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Q. Liang, X. Sun, S. Luo, Z. Wang, R. Li; Clinical Manifestation and Pathology Observation of Rabbits Non–Tuberculous Mycobacterial Keratitis . Invest. Ophthalmol. Vis. Sci. 2006;47(13):4375.
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© ARVO (1962-2015); The Authors (2016-present)
To observe clinical manifestation and pathology change of different time points of rabbit keratitis caused by non–tuberculous mycobacteria (NTM).
48 New Zealand White rabbits were randomly divided into 3 groups: subflap infection group, surface infection group, subflap infection group with corticosteroid. After infection, clinical manifestation of all rabbits were observed. 4 rabbits in each group were sacrificed on 5, 7, 14, 21 day. Bacterial quantitative culture and histopathological examination were performed. The latter included hematoxylin and eosin staining, acid–fast staining, and CD4+ and CD8+ T cells immunohistochemistrical staining.
All rabbits developed NTM keratitis in 4.0±1.2 days after surgery. The typical clinical feature included multifocal intense stromal infiltrates. In the course of this disease, the corticosteroid used may worsen the corneal infiltrates and make the cornea difficult to kill NTM. In the earliest stage, significant corneal epithelium proliferation was observed. In corneal stroma, There was infiltrates with polymorphonuclear (PMN) leukocytes, around which acid–fast bacilli was present. The infiltrates of plenty of lymphocytes in the cornea was characteristic to the middle stage of NTM keratitis. There were scattered PMN and a few of proliferated fibroblast cells beneath the epithelium. In the last stage, The fibroblast cells obviously proliferated and corneal cured. The number of CD4+, CD8+ T lymphocyte reached peak, then fell down gradually. CD4+ T lymphocyte decreased significantly in subflap infection group with corticosteroid compared with other two groups, and CD8+ T lymphocyte decreasing significantly on 7, 14 day (P<0.05).
The clinical feature of rabbit keratitis is multifocal dense superficial stromal infiltrates. The infiltration can be deteriorated with treatment of corticorsteroid. The pathogenesis of NTM keratitis is divided into three stages: Acute infection stage characterized with PMN infiltrates in earlier period (<7 days), immunoreaction stage characterized with lymphocyte accumulation in middle period (7∼14 days), and inflammation recession (>14 days). Acquired immunoreaction should play an important role in NTM keratitis.
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