Outbreaks of classical swine fever in Great Britain in 1986

Classical swine fever was confirmed in 10 herds in Britain between April 10 and June 25, 1986 and typical acute disease was seen in nine of them. Serological evidence of exposure to classical swine fever virus was found in a further seven herds which, together with another nine, were slaughtered as dangerous contacts. Altogether 7781 pigs in 26 herds were slaughtered at a cost of 450,101 pounds for compensation alone. In order to detect subclinical disease, the majority of traced herds were blood sampled as well as inspected. A total of 119,169 pigs were inspected in 506 herds and 8302 blood samples were collected. Three primary outbreaks were identified, all attributed to the feeding of unprocessed waste food containing imported pig meat products. There was no spread of disease from two of these primary outbreaks.     

筛选猪瘟抗体阴性猪检测方法的比较

评价ELISA法用于筛选猪瘟抗体阴性猪的可行性,分别采用两种商品化猪瘟抗体ELISA检测试剂盒检测了61份猪血清样品,并与兔体中和试验方法进行了比较。兔体中和试验法检测出4份阳性、2份可疑、55份阴性,而两种ELISA试剂盒均检测出6份阳性、55份阴性;两种ELISA方法与兔体中和试验检测结果阴性符合率均为100%（55/55）。结果表明,ELISA法更加敏感,可以替代兔体中和试验方法用于筛选猪瘟抗体阴性猪。     

Prevalence of African swine fever virus and classical swine fever virus antibodies in pigs in Benue State,Nigeria

Tropical Animal Health and Production - This study investigated the prevalence of African swine fever virus (ASFV) and classical swine fever virus (CSFV) antibodies in pigs in Benue State, Nigeria....     

Early pathogenesis of classical swine fever virus (CSFV) strains in Danish pigs

Host-virus interactions play an important role for the clinical outcome of classical swine fever virus (CSFV) infections in pigs. Strain virulence, host characteristics and environment are all factors that markedly influence disease severity. We tested CSFV strains of varying virulence in an experimental set-up, reducing the influence of host and environmental factors. Thus, weaner pigs were inoculated with one of 4 CSFV strains in order to compare the pathogenesis for a 3-week-period after infection. CSFV strains selected were 2 new and 2 previously characterized. None of these strains had been tested in Danish outbred pigs before. Clinical observations grouped the infected pigs into two different categories reflecting either non-specific, mainly gastro-intestinal, problems, or severe disease including high fever within the first week after inoculation. Gross-pathological findings varied between strains, however, lymphoid atrophy and growth retardation represented a consistent finding for all 4 strains. Virus distribution, viral load and in particular virus persistence differed, but supported present practice that recommends lymphoid tissue, most optimal tonsil and lymph nodes, as target material to be applied for early laboratory diagnosis. The present study demonstrated constraints associated with early detection of infections with CSFV strains of low virulence. Since neither clinical symptoms nor pathological lesions observed with these strains constituted characteristic signs of CSF, the risk of neglecting a CSF suspicion is immediate. Therefore, topical information on new outbreaks and continuous enhancement of an efficient surveillance system is of great importance to prevent further spread of CSF within the pig population.     

急性感染猪瘟病毒猪体外排毒规律的观察

为研究CSFV感染后在体外的传播途径、排毒规律,针对CSFV基因组设计了一对引物和一条探针,建立了一套CSFV荧光定量PCR(FQ-PCR)检测方法,并以质粒为标准品得到扩增标准曲线.对18个CSFV阳性质控样本检测全阳性,6个CSFV阴性质控样本检测全阴性,显示良好敏感性和特异性.应用此方法对石门株感染的16头60日龄长白猪和1头阴性对照猪的粪便、尿液、眼分泌物和唾液中病毒含量进行了动态测定,结果表明从感染后第1天到频死前第8天,粪便中均能检测出病毒;尿液和眼分泌物至少能从第3天,唾液从第4天开始检测出病毒,且病毒含量呈增加趋势.本研究对急性感染猪瘟病毒猪体外排毒规律进行了系统研究,为弄清CSFV感染病程、致病机理及临床诊断奠定了重要理论基础.     

Failure of protection and enhanced pneumonia with a US H1N2 swine influenza virus in pigs vaccinated with an inactivated classical swine H1N1 vaccine

Two US swine influenza virus (SIV) isolates, A/Swine/Iowa/15/1930 H1N1 (IA30) and A/Swine/Minnesota/00194/2003 H1N2 (MN03), were evaluated in an in vivo vaccination and challenge model. Inactivated vaccines were prepared from each isolate and used to immunize conventional pigs, followed by challenge with homologous or heterologous virus. Both inactivated vaccines provided complete protection against homologous challenge. However, the IA30 vaccine failed to protect against the heterologous MN03 challenge. Three of the nine pigs in this group had substantially greater percentages of lung lesions, suggesting the vaccine potentiated the pneumonia. In contrast, priming with live IA30 virus provided protection from nasal shedding and virus replication in the lung in MN03 challenged pigs. These data indicate that divergent viruses that did not cross-react serologically did not provide complete cross-protection when used in inactivated vaccines against heterologous challenge and may have enhanced disease. In addition, live virus infection conferred protection against heterologous challenge.     

Classical swine fever: virulence and tissue distribution of a 1986 English isolate in pigs

Following the recurrence of classical swine fever in the United Kingdom in 1986, a virus isolated from a single outbreak was studied. A major factor in the spread of this disease is considered to be the presence of infectious virus in tissues taken from animals at certain stages of infection, although their condition may escape detection by routine inspection either before or after slaughter. Intranasal inoculation of the isolate into eight-week-old pigs reproduced the acute form of the disease. The pigs were killed or died between seven and 25 days after inoculation. The virus concentration was determined in a wide range of tissues taken at different stages of infection. Infectious virus was present at high concentrations in all the tissues taken and at all stages of infection. Any porcine tissue is therefore a potential source of infection even when it is taken either before the animal displays detectable signs of disease of after it develops serum neutralising antibodies.     

Cytokines and acute phase proteins associated with acute swine influenza infection in pigs

This study set out to investigate the cytokines and acute phase proteins (APPs) associated with the acute stages of experimentally-induced swine influenza virus (SIV) infection in 3-week-old, colostrum-deprived, caesarean-derived piglets. The piglets were inoculated intratracheally with 10^7.5 50% egg infective dose [EID₅₀] Swine/Belgium/1/98 (H1N1) SIV and were euthanased at time-points between 0 and 120 h post-inoculation (PI). Broncho-alveolar lavage fluid (BALF), lung homogenates and sera were examined for inflammatory mediators by bioassay or ELISA. Interferon (IFN)-α, interleukin (IL)-6, IL-1 and tumour necrosis factor (TNF)-α peaked in BALF 24–30 h PI, when virus titres and the severity of clinical signs were maximal.Whereas IFN-γ and IL-12, but not IL-18, increased in tandem in BALF, serum cytokine concentrations were either undetectable or were up to 100-fold lower. The APP C-reactive protein (CRP) and haptoglobin peaked 24 h later than the cytokines and reached higher levels in serum than in BALF. In contrast, lipopolysaccharide (LPS)-binding protein (LBP) only increased in BALF. Lung virus titres tightly correlated with BALF IFN-α, IL-6, IL-1, TNF-α, IFN-γ and IL-12, as well as with serum IL-6, IFN-α and IFN-γ. Signs of disease correlated with the same cytokines in BALF and serum, as well as with BALF LBP and serum CRP. The findings suggest that IFN-γ and IL-12 play a role in the pathogenesis of SIV and that APPs are induced by cytokines. This influenza infection model may have value in assessing the therapeutic potential of cytokine antagonists.     

Efficacy of a live attenuated vaccine in classical swine fever virus postnatally persistently infected pigs

Classical swine fever (CSF) causes major losses in pig farming, with various degrees of disease severity. Efficient live attenuated vaccines against classical swine fever virus (CSFV) are used routinely in endemic countries. However, despite intensive vaccination programs in these areas for more than 20 years, CSF has not been eradicated. Molecular epidemiology studies in these regions suggests that the virus circulating in the field has evolved under the positive selection pressure exerted by the immune response to the vaccine, leading to new attenuated viral variants. Recent work by our group demonstrated that a high proportion of persistently infected piglets can be generated by early postnatal infection with low and moderately virulent CSFV strains. Here, we studied the immune response to a hog cholera lapinised virus vaccine (HCLV), C-strain, in six-week-old persistently infected pigs following post-natal infection. CSFV-negative pigs were vaccinated as controls. The humoral and interferon gamma responses as well as the CSFV RNA loads were monitored for 21 days post-vaccination. No vaccine viral RNA was detected in the serum samples and tonsils from CSFV postnatally persistently infected pigs for 21 days post-vaccination. Furthermore, no E2-specific antibody response or neutralising antibody titres were shown in CSFV persistently infected vaccinated animals. Likewise, no of IFN-gamma producing cell response against CSFV or PHA was observed. To our knowledge, this is the first report demonstrating the absence of a response to vaccination in CSFV persistently infected pigs.     

Expression of Mx protein and interferon-alpha in pigs experimentally infected with swine influenza virus

Expression of Mx protein and interferon-alpha (IFN-alpha) was examined by immunohistochemistry in pigs experimentally infected with swine influenza virus. In infected pigs euthanatized at 1 day postinoculation (dpi), the lumen of bronchioles were filled with large numbers of mononuclear cells, small numbers of neutrophils, sloughing epithelial cells, and proteinaceous fluid. Lesions at 3 and 5 dpi were similar but less severe. Alveolar spaces were filled with neutrophils. By 7 and 10 dpi, microscopic lesions were resolved. The immunohistochemical signals for Mx protein and IFN-alpha antigen were confined to cells in areas that had hybridization signal for swine influenza virus. In situ hybridization and immunohistochemistry of serial sections of lung indicated that areas containing numerous swine influenza virus RNA-positive cells also have numerous Mx and IFN-alpha antigen-positive cells. Mean immunohistochemical scores for Mx protein-positive cells were correlated with mean immunohistochemical scores for IFN-alpha antigen-positive cells (r(s) = 0.8799, P < 0.05). These results indicated that Mx protein and IFN-alpha antigen were expressed in the lung from pigs experimentally infected with swine influenza virus, but their biological functions remain to be examined.     

Antigenic variant of swine influenza virus causing proliferative and necrotizing pneumonia in pigs.

A new antigenic variant of swine influenza virus was isolated from the lungs of pigs experiencing respiratory problems in 7 different swine herds in Quebec. Pigs of different ages were affected, and the main clinical signs were fever, dyspnea, and abdominal respiration. Coughing was not a constant finding of the syndrome. At necropsy, macroscopic lesions included the overall appearance of pale animals, general lymphadenopathy, hepatic congestion, and consolidation of the lungs. Histopathologic findings were mainly proliferative pneumonia with a significant macrophage invasion, necrotic inflammatory cells in the alveoli and the airways, a marked proliferation of type II pneumocytes, and thickening of the alveolar septae. Fluorescent antibody examination of lungs of sick piglets did not demonstrate porcine parvovirus, transmissible gastroenteritis virus, or encephalomyocarditis virus. However, evidence of the presence of an influenza type A infection was demonstrated by indirect immunofluorescence (IIF) staining using monoclonal antibody directed to nucleocapsid protein (NP) of human type A influenza virus. The virus was isolated either by intra-allantoic inoculation of specific-pathogen-free embryonating hens' eggs or propagation in canine kidney (MDCK) cells in the presence of trypsin. By hemagglutination inhibition tests, no cross-reactivity was demonstrated with human influenza H1N1, H2N2, and H3N2 strains, and infected MDCK cells did not react by IIF with monoclonal antibodies to NP protein of type B influenza virus. The hemagglutination activity of plaque-purified isolates was only partly inhibited by hyperimmune serum produced to subtypes A/Wisconsin/76/H1N1 and A/New Jersey/76/H1N1 of swine influenza virus. Gnotobiotic piglets that were infected intranasally with egg-adapted isolates of this new antigenic variant of swine influenza virus developed the very same type of lesions observed in field cases.