樟子松松针锈病病原菌——春孢子形态及酯酶同工酶变异

樟子松松针锈病病原菌——鞘锈菌（Ｃｏｌｅｏｓｐｏｒｉｕｍ）的分类历来很乱。传统的分类方法都是依冬孢子形态和冬孢子寄主来进行的。但近年的研究表明１种鞘锈菌的春孢子可以侵染２种或２种以上的冬孢子寄主，所以按冬孢子寄主来划分鞘锈菌的种是不合理的。文中在病害症状观察和春孢子表面形态观察的基础上，首次对樟子松３种不同形态的春孢子的酯酶同工酶进行了分析，从而为鞘锈菌的分子分类学研究奠定了基础。     

常见儿科病红细胞免疫粘附功能检测的临床意义

检测儿科常见疾病患者中的红细胞免疫粘附功能发现：（１）新生儿的红细胞免疫粘附功能尚未发育完善，低于正常儿童水平；（２）急性肾炎患儿的红细胞免疫粘附功能呈现继发性增强；（３）肾病综合征、风湿性疾病、大叶性肺炎、秋季腹泻及急性白血病等患儿的红细胞免疫粘附功能呈继发性降低；（４）红细胞免疫粘附功能的变化与疾病的发展及转归有关。提示在儿科疾病的诊断和治疗中观察患儿的红细胞免疫粘附功能有重要意义。     

Studies on the mechanism of vaccinal immunity to Marek''s disease

Current knowledge of the nature of the antigens and of the host immune responses in vaccinal immunity to Marek's disease is reviewed. It is suggested that a two-step mechanism of resistance operates. The first step involves humoral and cell-mediated responses directed against viral antigens; the second step occurs after challenge with Marek's disease virus and consists of cellmediated responses directed against tumour cells.     

Etiology of patent ductus arteriosus in dogs

Patent ductus arteriosus (PDA) is the most common congenital heart disease in dogs and usually causes heart failure and death unless corrected at a young age. Previous histologic studies in a line of dogs derived from Miniature Poodles with hereditary PDA identified varying degrees of hypoplasia and asymmetry of ductus-specific smooth muscle and the presence of aortalike elastic tissue in the ductus wall sufficient to cause patency. To determine if similar structural abnormalities cause PDA in other dogs, serial-section, 3-dimensional histology of ductal architecture was studied in 8 non-Poodle purebred dogs with PDA with no immediate family history of PDA. Morphologic abnormalities were observed in 7 of 8 dogs with PDA and essentially were the same as those in dogs known to have a hereditary form of PDA. These findings suggest that apparently sporadic PDA in these breeds is caused by a genetic defect in the structure of the ductus arteriosus that is similar or identical to that in the Poodle. The relatives of dogs with PDA, particularly parents, offspring, and siblings, should be screened for evidence of PDA. Dogs with PDA should not be used for breeding, regardless of breed.     

NDV和IBV感染对肉鸡大肠杆菌病发病的影响

为了解新城疫弱毒苗和传染性支气管炎弱毒苗接种对肉鸡大肠杆菌病发病的影响。对8日龄肉仔鸡用不同剂量NDVclone-30株或IBV-H120株进行滴鼻及饮水,48h后相同途径接种2株不同“O”血清型的致病性大肠杆菌。结果表明,致病性大肠杆菌单独接种鸡死亡率在20%-25%之间,而NDVclone-30株或IBVH120株与致病性大肠杆菌联合接种鸡死亡率有明显增加达40%-75%。     

Seed treatment prevents vertical transmission of<Emphasis Type="Italic">Fusarium moniliforme</Emphasis>, making a significant contribution to disease control

Fusarium moniliforme is a widespread facultative endophyte, primarily associated with corn, where it causes extensive crop damage.F. moniliforme can be toxigenic, the carcinogenic fumonisins being accumulated predominantly when the fungus colonizes corn plants. The pathogen is transmitted both through contaminated seeds and through environmental inoculum. This study utilized markednit-mutantF. moniliforme inoculum in order to evaluate the quantitative significance of seedborne disease transmission. Greenhouse and field trials demonstrated that seedborne isolates were responsible for up to 50% ofF. moniliforme disease. Seed treatment with the fungicide prochloraz was found to control seedborne transmission and to protect againstF. moniliforme seedling blight. The elimination of seedborne inoculum resulted in reduced incidence of kernel rot and avoided the increment in soil inoculum accumulation associated with the introduction of infected seeds. http://www.phytoparasitica.org posting July 10, 2003.     

The Value of Tissue Imprint Hybridization for Rapid Detection of Infectious Bursal Disease Virus from Field Outbreaks

The use of a peroxidase labelled PCR generated probe followed by enhanced chemiluminescence hybridization assay detected infectious bursal disease virus directly from bursal imprints on a nylon membrane. Tissue imprint hybridization proved to be a simple, rapid and safe means of detecting IBD virus for screening large numbers of field samples. The PCR generated probe was highly specific for IBD virus and did not hybridize with cellular nucleic acids in control imprints. Tissue imprint hybridization was found to be a more sensitive method than conventional antigen detection assays.     

Canine leukocyte adhesion deficiency: presence of the Cys36Ser beta-2 integrin mutation in an affected US Irish Setter cross-breed dog and in US Irish Red and White Setters

Canine leukocyte adhesion deficiency (CLAD) is a primary immunodeficiency disease characterized by recurrent bacterial infections in the presence of marked leukocytosis. The disease was 1st described in the mid-1980s in a cross-breed Irish Setter Dog in the United States. It results from a defective beta-2 subunit of heterodimeric leukocyte adhesion proteins. The causative mutation for CLAD in Irish Setter Dogs from Europe has been identified as a missense mutation at base pair position 107 in the beta-2 integrin subunit gene (ITGB2) that results in an amino acid change from cysteine to serine at amino acid 36 (Cys36Ser) in the beta-2 integrin subunit protein. In the current work, the originally described dog with CLAD has been genetically tested and shown to have the same mutation as the European Irish Setters. This suggests that the mutation has been in the Irish Setter population for many generations spanning more than 2 decades. A related breed, the Irish Red and White Setter, has a history of interbreeding with Irish Setters and shares a common ancestry with the Irish Setter breed. DNA from Irish Red and White Setters residing in the United States was screened either by sequencing or by the newly developed restriction enzyme test for the Irish Setter Cys36Ser CLAD mutation. Seven of 54 dogs tested (13%) were found to be carriers of the Irish Setter CLAD mutation. Five of these were directly related to a sire from the UK, demonstrating the importation of an allele from another continent and establishing the need for genetic testing in this breed in the United States.     

Peste des petits ruminants has been widely present in southern India since, if not before, the late 1980s

Because previous authorities had suggested that small ruminants were playing a part in the dissemination of rinderpest, and a rinderpest-eradication campaign was about to begin, it was necessary to make precise virus identifications from a number of small-ruminant “rinderpest” outbreaks. When this was done using a database created from passive disease reports, we found that epidemics—reportedly due to rinderpest—were in fact due to peste des petits ruminants (PPRs). Although such cases had been common in India for a number of years, earlier clinical and laboratory reports no longer should be regarded as definitive. PPR outbreaks have been frequent in recent years. Further, we suggest that PPR is not a recent invader of India.     

Changes in platelet life span in dogs with mitral valve regurgitation

Platelet life span was measured in dogs with experimentally-induced mitral regurgitation (MR) by using an in vitro whole-blood biotinylation technique to evaluate the effects of shear stress induced by MR. Mitral regurgitation was created in healthy dogs by ablation of the mitral valve chordae tendineae. Mitral regurgitation was identified by auscultation and postoperative color Doppler echocardiography. Platelets were biotinylated. and derivatized blood was reinfused into the dogs. Biotinylated platelet disappearance was measured over time to determine platelet life span. Pre- and postablation platelet life span was compared in each dog. Platelet life span was shorter in dogs with experimentally induced MR. Shear stress from MR was postulated to shorten platelet life span. Alternations in platelet function and life span may contribute to the progression of cardiovascular disease in dogs with MR. Further studies are required to determine if platelet dysfunction is related to disease progression in these patients.