Antigenic variation between Newcastle disease viruses of goose and chicken origin.

Newcastle disease virus (NDV) is believed to infect only domestic avian species, with waterfowl such as geese either not being infected, even by virulent strains, or developing only inapparent infection. Since the late 1990s, a new infectious disease producing high morbidity and mortality among geese broke out in many provinces of China. This disease was caused by a serotype I avian paramyxovirus known as (APMV-1)-NDV. To investigate how NDV spreads between chickens and geese, the serological similarities of NDV strains (goose-origin NDV/NA-1 and chicken-origin NDV/F48E9, F48E8) were assessed by cross-neutralization assays both in vivo and in vitro. The results indicated that antigenic variation had occurred between NDV/NA-1 strains and NDV/F48E9, F48E8 strains. Notably, NDV/NA-1 effectively protected vaccinated birds from morbidity and mortality against NDV/NA-1 strain challenge and significantly reduced virus shedding from the vaccinated birds when compared with F48E9-vaccinated birds. This might provide clues to the evolution of the goose NDV.

ERIC-PCR genotyping of Pseudomonas aeruginosa isolates from haemorrhagic pneumonia cases in mink.

BACKGROUND: Pseudomonas aeruginosa is a significant pathogen of mink and the cause of haemorrhagic pneumonia, an acute fatal disease in farmed mink. RESULTS: Among 90 P. aeruginosa isolates from haemorrhagic pneumonia in mink from 16 farms in Shandong province, China, 43 genotypes were identified by enterobacterial repetitive intergenic consensus PCR (ERIC-PCR), with a diversity index of 0.96. The most prevalent ERIC-PCR types were type 18, found in 16 isolates, and type 39, found in 15 isolates. Four serotypes were detected, with serotype G (55.6 per cent) being the most frequent. CONCLUSIONS: These results showed that there was a high degree of clonal diversity among mink P. aeruginosa clinical isolates in this study.

Expression of interleukin 6 in brain and colon of rats with TNBS-induced colitis.

AIM: To characterise expression of interleukin 6 (IL-6), a potent proinflammatory cytokine, in the occurrence and development of inflammatory bowel disease (IBD) and investigate its effect on neuroimmunomodulation and immune homeostasis regulation. METHODS: In this study, rats with colitis induced by trinitrobenzene sulfonic acid (TNBS) were sacrificed on days 3, 7, 14, 21 and 28 after induction. In the controls, the TNBS was just replaced by equivalent amount of phosphate buffered solution (PBS, 0.01 mol/L). IL-6 mRNA expression in brain and colon tissues in each phase was evaluated by real-time reverse transcription-polymerase chain reaction, and cellular localisation and protein level of IL-6 was determined by immunohistochemistry. RESULTS: At day 7, mRNA expression of IL-6 was significantly higher in the colon and brain of IBD rats than that of the controls. The protein level was also significantly higher in colon, hypothalamus and cerebral cortex of IBD rats compared with the controls. So there are similar temporal trends in IL-6 mRNA expression and protein levels in all positions with a persistent increase to a peak at day 7, followed by a decline and gradual return to normal levels. CONCLUSION: These results revealed that changes in IL-6 expression in brain and colon tissues occur in different phases of IBD. Therefore, we propose that the nerve centre regulates and controls the occurrence and development of IBD via IL-6.