grey Parrot, Rainbow lory (Trichoglossus haematodus), Indian Ring-necked parakeet (Psittacula krameri manillensis) and peach-faced lovebird (Agapornis roseicollis). Two parrots (Amazona aestiva aestiva and Psittacus erithacus erithacus) and two budgerigars had intestinal cryptosporidiosis. Conjunctivitis associated with cryptosporidial infection was seen in a lovebird. Sarcocystis cysts containing crescent-shaped bradyzoites were found not only in the thigh and breast but also in the heart and cloacal muscles. Other organisms such as Ascaridia, tapeworm, microfilaria, Hexamita, and Spiroptera were clinically less significant. However, infections such as Giardia and Cryptosporidim might have zoonotic implications.

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Disseminated intravascular coagulation (DIC) in rabbit haemorrhagic disease.

Seven rabbits experimentally infected with rabbit haemorrhagic disease virus were examined haematologically and histologically. Haematologically, activated partial thromboplastin time and prothrombin time were markedly prolonged in the terminal phase of the disease, just prior to death (all the animals died between 27 and 40 hr after inoculation with rabbit haemorrhagic disease virus). There was an increase in the titre of fibrin degradation products and a decrease in antithrombin III activity during the same interval. Acute necrotic hepatitis and disseminated intravascular coagulation (DIC) in many organs, including the lung, kidney, spleen and heart were the characteristic histopathological changes. Thus, the haematological and histological changes suggested that DIC was induced by rabbit haemorrhagic disease virus infection. Severe liver necrosis was considered to be a factor causing DIC by inducing a hypercoagulable condition in the systemic blood circulation.

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Defective expression of neurofilament protein subunits in hereditary hypotrophic axonopathy of quail.

Hereditary hypotrophic axonopathy is an inherited, neuronal cytoskeletal disease of the "quiver" mutant quail (Quv). Nerve tissue pathology is characterized by axonal hypotrophy associated with neurofilament (NF) deficiency in the central and peripheral nervous system. To elucidate the biochemical mechanism of this disease, we examined the in vivo expression of NF triplet protein subunits and the assembly state thereof in neuronal cell bodies in adult Quv and controls. Gel electrophoresis and Western blot analysis indicated that low, middle and high molecular mass NF subunits were markedly deficient in the brain, cervical spinal cord and sciatic nerve of Quv. Immunohistochemically, the spinal cord of Quv had no immunoreactive products corresponding to low molecular mass NF. However, middle and high molecular mass NF antisera stained few axons in the white matter and bound to ventral horn cell bodies, which in the controls were not labeled. Furthermore, a 130-kDa subunit likely to be a non- or hypophosphorylated form of middle molecular mass NF was localized in neuronal cell bodies with considerably stronger intensity than those in the controls. Ultrastructurally, intermediate filaments were not seen in such neurons; instead amorphous matrix was increased between clusters of granular endoplasmic reticulum and in the peripheral cytoplasmic areas. Degenerative changes of the neurons were very rare. We hypothesize that the deficiency of NFs in Quv results from an alteration of filament assembly caused by defective expression of low molecular mass NF. This mutant presents direct evidence for the importance of NFs in achieving and/or maintaining normal axon caliber and provides a novel system for further studies on NF expression, metabolism and function.

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Modified Bielschowsky and immunohistochemical studies on senile plaques in aged dogs.

Aged dogs developed senile plaques (SP) in the brain which were similar to those occurring in aged humans. These SP were studied with a modified Bielschowsky stain and immunohistochemical methods using polyclonal antibodies raised against beta-protein and glial fibrillary acidic protein (GFAP). Serial sections stained by immunohistochemical and modified Bielschowsky stains showed that all areas of slight beta-protein immunoreactivity were intensely stained by the modified Bielschowsky stain. Most SP were observed in the neocortex of the cerebrum. Plaque densities were highest in the cingulate and temporal cortices. There were occasional SP in the subcortical nuclei including the caudate nucleus and putamen, and hippocampus. Based on the morphological characteristics demonstrated by the modified Bielschowsky stain, SP in the brains of the dogs were grouped into 3 types: diffuse, mature and perivascular plaques, of which diffuse plaques were predominant. Various degrees of astroglial reaction were observed in all subtypes of SP except diffuse plaques. These findings indicate that dog may serve as a model for study of the pathogenesis of SP.

Aging↗

Hereditary hypotrophic axonopathy with neurofilament deficiency in a mutant strain of the Japanese quail.

A primary axonal disease affecting the central and peripheral nervous system was discovered in a new mutant strain of the Japanese quail, named quiver (Quv). Quv showed significantly smaller cross-sectional areas of the cervical spinal cord and the optic and sciatic nerves, when compared with controls by light microscopic morphometry. In the cervical spinal cord, electron microscopic morphometry indicated that myelinated axons in Quv were significantly smaller in size than in controls, though greater in density. The axonal circularity was not significantly different from that of controls. Electron microscopically and immunohistochemically, neurofilaments were not detected in the axons or neuronal cell bodies. Axons in Quv were composed mainly of microtubules, which were increased in number in relation to the axonal size. From these findings, the lesions observed in Quv were regarded as axonal hypotrophy (growth arrest or retardation) due to altered neurofilament expression.

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Primary culture of chicken bursal plical epithelium.

Plical epithelial cells were obtained by trypsin-EDTA treatment of chicken bursa of Fabricius and cultured in the presence of type IV collagen. The culture became confluent six to seven days after seeding. The grown cells showed a positive reaction for cytokeratin by immunostaining and had ultrastructural characteristics of the epithelial cells in vivo. The cell culture will be useful for parasitological and virological studies.

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Glomerular lesions in spontaneously occurring diabetic WBN/Kob rats.

Glomerular lesions in WBN/Kob male rats with spontaneous diabetes were examined histopathologically. The glomerulopathy caused by diabetes was compared with lesions in chronic progressive nephropathy of non-diabetic SD and F344 male aged rats. Diffuse and global thickening of the mesangial area was observed only in WBN/Kob rats and showed a statistically significant correlation with serum glucose concentrations. Therefore, it suggested that the mesangial thickening was a result of hyperglycaemia. Fibrin cap-like lesions were seen in both WBN/Kob and non-diabetic SD or F344 male rats. The severity of these lesions was closely related to that of chronic progressive nephropathy and, therefore, the fibrin cap-like lesions were considered to be due to the chronic progressive nephropathy.

Age Factors↗

Chronic lesions of thrombo-embolic meningo-encephalomyelitis in calves.

Six calves showed neurological signs with recumbency for 5 to 30 days. Histologically, they had encephalomyelitis characterized by multiple minute foci of malacia and perivascular microgliosis throughout the central nervous system. Widespread degeneration of the white matter was also detected mainly in the spinal cord. Micro-abscesses and thrombophlebitis, which were occasionally observed in the malacic lesions, suggested that the disease was a feature of infectious thrombo-embolic meningo-encephalomyelitis modified by various factors, including antibiotic therapy.

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Renal lesions in rats infected with Rattus serotype hantavirus (SR-11 strain).

Hemorrhagic fever with renal syndrome (HFRS) virus, strain SR-11 (SR) was inoculated intraperitoneally into specific-pathogen-free (SPF) newborn rats, from which the kidney lesions were examined pathologically. The infected rats revealed proteinuria on and after 16 days postinoculation (PI). Histologically, the epithelial cells of the renal tubules showed mild vacuolar and granular degeneration with cytoplasmic inclusion bodies (CIB) on and after 16 days PI. Ultrastructurally, a decrease in number of mitochondria and endocytic vesicles was recognized in the epithelial cells of the proximal renal tubules. Occasionally, both the proximal and distal renal tubular cells had CIB near well-developed Golgi apparatus on and after 13 days PI. Immunohistochemically, CIB were positive for anti-SR nucleocapsid antibody, but negative for anti-SR envelope protein antibody. From the results obtained here, it was concluded that the proteinuria in rats infected with HFRS virus resulted from an insufficiency of reabsorption in the proximal renal tubules, and that CIB consisted of the viral nucleocapsid protein.

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Pathological studies on central nervous tissues of rats infected with Rattus serotype hantavirus (SR-11 strain).

Newborn rats inoculated intraperitoneally with a hantavirus strain (SR-11) developed neurological signs such as ataxia and limb paralysis. The main histological lesions were scattered and multiple neuronal degeneration and necrosis with eosinophilic cytoplasmic inclusion bodies (CIB) in the brain, spinal cord and ganglia. Immunohistochemically, the viral antigen was detected in neurons, capillary endothelial and glial cells throughout the nervous tissue and CIB were identified as consisting of hantaviral antigen (nucleocapsid protein). Ultrastructurally, CIB in the neurons consisted of an accumulation of granular or filamentous materials, or both. They were seen near a well-developed Golgi apparatus and associated with well-developed rough endoplasmic reticulum and increased numbers of ribosomes. The present results suggested that this virus strain was highly infective in neurons of the newborn rats and that excess production of viral antigen which accumulated as CIB resulted in the neuronal changes.

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Etiology of rabbit haemorrhagic disease spontaneously occurring in Korea.

Causative agent of rabbit haemorrhagic disease (RHD) was purified by CsCl density gradient centrifugation from the liver homogenate of rabbits infected with RHD virus which originated from Korea. The viral particles were 35-40 nm in diameter, and had hollow depressions on their surface. Protein A-gold immunoelectron microscopy clearly showed that the convalescent antisera of diseased rabbits reacted specifically with the virus particles. SDS-PAGE and Western blot analyses demonstrated that the structural protein of the virus was composed of a single major polypeptide of 63 kD. These findings indicate that the causative agent of RHD, tentatively named as picornavirus in Korea, belongs to calicivirus.

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Cryoglobulinemia in a horse.

Cryoglobulin was isolated from a horse which had glomerulo-nephritis and a history of swelling and skin ulcers of the limbs in the winter. The isolated cryoglobulin showed a single peak on a gel permeation chromatography column with an apparent molecular mass (Mr) of 180,000 which could be divided into two gamma bands by cellulose acetate electrophoresis. Immunoelectrophoretic analysis revealed that the cryoglobulin formed two precipitation lines with anti-horse IgG. Spur formation was observed when the cryoglobulin and the IgG purified from a normal healthy horse were cross-reacted with anti-horse IgG on a double diffusion gel. In addition, sodium dodecyl sulfate-polyacrylamide gel electrophoresis under the reduced conditions showed that the isolated cryoglobulin consisted of two doublets of polypeptides with Mr values of 52,000 and 50,000, and 31,000, and 30,000, corresponding to the heavy chain and the light chain of the horse IgG molecules, respectively. These results suggest that the isolated cryoglobulin might consist of two different IgG molecules, and that the manifestations such as foot swelling with skin ulcers and renal failures were all induced by the cryoglobulin in the serum.

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Glycogen accumulation in the renal tubular cells of spontaneously occurring diabetic WBN/Kob rats.

Cytoplasmic and nuclear accumulation of glycogen granules in the kidney cells of 72 male WBN/Kob rats with a long-term diabetic condition was studied histologically and by electron microscopy. The incidence and degree of the accumulation showed good correlation with the blood glucose concentration. In the kidneys, there was evidence of two types of lesion, cytoplasmic glycogen accumulation in the distal convoluted tubules and nuclear accumulation in the ascending thick segment of Henle's loops. Electron microscopically, the cytoplasmic glycogen accumulation was often associated with an increased number of lysosomal bodies containing lamellar bodies. Glycogen bodies, the halo of which was thought to be identical with that of nuclear bodies, were frequently observed in the nuclei containing the glycogen granules. These morphological and topographical differences between the two types of lesion were considered suggestive of different pathogenetic mechanisms for glycogen accumulation in the kidney cells.

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Histopathological development of equine cutaneous papillomas.

The histopathological development of equine cutaneous papillomas was studied in 78 warts naturally occurring in 50 one to 3-year-old Thoroughbred or Arab horses and in 54 warts experimentally induced in three 2-year-old Thoroughbreds. Lesions in the natural cases were categorized into three phases, growth, development and regression. Main lesions of the growing phase were marked hyperplasia of the basal cells and mild to moderate acanthosis, hyper- and parakeratosis with a few intranuclear inclusion bodies (IIB) which were positive with anti-bovine papillomavirus serum. In the developing phase, there was prominent acanthosis with cellular swelling and fusion, and marked hyper- and parakeratosis. Many IIB were also present in swollen or degenerative prickle cells and granular cells, with a high degree of parakeratosis in keratinocytes. In the regressing phase, epidermal layers were almost normal with only slight hyperplastic change. However, there was rete peg proliferation downward into the dermis with moderate proliferation of fibroblasts and collagen fibres. In addition, in 10 spontaneous and one experimental wart, the lesions were fibropapillomas and this has never been described in horses previously. It was concluded that papillomas were initiated by basal cell hyperplasia without viral antigen production, with formation of acanthosis and hyper- and parakeratosis with IIB production. These findings were confirmed by examination of the experimental cases on the basis of the gross diameter of the warts.

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Keratin expression in equine normal epidermis and cutaneous papillomas using monoclonal antibodies.

Keratin expressions in normal equine epidermis and experimentally induced equine papillomas were studied by immunohistochemical methods with three different human cytokeratin monoclonal antibodies, 34 beta B4 (directed against component 1), 34 beta E12 (directed against components 1, 5, 10, 11) and 35 beta H11 (directed against component 8). Staining patterns with 34 beta B4 and 34 beta E12 in the normal equine epidermis did not differ from those in the normal human epidermis. In the early developing papilloma, keratinocytes showed an abnormal suprabasal staining pattern and expressed an additional 56 kD keratin protein detected by 34 beta E12. In the advanced papilloma, cytolytic cells in the outer spinous and the granular layers did not stain positively with any of the three antibodies used. In both early and advanced papillomas, the expression of high molecular weight keratin proteins, as detected by 34 beta B4 and 34 beta E12, did not correlate with the degree of keratinization. By electron microscopy, keratinocytes in the advanced papilloma showed a marked decrease of tonofibrils and desmosome-tonofilament complex. These alterations may result from an abnormality in both proliferation and functional terminal differentiation of keratinocytes in the papilloma. There were obvious differences in staining patterns with 35 beta H11 between the normal human and equine epidermis; 54 kD keratin protein was expressed in suprabasal layers of the equine normal and papillomatous epidermis. Thus, this keratin protein may be regarded as a "permanent" marker for the equine epidermis.

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Ultrastructural morphology of hypomelanosis in equine cutaneous papilloma.

The morphology of hypomelanosis occurring in experimentally induced equine papillomas was investigated. Histologically, dopa-positive functioning melanocytes were decreased in number from the basal layer in the epidermis. Electron-microscopically, melanogenic organelles in the melanocytes were degenerate and melanosomes were decreased in number and size. In addition, the melanocytes had some abnormal melanosomes including melanosome complexes and giant melanosomes. Some abnormal melanosomes were also present in the keratinocytes. The hypomelanosis seemed to be related to a disturbance in melanin synthesis and melanocytic-keratinocytic interaction in the epidermal melanin unit.

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