Porcine infectious diseases characterized by respiratory abortion, premature birth, stillbirth, mummy and other reproductive disorders caused by respiratory syndrome virus (PRRSV), and severe respiratory symptoms and high mortality in piglets. Due to the rapid spread of PRRS and persistent infection in pigs, it is not easy to eliminate. Since the first outbreak of pigs in North Carolina, Iowa, and other states in 1987, it has been spread all over the world, and it has become a global pig farmer. Caused major economic losses. At the end of 1995, Guo Baoqing et al. in China isolated PRRSV from pigs suspected of this disease, confirming the existence of PRRS in China. Subsequently, the domestic research on various aspects of its pathogen PRRSV has also rapidly begun. The results of research in recent years are summarized as follows. 1 Pathogen PRRSV is an enveloped, single-stranded, positive-stranded RNA virus with viral particles of 55 to 60 nm in diameter. According to its morphological and physicochemical characteristics, cell tropism, strain variation, persistent infection, genome size, structure, ORF homology and transcription patterns, etc., the characteristics are obviously similar to members of the genus Arterivirus, and its virus taxonomic status is The genus Arteritis virus of the virus family. PRRSV is specialized in growth in porcine alveolar macrophages and can grow and multiply in the passaged cell lines CL-2621 and Marc145, Hs*2H, and can produce obvious cytopathic effects; PRRSV does not agglutinate red blood cells and has no hemagglutination activity; It is very sensitive to pH and temperature changes; when the pH value is greater than 7 or less than 5, its infectivity is reduced by more than 90%, and the alkali tolerance is extremely poor. pH 5.5-6.6 is the optimal pH for its preservation; room temperature and 37°C Immediately inactivated below, completely inactivated at 56°C for 45 minutes; resistance to disinfectants is not strong. Use these features to choose the right disinfectant or hot water to clean the environment. 2 Antigenicity According to the degree of genetic variation, PRRSV is currently divided into 2 different geographical groups: Group A represented by the European prototype virus Lelystad virus (abbreviated as LV) and B represented by the American prototype virus ATCC VR-2332 strain. group. The results of serological tests showed that there were common antigenic determinants among different isolates and it was a kind of virus. However, the difference in antigenicity between them makes them have only a few cross reactions in the serological reaction. Nucleic acid sequence comparisons also indicate a wide range of differences in their genomes. The antigenic differences between the two groups of viruses can be so great that only serological tests using the same antigenic type of virus can confirm PRRSV. Even among different strains in the same group, there are differences in virulence and antigenicity. The three major structural proteins of PRRSV are: a nucleocapsid protein (N) with a molecular weight of 15 KD, a matrix protein (M) of 18 KD, and an envelope protein (E) of 25 KD. The N protein was the most immunogenic. When PRRSV was infected in pigs, all infected pigs could detect anti-N antibody 7 days after challenge. 3 Epidemiology The main routes of transmission of PRRSV are contact infection, airborne transmission and semen transmission. Experiments show that a certain amount of virus is required in semen to infect sows. In addition, boar detoxification after infection can be as long as 90d. However, it is not clear how long the boar will be able to produce enough virus to infect the sow. The introduction of infected pigs, especially cryptogenic pigs, into susceptible herds is an important cause of the epidemic. In early pregnancy, the virus can infect the fetus through the placenta, which may be related to the passage of infected macrophages through the placenta into the fetus. Mid-pregnancy virus is difficult to infect the fetus through the placenta. 4 Pathogenic pigs are the only animals infected with PRRSV and present with clinical symptoms. The virus is mainly responsible for the breeding of sows and their piglets, causing serious sow reproductive problems and piglet respiratory diseases. Boar infection can cause semen quality to decline, and fattening pigs are mostly mild. 4.1 In the early stage of acute infection, the pigs showed symptoms of low appetite, fever, drowsiness, and mental insomnia, which generally lasted 1 to 3 weeks. The main features of peak incidence are sows' premature birth, late abortion, and increased mummification and debilitating rates; the mortality of piglets before weaning increases, and the peak period generally lasts 8 to 12 weeks. The following three indicators can be used to measure acute PRRS: 1 Abortion or preterm birth exceeds 8% 2 The rate of stillbirth exceeds 20% 3 The piglet mortality rate exceeds 25% in the first week after birth. At the end of the onset, sow reproductive function gradually recovered, reaching or approaching pre-illness levels. Piglets and finishing pigs have different degrees of respiratory symptoms. Healed pigs generally grow slowly and weigh less. If there are no secondary infections, gross lesions are not generally visible except for characteristic lesions such as interstitial pneumonia in the affected piglets. In addition, PRRS-prone pigs are prone to secondary infections such as Haemophilus, streptococcus, Salmonella cholera, Pasteurella multocida, Actinobacillus pleuropneumoniae, swine influenza virus, encephalomyocarditis virus, and pseudorabies virus, which aggravate the condition. development of. 4.2 The chronic type is more acute and the illness is longer. The main effect on the herd is secondary infection caused by other bacteria or viruses against the respiratory system, such as rhinitis and pneumonia. Infected pig growth rate, feed conversion rate decreased. 4.3 Subclinical serological surveys The positive rate of the pigs was as high as 40% to 50% but only 10% of the clinical symptoms. At present, the understanding of subclinical PRRS is still insufficient. 5 Diagnosis The diagnosis of PRRS currently relies mainly on the isolation and identification of the virus and the use of serological tests to detect PRRS antigens and their antibodies. Due to the cell preparation and the selective growth of different strains of PRRSV on the cells and the antigenic differences between the strains, the actual diagnosis work is complicated, difficult, time-consuming and laborious. Before the successful separation of PRRSV, the diagnosis of the disease mainly relied on the typical clinical symptoms of the pig, characteristic histological pathological changes, especially interstitial pneumonia. 5.1 Clinical symptoms When an outbreak of acute PRRS occurs, the clinically manifested late abortion, stillbirth, weak fetus, intractable diarrhea, and high mortality of pre-weaned piglets have important implications for the diagnosis of the disease. 5.2 Histopathological examination Since sows and finishing pigs do not show macroscopic pathological changes unless they are secondary to other pathogens. However, the incidence of interstitial pneumonia in piglets is characteristic. 5.3 Laboratory Diagnosis A number of serological methods have been established for the detection of PRRSV antigens and their antibodies in porcine sera: eg immunohistochemical cell monolayer assays (IPMA), indirect fluorescent antibody assays (IFA), and neutralization tests ( NT), immune enzyme technology (ELISA, Dot-ELISA) and the like. However, because of the difference in the antigenic type of PRRSV, one method can detect both A and B antigens or antibodies using only two antigenic subtypes, which inconveniences the actual operation. At present, serological methods can only be used to evaluate the status of PRRSV infection in pigs. If the diagnosis is still needed, virus isolation and identification must be performed. In the actual production, different methods or reagents provided by different units of the same method are used for detection, and the results are often quite different. Current monoclonal antibody technology and molecular biology diagnostic methods provide convenience for diagnosis of the disease. A variety of McAbs have been prepared against different epitopes on the nucleocapsid proteins. In addition to the McAb SDOWD prepared from VR2332 that recognizes a conserved epitope on the N protein, most McAbs can only recognize the US and European strains, respectively, for typing. Because PRRSV in vitro cultured laboratory host system PAMs, CL-2621, Marc-145 is not easy to obtain and the restriction of PRRSV different isolates on the adaptive growth of the above cells, the separation and culture of PRRSV is complicated and time-consuming. People began to make use of RT-PCR, nucleic acid probes, sequencing and in situ hybridization methods for molecular diagnosis and typing of PRRS, revealing the basis of antigenic variation and the evolution of strains at the molecular level. Universal primers for RT-PCR amplification of viral genomes were used to identify the specific primers of the European and American strains. The use of universal primers and specific primers in nested RT-PCR allows typing diagnosis in a single PCR reaction. It is also convenient and stable to use a cDNA fragment obtained by reverse transcription amplification to prepare a DNA probe after radioisotope or photobiotin labeling or digoxigenin labeling, and to detect RNA extracted from a PRRSV culture or a diseased material by Nerthern hybridization. diagnosis method. In addition, studies on gene sequence analysis of PRRSV showed that European and American types may be different genotypes evolved under pressure of environmental selection. PRRSV genotyping and antigen typing are basically the same, and the difference in gene sequence is antigen. The basis of type differences. 6 Control measures 6.1 Healthy pigs should adhere to self-cultivation and reduce the contact of healthy pigs with the virus. When the production needs to be introduced from the outside, strict quarantine should be conducted to prevent the introduction of susceptible pigs into vulnerable pigs. In combination with strict sanitization measures, it is possible to establish a herd without PRRSV infection. However, this practice has certain risks in the endemic areas of the disease. When the pigs are not protected by neutralizing antibodies produced by infection (wild virus or vaccine virus), the outbreak is often acute and the loss is greatest. . 6.2 PRRS can be controlled in PRRS affected farms by eliminating diseased pigs, preventing secondary infections, hot water washing, and sterilizing pig farms. In the weaning and fattening pig populations, there are usually a large number of viruses, and the disinfection work in these places should be especially emphasized in order to prevent the virus from spreading to the sow herds, which makes susceptible pigs infected and causes greater losses. 6.3 Active Immunity Because PRRS has an antibody-dependent infection-enhancement phenomenon, when the virus and antibody produce an antigen-antibody complex, the FC fragment of the Ab binds to the FC receptor of the target cell, thereby promoting the entry of the virus into the cell. And PRRSV in the pig long-term persistent infection. When the neutralizing antibody titer is high, the body can stop the virus from re-invasion. When the level of neutralizing antibodies is low, virus proliferation is further enhanced, further infecting surrounding susceptible pigs. Therefore, it is difficult for PRRSV to disappear from the farm. This poses some difficulties for the prevention of PRRS work. Recently, a variety of PRRS vaccines, inactivated vaccines, attenuated vaccines, and gene vaccines have been trial-produced at home and abroad. Because of the vaccine, neutralizing antibodies and cellular immunity produced by the body do not provide adequate and effective protection against PRRS infections. There is still some controversy about safety, and there are disagreements about the effectiveness of vaccines. Because the disease has many characteristics such as multiple routes of transmission, rapid transmission and long-term infection in pigs, the use of vaccines is the only best control method. It is imperative to develop a safe and effective PRRS vaccine by screening, transforming, and utilizing immunogenic genes that can cause the pig to produce a protective Ab against PRRSV. 6.4 Natural protection Most sows receive active immunity after the initial infection, and the sow group's symptoms are also relieved. The situation for finishing pigs is similar. However, weaned piglets are often infected with the virus as maternal antibodies are reduced. In addition, when the antibody level in pigs is uneven, the virus will re-infect pigs with low resistance, but the loss to production has been relatively small. However, as time passes, when all the pigs have relatively low antibody levels, all pigs become vulnerable. Once infected, the disease will recur again, and the loss will be quite heavy. Therefore, there is a certain risk that we hope to obtain a satisfactory immune effect through natural infections. In the absence of commercial vaccines, most pig farms generally adopt this practice passively. At present, most commercial vaccines have abandoned this practice since their inception. Because the husbandry and management factors determine to a large extent whether the naturally protected pigs will have the second outbreak. The feeding and management factors are related to various issues. Any farm owner does not dare to claim that there is no loophole in his farm management.
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