Effects of dual infection of chickens with Mycoplasma synoviae and Mycoplasma gallinaceum or infectious bursal disease virus on infectious synovitis.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to T Nunoya.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Seven-day-old chickens wee intratracheally inoculated with Mycoplasma gallisepticum. The tracheas collected 6 and 14 days after chickens were inoculated were subjected to titration of mycoplasma and examination by light and electron microscopy. The mycoplasma organisms grew well; 10(7) to 10(8) color-changing units in a milligram of tissue were determined. Tracheal lesions occurred in close association with the presence of mycoplasmas and were characterized by degeneration of the epithelial cells and inflammatory cellular infiltration of the mucosa. Mycoplasmas were predominantly found extracellularly and only rarely in phagocytic vacuoles of the epithelial cells. Although the mycoplasmas exhibited considerable pleomorphism in size and shape, most of them were oval or round, and the largest diameters were between 300 and 700 mn. Elongated and irregular forms were also observed, particularly in those mycoplasmas adhering to the epithelial cells. The organism had a limiting unit membrane, the fibrillar nuclear area, the peripheral cytoplasmic area containing numerous ribosomes, and a terminal bleb structure. Mycoplasmas attached to the epithelial cells by their blebs close to the host cell membrane. At the attachment site, neither fusion of the membranes of the mycoplasma and host cell nor injury to the host cell membrane could be demonstrated. Nevertheless, seemingly, the intimate association between the adhering mycoplasmas and the epithelial cells might be an important factor in pathogenesis of the disease.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Enzymatic and non-enzymatic pretreatments for antigen retrieval (AR) on formalin-fixed, paraffin-embedded, deparaffinised sections were compared and optimised by immunostaining of tissues infected with 13 different pathogens. Enzymatic pretreatment was achieved by incubating slides in 0.25 per cent trypsin (TR) and non-enzymatic pretreatments by heating them in a microwave oven (MWO) or an autoclave (AC). Three different buffers of different pH and molarity including phosphate buffer (PB), citrate buffer (CB) and acetate buffer (AB) were used as AR solutions. All of them were effective regardless of molarity, for the MWO with a processing time of 20 minutes, and the AC with a processing time of 15 minutes. The detectability of many viral antigens was significantly improved by MWO or TR pretreatment, but that of most bacterial antigens was not improved and that of some viral antigens was decreased by TR pretreatment. These results suggest that AR pretreatment is a prerequisite procedure for immunohistochemical detection of many infectious agents but the optimal pretreatment has to be individualised for each agent.
A new behavioral mutant showing either head or body quivering, or both, was found in Japanese quail. This trait was characterized by neurofilament deficiency in the axons of the cervical spinal cord and the optic and sciatic nerves and was named "hypotrophic axonopathy." This character was shown to be controlled by an autosomal recessive gene, for which the gene symbol hax was proposed.
The effect of beta-carotene (BC) on the development of pulmonary foam cells (PFCs) was studied in rats with diet-induced hyper beta-lipoproteinemia. Rats were fed a standard diet; a hyper-beta-lipoproteinemia diet (HB) consisting of the standard diet, 4% cholesterol, and 1% cholic acid; or the standard diet plus 0.1% BC; or the HB diet plus 0.1% BC diet (HBC). Rats in the HB and HBC groups developed hyper-beta-lipoproteinemia, but no significant differences were observed in serum levels of total cholesterol, phospholipid, and beta- lipoprotein (B-LP) between both groups. The percentages of foamy, lipid-ingested monocytes (FMs) to the number of blood monocytes (BMs), the number and size of lipid droplets in FMs, the percentages of PFCs to the number of alveolar macrophages from bronchopulmonary lavage fluid, and the score of PFC development in the lungs of rats in the HBC group were reduced compared to those of rats in the HB group. There were no differences in latex-phagocytotic activity of BMs among rats in the control, HB, BC, and HBC groups. BC suppressed the foamy transformation of BMs and development of PFCs deriving from the influx of FMs into the alveoli of hyper-beta-lipoproteinemic rats. Based on the present results, it is presumed that the antioxidative property of BC may prevent an oxidative modification of B-LP under the hyper-beta-lipoproteinemic condition, leading to a decrease in the uptake of oxidatively modified B-LP by BMs.
A spontaneous tumor in the nasal cavity, extending through the cribriform plate to the cranial cavity, was detected in a 103-wk-old female Fischer-344/DuCrj rat. The tumor appeared to arise from the olfactory epithelium and was composed of round to polygonal, undifferentiated cells arranged in solid sheet-like and lobular patterns with scant fibrovascular stroma. Ultrastructurally, the tumor cells often formed desmosomes between contiguous cells and had no neurosecretory granules. Immunohistochemically, the tumor cells did not react with any antibodies specific for intermediate filaments, neuronal, muscular, and endothelial elements. Based on these results, the tumor was diagnosed as undifferentiated olfactory epithelial carcinoma.
The effect of CCl4-hepatotoxicity on the development of pulmonary foam cells (PFCs) was studied using 4 groups of rats. Rats in the control group were fed a standard diet; rats in the second group were fed a hyper beta-lipoproteinemic (HB) diet consisting of the standard diet, 4% cholesterol, and 1% cholic acid; rats in the third group were fed the standard diet and administered with CCl4 (1.0 ml/kg, i.p., fortnightly) (CT); and rats in the fourth group were fed the HB diet and administered with CCl4 (HT). At feeding week 10, rats in the HB and HT groups developed hyper beta-lipoproteinemia. The ratios of foamy, lipid-ingested monocytes (FMs) to blood monocytes (BMs) and the histologic scores of PFC development were significantly greater in the HB and HT groups than in the control and CT groups, respectively. The ratio of PFCs to alveolar macrophages from bronchopulmonary lavage fluid was significantly higher in the HT group than in the CT group. At feeding week 20, rats in the CT and HT groups suffered hepatic injury and hypo beta-lipoproteinemia. Despite hypo beta-lipoproteinemia, the FM and PFC development, the ratio of BMs in differential leukocyte counts, and latex-phagocytotic activity of BMs were enhanced in the HT group. Furthermore, markedly enlarged FMs, described here as giant-FMs, that contained numerous lipid droplets in their abundant cytoplasm appeared in the peripheral blood from rats in the HT group. Histologically, embolism caused by giant-FMs in the pulmonary blood vessels and intraalveolar accumulation of PFCs were detected with a high incidence in the HT group. The present study suggests that CCl4-hepatotoxicity may affect lipoprotein synthesis in the liver of hyper beta-lipoproteinemic rats and defective or modified lipoproteins can be phagocytosed actively by BMs, and then BMs transform into FMs or giant-FMs, resulting in the PFC development and pulmonary embolism by giant-FMs.
Highly virulent infectious bursal disease virus (IBDV) was isolated from field cases, and the pathogenicity of the isolates was examined in specific-pathogen-free chickens. Chickens inoculated with the isolates developed severe clinical disease with a high mortality rate. Histopathologically, infectious bursal disease was characterized by bursal and thymic necrosis, aplastic anemia, acute hepatitis with fatty change, and systemic inflammatory response. In addition to functional abnormalities in the liver, a hypoxic state was induced by aplastic anemia and severe inflammation in the pulmonary air capillary walls. These pathological changes appeared to be closely related to the cause of death.
The immunosuppressive effect of infectious bursal disease virus (IBDV) on vaccination against Newcastle disease (ND) was compared among 2-, 3-, and 4-week-old chickens inoculated with the highly virulent IBDV field isolate 90-11 and the reference serotype 1 strain GBF-1. In all age groups, isolate 90-11 severely suppressed antibody response to ND vaccination and protective vaccinal immunity against ND. In contrast, chickens inoculated with strain GBF-1 and vaccinated with ND vaccine were well protected from the ND virus challenge. The mitogenic response to phytohemagglutinin of splenic lymphocytes from chickens inoculated with isolate 90-11 or strain GBF-1 was significantly lower than that of uninoculated controls. There was no difference between the two inoculated groups in responsiveness, although lymphocyte depletion in the thymus was more severe in chickens inoculated with isolate 90-11 than in chickens inoculated with strain GBF-1.
Chickens of the high-responder line GSP and low-responder line BM-C, which had been known to have different antibody responses to Mycoplasma gallisepticum (MG) antigen, were immunized by intramuscular injection and by subsequent intratracheal instillation of MG bacterin. They were then challenged with the pathogenic strain SAS of MG. The preventive effects of local antibodies detectable in the trachea, saliva, and lacrima were compared between the two lines of chickens. The local antibody responses, as determined by an enzyme-linked immunosorbent assay, were higher in line GSP than in line BM-C before and after challenge. Following challenge, chickens of both lines were protected from colonization by MG and the development of respiratory lesions. The degree of protection in line GSP was higher than that of line BM-C. The results suggest that local antibodies may play an important role in the host defense mechanism to respiratory MG infection.
Abnormal feathers, characterized by thinness and increased transparency of the calamus and rachis, and loss of barbs, were induced at a high frequency by inoculating day-old chicks with reticuloendotheliosis virus (REV) propagated in chicken-embryo fibroblast (CEF) cultures. The few birds that survived inoculation with oncogenic stock of REV derived from liver tissue of an infected chick developed similar abnormalities. Lesions of an inflammatory-degenerative type were observed in close association with the presence of viral antigen and numerous c-type virus particles, characteristic of REV, in the intermediate and cylindrical cell layers of all abnormal feathers examined. These findings, first detected in the intermediate and cylindrical cell layers of developing feathers 6--9 days after infection, suggest that degeneration and necrosis of feather-forming cells result from productive infection of REV, resulting in the development of the abnormal feathers.
Four monoclonal antibodies (MAbs) were developed against serotype 3:A, P-1059 strain of Pasteurella multocida. Enzyme-linked immunosorbent assays were used to screen those hybridomas producing antibodies to either a surface protective (2.5 S) or lipopolysaccharide (LPS) antigen. MAbs 6EE11, D7H10, E11E3, and C11H2 were positive against 2.5 S antigen, and two of them, E11E3 and C11H2, were positive for the LPS antigen. MAbs 6EE11 and D7H10 reacted with a major protein band of molecular weight of 35,500, whereas E11E3 and C11H2 recognized a band with a molecular weight of 12,500 of the 2.5 S antigen. Treatment of the 2.5 S antigen with periodic acid abolished epitopes reacting with E11E3 but not with 6EE11. MAb 6EE11 did not recognize any band in Western blot after proteinase K treatment of the 2.5 S antigen, whereas antibody activity of E11E3 did not change. MAb 6EE11 reacted with serotypes 3, 4, 9, 10, 11, 12, and with M-9 strains in the immunofluorescence test. MAb E11E3 was positive only with serotype 3 or 10 strains, excluding M-9 strain. Electron microscopic studies with P-1059 strain indicated that antigens binding to 6EE11 and/or E11E3 were present in the capsule.
The protective effect of an inactivated Mycoplasma gallisepticum (MG) bacterin was evaluated in chickens subsequently challenged intratracheally (IT) with the homologous strain. Antibody responses in sera and tracheal washings (TWs) from these chickens were determined by an enzyme-linked immunosorbent assay. A group of chickens was vaccinated intramuscularly (IM) with two doses of the bacterin containing aluminum hydroxide gel (IM + IM). Another group was vaccinated IM with the same bacterin followed by IT with bacterin lacking the adjuvant (IM + IT). Chickens of both vaccinated groups had similar levels of antibody in TWs at the time of challenge. MG was eliminated from the trachea at higher rates and inflammatory lesions in the trachea were less severe in vaccinated chickens than in unvaccinated controls. The protective effect in chickens vaccinated IM + IT was greater than that in chickens vaccinated IM + IM. Perhaps vaccinal immunity is mediated by local rather than systemic antibody responses, or perhaps resistance provided by vaccination IM + IT is conferred partly by another immune mechanism such as cell-mediated immunity.
The titer of antibody specific to infectious bursal disease virus (IBDV) was measured by a new method and correlated with protection. Challenge was carried out in chickens with various antibody titers, which were measured using a latex agglutination-inhibition (LI) test, a rapid and easy technique for measuring IBDV VP2-specific antibody. When actively immunized chickens had LI titers of 1:2 or more, almost all were protected from subsequent challenge with highly virulent IBDV. In contrast, even when chickens passively immunized with maternally derived antibody had LI titers of 1:4, half were susceptible to the same challenge.