Study On The Pathogenesis Of Chicken Viral Proventriculitis

Chicken viral proventriculitis was first isolated from chicken flocks in Tai'an. The isolated virus was identified typical coronavirus by chicken-embroy-passage test, morphology observing, PCR and artificial infection test. The viral particles were about 80-160nm in diameter,and they had capsules and ciliary process. The chicken-embroy vaccinated virus allantoid fluid did not have directly hemagglutination activity .The PCR result indicated that the isolated virus had the same band with the identified SI gene of QX strain, whichwas about 1.7 kb.CVP spreaded widely in our country recent years. The lab model of disease was difficult to copy so in this study we set up multi-factors pathogenicity model, infected CVP or correlative viruses.The pathogenisis of CVP was studied by clinic observing , pathologic examination and blood biochemistry indexs test. This test used four kinds of viruses: QX strain, REV, FDV and IBDV vaccine. The 1-day old SPF chickens were divided into 8 groups at random . One group was control and the others were divided into singleness or commixed infective groups, setting multi-factors disease model of avian infectious proventriculitis. Through this method we copied the CPV disease successfully. The mortality was most highest with four kinds of viruses total infection group(78%), the QX strain infected group was lightest(35%).Some chickens were killed at 35 and 60 day after infection, collecting the serum then measuring the difference serum enzyme, protein, electrolyte and blood sugar etc. The results showed that, the content of total albumin and glucose in all infected groups were lower than matched control(P>0.05) at 35 day;the content of the LDH. CK and the serum carbamide nitrogen in allinfected groups were lower than control significantly(P>0.05),the content of electrolyte such as Ca2+, P6+,K+, Na+, Cl- in all infected groups were lower than control significantly (P>0.05). For the 60 days chicken , the content of serum protein, the serum carbamide nitrogen, LDH, CK in all infected groups were lower than control significantly (P<0.01),but the content of electrolyte in all infected groups were higher than control,however the difference of the content of serum K in all infected groups were significant than control.At the same time, the indexes of all the infected groups were not consistent. The ranking from light to heavy is Q →QF→QI→QR→QRF→QRI→QRIF.The lymphoid cell apotosis of chickens immunity organs were studied by using immunohistochemstry electromicroscopy and H.E. dyed technique.We discovered that each virus infected groups could cause lymphoid cell apotosis obviously, especially in the earlier period infected. Cell apotosis degree in the group with four kinds of viruses infected together was most heavy, and the QX strain infected group is most light.The dynamic pathology of each groups' immunity organs and gland stomach, small intestines and part of internal organs ( liver, kidney, lung, myocardial, brain...etc.) was studied by H.E. dyed method, the results showed that the character of pathological changes was same, but the degree of pathological changes was not same. The pathological changes in kidney is serious in early days,including the epithelium of nephric tubule denaturalization and necrosis, internal inflammatory cell soakage and accumulation of uric acid salt. In later days the pathological changes of gland stomach and intestines became serious gradually, the gland stomach intumescence, hyperplasia of lymphocyte in mucoderm and gland. Pathological changes degree in all viruses infected groups was not same in other organs. The pathological lesion was most heavy with four kinds of viruses total infected group,and the QX strain infected group was the lightest.The result show that other pathogen factors can strengthen the pathogenesis action, and it can weaken the chichen condition, diminish theimmune function and result in the local pathological changes in gland stomach. This is just the main renson why other pathogen factors can cause or accelerate pathogenesis action of CPV.