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     

Postweaning multisystemic wasting syndrome (PMWS) in pigs. A review

Postweaning multisystemic wasting syndrome, caused by porcine circovirus type 2 (PCV2), is a recently described clinical condition which affects nursery and growing pigs. PMWS was initially recognized in Canada in 1991 and nowadays is considered to be worldwide distributed. Clinically, PMWS most representative symptoms include wasting, unthriftness, paleness of the skin, respiratory distress, diarrhea and sometimes icterus. PCV2 infection occurs in both PMWS affected and non-affected farms, and viral seroconversion shows a typical pattern, with declining of colostral antibodies during the lactating and nursery periods, with the lowest levels at the end of the nursery period, and active seroconversion of almost all pigs during the grower period. Although antibodies to PCV2 have been detected as early as 1969, no explanation for the emergence of this disease in the 90s has been established. Macroscopic lesions associated with PMWS are quite unspecific, but histopathological lesions in lymphoid tissues (lymphocyte depletion with histiocytic infiltration) are almost unique for this disease. These lesions together with other clinical and laboratorial findings suggest that severely affected pigs may be immunosuppressed. The criteria used for the diagnosis of PMWS include the existence of compatible clinical signs, presence of characteristic microscopic lesions and detection of PCV2 within these lesions. Because of the lack of appropriate treatment or vaccination against PCV2, zootechnical changes have been proposed in affected farms to reduce the so-called "infection pressure" due to PCV2 as well as to any other pathogen.     

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.     

Brain lesions in pigs affected with postweaning multisystemic wasting syndrome.

Anti-porcine circovirus type 2 (anti-PCV2) immunostaining was associated with cerebellar lymphohistiocytic vasculitis combined with hemorrhages (50 pigs) or with lymphohistiocytic meningitis (23 pigs) in pigs naturally affected with postweaning multisystemic wasting syndrome (PMWS). The animals originated from 12 farms in Rio Grande do Sul, Brazil. In total, 456 unthrifty 3- to 5-month-old postweaning pigs confirmed as PMWS cases were necropsied. Although most findings mimicked those extensively reported in PMWS-affected pigs, there were distinctive brain lesions that included multiple hemorrhages in the cerebellar leptomeninges associated with lymphohistiocytic vasculitis and fibrinoid degeneration in vessels of the cerebellum and periventricular areas (69 pigs). These vascular lesions were also seen in conjunction with lymphohistiocytic meningitis (38 additional pigs). PCV2 antigen was immunohistochemically demonstrated in the cytoplasm and nuclei from intralesional perivascular macrophages and endothelial-like cells in brain tissues. Together these findings suggest that these lesions were caused by PCV2.     

Postweaning multisystemic wasting syndrome in Danish pig herds: productivity, clinical signs and pathology

A case-control study of 74 herds with postweaning multisystemic wasting syndrome (pmws) and 74 matched control herds was carried out. In the case herds the mortality rates of weaner and finisher pigs were 11.2 and 5.2 per cent respectively, compared with 3.1 and 3.2 per cent in the control herds. In most case herds, pmws developed within the first four weeks after weaning. Wasting, diarrhoea and respiratory signs were observed in 10 per cent of the weaner pigs (7 to 30 kg) in the case herds compared with 7 per cent in the control herds. The average daily gains of the weaner pigs and finisher pigs were 36 g and 52 g less in the case herds than in the control herds. By examining three weaner pigs from each herd the pmws diagnosis was confirmed by histopathology and immunohistochemistry in 78 per cent of the case herds, but at least one pmws-positive weaner pig was found in 19 of the control herds. The prevalence of pmws-positive pigs among illthriven weaner pigs was 45 per cent (101/222) in the case herds, and 12 per cent (27/222) in the control herds. Specific gross pathological findings were associated with a positive pmws diagnosis; pigs with heavy, rubber-like lungs, atonic intestines, and enlarged bronchial and inguinal lymph nodes, had a 0.7 probability of a positive pmws diagnosis by laboratory examinations. However, for illthriven pigs, this probability of having pmws was equal in the case herds and the control herds.     

Immunosuppression in postweaning multisystemic wasting syndrome affected pigs

The present review concentrates on the clinical, pathological and immunological aspects of pigs suffering from PMWS which strongly suggest that PCV2 may be, in particular conditions, a cause of secondary immunodeficiency in pigs. From a clinical point of view, the lack of antibiotic therapy response against the disease, the existence of a litter effect and the concurrence of other disease syndromes and well-known secondary pathogens, such as Pneumocystis carinii, Chlamydia spp. and Aspergillus spp., may account as features of immunosuppression in PMWS. Furthermore, pathologic, immunohistologic and flow cytometric studies also suggest that pigs with PMWS may be immunosuppressed. Lymphocyte depletion of follicular and interfollicular areas together with macrophage infiltration of lymphoid tissues is a unique lesion, which is the basic feature of PMWS affected pigs. These findings are highly correlated with the decrease of circulating B- and T-cells and the diminution of these cell types in lymphoid organs, and with the increase of macrophage/monocytes lineage cells both in peripheral blood and lymphoid tissues in both naturally and experimentally PMWS affected pigs. The altered populations of cells participating in the immune system response both in blood and tissues suggests, at least in those severely PMWS affected pigs, a transient inability of diseased pigs to mount an effective immune response. From these points of view, strong suspicions on the immunosuppressive status of PMWS affected pigs do exist; however, future studies are needed to characterise the exact role of PCV2 on the immune system of pigs affected with PMWS.     

Isolation of circovirus from lesions of pigs with postweaning multisystemic wasting syndrome.

Postweaning multisystemic wasting syndrome (PMWS), an apparently new disease, has been recognized in swine herds in western Canada. Young pigs with this disease have progressive weight loss, tachypnea, dyspnea, and jaundice, accompanied by interstitial pneumonia, lymphadenopathy, hepatitis, and nephritis. We examined more than 400 pigs from more than 70 herds in Alberta, Saskatchewan, and Manitoba with cases of PMWS. A small virus was isolated from a range of tissues from 8 of 8 affected pigs examined. The agent was identified as a circovirus-like virus using electron microscopy, immunohistochemical staining with porcine and rabbit immune serum, and in situ hybridization. Immunohistochemical examination of tissues from more than 100 affected pigs has revealed widespread viral antigen, often contained in circovirus-like inclusion bodies, in lesions from numerous organs. Although Koch's postulates remain to be fulfilled, these results demonstrate a high degree of association between the presence of the circovirus-like virus and PMWS in affected swine.     

Muco-cutaneous candidiasis in two pigs with postweaning multisystemic wasting syndrome

In two distinct commercial swine herds, poor weight gain and an increased number of animals showing wasting were observed among nursery and growing pigs. Cases of postweaning multisystemic wasting syndrome (PMWS) and infection with Haemophilus parasuis had been previously diagnosed in these herds. One growing wasted pig from each herd was necropsied and showed enlarged lymph nodes. Pseudomembranous material adhered to the dorsum of the tongue, soft and hard palate in case 1, and in case 2, fibrinous material was seen as whitish plaques on the oesophageal surface with hyperkeratosis of the non-glandular stomach. The main histological lesions in both cases were found in lymphoid tissues with a multifocal accentuated lymphohistiocytic infiltrate, areas of lymphoid depletion and intracytoplasmic inclusions in histiocytic cells in lymph nodes and Payer's patches. Focally, extensive ulceration was found in the stratified pavement epithelium of the tongue with necrosis and necrosuppurative infiltrate in case 1; in case 2, there was ulceration in the stomach with lymphohistiocytic infiltrate in the submucosa and ulceration in the mucosa of the oesophagus associated with yeast cells and pseudo-hyphae. Candida albicans was isolated from the oral cavity lesions. Immunohistochemistry of the lymph nodes was positive for porcine circovirus 2 (PCV2). The association between PMWS and mucocutaneous candidiasis reported here supports the potential immunosuppressive state of PMWS infected pigs.     

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.     

Clinical and pathological observations on pigs with postweaning multisystemic wasting syndrome

The aim of this work was to characterise the lesions and agents present in clinically normal and clinically affected pigs on a farm during an outbreak of postweaning multisystemic wasting syndrome (PMWS), and to evaluate the diagnostic techniques for detecting porcine circovirus type 2 (PCV-2) and other microorganisms. Four pigs in the early stage and 11 pigs in the late stage of the disease, and eight clinically normal pigs were necropsied. Samples of lymphoid tissue and serum were also obtained from 12 slaughter pigs from the same farm. The tissues were examined histopathologically, and in situ hybridisation, serology and PCR were used to detect porcine circovirus type 1 (PCV-1) and/or PCV-2 in tissues and/or sera. The presence of porcine reproductive and respiratory syndrome virus (PRRSV), Aujeszky's disease virus (ADV) and porcine parvovirus (PPV) were also investigated. Characteristic microscopical lesions of PMWS were observed in the lymphoid tissues of the pigs in all three necropsied groups; the lesions were most common and severe in the pigs in the early stage of the disease, less so in the pigs in the late stage of the disease, and least in the clinically normal pigs. PCV-2 infection was detected in all the necropsied pigs by in situ hybridisation and PCR. Only three pigs had the PCV-1 genome in serum or lymph node tissue. In contrast, the slaughter pigs had no microscopical lesions and no PCV-2 nucleic acid in their serum or tissues, and only one of them had the pCV-1 genome in its serum. Immunohistochemical, serological and PCR studies revealed that PRRSV and ADV were also present on the farm during the outbreak.     

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 produced in gnotobiotic pigs following exposure to various amounts of porcine circovirus type 2a or type 2b

In late 2005, a postweaning, high mortality syndrome spread rapidly through finishing barns in swine dense areas of the United States. Diagnostic investigations consistently detected porcine circovirus type 2 (PCV2) from diseased tissues. Subsequent genetic analysis revealed that the infectious agent was a PCV2 type termed "PCV2b". Prior to late 2004, only the PCV2a type, but not PCV2b, had been reported in North America. In this communication, we produce severe postweaning multisystemic wasting syndrome (PMWS) in gnotobiotic pigs using infectious PCV2a and PCV2b generated from DNA clones constructed from field isolates identified in the 2005 outbreak. Clinical signs exhibited by diseased pigs included anorexia, dyspnea and listlessness. Mortality was typically observed within 12h of onset of dyspnea. The most striking microscopic lesions in affected animals were severe hepatic necrosis and depletion of germinal centers in lymph nodes with associated abundant PCV2 viral antigen. Clinical signs and lesions observed in these studies were comparable to those reported in experiments with gnotobiotic pigs inoculated with a PCV2a isolate while concurrently receiving immune-stimulation or co-infection with porcine parvovirus or torque teno virus. The animals in these studies were confirmed to be free of detectable porcine parvovirus, porcine reproductive and respiratory syndrome virus, bovine viral diarrhea virus, swine hepatitis E virus, and aerobic and anaerobic bacteria. Seven out of 24 PCV2 inoculated pigs had a detectable congenital torque teno virus infection with no correlation to clinical disease. Thus, in these studies, both PCV2a and PCV2b isolates were singularly capable of inducing high mortality in the absence of any detectable infectious co-factor.     

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.