断奶仔猪多系统消耗综合征

断奶仔猪多系统消耗综合征是由猪圆环病毒Ⅱ型感染所引起的一种新传染病。近几年来 ,该病呈不断蔓延趋势 ,已给世界养猪业带来了巨大的经济损失。本文就该病的病原、流行病学、临床症状、病理变化、致病机理、危害及防治等方面作简单介绍 ,希望引起有关部门的重视     

Pathological investigations of pigs with porcine multisystemic wasting syndrome (PMWS)

Extract

Pathological changes and immunohistochemical (IHC) examination for porcine circovirus-2 (PCV-2) in nine weaner pigs from a property with PMWS are reported. The pigs were in moderate to poor body condition, and several had diarrhoea and noisy respiration. The outstanding pathological changes related to microscopic lesions in lymphoid tissues, including lymph nodes, palatine tonsils, Peyer's patches, peribronchial lymphoid aggregates and spleen. While there was variability of expression of change between and within cases, the main features of lesions could be summarised as depletion of lymphoid cells, infiltration of histiocytes (often syncytial), and the presence of botryoid intra-cytoplasmic inclusion bodies in macrophages. The changes in lymphoid tissue were typical of those described in PMWS. Also characteristic of this syndrome were histiocyte-dominated cellular inflammatory infiltrates in kidney, liver and lung. There was strong correlation between IHC positivity for PCV-2 and the lesions in lymphoid, pulmonary and renal tissues. Concurrent diseases that are probably promoted by immune suppression may complicate the diagnosis of PMWS. In the present cases, salmonellosis, attaching and effacing Escherichia coli infections, and secondary bacterial bronchopneumonia were identified.     

Postweaning multisystemic wasting syndrome (PMWS) in Sweden from an exotic to an endemic disease

Postweaning multisystemic wasting syndrome (PMWS) is causally associated with porcine circovirus type 2 (PCV2) infection of pigs. PCV2 was first demonstrated in Swedish pigs in 1993, although the virus was almost certainly present in pigs in the country before that. Despite this, no signs of PMWS were observed in pigs of Sweden until the first outbreak was reported in 2003. The accumulated number of PMWS-affected herds have increased via 16 (2004) and 41 (2005) to 123 in December 2006. Of these herds, 30 (25%) have now been declared free from PMWS. However, a number of other herds have had individual pigs that have fulfilled the demands for PMWS at necropsy and 52 of these herds have been declared negative on herd basis after treatment for intestinal or respiratory diseases, and/or by correcting shortcomings in management of the herd including feed. Thus, individual cases of the disease have been observed in around 200 herds by the end of 2006 and PMWS is now regarded as an endemic disease in Sweden. The pig population of Sweden is geographically isolated, the density of pigs and the pathogen load in the country is low and the use of growth promoters (low dose antibiotics in feed) was prohibited in 1986. Additionally, the trade of animals in Sweden is organised in a restricted way. Because of these factors it is possible to conduct meaningful real-time studies on the transformation of PMWS in Sweden from being an exotic to an endemic disease in a three year time scale. Initially the PMWS cases were concentrated in the southern part of Sweden, but have gradually spread north. The PMWS-positive herds have, in general, had an effective production, but some management errors have constantly been observed in affected herds. Physical links between affected herds are often missing, and the data generated to date on the PMWS outbreaks in Sweden do not suggest an introduction of a new contagious microbe into the country that is responsible for the PMWS outbreaks, nor does PMWS appear to be spread via semen. In Sweden, intensity in rearing, disease preventing measures and immaturity of the piglets appear to be important as predisposing factors to PMWS and, as such, are discussed in this article.     

Postweaning multisystemic wasting syndrome (PMWS) in pigs in Croatia: detection and characterisation of porcine circovirus type 2 (PCV2)

The objective of this study was to characterise porcine circovirus type 2 (PCV2) from pigs with naturally occurring postweaning multisystemic wasting syndrome (PMWS) in Croatia, and to determine the epizootiological, clinical and pathomorphological features of the disease. During a systematic health monitoring programme conducted in the period from January 2002 to June 2003, PMWS was suspected on eight different pig-producing farms in Croatia. The diagnosis of PMWS met all three key criteria: the presence of compatible clinical signs, the presence of the characteristic microscopic lymphoid lesions, and the detection of PCV2 within the lesions by polymerase chain reaction (PCR) and by in situ hybridisation (ISH). Moreover, PCV2 DNA from swine tissues was extracted and sequenced. The phylogenetic analysis of 4 Croatian PCV2 strains showed close relationship to PCV2 strains isolated in Slovenia, France, the Netherlands, the United Kingdom, China and Hungary. PCV2 was also demonstrated by electron microscopy in the lymph node of an affected animal. This is the first demonstration of PMWS in Croatia based on all scientifically accepted diagnostic criteria.     

Detection of neutralizing antibodies in postweaning multisystemic wasting syndrome (PMWS)-affected and non-PMWS-affected pigs

The notion that postweaning multisystemic wasting syndrome (PMWS)-affected pigs develop an impaired humoral response against porcine circovirus type 2 (PCV2) has been reported in several studies. However, little information is available regarding the presence of neutralizing antibodies (NA) in PCV2-infected pigs and their role in the pathogenesis of the disease. The aim of the present work was to further characterize the humoral response, and in particular the production of NA, in pigs with different PCV2-infection status. Seventy-two conventional pigs from different farms were classified into three groups based on PCV2 infection and clinico-pathological status, namely: PCV2-negative, non-PMWS PCV2-positive and PMWS-affected animals. In addition, 9-week old pigs from an experimental infection (6 controls and 14 PCV2-inoculated pigs) were also studied. NA and total PCV2 antibodies (TA) as well as viral load in serum were determined and correlated with the clinico-pathological status of pigs. Results indicated that PMWS-affected pigs had lower NA titres, if any, than healthy animals. NA titres were also inversely correlated with PCV2 load in serum. NA and TA titres were positively correlated; however, correlation differed among infection status, being lower in PCV2-positive pigs. Also, the diagnostic performance of each test was evaluated, indicating that the combination of viral neutralization and quantitative PCR in serum was useful to discard PMWS (specificity 92%). In experimentally infected animals, the evolution of NA paralleled the course TA, although a slight delay in NA production was seen in some animals. The increase of NA coincided with the drop in viral load. Results from this work further support that PMWS-affected pigs show an impaired humoral immune response and, particularly, an inefficient NA response against PCV2.     

Induction of porcine post-weaning multisystemic wasting syndrome (PMWS) in pigs from PMWS unaffected herds following mingling with pigs from PMWS-affected herds

In this paper we present the results from two experimental studies (I and II) investigating whether post-weaning multisystemic wasting syndrome (PMWS) can be induced in pigs from PMWS unaffected herds by mingling with pigs from PMWS-affected herds and to observe whether transportation and/or mingling of healthy pigs from unaffected herds could induce PMWS.The studies comprised pigs from 12 different herds. Eight herds had PMWS while four were unaffected. All 12 herds were found to be infected with PCV2. Pigs from PMWS-affected herds were mingled with pigs from unaffected herds in four separate compartments in both study I and study II. In addition, in study II, four groups of pigs from unaffected herds were included. Two groups with pigs transported and mingled from unaffected herds and two groups with pigs which were only transported. The PMWS diagnoses on the individual pigs were based on lymphoid depletion, histiocytic proliferation and the presence of giant cells or inclusion bodies together with the demonstration of PCV2 in lymphoid tissue.Healthy pigs, in both studies, developed PMWS 4–5 weeks after mingling with pigs clinically affected with PMWS. None of the pigs from unaffected herds which had no contact with pigs from PMWS-affected herds developed clinical signs of PMWS. Transportation and mingling of pigs from PMWS unaffected herds in combination or alone was insufficient to provoke PMWS.     

Postweaning mulstisystemic wasting syndrome (PMWS) in pigs and porcine circovirus (PCV). An indexed bibliography

Summary This bibliography contains the bibliographic data, including the abstracts (if available), the post addresses and as far as available also the E-mail addresses of the authors, of 177 articles on postweaning multisystemic wasting syndrome (PMWS) in pigs and porcine circovirus (PCV). The bibliography concerns the period 1982-2002. The vast majority of the articles (151 of 177 being 85%) were published in the period 1998-2002. All publications except one are taken from easily accessible journals. The exception concerns reference 52 being the first report on PMWS, which has been published in a congress proceedings. To improve the accessibility of the bibliography five indices are given referring to the authors, the subjects, the serials, the years of publication and the countries.     

Haptoglobin and pig-major acute protein are increased in pigs with postweaning multisystemic wasting syndrome (PMWS)

The objective of this study was to determine the serum concentration levels of selected acute phase proteins (APP), haptoglobin (HPT) and pig-major acute phase protein (pig-MAP), in postweaning multisystemic wasting syndrome (PMWS) affected pigs and PCV2-subclinically infected pigs. In a first study, a group of 15 eight-week-old conventional pigs from a PMWS affected farm were bled and a complete necropsy, histopathology and in situ hybridisation to detect PCV2 were performed. Based on the results, pigs were classified as suffering from PMWS (n = 10) or healthy animals (n = 5). In a second study, a group of 45 pigs from another PMWS affected farm were selected and bled at 3, 7, 12 and 28 weeks of age. The assessment of PCV2 infection status in these pigs was retrospectively done by PCV2 PCR in serum samples. Selected APP were measured in the serum of all studied pigs by means of radial immunodiffusion. Mean HPT and pig-MAP levels were significantly increased (p = 0.004 and p = 0.0006 respectively) in PMWS-affected pigs when compared to levels found in healthy pigs (2.52 +/- 0.88 mg/mL vs. 1.06 +/- 0.73 mg/mL for HPT and 3.81 +/- 1.53 mg/mL vs. 0.76 +/- 0.34 mg/mL for pig-MAP). In the second study, no significant difference in mean HPT and pig-MAP values were observed between PCV2 PCR positive and negative pigs of any age. However, both APP increased significantly with age in PCV2 PCR negative pigs. Altogether, the present results suggest that APP levels are significantly increased in pigs that develop PMWS, but not in animals with a PCV2 subclinical infection.     

Changes in peripheral blood leukocyte populations in pigs with natural postweaning multisystemic wasting syndrome (PMWS)

The objective of the present study was to analyze, by flow cytometry, changes in PBMC subsets in pigs having postweaning multisystemic wasting syndrome (PMWS), a new condition associated to porcine circovirus type 2 (PCV2) infection. Thirteen acutely PMWS affected pigs were selected from a farm seronegative to porcine reproductive and respiratory syndrome virus (PRRSV) and to Aujeszky's disease virus (ADV); 11 clinically healthy pigs were selected from a high health farm with no history of PMWS and free of the major swine pathogens, and used as a control group. All pigs were necropsied, and tissue samples were fixed in formalin; blood with EDTA anticoagulant was used to perform the flow cytometric analysis. PBMC were incubated with mAb against porcine CD3, CD4, CD8, CD25, CD45, IgM, SWC3, and SLA-Class II. Flow cytometric analysis showed substantial changes in leukocyte subsets in the peripheral blood of PMWS-affected pigs, which were characterized by an increase of monocytes, a reduction of T (mainly CD4(+)) and B-lymphocytes, and the presence of low-density immature granulocytes. Altogether, these changes would suggest an inability of acutely PMWS-affected pigs to mount an effective immune response.     

Postweaning multisystemic wasting syndrome (PMWS) in pigs with particular emphasis on the causative agent, the mode of transmission, the diagnostic tools and the control measures. A review

Postweaning multisystemic wasting syndrome (PMWS) is a worldwide emerging disease of weaned piglets. The objective of this review is to summarize the current knowledge regarding PMWS, its causative agent, mode of transmission, diagnostic techniques to detect PCV-2, the possible control measures, and the association of PMWS and PCV-2 with porcine dermatitis and nephropathy syndrome (PDNS). The causative agent of PMWS is porcine circovirus type 2 (PCV-2), however, not all pigs infected with PCV-2 develop the syndrome. PCV-2 is consistently associated with PMWS and PMWS is considered not to occur without it. Both the syndrome and the virus are not regarded as new. Co-factors that could activate PCV-2 to cause PMWS are considered. This enigmatic nature of both the syndrome and the virus is triggering a concern towards uncertainties of the viral transmission, its introduction in to the herd, effective tools of diagnosis, and control strategies.     

Porcine circovirus type 2-associated cerebellar vasculitis in postweaning multisystemic wasting syndrome (PMWS)-affected pigs

Porcine circovirus type 2 (PCV2) is associated with several syndromes in growing pigs, including postweaning multisystemic wasting syndrome and porcine dermatitis and nephropathy syndrome. In the present study, a previously undescribed neurovascular disorder associated with a PCV2 infection is described. Sixteen pigs showed clinical signs of wasting and neurologic deficits. Acute hemorrhages and edema of cerebellar meninges and parenchyma due to a necrotizing vasculitis resulted in degeneration and necrosis of the gray and white matter. Few to numerous PCV2 DNA and antigen-bearing endothelial cells were detected in affected areas of the brain using in situ hybridization and immunohistochemistry. Conventional histochemical stains, as well as the detection of caspase 3 activity and DNA strand breaks by the terminal transferase dUTP nick end labeling assay, showed numerous apoptotic endothelial cells in the vascular lesions observed. Sequencing of various brain-derived PCV2-specific amplicons revealed a strong identity between different isolates and an 89 to 100% identity to previous isolates. The phylogenetic tree showed that there was no clustering of isolates correlating to clinical signs or geographic distribution. This previously undescribed PCV2-associated neurologic disease has features of both postweaning multisystemic wasting syndrome and, to a lesser extent, porcine dermatitis and nephropathy syndrome. The available evidence suggests that direct virus-induced apoptosis of endothelial cells plays a role in the pathogenesis of this unusual PCV2-associated cerebellar vasculitis.     

Examination for a viral co-factor in postweaning multisystemic wasting syndrome (PMWS)

In order to test the hypothesis that a putative co-factor for the development of postweaning multisystemic wasting syndrome (PMWS) in pigs could be of viral origin, we performed extensive virological examinations on organ material from pigs diagnosed with PMWS originating from within a Danish PMWS-transmission study. Virus isolation attempts were carried out on a large panel of different cell types including primary pig kidney cells and lung macrophages, primary rabbit kidney cells and seven established cell lines (MARC-145, ST117, PK15, BHK21, HeLa, Vero, and MDCK). Although these represent cells with susceptibility to a wide range of known viruses, the results did not provide evidence for a specific virus other than PCV2 contributing to the development of PMWS. Furthermore, in order to test whether specific genotypes of PCV2 may trigger the switch from PCV2 infection to clinical disease, we compared complete DNA genome sequences of PCV2 derived from PMWS-positive as well as PMWS-negative pigs. On the basis of the DNA sequences, the PCV2 isolates were divided into two groups. Group 1 consisting of one isolate originating from a herd unaffected by PMWS, with group 2 consisting of nine isolates originating from four PMWS-affected herds, four PMWS-positive pigs plus one unaffected herd. The PCV2 genomes from the two groups showed 95.5% identity. Alignment analyses of the sequences encoding the replicase and capsid protein from group 1 and group 2 PCV2 isolates showed two amino acid differences encoded in the replicase protein, while 19 amino acid differences were predicted among the capsid protein sequences. The PCV2 DNA sequence analysis supports recent observations from studies in USA as well as Europe, which suggest that strain variations may influence the clinical outcome of PCV2 infection.     

Postweaning multisystemic wasting syndrome: a review of aetiology, diagnosis and pathology

This review paper concentrates on the aetiology, diagnosis, and pathological aspects of postweaning multisystemic wasting syndrome (PMWS). PMWS was first recognized in Canada in 1996 as a new emerging disease which caused wasting in postweaned pigs. Since then, PMWS has been recognized in pigs in many countries. The syndrome is caused by a DNA virus referred to as porcine circovirus 2 (PCV2), which is classified in the family Circoviridae. PMWS primarily occurs in pigs between 25 and 120 days of age with the highest number of cases occurring between 60 and 80 days of age. The diagnosis of PMWS must meet three criteria: (i) the presence of compatible clinical signs, (ii) the presence of characteristic microscopic lesions, and (iii) the presence of PCV2 within these lesions. In order to establish the diagnosis, techniques are required that link virus and tissue lesions, such as immunohistochemistry and in situ hybridization, but not polymerase chain reaction or virus isolation. The three criteria considered separately are not diagnostic of PMWS. For example, the detection of PCV2 alone does not indicate PMWS but merely PCV2 infection. A hallmark of microscopic lesions of PMWS is granulomatous inflammation in the lymph nodes, liver, spleen, tonsil, thymus, and Peyer's patches. Large, multiple, basophilic or amphophilic grape-like intracytoplasmic inclusion bodies are often seen in the cytoplasm of macrophages and multinucleated giant cells.     

Association of hepatitis E virus (HEV) and postweaning multisystemic wasting syndrome (PMWS) with lesions of hepatitis in pigs

The aim of the study was to determine the presence of swine hepatitis E virus (HEV) RNA and antibodies in postweaning multisystemic wasting syndrome-affected (n=114) and non-affected (n=46) pigs and the possible association with hepatitis lesions. Forty-four pigs were RT-PCR positive (28.2%); 25 of them were PMWS cases, while 19 were non-PMWS pigs. In both groups, HEV RT-PCR results were associated with hepatitis (OR=5.61 for PMWS-affected pigs and OR=5.17 for non-PMWS affected pigs; p=0.01). No interaction was detected in a logistic regression between PMWS occurrence and HEV infection for the development of hepatitis lesions. Seropositivity to HEV was more likely to occur in pigs with hepatitis (51.9%) compared to pigs without hepatitis (36.1%; p=0.03). Significant differences in optical densities were notices comparing the lesional stage of pigs (p=0.009). While pigs with slight or moderate hepatitis were seropositive, pigs with more severe lesions were seronegative to HEV. These results indicate that swine HEV infection can be a significant contributor to the development of moderate hepatitis in pigs regardless of the PMWS status.