犬细小病毒病流行病学调查

犬细小病毒感染是由犬细小病毒引起的一种急性、热性、传染性疾病,临床上以出血性肠炎或心肌炎为主要特征。本研究对泰州某宠物门诊2010年1月－2011年3月期间接诊的260例犬细小病例进行了分析研究,旨在了解泰州地区犬细小病毒病发病率、死亡率与犬年龄、品种、免疫接种、季节等因素之间的关系,并总结防控犬细小病毒病最有效的方法。结果表明,犬细小病毒病发病率及死亡率与犬的年龄、品种、免疫接种、季节有很大的相关性,依此提出了防制对策,以期为防制犬细小病毒病提供参考。     

犬细小病毒病流行病学调查及治疗措施

犬细小病毒病是由犬细小病毒引起的犬的一种急性传染病,临床上常表现为剧烈呕吐、出血性肠炎、血性水样便、脱水、白细胞显著性减少和心肌炎。对宁夏银川海俊宠物诊疗所2012年1月至2013年1月跟踪记录调查360例犬细小病毒病进行了研究分析,旨在阐明银川地区犬细小病毒病的发病率、死亡率与品种、年龄、免疫接种、季节等因素之间的关系,并对犬细小病毒病的治疗及预防措施进行了讨论。     

新疆哈密地区犬细小病毒病的诊断与防制

1哈密地区犬细小病毒病的流行状况通过对哈密地区100例重症犬统计分析得知:该病发病率为34%,治愈率为14.7%,死亡率为85.29%。本地未免疫的哈萨犬及从青海引进的藏獒发病率,死亡率均比其它犬高,也有极少数免疫过的犬发病。2008年1月至今该病呈上升趋势。2病原与流行病学犬细小病毒病是由犬细小病毒(CPV)引起的一种急性热性传染病,该病毒属于细小病毒科细小病毒属RNA型病     

兰州地区犬瘟热流行病学调查及其治疗

为了解兰州地区犬瘟热发病率、死亡率与犬年龄、品种、免疫接种、季节之间的关系,并总结出一套治疗犬瘟热最有效的方法,收集108例临床犬瘟热病例,从流行病学、临床鉴别诊断、病理剖检、治疗等方面进行深入、全面的研究。结果表明,犬瘟热发病率及死亡率与犬的年龄、品种、免疫接种、季节有很大的关系;通过应用被动免疫（犬瘟热血清、犬瘟热单克隆抗体）联合主动免疫（弱毒疫苗）的治疗方法取得了良好的治疗效果。     

藏獒犬细小病毒病的诊治

<正>犬细小病毒病主要侵害幼犬,是由犬细小病毒引起的一种具有高度接触性传染的烈性传染病,死亡率极高,对养犬业的危害相当大。该病多发于冬春寒冷季节,临床上以剧烈呕吐、非化脓性心肌炎和出血性肠炎为特征。近年来,随着藏獒饲养量的逐年上升,犬细小病毒病在藏獒中呈暴发趋势,6周龄到6月龄藏獒幼犬的发病率和死亡率比一般的犬种还要高,已成为当前藏獒养殖业危害最大的疫病之一。2014年2月,笔者诊治一起以呕吐、拉稀、拉血便为特征的藏獒犬细     

广西南宁市某宠物医院犬细小病毒病的临床调查

对2012年到广西南宁市某宠物医院就诊的956例病犬进行临床调查,调查内容主要包括犬细小病毒病的发病率、发病季节、发病年龄、犬品种纯度与犬细小病毒病发病率的关系、免疫对犬细小病毒病的影响等。结果表明,犬细小病毒病发病率达14.3%;发病季节主要以春季、秋末和冬季为主;各种年龄阶段的犬均可发生,但以幼犬的发病率和死亡率较高;免疫是预防该病最有效的方法。     

广西南宁市某宠物医院犬细小病毒病的临床调查

对2012年到广西南宁市某宠物医院就诊的956例病犬进行临床调查,调查内容主要包括犬细小病毒病的发病率、发病季节、发病年龄、犬品种纯度与犬细小病毒病发病率的关系、免疫对犬细小病毒病的影响等.结果表明,犬细小病毒病发病率达14.3％;发病季节主要以春季、秋末和冬季为主;各种年龄阶段的犬均可发生,但以幼犬的发病率和死亡率较高;免疫是预防该病最有效的方法.     

犬细小病毒病的诊断和治疗

犬细小病毒是由犬细小病毒(CPV)引起的一种急性传染病。近几年来,在甘南藏族自治州和临夏回族自治州呈地方性流行。其临床症状差异较大,主要表现为出血性胃肠炎和非化脓性心肌炎,且往往伴有细菌性继发感染。确诊后,采取一系列综合治疗措施,取得了较好的疗效。1流行病学各种年龄和性别的狗均可感染此病,在甘南、临夏地区一年四季均有此病发生,特别在藏獒繁殖的冬春季节呈大的流行趋势。不同年龄的狗都能被感染,但以断奶后2~3月龄的幼犬最为常见,尤其是断奶后长途贩运、离母易地饲养的小藏獒发病率、死亡率最高。同窝的狗崽一旦一个发病,一…     

藏獒犬弓形虫病的血清学调查

为初步了解青海省大通县3个地区藏獒犬弓形虫病感染的流行病学特征,本试验采用间接血凝试验(IHA)方法检测了采集自大通县桥头镇、城关镇和多林镇地区的80份藏獒犬血清样本。结果提示:大通县藏獒犬的弓形虫抗体阳性率为3.75%,且均为散养的成年护院藏獒犬,在养殖场中未检测出弓形虫阳性;其中1岁内的藏獒犬未检出阳性,检出1岁以上的藏獒犬阳性率为6.98%(3/43),不同年龄藏獒犬间存在显著差异(P0.05)。随着年龄的增长,藏獒犬感染弓形虫的几率增加,且夏季是弓形虫病的高发季节。调查结果表明弓形虫的感染与犬的饮食、环境有一定的关系,应加强对散养户的饲养管理,确保人和藏獒犬的安全,防止人畜间的互相传播。     

酒泉地区犬细小病毒病流行病学调查

为研究甘肃酒泉地区犬细小病毒(Canine parvovirus,CPV)病的流行规律,本研究对酒泉沂蒙动物医院、酒泉职业技术学院动物医院自2014年5月~2017年4月期间接诊的527例CPV病例进行了调查分析。结果表明,酒泉地区CPV病发病率与犬的年龄、品种、免疫接种、季节有很大的相关性,本研究调查在一定程度上代表了CPV病在甘肃酒泉地区的实际发病情况,以期为防制CPV病提供参考。     

藏獒细小病毒病的诊断

藏獒作为犬类的一种,也受到犬类病毒感染的威胁。据调查,侵害藏獒的主要病毒有犬细小病病毒和犬瘟热病毒两大类。作者对青海某藏獒养殖户的病死藏獒进行临床症状观察,病理剖检及实验室诊断,通过病毒的分离培养及鉴定,确诊病死藏獒为犬细小病毒感染。鉴于养殖场中该病的存在及对养犬业的危害,建议加强对犬细小病毒的诊断及监控。     

Risk factors for death from canine parvoviral-related disease in Australia

Canine parvovirus (CPV) is a highly contagious cause of serious and often fatal disease in dogs worldwide despite the availability of safe and efficacious vaccines. Although a number of studies have focussed on identifying risk factors in disease development, risk factors associated with death from CPV are largely unknown. In this study we analysed a total of 1451 CPV cases reported from an Australian surveillance system - using univariate and multivariate techniques - to determine significant risk factors associated with death and euthanasia. A crude case fatality rate of 42.3% was estimated - higher than has been reported previously. We found that 3.3% of CPV cases had a history of vaccination in the previous 12 months, despite having completed the primary puppy vaccination course. The majority (89.5%) of these cases occurred in dogs <12 months of age, indicating failure of the primary vaccination course to provide protective immunity (most likely due to interference of the vaccine antigen with maternal antibodies but other reasons are discussed). Extending the age at which the final puppy vaccination is administered might be one of several strategies to consider. The final multivariate model showed that in non-litter CPV cases, risk of death was significantly associated with season of diagnosis (summer) and pedigree type (hounds and non-sporting dogs). Euthanasia in non-litter CPV cases was significantly associated with season of diagnosis (summer), state of residence (Northern Territory/South Australia/Tasmania combined), age (相似文献   

Canine parvoviral enteritis: a review of diagnosis, management, and prevention

Objective: To review and summarize current information regarding epidemiology, risk factors, and pathophysiology associated with canine parvoviral infection, and to outline diagnostic and treatment modalities for this disease. Preventative and vaccination strategies will also be discussed, as serologic documentation of immunocompetence and adoption of safe and effective vaccination protocols are crucial in limiting infection and spread of canine parvoviral enteritis. Etiology: Parvoviruses (Parvoviridae) are small, nonenveloped, single‐stranded DNA viruses that replicate in rapidly dividing cells. Canine parvovirus 2 (CPV‐2) remains a significant worldwide canine pathogen and the most common cause of viral enteritis in this species. Diagnosis: Classic presentation of CPV infection includes acute‐onset enteritis, fever, and leukopenia. Definitive diagnostic tests include detection of CPV in the feces of affected dogs, serology, and necropsy with histopathology. Therapy: Standard therapeutic practices for both mildly and severely affected puppies will be discussed. The ability of this virus to incite not only local gastrointestinal injury, but also a significant systemic inflammatory response has recently been reviewed in the literature, and novel innovative experimental and clinical therapeutic strategies, such as antagonism of proinflammatory cytokines and immunostimulation, are introduced in this article. Prognosis: CPV remains a significant worldwide canine pathogen. In experimentally affected dogs, mortality without treatment has been reported as high as 91%. However, with prompt recognition of dogs infected with CPV‐2, and aggressive in‐hospital supportive therapy of severely affected puppies, survival rates may approach 80–95%.     

Canine parvovirus 2c infection in central Portugal

Canine parvovirus (CPV) has been evolving, generating new genetic and antigenic variants throughout the world. This study was conducted to determine the types of CPV circulating in dogs in Figueira da Foz, Portugal. Thirty fecal samples, collected between 2006 and 2007 from dogs with clinical signs of CPV infection, were tested for CPV by a rapid, in-clinic, enzyme-linked immunosorbent assay (ELISA)/immunomigration test, by conventional real-time polymerase chain reaction (PCR), and by minor-groove binding TaqMan PCR. Of the 29 PCR-positive samples, 15 were identified as CPV-2b and 14 as CPV-2c. No CPV-2a was detected. The sensitivity of the ELISA test was 82.76% compared with the PCR assays. No significant associations were found between CPV type, clinical outcome, breed, vaccination status, or age.     

Use of modified live feline panleukopenia virus vaccine to immunize dogs against canine parvovirus

Modified live feline panleukopenia virus (FPLV) vaccine protected dogs against canine parvovirus (CPV) infection. However, unlike the long-lived (greater than or equal to 20-month) immunity engendered by CPV infection, the response of dogs to living FPLV was variable. Doses of FPLV (snow leopard strain) in excess of 10(5.7) TCID50 were necessary for uniform immunization; smaller inocula resulted in decreased success rates. The duration of immunity, as measured by the persistence of hemagglutination-inhibiting antibody, was related to the magnitude of the initial response to vaccination; dogs with vigorous initial responses resisted oronasal CPV challenge exposure 6 months after vaccination, and hemagglutination-inhibiting antibodies persisted in such dogs for greater than 1 year. Limited replication of FPLV in dogs was demonstrated, but unlike CPV, the feline virus did not spread to contact dogs or cats. Adverse reactions were not associated with living FPLV vaccination, and FPLV did not interfere with simultaneous response to attenuated canine distemper virus.     

A history of canine parvovirus in Australia: what can we learn?

Canine parvovirus (CPV) has been reported throughout the world since the late 1970s. Published information was reviewed to draw insights into the epidemiology, pathogenesis, diagnosis, treatment and outcomes of CPV disease in Australia and the role of scientific research on CPV occurrence, with key research discoveries and knowledge gaps identified. Australian researchers contributed substantially to early findings, including the first reported cases of parvoviral myocarditis, investigations into disease aetiopathogenesis, host and environmental risk factors and links between CPV and feline panleukopenia. Two of the world's first CPV serological surveys were conducted in Australia and a 1980 national veterinary survey of Australian and New Zealand dogs revealed 6824 suspected CPV cases and 1058 deaths. In 2010, an Australian national disease surveillance system was launched; 4940 CPV cases were reported between 2009 and 2014, although underreporting was likely. A 2017 study estimated national incidence to be 4.12 cases per 1000 dogs, and an annual case load of 20,110 based on 4219 CPV case reports in a survey of all Australian veterinary clinics, with a 23.5% response rate. CPV disease risk factors identified included socioeconomic disadvantage, geographical location (rural/remote), season (summer) and rainfall (recent rain and longer dry periods both increasing risk). Age <16 weeks was identified as a risk factor for vaccination failure. Important knowledge gaps exist regarding national canine and feline demographic and CPV case data, vaccination coverage and population immunity, CPV transmission between owned dogs and other carnivore populations in Australia and the most effective methods to control epizootics.     

Three-year rabies duration of immunity in dogs following vaccination with a core combination vaccine against canine distemper virus, canine adenovirus type-1, canine parvovirus, and rabies virus

Thirty-two seronegative pups were vaccinated at 8 weeks of age with modified-live canine distemper virus (CDV), canine adenovirus type-2 (CAV-2), and canine parvovirus (CPV) vaccine and at 12 weeks with a modified-live CDV, CAV-2, CPV, and killed rabies virus vaccine. An additional 31 seronegative pups served as age-matched, nonvaccinated controls. All test dogs were strictly isolated for 3 years after receiving the second vaccination and then were challenged with virulent rabies virus. Clinical signs of rabies were prevented in 28 (88%) of the 32 vaccinated dogs. In contrast, 97% (30 of 31) of the control dogs died of rabies infection. These study results indicated that no immunogenic interference occurred between the modified-live vaccine components and the killed rabies virus component. Furthermore, these results indicated that the rabies component in the test vaccine provided protection against virulent rabies challenge in dogs 12 weeks of age or older for a minimum of 3 years following vaccination.     

Dog response to inactivated canine parvovirus and feline panleukopenia virus vaccines

Inactivated canine parvovirus (CPV) and inactivated feline panleukopenia virus (FPV) vaccines were evaluated in dogs. Maximal serologic response occurred within 1-2 weeks after vaccination. Antibody titers then declined rapidly to low levels that persisted at least 20 weeks. Immunity to CPV, defined as complete resistance to infection, was correlated with serum antibody titer and did not persist longer than 6 weeks after vaccination with inactivated virus. However, protection against generalized infection was demonstrated 20 weeks after vaccination. In unvaccinated dogs, viremia and generalized infection occurred after oronasal challenge with virulent CPV. In contrast, viral replication was restricted to the intestinal tract and gut-associated lymphoid tissue of vaccinated dogs. Canine parvovirus was inactivated by formalin, beta-propiolactone (BPL), and binary ethylenimine (BEI) in serum-free media; inactivation kinetics were determined. Formalin resulted in a greater loss of viral HA than either BEI of BPL, and antigenicity was correspondingly reduced.     

Serum antibody response to canine parvovirus, canine adenovirus-1, and canine distemper virus in dogs with known status of immunization: study of dogs in Sweden

Serum antibody titers to canine parvovirus (CPV), canine adenovirus-1 (CAV-1), and canine distemper virus (CDV) were measured in dogs with known immunization status. The dogs represented 3 groups: nonvaccinated dogs less than 12 months old; vaccinated dogs less than 12 months old; and adult dogs greater than 12 months old. For practical reasons, the population from which the specimens were obtained could be considered as free from natural infection with CAV-1 and CDV. In nonvaccinated dogs less than 12 months old, antibodies against all 3 viruses were measured at the time the dogs were given their first vaccination. Altogether, 50.7% of the dogs had titer greater than or equal to 1:10 to CPV, and 26.1 and 46.2% had titer greater than or equal to 1:8 to CAV-1 and CDV, respectively. The concentration of maternal antibody seemed to be of major importance for failure of immunization with use of inactivated CPV vaccine, but not with CAV-1 and CDV vaccination. In dogs less than 12 months old and vaccinated against CPV infection with inactivated virus, only 11.5% had titer greater than or equal to 1:80. In dogs vaccinated against infectious canine hepatitis and canine distemper, 63.2 and 78.3%, respectively, had titer greater than or equal to 1:16. In adult dogs greater than 2 months old and vaccinated against CPV infection, less than 50% had titer greater than or equal to 1:80, regardless of time after vaccination. There was no significant difference in titer between vaccinated and nonvaccinated dogs.(ABSTRACT TRUNCATED AT 250 WORDS)     

Active use of coyotes (Canis latrans) to detect Bovine Tuberculosis in northeastern Michigan, USA

Seroconversion after early vaccination at four weeks against canine parvovirus (CPV) using a high antigen titre vaccine was evaluated in 121 puppies from three breeds of dogs housed in kennels representative of the private practitioner's environment. The trial included 52 German shepherd pups, 25 Rottweiler pups and 44 Boerboel pups. From each group 11, 4, and 18 puppies acted as control dogs, respectively. Depending on the different groups, puppies were vaccinated at 4, 6, 9 and 12 weeks. The experimental group differed from the control group in that they received the high titre vaccine at 4 weeks of age, whereas the control group was not vaccinated at 4 weeks. Blood was collected from all pups prior to vaccination to measure maternally derived colostral antibody. The results indicated that vaccination at 4 weeks of age in pups with high maternally derived antibody levels, results in seroconversion rates that may lead to a reduction in the window of susceptibility with respect to CPV infection. The implications of the findings with respect to dogs in heavily contaminated environments are discussed.