Schuller Simone, Callanan John J, Worrall Sheila, Francey Thierry, Schweighauser Ariane, Kohn Barbara, Klopfleisch Robert, Posthaus Horst, Nally Jarlath E
University College Dublin, School of Veterinary Medicine, Dublin, Ireland; Vetsuisse Faculty Bern, Länggassstrasse 128, 3012 Bern, Switzerland.
University College Dublin, School of Veterinary Medicine, Dublin, Ireland; Ross University School of Veterinary Medicine, St Kitts, West Indies.
Comp Immunol Microbiol Infect Dis. 2015 Jun;40:47-53. doi: 10.1016/j.cimid.2015.04.002. Epub 2015 Apr 30.
Leptospiral pulmonary haemorrhage syndrome (LPHS) is a severe form of leptospirosis. Pathogenic mechanisms are poorly understood. Lung tissues from 26 dogs with LPHS, 5 dogs with pulmonary haemorrhage due to other causes and 6 healthy lungs were labelled for IgG (n=26), IgM (n=25) and leptospiral antigens (n=26). Three general staining patterns for IgG/IgM were observed in lungs of dogs with LPHS with most tissues showing more than one staining pattern: (1) alveolar septal wall staining, (2) staining favouring alveolar surfaces and (3) staining of intra-alveolar fluid. Healthy control lung showed no staining, whereas haemorrhagic lung from dogs not infected with Leptospira showed staining of intra-alveolar fluid and occasionally alveolar septa. Leptospiral antigens were not detected. We conclude that deposition of IgG/IgM is demonstrable in the majority of canine lungs with naturally occurring LPHS, similar to what has been described in other species. Our findings suggest involvement of the host humoral immunity in the pathogenesis of LPHS and provide further evidence to support the dog as a natural disease model for human LPHS.
钩端螺旋体肺出血综合征(LPHS)是钩端螺旋体病的一种严重形式。其致病机制尚不清楚。对26只患有LPHS的犬、5只因其他原因导致肺出血的犬以及6个健康肺组织进行了IgG(n = 26)、IgM(n = 25)和钩端螺旋体抗原(n = 26)标记。在患有LPHS的犬肺中观察到三种IgG/IgM的一般染色模式,大多数组织呈现不止一种染色模式:(1)肺泡间隔壁染色,(2)偏向肺泡表面的染色,(3)肺泡内液体染色。健康对照肺无染色,而未感染钩端螺旋体的犬出血性肺呈现肺泡内液体染色,偶尔肺泡间隔也有染色。未检测到钩端螺旋体抗原。我们得出结论,在大多数自然发生LPHS的犬肺中可证实IgG/IgM的沉积,这与在其他物种中所描述的情况类似。我们的研究结果表明宿主体液免疫参与了LPHS的发病机制,并为支持犬作为人类LPHS的自然疾病模型提供了进一步的证据。