犬细小病毒病防治难点与对策

犬细小病毒病是由犬细小病毒(CPV)引起犬的一种接触性、急性、致死性传染病,特征为出血性肠炎或非化脓性心肌炎。本病无明显发病季节,各年龄段犬均可发生,发病率50%～100%,死亡率10%～50%。2～4月龄幼犬感染率     

犬细小病毒病的免疫效果分析

<正>犬细小病毒病是由犬细小病毒(CPV)引起的一种高度接触性急性传染病,传染性极强,死亡率极高。近年来,随着免疫疫苗的增加,其发病比例有所下降,但其免疫效果并不理想,影响犬业发展。1疫苗类型免疫犬细小病毒疫苗仍是控制本病的主要方法,选择合理的疫苗是成功免疫的第一步。疫苗主要分类传统疫苗和新型疫苗,在传统疫苗研究上,猫泛白细胞减少症病毒(FPV)灭活苗、弱毒苗免疫CPV,但免疫效果远不理想;1990年,徐汉坤等研制成     

犬细小病毒病的快速诊断及防治对策

犬细小病毒病是由犬细小病毒（canine parvovirus cpv)引起的危害犬业极大的疫病之一。犬感染CPV，临床多见肠炎型，发病年龄以3－6月龄为主，以严重呕吐、腹泻、恶臭血便为主要特征；心肌炎型发病较少，发病年龄多为2－3月龄，发病快、病程短、昏迷、体温低、衰竭、心动过速而无力为主要特征。同一疗法，肠炎型治愈率极高，几乎全愈。但心肌炎型却死亡率高。用快速诊断试纸可在5－10min内确诊该病。肌注犬细小病毒单克隆抗体及1％口服补液盐等体温灌肠，治愈本病有独特作用。     

母犬产前接种疫苗对犬细小病毒抗体效价的影响

犬细小病毒病（CPV）具有感染率高、发病急、病程短、死亡率高等特点,已成为目前危害我国养犬业的主要疫病之一。目前针对犬细小病毒,尽管大量采用疫苗进行免疫,但免疫失败现象屡有发生,许多国家均有犬群免疫后暴发CPV的报道．引起了世界各国的重视。其主要原因极有可能与毒株发生变异有关,尤其是2003年以来CPV地方变异的问题日益突出。     

犬细小病毒流行病学调查诊断研究

犬细小病毒病是由犬细小病毒(CPV)引起的一种发病急、死亡率高、高度传染性疾病,临床主要表现为出血性肠炎和心肌炎两种类型,对养犬业和宠物犬行业造成较大危害,目前该病主要通过接种疫苗进行免疫预防。犬细小病毒病感染率与犬的年龄、品种、免疫情况、环境、季节等因素密切相关,本文主要阐述犬细小病毒的病原学特征、临床症状、常见检测方法、防治措施等。     

犬细小病毒病的临床诊断与治疗

犬细小病毒病（CPV）是一种由细小病毒引起的急性、高度致死性传染病，对犬只造成严重危害。感染犬和康复犬是主要传染源。不同年龄、性别犬均可发病，但以幼犬为主，断奶前后的仔犬易感性最高。本病的发生无明显季节性。     

犬发生细小病毒性肠炎的综合疗法

<正>犬细小病毒简称(CPV)是由犬细小病毒引起的一种急性传染病,临床上以出血性肠炎和心肌炎为特征,且以肠炎型多见。其主要发病原因是由于自然感染了犬细小病毒或潜伏期内注射了几种疫苗所致,发病率较高。目前,由于对本病尚无特殊疗法,致     

犬发生细小病毒性肠炎的综合疗法

<正>犬细小病毒简称(CPV)是由犬细小病毒引起的一种急性传染病,临床上以出血性肠炎和心肌炎为特征,且以肠炎型多见。其主要发病原因是由于自然感染了犬细小病毒或潜伏期内注射了几种疫苗所致,发病率较高。目前,由于对本病尚无特殊疗法,致     

中西医结合防制犬细小病毒性肠炎

犬细小病毒性肠炎是南犬细小病毒引起的一种急性传染病，临床上以剧烈呕吐、腹泻排血样便为主要特征。本病一年四季均可发生，以晚春和夏季多发，任何品种、年龄的犬均可发病，但以2～5月龄的幼犬多发，此病发病急，死亡率高，对养犬业危害较大：笔者近几年来采用中西药结合疗法治愈262例，     

浅议犬细小病毒病的诊治要点

正随着宠物行业的发展,病毒性疾病在临床上有逐渐减少的趋势,但犬细小病毒(Canine Parvovirus Disease,CPV)在宠物临床的发病与死亡率却一直居高不下。现就其诊治做一简单总结。犬细小病毒病是由CPV引起的一种急性传染病,临床上以出血性肠炎或非化脓性心肌炎为其主要特征。本病一年四季都有发生,常发生于2~6月龄犬,感染率有时可达100%,致死率为10%~50%不等。1临床症状     

A modified live canine parvovirus vaccine. II. Immune response

The safety and efficacy of an attenuated canine parvovirus (A-CPV) vaccine was evaluated in both experimental and in field dogs. After parenteral vaccination, seronegative dogs developed hemagglutination-inhibition (HI) antibody titers as early as postvaccination (PV) day 2. Maximal titers occurred within 1 week. Immunity was associated with the persistence of HI antibody titers (titers greater than 80) that endured at least 2 years. Immune dogs challenged with virulent CPV did not shed virus in their feces. The A-CPV vaccine did not cause illness alone or in combination with living canine distemper (CD) and canine adenovirus type-2 (CAV-2) vaccines, nor did it interfere with the immune response to the other viruses. A high rate (greater than 98%) of immunity was engendered in seronegative pups. In contrast, maternal antibody interfered with the active immune response to the A-CPV. More than 95% of the dogs with HI titers less than 10 responded to the vaccine, but only 50% responded when titers were approximately 20. No animal with a titer greater than 80 at the time of vaccination became actively immunized. Susceptibility to virulent CPV during that period when maternal antibody no longer protects against infection, but still prevents active immunization, is the principal cause of vaccinal failure in breeding kennels where CPV is present. Reduction, but not complete elimination, of CPV disease in large breeding kennels occurred within 1-2 months of instituting an A-CPV vaccination program.     

The emergence of parvoviruses of carnivores

The emergence of canine parvovirus (CPV) represents a well-documented example highlighting the emergence of a new virus through cross-species transmission. CPV emerged in the mid-1970s as a new pathogen of dogs and has since become endemic in the global dog population. Despite widespread vaccination, CPV has remained a widespread disease of dogs, and new genetic and antigenic variants have arisen and sometimes reached high frequency in certain geographic regions or throughout the world. Here we review our understanding of this emergence event and contrast it to what is known about the emergence of a disease in mink caused by mink enteritis virus (MEV). In addition, we summarize the evolution of CPV over the past 30 years in the global dog population, and describe the epidemiology of contemporary parvovirus infections of dogs and cats. CPV represents a valuable model for understanding disease emergence through cross-species transmission, while MEV provides an interesting comparison.     

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.     

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。     

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)     

Changes in blastogenic responses of lymphocytes and delayed type hypersensitivity responses after vaccination in dogs.

To clarify the immunologic effects of vaccination in dogs, we monitored total leukocyte and lymphocyte counts, humoral antibody responses, blastogenic responses of lymphocyte, and delayed type hypersensitivity (DTH) responses after vaccination. Mixed vaccines were administered on day 0 except for canine parvovirus (CPV) vaccine which was readministered on day 21. The puppy and adult dogs had a significant decrease in leukocyte and lymphocyte counts on day 7. The puppies showed a significant increase in the blastogenesis of lymphocytes after each vaccination, whereas the adult dogs had no significant changes. However, the adult dogs were divided into two groups, high responders and low responders in blastogenesis of lymphocytes. The dogs with higher or lower response in SI values on day 0 tended to show decrease or increase after the first vaccination, respectively. Since almost all dogs developed high titers of humoral antibody, it is considered that vaccination acts in an immunomodulative fashion. DTH responses to phytohemagglutinin (PHA) and CPV vaccine monitored at 0, 3, and 8 weeks after the first vaccination produced strong reactions, in particular those to CPV vaccine rose significantly after vaccination and maintained the higher responses for at least 2 months. These results suggest that DTH responses to PHA and CPV vaccine are helpful to monitoring non-specific and specific immune functions in vivo, therefore, DTH could be used as simple and rapid immunologic tests in canine practice.     

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%.     

Three-year duration of immunity in dogs following vaccination against canine adenovirus type-1, canine parvovirus, and canine distemper virus

A challenge-of-immunity study was conducted to demonstrate immunity in dogs 3 years after their second vaccination with a new multivalent, modified-live vaccine containing canine adenovirus type 2 (CAV-2), canine parvovirus (CPV), and canine distemper virus (CDV). Twenty-three seronegative pups were vaccinated at 7 and 11 weeks of age. Eighteen seronegative pups, randomized into groups of six dogs, served as challenge controls. Dogs were kept in strict isolation for 3 years following the vaccination and then challenged sequentially with virulent canine adenovirus type 1 (CAV-1), CPV, and CDV. For each viral challenge, a separate group of six control dogs was also challenged. Clinical signs of CAV-1, CPV, and CDV infections were prevented in 100% of vaccinated dogs, demonstrating that the multivalent, modified-live test vaccine provided protection against virulent CAV-1, CPV, and CDV challenge in dogs 7 weeks of age or older for a minimum of 3 years following second vaccination.     

Application of a dot enzyme-linked immunosorbent assay for evaluation of the immune status to canine parvovirus and distemper virus in adult dogs before revaccination.

A growing body of literature has been published indicating that the current practice of annual vaccination of dogs may not be beneficial and in some cases may even be harmful. A number of publications have proposed assessing the immune status of dogs before annual revaccination. In this study the usefulness of a commercially available dot-ELISA kit was evaluated to determine the duration IgG antibody titers to canine parvovirus (CPV) and canine distemper virus (CDV) in 158 dogs vaccinated at least one year ago. Overall, the percentage of dogs with protective antibody titers to both CPV and CDV was 84%. The percentage of dogs with borderline antibody titers was 11% for CPV and 10% for CDV. Four percent of the dogs had no detectable antibody to CPV and 6% had no antibody to CDV. The results reported here are in good agreement with other studies measuring IgG antibody levels. It is concluded that the kit offers veterinarians the opportunity of determining antibody titers and revaccinating only those pets whose antibody titers to specific diseases have waned.