[Cephalometric analysis on anterior crossbite treated using activator].
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Biomedical subjects
Publications and source records attributed to Y Imada.
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Outbreaks of Mycoplasma bovis-associated otitis media and pneumonia occurred on four beef cattle farms in Hokkaido, Japan between 2000 and 2001. The morbidity and mortality were estimated at 8-40 and 30-100%, respectively. Eight calves with bilateral ear droop and exudative otitis media were examined bacteriologically and histopathologically. M. bovis was isolated post mortem from nasal swabs and from the ears, lungs, lymph nodes (cranial and pulmonary), brain and heart of all calves. At necropsy, suppurative exudates were observed in the tympanic bullae of all cases. Numerous abscesses were also found in the petrous portion of the temporal bone and lungs in seven cases. Histopathologically, the exudates within the tympanic bullae consisted of a mixture of neutrophils, necrotic cell debris and fibrin, and the tympanic mucosa was thickened with neutrophil and macrophage infiltration and proliferation of fibrous connective tissue. Pulmonary lesions included extensive foci of coagulative necrosis surrounded by numerous neutrophils. Hepatocytes or renal tubular epithelial cells were enlarged with hyaline cytoplasmic inclusions in four calves. Immunohistochemical labelling confirmed the presence of M. bovis antigen in the cytoplasm of the inflammatory cells in the middle ear, temporal bone and lungs, and was also demonstrated within the cytoplasmic inclusions of the hepatocytes and renal tubular epithelial cells. Ultrastructurally, mycoplasma-like organisms, 200-500 microm in diameter, were found within not only hepatocytes and renal tubular epithelia but also within axons of the facial nerves. The present results show that M. bovis spreads to multiple organs and is capable of invading various kinds of host cell. The intracellular localization may be favourable for evading host immune responses.
Temperature-sensitive (ts) mutants of Mycoplasma synoviae were produced by treating the wild 1-3SN strain with N-methyl-N'-nitro-N-nitrosoguanidine. Twelve ts mutants were selected at 39.5 C as a restrictive and 33 C as a permissive temperature. Among the mutants, MSts44 was proven to be nonpathogenic but immunogenic. MSts44 did not induce airsacculitis in bursectomized or normal chickens, and it was stable after five passages through chicken. Chickens immunized intranasally with MSts44 were protected against airsacculitis for at least 21 weeks. A dose of 10(4.1) colony-forming units or more of the mutant per bird was needed to induce protection in 3-week-old chickens.
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