Economic analysis of outbreaks of porcine reproductive and respiratory syndrome virus in nine sow herds

The economic losses due to porcine reproductive and respiratory syndrome virus (PRRSv) outbreaks are reported in the literature to be substantially high, but recent figures are not available. The aim of this study was to quantify the economic effects of epidemic PRRSv outbreaks in Dutch sow herds. Nine sow herds were selected based on a confirmed PRRSv outbreak within those populations. The economic impact during the first 18 weeks after the outbreak was estimated by comparing the overall costs between pre- and postoutbreak periods, using different factors (production data, medication, diagnostics, labour, etc.). An outbreak of PRRSv resulted in a reduced number of sold pigs per sow of 1.7. The economic loss varied between €59 and €379 for one sow per 18-week period outbreak. The mean loss per sow per outbreak was €126. The costs after the outbreak varied significantly from €3 to 160 per sow, due to the different methods used by farmers to tackle PRRSv outbreaks. The calculated costs in this study correlate with the costs of the initial outbreak in The Netherlands of 98 per sow.     

Genetic analysis of reproductive performance in sows during porcine reproductive and respiratory syndrome(PRRS) and porcine epidemic diarrhea(PED)outbreaks

Background: Porcine reproductive and respiratory syndrome(PRRS) is one of the most infectious swine diseases in the world, resulting in over 600 million dollars of economic loss in the USA alone. More recently, the USA swine industry has been having additional major economic losses due to the spread of porcine epidemic diarrhea(PED).However, information regarding the amount of genetic variation for response to diseases in reproductive sows is still very limited. The objectives of this study were to identify periods of infection with of PRRS virus(PRRSV) and/or PED virus(PEDV), and to estimate the impact their impact on the phenotypic and genetic reproductive performance of commercial sows.Results: Disease(PRRS or PED) was significant(P 0.05) for all traits analyzed except for total piglets born.Heritability estimates for traits during Clean(without any disease), PRRS, and PED ranged from 0.01(number of mummies; Clean and PED) to 0.41(abortion; PED). Genetic correlations between traits within disease statuses ranged from-0.99(proportion born dead with number weaned; PRRS) to 0.99(number born dead with born alive;Clean). Within trait, between disease statuses, estimates ranged from-0.17(number weaned between PRRS and PED) to 0.99(abortion between Clean and PRRS).Conclusion: Results indicate that selection for improved performance during PRRS and PED in commercial sows is possible and would not negatively impact performance in Clean environments.     

Interaction between innate immunity and porcine reproductive and respiratory syndrome virus

Innate immunity provides frontline antiviral protection and bridges adaptive immunity against virus infections. However, viruses can evade innate immune surveillance potentially causing chronic infections that may lead to pandemic diseases. Porcine reproductive and respiratory syndrome virus (PRRSV) is an example of an animal virus that has developed diverse mechanisms to evade porcine antiviral immune responses. Two decades after its discovery, PRRSV is still one of the most globally devastating viruses threatening the swine industry. In this review, we discuss the molecular and cellular composition of the mammalian innate antiviral immune system with emphasis on the porcine system. In particular, we focus on the interaction between PRRSV and porcine innate immunity at cellular and molecular levels. Strategies for targeting innate immune components and other host metabolic factors to induce ideal anti-PRRSV protection are also discussed.     

Persistence of porcine reproductive and respiratory syndrome virus in intensive farrow-to-finish pig herds.

An epidemiological study of porcine reproductive and respiratory syndrome (PRRS) within pig herds was conducted in 8 intensive farrow-to-finish pig farms. Persistence of PRRS virus (PRRSV) in pig herds was demonstrated by regular postmortem examination on 2 farms for a period of 2 y. Virus isolation and serum neutralization (SN) tests were performed on the sera collected from 9 groups of pigs (10 pigs/group) of various ages on 8 pig farms. Except for 1 farm, isolation rates of PRRSV reached the highest level of 70 to 100% of pigs 6 to 8 wk of age, which coincided with the lowest levels of maternal immunity. In 1 pig herd, sows (39 in total) with SN titers of < or = 1:2, 1:4-1:8, and > or = 1:16 were designated as groups 1, 2, and 3, respectively. Sera were obtained from their progeny (3 pigs randomly selected from each litter) at various ages from 0 to 22 weeks. A positive correlation (r = 0.377, P < 0.001) between the SN titers of sows and those of their progeny (1-week-old piglets) was observed. Pigs at the age of 6 wk, only 7.9% of group 1 pigs compared to 72.4% of group 3 pigs were seropositive. A significant difference (P < 0.01) in the percentage of pigs with PRRSV viremia among the 3 groups was observed, with the lowest level found in group 3 pigs. The isolation rates of PRRSV from serum reached the maximum at the age of 9 wk for all 3 groups. The results indicated that passively acquired serum antibodies conferred a protective effect for piglets; however, loss of passive immunity at various ages of pigs produced susceptible pigs that resulted in PRRSV persistence in the pig herds. Pigs 6 to 9 weeks old were the major reservoir for PRRSV in farrow-to-finish pig herds.     

Long-term administration of a commercial porcine reproductive and respiratory syndrome virus (PRRSV)-inactivated vaccine in PRRSV-endemically infected sows

The purpose of this study was to investigate the safety and efficacy of a commercial European porcine reproductive and respiratory syndrome virus (PRRSV)-inactivated vaccine after 18-month use in gilts/sows at a farm with high seroprevalence. In a farrow-to-finish farm with 1100 sows, all sows and gilts were systematically vaccinated with the PRRS-inactivated PROGRESSIS vaccine for a period of 18 months. Farm's reproductive and litter characteristics were longitudinally recorded for this period and historically compared with those of the year prior to vaccination. Serology, employing immunoperoxidase monolayer assay, had confirmed a high prevalence of PRRS-specific antibodies in most age groups within the farm prior to vaccination. Seroprevalence during the experiment ranged between 0% and 100% in weaners and growers, but remained at stable high levels (> 93%) in finishing pigs and gilts throughout all 2-year period of serology measurements. No local or systemic vaccine side effects were noted throughout the trial period. Vaccinations had resulted over time in a significant improvement of sow reproductive performance (e.g. reduction of premature farrowings, abortions and increase of farrowing rate) and litter characteristics (e.g. increase of the number of live born and weaned pigs and decrease of stillborn, mummified, weak and splay-legged piglets). It has also been observed that the higher the degree of immunization of a sow, the better the improvement of her reproductive parameters. Sows after vaccination have shown improved characteristics compared to homoparous sows prior to the application of vaccinations in the farm.     

Pathogenesis of porcine reproductive and respiratory syndrome virus infection in mid-gestation sows and fetuses.

Two experiments were undertaken to evaluate whether porcine reproductive and respiratory syndrome (PRRS) virus was able to cross the placenta and infect midgestation fetuses following intranasal inoculation of sows and whether PRRS virus directly infected fetuses following in utero inoculation. In experiment 1, eight sows between 45 and 50 days of gestation were intranasally inoculated with PRRS virus (ATCC VR-2332), and four control sows were inoculated with uninfected cell culture lysate. Virus inoculated sows were viremic on postinoculation (PI) days 1, 3, 5, 7 and 9, shed virus in their feces and nasal secretions, and became leukopenic. Sixty-nine of 71 fetuses from principal sows euthanized on PI day 7, 14 or 21 were alive at necropsy and no virus was isolated from any of the fetuses. Two principal sows that farrowed 65 and 67 days PI delivered 25 live piglets and three stillborn fetuses. The PRRS virus was isolated from two live piglets in one litter. In experiment 2, laparotomies were performed on five sows between 40 and 45 days of gestation and fetuses were inoculated in utero with either PRRS virus alone, PRRS virus plus a swine serum containing PRRS antibodies, or uninfected cell culture lysate. Three sows were euthanized on PI day 4 and two sows on PI day 11. Viral replication occurred in fetuses inoculated with virus alone and was enhanced in fetuses inoculated with virus plus antibody. No virus was isolated from control fetuses.(ABSTRACT TRUNCATED AT 250 WORDS)     

Shedding of porcine reproductive and respiratory syndrome virus in mammary gland secretions of sows.

OBJECTIVE: To document shedding of porcine reproductive and respiratory syndrome (PRRS) virus in mammary gland secretions of experimentally inoculated sows, to evaluate effects of vaccination during gestation on virus shedding during the subsequent lactation, and to evaluate shedding of PRRS virus in milk of sows in commercial herds. ANIMALS: 6 sows seronegative for PRRS virus were used for experiment 1, and 2 sows were retained for experiment 2. For experiment 3, 202 sows in commercial herds were used. PROCEDURE: In experiment 1, 2 sows were inoculated with PRRS virus, 2 sows were vaccinated with modified-live PRRS virus vaccine, and 2 sows served as control pigs. Mammary gland secretions were assayed for PRRS virus. In experiment 2, pregnant vaccinated sows from experiment 1 were vaccinated with another modified-live PRRS virus vaccine. Mammary gland secretions were assayed in the same manner as for experiment 1. For experiment 3, milk collected from 202 sows in commercial herds was assayed for PRRS virus. RESULTS: In experiment 1, PRRS virus was detected in mammary gland secretions of both vaccinated and 1 of 2 virus-inoculated sows. In experiment 2, virus was not detected in samples from either vaccinated sow. In experiment 3, all samples yielded negative results. CONCLUSIONS AND CLINICAL RELEVANCE: Na?ve sows inoculated late in gestation shed PRRS virus in mammary secretions. Previous vaccination appeared to prevent shedding during the subsequent lactation. Results for samples obtained from sows in commercial herds suggested that virus shedding in mammary gland secretions of such sows is uncommon.     

Genetic diversity of porcine reproductive and respiratory syndrome virus strains circulating in Hungarian swine herds

Analysis of 37 ORF5 sequences of Hungarian porcine reproductive and respiratory syndrome virus (PRRSV) strains revealed that most of them (35) belonged to the European genotype, forming distinct subgroups, reflecting the exceptional diversity of Eastern European strains. Twelve vaccine-like strains were also found in non-vaccinated animals. Two strains belonged to the American genotype showing 90-91% nucleotide identity to the "Quebec" Canadian reference strain. The analysis of the putative ectodomains and their N-linked glycosylation sites of the vaccine strain and its variants suggested selective pressure on the first ectodomain, by a consistent amino acid change on epitope B and by loosing a glycosylation site in the otherwise conserved N-46 position.     

Randomised, placebo-controlled trial of a live vaccine against porcine reproductive and respiratory syndrome virus in sows on infected farms

A randomised, double-blinded, placebo-controlled study into the effectiveness and safety of a vaccine against porcine reproductive and respiratory syndrome virus (PRRSV) was carried out on three farms with a history compatible with chronic PRRSV infection; representative groups of sows and gilts were injected with a live vaccine against PRRSV, and during the next six weeks no side effects were observed. The remaining sows and gilts on the three farms were then vaccinated with the same vaccine. Again, no side effects were observed. There were significant reductions in abortion, reproductive disease, returns to oestrus and the numbers of stillborn pigs per sow, and significant increases in the numbers of liveborn pigs per sow and weaned pigs per sow among the vaccinated animals.     

Risk factors for infection of sow herds with porcine reproductive and respiratory syndrome (PRRS) virus

In 1992, the porcine reproductive and respiratory syndrome virus (PRRSV) of European type (PRRSV-EU) was introduced in Denmark. By 1996, the virus had spread to approximately 25% of the Danish herds. In January 1996, a modified-live vaccine based on the American type of the virus (PRRSV-US) was used in replacement boars for Danish artificial insemination (AI) centres and from July 1996, the vaccine was used in PRRSV-EU infected herds for prevention of disease. Soon after vaccine introduction, PRRSV non-infected herds experienced outbreaks of disease due to infection with PRRSV-US. In this study, we investigated the risk factors (biosecurity level, animals, exposure from PRRSV-US-infected neighbour herds, semen, herd size, pig density and herd density) for infection with PRRSV-US in a cohort of 1071 sow herds; we used a nested case-control study. The retrospective observation period lasted from June 1996 (when they all were non-infected) to October 1997. Seventy-three non-vaccinated, closed sow herds became infected with the vaccine strain during this period. Each case herd was matched with two control herds from the cohort (controls had not been infected at the time of infection in the case herds). The data were analysed using a Cox-regression model. The hazard of infection increased significantly with exposure from PRRSV-US-infected neighbouring herds, purchase of animals from herds incubating PRRSV-US infection, increasing herd size and purchase of semen from boars at PRRSV-US-infected AI centres. The results are consistent with the modified-live vaccine strain spread to other herds by trade with animals and semen and by neighbour (area) transmission. We suggest that virus spread by aerosols was a frequent mode of transmission.     

Transmission of porcine reproductive and respiratory syndrome virus from persistently infected sows to contact controls.

The objective of this study was to determine if porcine reproductive and respiratory syndrome virus (PRRSV) could persist in non-pregnant sows and if persistently infected sows could transmit virus to naive contact controls. Twelve PRRSV-naive, non-pregnant sows (index sows) were infected with a field isolate of PRRSV and housed in individual isolation rooms for 42 to 56 days postinfection. Following this period, 1 naive contact sow was placed in each room divided by a gate allowing nose-to-nose contact with a single index sow. Index sows were not viremic at the time of contact sow entry. Virus nucleic acid was detected by polymerase chain reaction, and infectious virus was detected by virus isolation in sera from 3 of the 12 contact sows at 49, 56, and 86 days postinfection. All 3 infected contacts developed PRRSV antibodies. Virus nucleic acid was detected in tissues of all of the 12 index sows at 72 or 86 days postinfection. Nucleic acid sequencing indicated that representative samples from index and infected contacts were homologous (> 99%) to the PRRSV used to infect index sows at the onset of the study. This study demonstrates that PRRSV can persist in sows and that persistently infected sows can transmit virus to naive contact animals.     

猪α干扰素的原核表达及抗高致病性猪繁殖与呼吸综合征病毒活性测定

为了研究高效广谱的基因工程抗病毒制剂,本研究采用PCR技术自猪肝脏总DNA中扩增、克隆猪α干扰素（PoIFN-α）成熟肽基因并亚克隆入pQE30载体进行原核表达,对表达的融合重组猪α干扰素（rPoIFN-α）蛋白通过尿素变性、低浓度蛋白复性液复性、PBS溶液透析等步骤进行纯化,采用细胞病变抑制法分别测定rPoIFN-α蛋白在PK15细胞上抗水泡性口炎病毒（VSV）增殖活性及在Marc-145细胞上抑制高致病性猪繁殖与呼吸综合征病毒（PRRSV）的增殖活性,以分别评价rPoIFN-α的活性单位及其体外抑制高致病性PRRSV增殖所需的最低浓度。结果表明,克隆的PoIFN-α成熟肽基因全长501bp,编码166个氨基酸;表达的rPoIFN-α蛋白分子量大小20.7ku左右,与预期大小相一致;经纯化后的蛋白纯度在95%以上;纯化的rPoIFN-α蛋白在PK15细胞上抗VSV病毒活性单位为1.4482&#215;10^4IU/mL（5.2&#215;10^6IU/mg）,在Marc-145细胞上能完全抑制高致病性PRRSV增殖所需的rPoIFN-α蛋白最低有效剂量为640U/mL（2.3&#215;10^4U/mg）。这些研究结果为新型基因工程抗病毒制剂的开发以及用于高致病性PRRSV性疾病的预防和治疗奠定了基础。     

猪繁殖与呼吸综合征DNA重组质粒对猪的免疫效应

猪繁殖与呼吸综合征病毒(PRRSV)灭活疫苗、表达GP5蛋白的DNA重组质粒分别与表达IL-2和IL-4的重组质粒(pcDNA-IL-2和pcDNA-IL-4)联合免疫健康仔猪,经3次免疫后人工感染PRRSV HB-2株,检测仔猪体液免疫以及攻毒保护性反应。研究结果显示,重组质粒pCI-GP5可诱导免疫猪产生抗GP5抗体,最高ELISA抗体效价可达1∶285。攻毒后组织中PRRSV核酸的检出率下降30.3%,与对照组相比,差异显著(P<0.05),表明表达PRRSV GP5的DNA重组质粒pCI-GP5可诱导一定的免疫效力。pcDNA-IL-2与pCI-GP5联合免疫后,病毒血症的出现频率减少38.9%,PRRSV阳性组织检出率下降28.8%,与对照组差异显著(P<0.05);pcDNA-IL-4与pCI-GP5联合免疫后,最高ELISA抗体效价可达1∶320,病毒血症的出现频率下降38.9%,PRRSV阳性组织检出率减少34.8%,与对照组相比差异极显著(P<0.01)。本研究表明,PRRS DNA重组质粒pCI-GP5对猪的免疫保护力是稳定的,真核表达的细胞因子pcDNA-IL-2与pcDNA-IL-4能够显著增强pCI-GP5的免疫保护力。     

论商品群中母猪高繁殖性能的影响因素

<正>随着信息技术的应用与发展,猪场收集了商品猪群大量的数据信息,新技术可以最大程度的采集、交换和分析数据。然而,这种数据的作用受到了制约,因为农场的数据分析仅仅可以帮助兽医和生产人员发现生产中的问题,不能确定更好地解决问题的方案。不仅如此,数据分析还可以加大繁殖群中可以提高群体生产率和稳定产出的有用信息的传播。为充分发挥母猪的繁殖潜能,使其最大化,通过数据分析,可以识别与繁     

Differential immunity in pigs with high and low responses to porcine reproductive and respiratory syndrome virus infection

One hundred Hampshire x Duroc cross-bred pigs (HD) and 100 NE Index line (I) pigs were infected with porcine reproductive and respiratory syndrome (PRRS) virus and evaluated for resistance/susceptibility. Controls (100/line) were uninfected littermates to the infected pigs. Viremia, change in weight (WTdelta), and rectal temperature at 0, 4, 7, and 14 d postinfection were recorded. Lung, bronchial lymph node (BLN), and blood tissue were collected at necropsy (14 d postinfection). The first principal component from principal component analyses of all variables was used to rank the pigs for phenotypic response to PRRS virus. Low responders (low PRRS burden) had high WTdelta, low viremia, and few lung lesions; high responders (high PRRS burden) had low WTdelta, high viremia, and many lesions. The RNA was extracted from lung and BLN tissue of the 7 highest and 7 lowest responders per line and from each of their littermates. Expression of 11 innate and T helper 1 immune markers was evaluated with cDNA in a 2 x 2 x 2 factorial design. Significant upregulation in lung, lymph, or both of infected pigs relative to controls occurred for all but one gene. Expression differences were greater in HD than I pigs. Significant downregulation for certain immune genes in low pigs, relative to littermate controls, was detected in lung and BLN, particularly in line I. Serum levels of the immune cytokines affirmed the gene expression differences. High preinfection serum levels of IL 8 were significantly associated with PRRS virus-resistant, low pigs. After infection, low expression of interferon gamma in cDNA and in serum was also correlated with PRRS virus resistance. Important genetic associations were revealed for fine mapping of candidate genes for PRRS virus resistance and determining the causative alleles.     

An assessment of sanitation protocols for commercial transport vehicles contaminated with porcine reproductive and respiratory syndrome virus

The objective of this study was to develop and test a rapid (< 2 h) sanitation protocol designed for porcine reproductive and respiratory syndrome virus (PRRSV) positive commercial transport vehicles involving cold water washing and disinfection via fumigation using scale models of weaned pig trailers. The study consisted of 2 phases. Following experimental contamination of model trailers with PRRSV MN 30-100 (5 x 10(5)TCID50), phase 1 evaluated the presence or absence of PRRSV RNA by polymerase chain reaction (PCR) on swabs collected from the trailer interiors 0, 60, and 90 min after treatment. Phase 2 consisted of evaluating the infectivity of trailers 90 min posttreatment by monitoring changes in the PRRSV-status of naive sentinel pigs housed for 2 h. Treatments included washing only (treatment 1), washing plus formaldehyde fumigation (treatment 2), washing plus fumigation with glutaraldehyde-quaternary ammonium chloride (treatment 3), and washing plus overnight drying (treatment 4). Porcine reproductive and respiratory syndrome virus RNA was detected in all trailers (20 out of 20 replicates) at 60 and 90 min following the application of treatments 1 and 2. These trailers also contained infectious PRRSV, as determined by the infection of naive pigs housed in treated trailers and the testing of organic debris collected from the interior of trailers by swine bioassay. At 90 min posttreatment, all trailers treated with glutaraldehyde-quaternary ammonium chloride were PCR-negative, non-infectious to sentinel pigs, and swine bioassay negative. Similar results were observed in trailers allowed to dry for 8 h. Under the conditions of this study, it appears certain disinfectants may possess different levels of efficacy against PRRSV and PRRSV-positive models may be effectively sanitized in the absence of overnight drying.     

Genetic parameters for performance traits in commercial sows estimated before and after an outbreak of porcine reproductive and respiratory syndrome

Porcine reproductive and respiratory syndrome (PRRS), caused by the PRRS virus (PRRSV), is globally the most economically important disease in commercial pigs, and novel control strategies are sought. This paper explores the potential to use host genetics to decrease the impact of PRRS on reproductive sows. Commercial pig data (7,542 phenotypic records) from a farm undergoing an outbreak of PRRSV were analyzed to assess the impact of PRRS on reproductive traits and the inheritance of such traits. First, differing methodologies were used to partition the data into time periods when the farm was disease free and when the farm was experiencing PRRSV outbreaks. The methods were a date/threshold method based on veterinary diagnosis and a threshold/threshold method based on trends in underlying performance data, creating the DTD and TTD data sets, respectively. The threshold/threshold method was more stringent in defining periods when PRRS was likely to be having an impact on reproductive performance, resulting in a data set (TTD) that was slightly smaller (1,977 litters from 1,526 sows) than that from the date/threshold method (3,164 litters and 1,662 sows), and it showed more pronounced impacts of PRRS on performance. Impacts on performance included significant increases in mean values of mummified and stillborn piglets (0.04 to 1.13 and 0.63 to 1.02, respectively) with a significant decrease in total born alive (10.3 to 9.08). Estimated heritabilities during the healthy phase were generally less (mummified piglets = 0.03 +/- 0.01, matings per conception = 0.04 +/- 0.01) than during the PRRSV outbreak (TTD data set; mummified piglets = 0.10 +/- 0.03, matings per conception = 0.46 +/- 0.04). These results imply genetic variation for host resistance to, or tolerance of, PRRSV, particularly with the TTD data set. Genetic correlations between reproductive traits measured in the healthy phase and TTD data set varied from effectively zero for traits describing numbers of mummified or dead piglets to strongly positive for litter size traits. This indicates genetic variation in piglet losses during PRRSV outbreaks is independent of genetic variation in the same traits in healthy herds. In summary, our findings show that there is within-breed genetic variation for commercially relevant traits that could be exploited in future breeding programs against PRRSV infection. Selection for increased PRRS resistance would be desirable to the industry because effective control measures remain elusive.