Ocular defects and age-related lesions in mutant (GUB strain) Japanese quail (Coturnix coturnix japonica), phenotypically characterised by silver plumage, are described. Grossly, a circular area of hypopigmentation in the posterior retina with thinning of the subjacent sciera was observed in all GUB quails. As the birds matured, the thinned sciera progressed to scierai ectasia. Histologically, the sciera at the ectatic area consisted of an outer fibrous layer and was devoid of the inner cartilaginous shell. Atypical differentiation and duplication of the retina with absence of the choroid was common at the ectatic area. The retina, choroid, ciliary body and iris were all poorly pigmented. With increasing age, the ectatic area became cystic, and the duplicated retina degenerated and atrophied. In addition, there were mononuclear cell infiltration in the stroma of the iris and ciliary body, anterior and posterior synechiae, cataract and/or glaucoma in aged GUB quails. These findings suggest that posterior scierai ectasia in the GUB strain of Japanese quails may have developed secondarily to a congenital structural defect of the posterior portion of sciera associating with general ocular defects.
SUMMARY The effect of immunosuppression on Mycoplasma hyopneumoniae infection was evaluated by comparing data from infected, thymectomized, and antithymocyte serum-treated pigs (group 1) with data from infected (group 2) and noninfected (group 3) healthy pigs. After groups 1 and 2 pigs were inoculated intranasally with M hyopneumoniae, mycoplasmas tended to multiply slightly more in the lungs and bronchial lymph nodes of group 1 pigs than that of group 2 pigs. Organisms were also isolated from the spleen of 1 of 3 group 1 pigs. Pneumonia developed in group 2 pigs and was characterized by massive peribronchial, peribronchiolar, and perivascular lymphoid hyperplasia and exudate consisting mainly of polymorphonuclear leukocytes in the alveoli and lumina of the bronchioles and bronchi. In group 1 pigs, perivascular and peribronchiolar cuffings by lymphocytes were less prominent, and the extent of intraluminal exudate was severe and widespread. Bronchial lymph nodes from group 2 pigs had marked hyperplasia of germinal centers and paracortical areas. In group 1 pigs, germinal centers were hyperplastic, whereas in the paracortical areas, depletion of lymphocytes was evident. Seemingly, cell-mediated immune mechanisms are important in the development of pneumonic lesions in enzootic pneumonia of pigs.
Natural cases of keratoconjunctivitis, apparently caused by Mycoplasma gallisepticum (MG), in layer chickens are described. The disease occurred in a commercial flock consisting of 36,000 pullets (Babcock), first appearing around 30 days of age. Clinically, affected chickens showed unilateral or bilateral swelling of the facial skin and the eyelids, increased lacrimation, congestion of conjunctival vessels, and respiratory rales. Some of the severely affected chickens closed their eyes. The morbidity reached 27.8%, and it was estimated that approximately 10% died from reduced feed intake due to impaired vision. Ten 70-day-old chickens with clinical diseases were examined for lesions. There was acute to subacute keratoconjunctivitis in all of the chickens, and some exhibited laryngitis. Adherence of mycoplasma organisms to epithelial cells of the conjunctiva, cornea, and larynx was frequently observed. These organisms had an ultrastructure characteristic of MG and showed a positive reaction with rabbit polyclonal antibodies against the S6 strain of MG by immunohistochemical analysis. MG was isolated from tissue homogenates of the eyelids and tracheas of the affected chickens. Many of the chickens had atrophic bursae, and infectious bursal disease virus antigens were detected in necrotic bursal follicles by immunostaining. Therefore, immunosuppression due to infectious bursal disease was implicated in the pathogenesis of keratoconjunctivitis in the present cases.
A ruthenium red-staining capsule was observed on two pathogenic strains, but not on one nonpathogenic strain of Mycoplasma gallisepticum. The capsule appeared to mediate cytadsorption of mycoplasmas to the chicken tracheal epithelium without evidence of membrane fusion. No relationship was seen between the presence of capsule and hemagglutination titers of the strains examined.
HypothesisAlthough rheumatoid arthritis (RA) is believed to be primarily an inflammatory disease of synovium, there is a good possibility that the initiation of the rheumatoid process is triggered by the autoimmune reaction involving type II collagen in the articular cartilage as a consequence of an unknown aetiological agent.Synovitis and other extra-articular features may be induced secondary to the immune complex formation in the subchondral area.Extensive scientific data on the immune nature of RA have been accumulated. 1 According to this, RA is considered to be an autoimmune disease that is presently incurable.Although its aetiology remains unknown, most investigators believe that RA is primarily an inflammatory disease of synovial membrane of the joints.However, here we show evidence that RA primarily involves articular cartilage and subchondral bone, not the synovium; this new direction of research may allow for the development of a specific treatment for the disease.It is generally accepted that the initial events in the development of articular damage is the proliferation of synovial cells together with inflammation and vascular neoformation in the stroma of synovial tissue. 2 As the disease progresses, the proliferating synovial tissue extends over the articular cartilage and erodes from the joint surface down to the subchondral bone.Eventually, small and large joints of the patient are destroyed, deformed and ankylosed.Recently, we have focused on the following clinical facts that raise an important question: Is RA really a synovial disease?Firstly, although administration of non-steroidal antiinflammatory drugs, anti-rheumatic medicines and corticosteroids is recognised as a fundamental conservative treatment for RA, these cannot completely suppress the synovitis of aVected joints.4][5] Secondly, synovitis progression tends to gradually decrease when articular cartilage and bone are severely destroyed in the advanced stages. 6Thirdly, active synovitis remarkably diminish after excision of articular cartilage and subchondral bone during prosthetic joint replacement even
