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1.
OBJECTIVE: To describe the pathological findings in stillborn piglets and fetuses delivered by sows naturally infected with Menangle virus, a recently recognised Paramyxovirus. DESIGN: Observations of the gross and microscopic pathology of natural disease. PROCEDURE: Postmortem examinations were performed on 49 stillborn piglets, 35 mummified or semi-mummified full-term fetuses and 6 aborted fetuses from 20 litters at a 2600-sow intensive piggery in New South Wales during an outbreak of reproductive disease from June to September 1997. Body weights, crown-rump lengths and gross pathological changes were recorded. Tissues, including brain and spinal cord, were processed for histopathological examination. RESULTS: Litters with reduced numbers of live born piglets had mummified fetuses and stillborn piglets. Affected stillborn and aborted piglets frequently had arthrogryposis, craniofacial and spinal deformities, pulmonary hypoplasia and degeneration of the brain and spinal cord. Intranuclear and intracytoplasmic inclusion bodies were observed in neurones and other cells in the brain and spinal cord in association with extensive degeneration, necrosis, infiltration of macrophages and gliosis. CONCLUSIONS: In utero infection of piglets with Menangle virus is associated with severe skeletal and neurological malformations.  相似文献   

2.
An outbreak of reproductive failure, characterised by mummified foetuses and stillbirths, was investigated in an intensive piggery. Six foetuses that died towards the end of gestation had multifocal myocardial necrosis and encephalomyocarditis virus was recovered from 4 of these foetuses but not from 6 mummified foetuses. There was also a significant increase in failure of conception or early embryonic deaths in sows mated at the same time as sows which produced affected litters.  相似文献   

3.
Epidemiology and control of Menangle virus in pigs   总被引:6,自引:0,他引:6  
OBJECTIVE: To describe the epidemiology and eradication of Menangle virus infection in pigs. DESIGN: Field observations and interventions, structured and unstructured serological surveys, prospective and cross-sectional serological studies and laboratory investigations. PROCEDURE: Serum samples were collected from pigs at a 2600-sow intensive piggery in New South Wales that experienced an outbreak of reproductive disease in 1997. Serum samples were also collected from piggeries that received pigs from or supplied pigs to the affected piggery and from other piggeries in Australia. Serum and tissue samples were collected from pigs at piggeries experiencing reproductive disease in New South Wales. Sera and faeces were collected from grey-headed flying foxes (Pteropus poliocephalus) in the region of the affected piggery. Serum samples were tested for neutralising antibodies against Menangle virus. Virus isolation was attempted from faeces. RESULTS: Following the outbreak of reproductive disease, sera from 96% of adult pigs at the affected piggery, including sows that produced affected litters, contained neutralising antibodies against Menangle virus. Neutralising antibodies were also detected in sera from 88% of finisher pigs at two piggeries receiving weaned pigs from the affected piggery. No evidence of Menangle virus infection was found in other piggeries in Australia. In cross-sectional studies at the affected piggery, colostral antibodies were undetectable in most pigs by 14 to 15 weeks of age. By slaughter age or entry to the breeding herd, 95% of pigs developed high antibody titres (> or = 128) against Menangle virus in the virus neutralisation test. Menangle virus was eradicated from the affected piggery following a program of serological testing and segregation. Neutralising antibodies against Menangle virus were also detected in P poliocephalus from two colonies in the vicinity of the affected piggery. Two piggery workers were infected with Menangle virus. There was no evidence of infection in cattle, sheep, birds, rodents, feral cats and a dog at the affected piggery. CONCLUSIONS: Serological evidence of infection with Menangle virus was detected in pigs at a piggery that had experienced reproductive disease, in pigs at two associated piggeries and in fruit bats in the region of the piggery. Two humans were infected. The mode of transmission between pigs is unknown, but spread by faecal or urinary excretion is postulated. This virus can be eradicated by the segregation of pigs into discrete age groups.  相似文献   

4.
Causes of preweaning mortality were examined on a large intensive piggery. Diagnosis was made using comprehensive clinical histories combined with post-mortem data. Two thousand four hundred and twenty-six piglets were born in 238 litters. Pre-parturient and parturient losses were 2.9% and 5.4% of the total numbers of piglets born. Birth to weaning mortality was 11.3%. Among piglets born alive, overlaying was the most frequent cause of death (2.1%), followed by deaths due to diarrhoea (1.7%), anaemia (1.2%), savaging (1.1%) and losses of small weak piglets (0.9%). Most deaths, including stillbirths, were associated with below average birth weight, and two-thirds of all deaths of liveborn pigs occurred within 4 days of birth. Increased litter size resulted in decreased birth weights, an increased percentage of stillborn piglets and mummified foetuses, but duration of parturition was not affected. Stillborn piglets were born late in the litter and after a longer interval between pigs born (interpig interval). Over 70% of deaths due to overlay were in previously healthy piglets, but some were associated with illness of the sow (18%) or both sow and piglet (3%). Savaging was confined mainly to first parity sows and was responsible for 20% of all deaths in these litters. Sixty-two per cent of all piglets with a birth weight of less than 800g were stillborn or died before weaning compared with 18.7% mortality for all piglets. Anaemia in piglets was considered to be due to umbilical haemorrhage. Anaemic piglets had a 36% mortality to weaning compared with 10% for non-anaemic piglets.(ABSTRACT TRUNCATED AT 250 WORDS)  相似文献   

5.
The time of development of demonstrable antibody to porcine parvovirus (PPV) was determined for 661 gilts entering the breeding herd in a 2800 sow intensive piggery; 13.2% of these gilts did not have detectable antibody to PPV when first introduced into the breeding herd at 25 to 26 weeks of age. Exposure to PPV was found to vary in different sheds and even in different areas within a shed. Gilts that developed antibody to PPV during the first third of pregnancy were not adversely affected. Those that developed antibody during the middle third of pregnancy had fewer piglets born alive, more stillborn piglets and more mummified foetuses.  相似文献   

6.
We evaluated stillbirth risk factors in two commercial swine farms of the Rio Grande do Sul State (south of Brazil). The study was conducted during 1 month in Farm A and during 2 months in Farm B, both during 1999. Data for all farrowings that occurred during the study period were recorded (101 for Farm A and 373 for Farm B), without interference in the farm management. In Farm A, 39% of all litters born during the period of interest had stillborn piglets and the stillborn risk for piglets was 12%. In Farm B, 25% of all litters had stillborn piglets whereas the stillborn risk was 2%. Variables considered as potential risk factors for stillbirths were: parity (1, 2–3, 4+); breed (purebred or crossbred); sow body-condition (normal or fat); use of oxytocin during parturition (yes or no); obstetric intervention through vaginal palpation (yes or no); farrowing duration (<4 or ≥4 h); mummified fetuses (yes or no); total litter size (<12 or ≥12 piglets); and litter birth weight (<11 or ≥11 kg). All stillborn piglets had their classification validated by necropsy. In multivariable logistic-regressions, the cases were the litters having at least one stillborn piglet. In Farm A, litters having at least 12 pigs and in which oxytocin was used during the parturition had 20.8-times-higher odds of stillborn occurrence. In Farm B, litters from sows having parity ≥4 had 2.2-times-higher odds of stillborn occurrence than litters from parity 2 to 3 females, litters having ≥12 pigs had 2.0-times-higher odds of a stillborn piglet than smaller litters and farrowings in which vaginal palpation was performed had 8.0-times-higher odds. Farrowing room management to minimize stillborn risk should target higher-parity females, large litters and optimization of practices of obstetric interventions.  相似文献   

7.
Menangle病毒研究进展   总被引:2,自引:0,他引:2  
Menangle病毒(MenV)是近几年出 现的一种能导致新生仔猪繁殖障碍综合征和 人类类似流感症状的副黏病毒科的病原体。 MenV于1997年首次在澳大利亚新南威尔 士商品化猪场分离得到。生物分类、分子生 物学、系统发育树分析和流行病学等多方面 综合研究表明,MenV具有腮腺炎病毒属的 基本特征,并与腮腺炎病毒属(Rubulavirus)的另一成员Tiomanvirus(TiV)亲源关系最 近,从而证实MenV为腮腺炎病毒属的新成 员。文章重点对Menangle病毒分子生物学、 流行病学和诊断等方面内容进行了综述。  相似文献   

8.
9.
SUMMARY A parvovirus was isolated during an outbreak of mummifications and abortions in a commercial piggery. Stillborn piglets from which virus was isolated or in which parvovirus antibody was detected had widespread inflammatory lesions. Lesions were also seen in apparently healthy piglets from affected titters.  相似文献   

10.
An outbreak of abortions, stillbirths, mummified piglets and neonatal deaths in a pig herd in Arequipa, Peru is described. A total of 31 of 240 sows aborted between May and September 1988. When sera were examined 12 of 14 had very high titres of antibody to canicola PC125 and canicola Hond Utrecht, but there were also high titres of antibody to other leptospiral serovars. A detailed investigation was made and serovar canicola PC125 was isolated from the urine of four sows which had aborted and the kidney of one slaughter pig. Antibodies to various serovars of Leptospira were demonstrated in 11 of 17 sows which had aborted, two of six sows which had normal litters, nine of 18 boars, four of 39 slaughter pigs and four of 14 workers on the farm. The outbreak was brought under control by treatment and vaccination coupled with a thorough cleaning of the farm and control of the wild animal population. It is suggested that the infection was brought onto the farm by wild animals and that the disease is more common in Arequipa than was previously supposed.  相似文献   

11.
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.  相似文献   

12.
The use of a live attenuated porcine reproductive and respiratory syndrome virus (PRRSV) vaccine in piglets has been associated with reproductive disorders in non-vaccinated sows. Vaccine-derived virus (VDV) has been isolated from foetuses, stillborn pigs, and dead piglets, indicating that the live vaccine spread from vaccinated piglets to non-vaccinated sows, and that the virus might be implicated in the severe reproductive problems observed. In the present study, one such VDV isolate was used to experimentally infect pregnant sows in the last trimester. The chosen isolate, which had more than 99.6% identity to the attenuated vaccine virus, originated from the lungs of a stillborn pig from a swine herd with a sudden high level of stillborn pigs and increased piglet mortality in the nursing period. Intranasal inoculation of sows with the virus isolate resulted in congenital infection, foetal death, and preweaning pig mortality. As such, the present study showed that vaccine-derived PRRSV can cause disease in swine consistent with PRRS.  相似文献   

13.
The objective of this study was to detect the presence of porcine parvovirus (PPV) and porcine circovirus 2 (PCV2) in a farm showing reproductive failure and increased mortality in neonatal piglets by histopathological examination, polymerase chain reaction, and demonstration of viral antigen and nucleic acid. Out of 594 piglets farrowed by 70 first-parity gilts, nine (1.51%) mummified fetuses, 13 (2.19%) stillborn, and 572 (96.3%) live-born piglets were recorded. The average litter size at birth was 8.48 piglets per litter. One hundred ninety-four (33.91%) piglets died within 7 days of age. PPV was detected in five litters (7.14%) and two of them revealed coinfection with PCV2. The pathological lesions in the coinfected litters were more severe, indicating a synergistic action between the two viruses. Results of this study suggest for the first time occurrence of PPV and coinfection with PCV2 in crossbred Indian pigs affected with reproductive problem and neonatal mortality.  相似文献   

14.
During a period of 1.5 months, a newly established pig herd experienced a high number of mummifications and stillbirths, a high neonatal mortality rate, and many piglets with congenital tremors or hind leg ataxia. After clinical and histological investigations, the submitted animals were divided into 4 groups: mummified or stillborn (N = 6), live born with myocarditis (N = 5) (average age 22.8 days), live born without myocarditis (N = 14) (average age 20.0 days), and control animals from a different herd (N = 5) (newborn). Statistically significant differences were observed in the mean porcine circovirus 2 (PCV2) load among the 4 groups in the liver (P < 0.0001). The presence of PCV2 antigen within the myocardial lesions was confirmed by immunohistochemistry. A high load of PCV2 DNA was observed in myocardium, liver, and spleen from mummified or stillborn piglets (>1 x 10(7) copies per 500 ng DNA), lower in piglets with myocarditis (>1 x 10(5) copies per 500 ng DNA), and even further lower in pigs without myocarditis (<1 x 10(5) copies per 500 ng DNA), whereas no PCV2 DNA was detected in the control animals. Myocardium, liver, and spleen were well suited for routine testing of fetuses and young piglets by quantitative real-time polymerase chain reaction. Neither porcine parvovirus nor encepaholomyocarditis virus was detected. These results indicate that the PCV2 infection might have been of etiological importance for the fetal deaths and piglet mortality observed in this herd.  相似文献   

15.
SUMMARY An inactivated porcine parvovirus (PPV) vaccine for the prevention of PPV-induced reproductive failure in pigs was developed, using virus grown in cell culture, inactivated with beta-propiolactone and adjuvanted with aluminium hydroxide. The vaccine was tested for safety by subcutaneous injection into pregnant gilts. There were no signs of abnormal reactions nor evidence of PPV infection in the gilts or their foetuses when they were sacrificed 6 weeks after vaccination. To demonstrate that the vaccine was immunogenic, pigs were immunised either once or twice with 4 weeks between doses. Resulting antibody titres (haemagglutination inhibition — HAI) ranged from < 8 to 64 (geometric mean of 30) after one dose of vaccine, and from 128 to 512 (geometric mean 256) after two doses. To demonstrate that the vaccine was protective, antibody-negative gilts were vaccinated twice, with 4 weeks between doses, joined after the second dose, and were then infected with virulent PPV 40 to 50 days after joining. In litters from 10 vaccinated gilts, none of 93 foetuses showed evidence of PPV infection. In contrast, in litters from two unvaccinated gilts, all 13 foetuses showed evidence of PPV infection and 10 of these were mummified. The average number of live piglets per litter was 9.2 from vaccinated gilts and 1.5 from unvaccinated gilts. The vaccine was therefore considered to be effective in preventing PPV reproductive failure in susceptible gilts.  相似文献   

16.
Leptospirosis outbreak in a piggery in southern alberta   总被引:2,自引:1,他引:1       下载免费PDF全文
Fourteen abortions, stillbirths and neonatal deaths occurred over an interval of one month in crated sows in a farrow-to-finish swine operation. Leptospira interrogans serovar pomona (kennewicki by DNA analysis) was demonstrated by culture and fluorescent antibody test to be present in sows, piglets, boars, feeders, drinking water and skunks on the premises.

Antibody was found in all clinically affected sows, at serum dilutions ranging from 1/800 to 1/25,600, and in all breeding boars at titers from 1/50 to 1/1600. Pomona antibody was present in 118 sow sera collected nine months before the outbreak, at a prevalence of 21.3%. Parvovirus infection in fetuses was intercurrent with the leptospirosis epizootic, despite vaccination for the former. Environmental contamination, feedback through skunks via drinking water, and dissemination through the piggery are discussed.

  相似文献   

17.
The objectives of this study were to analyze the incidence of different categories of stillborn piglets in relation to genetic merit for farrowing survival of sows and litters and to analyze relationships of total number of piglets born per litter, average BW of the litter, and within-litter variation in BW with genetic merit for farrowing survival of sows and litters. Records of 336 purebred litters, produced by 307 first-to eighth-parity sows, were collected on a nucleus farm in Brouennes, France. Breeding values for farrowing survival were estimated for sows (EBVfs_maternal) and litters (EBVfs_direct) using a large data set from which information obtained in the current study was excluded. For each litter, BW, number of stillborn piglets (classified as nonfresh stillborn, prepartum stillborn, intrapartum stillborn, and postpartum stillborn), and number of live-born piglets were recorded. Birth weights of stillborn piglets were lower than BW of live-born piglets (P < 0.0001), except for prepartum stillbirths. The total number of stillborn piglets per litter and the number of stillborn piglets in each category decreased with increasing EBVfs_maternal (P < 0.01). An increase in EBVfs_direct was also associated with a decrease in the total number of stillborn piglets per litter (P < 0.01). This decrease was due to a decrease in the number of nonfresh, prepartum, and postpartum stillborn piglets but not to a decrease in the number of intrapartum stillborn piglets. Probabilities of stillbirth in relation to EBVfs_maternal were higher than probabilities of stillbirth in relation to EBVfs_direct. Total number of piglets born decreased with increasing EBVfs_direct (P = 0.0003), but was not related to EBVfs_maternal. Average BW of the litter (P < 0.0001) and within-litter variation in BW (P = 0.05) decreased with increasing EBVfs_maternal but were not related to EBVfs_direct. Selection for the maternal genetic component of farrowing survival seems a better strategy than selection for the direct genetic component. Selection for the maternal genetic component of farrowing survival reduces stillbirth in all categories and does not affect litter size.  相似文献   

18.
An outbreak of exudative epidermitis (EE) among piglets in a Swedish SPF-herd initiated a survey for indications as to the cause of disease.The herd was established by caesarean section and has been closed to all new animal material, with the exception of semen for artificial insemination (AI). The study comprised serum samples from the SPF-herd over a 10-year period (n=109) and a close monitoring of animals in the herd during the period after the EE outbreak. Serum samples from conventional boars at the AI-station servicing the herd were also included (n=9). All serum samples were tested for antibodies to porcine circovirus-2 (PCV-2). In addition, 3-week-old piglets from three litters (n=24) farrowed close after the initial EE outbreak were closely monitored for clinical signs of skin disease, sampled for Staphylococcus hyicus, tested for antibodies to porcine parvovirus and in sequentially collected serum samples tested for interferon-alpha (IFN-alpha) and interleukin-6.The PVC-2 serology showed that animals in the herd were sero-negative at least until 2 months prior to the EE outbreak. During the period close after the EE outbreak the animals showed varying levels of antibodies to PCV-2 but all the tested animals had sero-converted 4 months later. The AI boars were also sero-positive to PCV-2 at the time of the EE outbreak. Animals in the SPF-herd remained sero-positive to PCV-2 during the following 7 years. In the monitored litters, one piglet had clinical EE and 15 piglets displayed defined erythemas on the abdomen. Fourteen of the piglets also had IFN-alpha in serum on one or more occasions during the study, indicating viral activity among the animals. S. hyicus was isolated from all of the piglets from the earliest sampling point (3 days of age) and onwards, irrespective of clinical signs. PCV-2 was isolated from lymph node tissue collected from one of the EE affected pigs.Further, increases in the number of stillborn piglets, small litters (<6 piglets) and repeat breeders could be correlated to the time of PCV-2 sero-conversion. Coincidence of active viral infection and sero-conversion to PCV-2 points to the virus as the cause of the EE outbreak and reproductive disturbances.  相似文献   

19.
A possible infection with encephalomyocarditis virus was investigated on two Minnesota pig farms which experienced an increase in stillborn and mummified fetuses, high pre-weaning mortality and reduced farrowing rates. The monthly averages for the numbers of piglets born dead per litter on farms A and B reached 4-6 and 3-6, the pre-weaning mortalities 50 per cent and 31 per cent, and the farrowing rates 52 per cent and 63 per cent, respectively. Serological and histopathological examinations supported a diagnosis of infection with encephalomyocarditis virus, but attempts to isolate the virus failed. Specific antibody to the virus was detected in both fetal and neonatal sera collected from abnormal litters. The predominant histopathological finding was myocarditis consisting of focal or diffuse mononuclear cell infiltration. The detection of specific antibody, and the myocardial lesions in stillborn fetuses, suggested that the problems were associated with infection by encephalomyocarditis virus.  相似文献   

20.
Six pregnant gilts were purchased from a high health herd and were found to be serologically positive for swine influenza virus (SIV) subtype H3N2. Three of the gilts, at 80 to 82 days of gestation, were experimentally exposed a second time to the same SIV subtype--H3N2. No clinical signs resulted from the second exposure to SIV and hemagglutination-inhibition (HI) titers for SIV at 4 weeks postexposure were unchanged suggesting that the gilts had not been reinfected. However, the second exposure to SIV affected the number of pigs born alive. Each of the 3 litters from the twice exposed gilts suffered 2 or 3 stillborn piglets per litter. In contrast the 3 matched, sero-positive gilts that were not exposed to SIV (controls) had no stillborn piglets. These differences were statistically significant using a t-test for unequal variances (P = 0.0086). Sera from 2 of the stillborn piglets were negative for HI antibodies and there was no indication from the pigs born alive that the H3N2 virus had crossed the placenta.  相似文献   

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