porcine reproductive and respiratory syndrome
- Host Animals
- Hosts/Species Affected
- Systems Affected
- Distribution Table
- List of Symptoms/Signs
- Disease Course
- Impact: Economic
- Zoonoses and Food Safety
- Disease Treatment
- Prevention and Control
- Links to Websites
- Distribution Maps
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PicturesTop of page
IdentityTop of page
Preferred Scientific Name
- porcine reproductive and respiratory syndrome
International Common Names
- English: blue ear disease; blue eared pig disease; new pig disease; porcine proliferative and necrotizing pneumonia; porcine reproductive and respiratory syndrome, prrs
- Spanish: sindrome disgenésico y respiratorio del cerdo; sindrome respiratorio y de infertilidad porcina
- French: maladie bleue du porc; maladie mystérieuse du porc; syndrome dysgénésique et respiratoire porcin
Local Common Names
- Canada: syndrome HAAT; syndrome reproducteur et respiratoire porcin
- Germany: Epidemisch Spätabort der Sauen; Rätselhafte Schweinekrankheit; Seuchenhafter Spätabort der Schweine
- Netherlands: abortus blauw
- USA: disease '89; mystery disease syndrome; mystery pig disease; mystery swine disease; pig plague 1989; porcine viral syndrome; reproductive failure syndrome; swine reproductive and respiratory syndrome; swine reproductive failure syndrome
OverviewTop of page
In the early 1980s a previously unrecognized disease syndrome started causing heavy production losses in pig herds in North America. In the following decade, this syndrome (subsequently named porcine reproductive and respiratory syndrome: PRRS) appeared in most of the major pig-producing areas of North America and Europe. During an outbreak, which can last for 2-6 months, there are increased stillbirths and mummification rates, high preweaning mortality, and respiratory disease particularly in the growing pigs. Sows and gilts go off feed about 2 weeks before reproductive losses begin, and some sows have decreased thirst.
A particularly severe epizootic of PRRS, with an estimated loss of one million or more pigs, occurred in Europe in the winter of 1990/91. In more recent years, PRRS has been detected in most parts of the world, with notable exceptions such as Australia, New Zealand and Ireland. Not all countries have surveyed their pig populations, so many could be infected without knowing; the varied clinical effects of PRRS necessitate specialized laboratory techniques for accurate diagnosis.
In 1991, Wensvoort, Terpstra and colleagues at the ID-DLO research centre in the Netherlands, identified a new RNA virus as the principal causative agent of PRRS. The virus was named ‘Lelystad virus’, but is now generally known as ‘PRRS virus (PRRSV)’. Virologists in Germany and the USA identified similar viruses later that year. Blood samples from PRRS outbreaks in the UK, USA and Germany were sent to the Netherlands and found, in most cases, to show a rise in antibodies to the newly recognized Lelystad virus. Lelystad virus and similar viral strains (PRRS viruses/PRRSV) are currently believed to be the primary cause of PRRS syndromes in Europe and North America. Virus isolates have been investigated in Germany (Ohlinger et al., 1991), France, the UK, USA, Canada and Spain (Plana et al., 1991) and have been used to reproduce the typical PRRS clinical effects (Christianson et al., 1991; Paton et al., 1991; Dee et al., 1992; Joo et al., 1992; Plana et al., 1992a; Plana et al., 1992b).
PRRSV infection is not always sufficient, on its own, to cause clinical and production problems in pig herds. Field experience in many countries repeatedly points to the fact that environment, management and secondary infection factors have an important role in manifestation of the clinical syndrome. For example, respiratory disease in weaners is often seen when PRRSV infection combines with rapid generation turnover, overcrowding, poor air quality and constantly occupied buildings.
The origin of the PRRSV epidemic is uncertain. The virus may have been present for many years somewhere in the world, in a porcine ecological niche, without causing serious problems to its host. Changes in pig husbandry may have favoured its multiplication and spread. Alternatively, it may have arisen as a mutation of an existing arterivirus, for example, the mouse virus LDV.
Wherever and however the virus originated, its spread has been facilitated by the widespread implementation of genetic improvement programmes in the past two decades. The virus has particularly become established in regions where farm-to-farm and international movements of pigs are commonplace.
The spread of PRRSV and the occurrence of PRRSV-related health problems are also particularly likely in pig populations that are large and dense. Indeed, the past two decades have seen a trend towards increased size and density of pig populations, both in individual herds and in geographical regions. A further factor facilitating the multiplication and spread of PRRSV is the increasingly rapid generation turnover of pig farms providing a constant stream of young vulnerable animals for the virus to replicate in.
The varied clinical picture of PRRSV infection suggests that the disease is multifactorial in nature and that management factors and the presence of other infectious agents play an important role (White, 1992). Infection with PRRSV, as judged by seroconversion and virus isolation, in either individuals or populations can sometimes occur without any detectable effect on health or performance.
Viruses other than PRRSV (particularly influenza strains and encephalomyocarditis [EMCV] viruses) are frequently detected in pigs involved in PRRS type syndromes (for example, Carlson, 1992). It has also been suggested that a paramyxovirus-like agent, isolated from an affected herd in France, may contribute to the aetiology of PRRS (Brun et al., 1992).
PRRS may be viewed as a syndrome of clinical and production effects in pig herds, which results from a combination of management and microbial factors. PRRSV infection is just one factor that can produce PRRS, although, at present, it seems to be a common and very influential factor.
This disease is on the list of diseases notifiable to the World Organisation for Animal Health (OIE). The distribution section contains data from OIE's WAHID database on disease occurrence. Please see the AHPC library for further information on this disease from OIE, including the International Animal Health Code and the Manual of Standards for Diagnostic Tests and Vaccines. Also see the website: www.oie.int.
Host AnimalsTop of page
|Animal name||Context||Life stage||System|
|Sus scrofa (pigs)||Domesticated host, Experimental settings||Pigs: All Stages|
Hosts/Species AffectedTop of page
PRRS is a multifactorial disease. PRRSV infection is not always sufficient, on its own, to cause clinical and production problems. Field experience in many countries repeatedly points to the fact that environmental, management and secondary infection factors have an important role in the manifestation of the clinical syndrome. For example, respiratory disease in weaners, is often seen when PRRSV infection combines with rapid generation turnover, overcrowding, poor air quality and constantly occupied buildings. PRRS does occur in extensively kept pigs, but is less common and less severe. PRRSV can infect pigs of any age.
Systems AffectedTop of page blood and circulatory system diseases of pigs
reproductive diseases of pigs
respiratory diseases of pigs
DistributionTop of page
The disease was first detected in pig herds in North America in the 1980s. In the following decade PRRS appeared in most of the major pig-producing areas of North America and Europe. A particularly severe epizootic of PRRS, with an estimated loss of one million or more pigs, occurred in Europe in the winter of 1990/91. In more recent years, PRRS has been detected in most parts of the world, with notable exceptions such as Australia, New Zealand and the rest of Australasia, and Ireland. Not all countries have surveyed their pig populations, so many could be infected without knowing; the varied clinical effects of PRRS necessitate specialized laboratory techniques for accurate diagnosis.
For current information on disease incidence, see OIE's WAHID Interface.
Distribution TableTop of page
The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.Last updated: 10 Jan 2020
|Continent/Country/Region||Distribution||Last Reported||Origin||First Reported||Invasive||Reference||Notes|
|Algeria||Absent, No presence record(s)||OIE (2009)|
|Angola||Absent, No presence record(s)||OIE (2009)|
|Central African Republic||Absent, No presence record(s)||OIE Handistatus (2005)|
|Congo, Democratic Republic of the||Absent, No presence record(s)||OIE Handistatus (2005)|
|Côte d'Ivoire||Absent, No presence record(s)||OIE Handistatus (2005)|
|Djibouti||Absent, No presence record(s)||OIE (2009)|
|Eswatini||Absent, No presence record(s)||OIE (2009)|
|Kenya||Absent, No presence record(s)||OIE (2009)|
|Lesotho||Absent, No presence record(s)||OIE (2009)|
|Libya||Absent, No presence record(s)||OIE Handistatus (2005)|
|Madagascar||Absent, No presence record(s)||OIE (2009)|
|Mauritius||Absent, No presence record(s)||OIE (2009)|
|Namibia||Absent, No presence record(s)||OIE (2009)|
|Réunion||Absent, No presence record(s)||OIE Handistatus (2005)|
|São Tomé and Príncipe||Absent, No presence record(s)||OIE Handistatus (2005)|
|South Africa||Absent, No presence record(s)||OIE (2009)|
|Sudan||Absent, No presence record(s)||OIE (2009)|
|Tunisia||Absent, No presence record(s)||OIE (2009)|
|Zimbabwe||Absent, No presence record(s)||OIE (2009)|
|Armenia||Absent, No presence record(s)||OIE (2009)|
|Azerbaijan||Absent, No presence record(s)||OIE (2009)|
|Bahrain||Absent, No presence record(s)||OIE (2009)|
|Bangladesh||Absent, No presence record(s)||OIE (2009)|
|Brunei||Absent, No presence record(s)||OIE Handistatus (2005)|
|Georgia||Absent, No presence record(s)||OIE Handistatus (2005)|
|Hong Kong||Present||OIE (2009)|
|India||Absent, No presence record(s)||OIE (2009)|
|Indonesia||Absent, Unconfirmed presence record(s)||OIE (2009)|
|Iran||Absent, No presence record(s)||OIE (2009)|
|Iraq||Absent, No presence record(s)||OIE (2009)|
|Israel||Absent, No presence record(s)||OIE (2009)|
|Kazakhstan||Absent, No presence record(s)||OIE (2009)|
|Kuwait||Absent, No presence record(s)||OIE (2009)|
|Kyrgyzstan||Absent, No presence record(s)||OIE (2009)|
|Laos||Absent, No presence record(s)||OIE (2009)|
|Lebanon||Absent, No presence record(s)||OIE (2009)|
|Malaysia||Absent, No presence record(s)||OIE (2009)|
|-Peninsular Malaysia||Absent, No presence record(s)||OIE Handistatus (2005)|
|-Sabah||Absent, No presence record(s)||OIE Handistatus (2005)|
|-Sarawak||Present, Serological evidence and/or isolation of the agent||OIE Handistatus (2005)|
|Myanmar||Absent, No presence record(s)||OIE (2009)|
|North Korea||Absent, No presence record(s)||OIE Handistatus (2005)|
|Oman||Absent, No presence record(s)||OIE (2009)|
|Saudi Arabia||Absent, No presence record(s)||OIE (2009)|
|Singapore||Absent, No presence record(s)||OIE (2009)|
|South Korea||Present||OIE (2009)|
|Sri Lanka||Absent, No presence record(s)||OIE (2009)|
|Syria||Absent, No presence record(s)||OIE (2009)|
|Taiwan||Present||OIE Handistatus (2005)|
|Tajikistan||Absent, No presence record(s)||OIE (2009)|
|Uzbekistan||Absent, No presence record(s)||OIE Handistatus (2005)|
|Belarus||Absent, No presence record(s)||OIE (2009)|
|Belgium||Absent, No presence record(s)||OIE (2009); ESAVS (1992)|
|Bosnia and Herzegovina||Absent, No presence record(s)||OIE Handistatus (2005)|
|Bulgaria||Absent, No presence record(s)||OIE (2009)|
|Denmark||Present||OIE (2009); ESAVS (1992)|
|Finland||Absent, No presence record(s)||OIE (2009)|
|Greece||Absent, No presence record(s)||OIE (2009)|
|Hungary||Present, Localized||OIE (2009)|
|Iceland||Absent, No presence record(s)||OIE (2009)|
|Isle of Man||Present||OIE Handistatus (2005)|
|Jersey||Absent, No presence record(s)||OIE Handistatus (2005)|
|Latvia||Absent, No presence record(s)||OIE (2009)|
|Liechtenstein||Absent, No presence record(s)||OIE (2009)|
|Lithuania||Absent, No presence record(s)||OIE (2009)|
|Luxembourg||Absent, No presence record(s)||OIE (2009)|
|Malta||Present||OIE (2009); ESAVS (1992)|
|Moldova||Absent, No presence record(s)||OIE Handistatus (2005)|
|Montenegro||Absent, No presence record(s)||OIE (2009)|
|Netherlands||Present||OIE (2009); ESAVS (1992)|
|North Macedonia||Absent, Unconfirmed presence record(s)||OIE (2009)|
|Norway||Absent, No presence record(s)||OIE (2009)|
|Portugal||Absent, No presence record(s)||OIE (2009)|
|Russia||Present, Localized||OIE (2009)|
|Serbia and Montenegro||Absent, No presence record(s)||OIE Handistatus (2005)|
|Slovakia||Absent, No presence record(s)||OIE (2009)|
|Slovenia||Absent, No presence record(s)||OIE (2009)|
|Spain||Present||OIE (2009); ESAVS (1992)|
|Sweden||Absent, No presence record(s)||OIE (2009)|
|Switzerland||Absent, No presence record(s)||OIE (2009)|
|Ukraine||Absent, No presence record(s)||OIE (2009)|
|United Kingdom||Present||OIE (2009); ESAVS (1992)|
|-Northern Ireland||Present||OIE Handistatus (2005)|
|Barbados||Absent, No presence record(s)||OIE Handistatus (2005)|
|Belize||Absent, No presence record(s)||OIE (2009)|
|Bermuda||Absent, No presence record(s)||OIE Handistatus (2005)|
|British Virgin Islands||Absent, No presence record(s)||OIE Handistatus (2005)|
|-Quebec||Present||Voicu et al. (1992)|
|Cayman Islands||Absent, No presence record(s)||OIE Handistatus (2005)|
|Costa Rica||Present||OIE (2009)|
|Cuba||Absent, No presence record(s)||OIE (2009)|
|Curaçao||Absent, No presence record(s)||OIE Handistatus (2005)|
|Dominica||Absent, No presence record(s)||OIE Handistatus (2005)|
|Dominican Republic||Present||OIE (2009)|
|El Salvador||Absent, No presence record(s)||OIE (2009)|
|Greenland||Absent, No presence record(s)||OIE (2009)|
|Guatemala||Absent, No presence record(s)||OIE (2009)|
|Haiti||Absent, No presence record(s)||OIE (2009)|
|Jamaica||Absent, No presence record(s)||OIE (2009)|
|Martinique||Absent, No presence record(s)||OIE (2009)|
|Saint Vincent and the Grenadines||Absent, No presence record(s)||OIE Handistatus (2005)|
|Trinidad and Tobago||Absent, No presence record(s)||OIE Handistatus (2005)|
|United States||Present||OIE (2009); USDA (1997)|
|Australia||Absent, No presence record(s)||OIE (2009)|
|French Polynesia||Present||OIE (2009)|
|New Caledonia||Absent, No presence record(s)||OIE (2009)|
|New Zealand||Absent, No presence record(s)||OIE (2009)|
|Samoa||Absent, No presence record(s)||OIE Handistatus (2005)|
|Vanuatu||Absent, No presence record(s)||OIE Handistatus (2005)|
|Argentina||Absent, No presence record(s)||OIE (2009)|
|Brazil||Absent, No presence record(s)||OIE (2009)|
|Chile||Absent, No presence record(s)||OIE (2009)|
|Ecuador||Absent, No presence record(s)||OIE (2009)|
|Falkland Islands||Absent, No presence record(s)||OIE Handistatus (2005)|
|French Guiana||Absent, No presence record(s)||OIE (2009)|
|Guyana||Absent, No presence record(s)||OIE Handistatus (2005)|
|Paraguay||Absent, No presence record(s)||OIE Handistatus (2005)|
|Peru||Absent, No presence record(s)||OIE (2009)|
|Uruguay||Absent, No presence record(s)||OIE (2009)|
PathologyTop of page
Field cases of PRRS are often grossly normal at autopsy unless complicated by secondary infection. Similarly, histological changes may be slight and confined to the respiratory tract. Pathological changes in PRRS are not pathognomic. In a study of PRRS effects on finishing herds (Blaha, 1993), it was concluded that there is no typical ‘PRRS pneumonia’, the clinical and pathological disease observed depended on the predominant respiratory pathogens enzootic in a herd.
In pure experimental PRRSV infections (Lelystad strain), diffuse interstitial pneumonia with focal areas of catarrhal pneumonia may occur (Paton and Done, 1992). There was also enlargement and vacuolation of splenic red pulp macrophages. Ultrastructurally there was degeneration of alveolar macrophages and of epithelial cells in the lungs and nasal mucosa. Excessive vacuolation of endoplasmic reticulum has also been detected. Researchers studying the UK virus strain, have reported interstitial pneumonia and loss of cilia and microvilli in bronchiolar epithelium as typical findings in both experimental and field infections with UK strains of PRRSV (Done and Paton, 1995).
In a US study, infected 3-week-old pigs developed moderate multifocal proliferative interstitial pneumonia with pronounced type II pneumocyte hypertrophy and hyperplasia, moderate infiltration of alveolar septa with mononuclear cells and abundant accumulation of necrotic cell debris and mixed inflammatory cells in the alveolar spaces. No bronchial or bronchiolar epithelial damage was detected, but there was necrotic cell debris in smaller airway lumina (Halbur et al., 1994).
Spanish researchers have studied the effects of experimental intranasal infection of 12 weaned pigs (6-7 kg) with the Huesca 1 isolate of PRRSV (Ramos et al., 1992). Only one out of four infected animals killed at day 2 had gross lung lesions (consolidated lobules especially in the ventral aspects of middle and caudal lobes - unilaterally). At day 5, two pigs out of four had lung consolidation and at day 9, all pigs examined had developed consolidation of isolated or contiguous lobules (especially pronounced in the ventral aspects of the middle and accessory lobes, but also the cranial part of the caudal lobe or apical lobe). Gross lesions were not found in other organs. Histologically there was interstitial pneumonia, progressing towards necrosis of cells in the alveolar lumina or septae. Electron microscopy revealed many degenerated and necrotic cells in the interstitial infiltrate (neutrophils, plasma cells and type-II alveolar cells). There was also type II alveolar hyperplasia. Sometimes bronchiolar epithelial cells were also degenerated. One pig, at day 9 after infection, had severe suppurative broncho-interstitial pneumonia.
After an experimental infection of pregnant sows with PRRSV, stillborn and weakborn piglets were found to have abundant clear liquid in the thoracic cavity (Plana et al., 1992a; Plana et al. 1992b). Healthy piglets born to these infected sows were found to have small greyish foci of pulmonary consolidation when killed at 8-12 days old. Microscopically there was a multifocal, mild interstitial pneumonia with thickening of alveolar septa by infiltration of mononuclear cells. Virus-like structures are present on endothelial cells of fetal and maternal placental capillaries and occasionally between epithelial cells.
DiagnosisTop of page Introduction
A diagnosis of PRRS is based on subjective (history, clinical signs, gross and microscopic lesions) and objective (production record analysis, serology, virus detection) factors. PRRS should be considered when there are clinical signs of respiratory disease occurring at any stage of production, when reproductive failure occurs, and when herd performance is sub-optimal. Mild or subclinical disease is common, so absence of clinical signs does not ensure a PRRSV-free herd.
Common signs of PRRS are inappetence, abortions, premature farrowings, stillbirths, pre-weaning mortality, respiratory disease and increased mortality (see Symptoms).
Gross lesions are present in the lungs; less noticeable lesions are found in the lymph nodes. Any additional lesions are likely to be caused by secondary infections. Inflammatory and degenerative lesions have been seen in the placentas from PRRS-infected sows (Stockhofe-Zurwieden et al., 1992).
Laboratory diagnosis of PRRSV infection is crucial in the diagnosis of disease. Serological tests for PRRSV are generally by immunoperoxidase monolayer assay (IPMA), ELISA test and indirect fluorescent antibody test. Isolation of virus particles may be made from serum, plasma, lungs, spleen and ascitic fluid (from foetuses). Virus isolation in alveolar macrophages or cell line 2621 can be undertaken by specialized laboratories. Histological tests for viral antigen include immunofluorescence and immunoperoxidase tests. Serological diagnosis is most widely used, for speed and simplicity. Ideally it should be based on paired acute and convalescent sera, but in an emergency, a range of titres in a group of pigs is taken to be indicative of active infection.
Serological tests for PRRS antibodies
|IPMA||Immuno-peroxidase monolayer assay||Highly specialised||Very high||Very high||Very slow||Wensvoort et al. (1992)|
|SN(T)||Serum neutralisation test||Specialised||High||High||Slow||Morrison et al. (1992)|
|IFA||Indirect immuno-fluorescent antibody test||Specialised||High||High||Slow||Frey et al. (1992)|
|IPT||Immuno-peroxidase test||Specialised||Very high||Very high||Very slow||Frey et al. (1992)|
|ELISA||Enzyme-linked immuno-sorbent assay||Specialised at present; field use in future?||Low||Very low||Very rapid||Albina et al. (1992a); Houben et al. (1995)|
|LT||Latex test||Specialised||Low||Low||Rapid||Boeckman (1993)|
Immunology of disease
PRRSV antibodies are found in the colostrum of immune sows and their offspring are seropositive and have passive immunity for some weeks after birth (Chung et al., 1997; Senn et al., 1998). Antibodies can be detected at 4 days after birth and often disappear by 3 weeks, but have been known to last as long 16 weeks. The half-life of these antibodies has been estimated as 16 days. However, passive immunity is not due solely to antibodies; artificially administered antibodies are not protective. It may be that white blood cells present in colostrum and milk play a part. On persistently infected farms, growing pigs seroconvert actively at about 6-7 weeks of age and maintain titres of about 1:1024 up to 6 months of age (Dee et al., 1993).
Non-infectious differential diagnosis
- Colostrum problems; poor hygiene.
Important agents for differential diagnosis
- Atypical influenza A virus (proliferative and necrotizing pneumonia); Aujeszky (pseudorabies) virus; Chlamydia psittaci; Encephalomyocarditis virus V; Leptospira interrogans serovars e.g. pomona, bratislava; Swine influenza virus (sub-types H1N1 and H3N2).
Uncommon agents for differential diagnosis
- African swine fever virus; Classical swine fever virus; Erysipelothrix rhusiopathiae; Haemagglutinating encephalomyelitis virus; Porcine cytomegalovirus; Porcine epidemic diarrhoea virus; Porcine parvovirus; Talfan disease virus; Transmissible gastroenteritis virus (respiratory coronavirus).
List of Symptoms/SignsTop of page
|Cardiovascular Signs / Tachycardia, rapid pulse, high heart rate||Pigs:All Stages||Sign|
|Digestive Signs / Anorexia, loss or decreased appetite, not nursing, off feed||Pigs:All Stages||Diagnosis|
|Digestive Signs / Decreased amount of stools, absent faeces, constipation||Pigs:Piglet,Pigs:Weaner||Sign|
|Digestive Signs / Diarrhoea||Pigs:Piglet,Pigs:Weaner||Diagnosis|
|Digestive Signs / Vomiting or regurgitation, emesis||Sign|
|General Signs / Ataxia, incoordination, staggering, falling||Pigs:Piglet,Pigs:Weaner,Pigs:Growing-finishing pig||Diagnosis|
|General Signs / Cyanosis, blue skin or membranes||Pigs:All Stages||Diagnosis|
|General Signs / Decreased, absent thirst, hypodipsia, adipsia||Sign|
|General Signs / Dehydration||Pigs:Piglet||Sign|
|General Signs / Empty abdomen on internal palpation||Pigs:Piglet,Pigs:Weaner||Sign|
|General Signs / Exercise intolerance, tires easily||Pigs:Piglet,Pigs:Weaner||Sign|
|General Signs / Fever, pyrexia, hyperthermia||Pigs:All Stages||Diagnosis|
|General Signs / Forelimb lameness, stiffness, limping fore leg||Sign|
|General Signs / Forelimb swelling, mass in fore leg joint and / or non-joint area||Sign|
|General Signs / Generalized lameness or stiffness, limping||Sign|
|General Signs / Generalized weakness, paresis, paralysis||Pigs:Piglet,Pigs:Weaner||Diagnosis|
|General Signs / Haemorrhage of any body part or clotting failure, bleeding||Sign|
|General Signs / Hindlimb lameness, stiffness, limping hind leg||Sign|
|General Signs / Hindlimb swelling, mass in hind leg joint and / or non-joint area||Sign|
|General Signs / Hypothermia, low temperature||Pigs:Piglet,Pigs:Weaner||Sign|
|General Signs / Inability to stand, downer, prostration||Pigs:Piglet,Pigs:Weaner,Pigs:Growing-finishing pig||Diagnosis|
|General Signs / Lack of growth or weight gain, retarded, stunted growth||Pigs:Piglet,Pigs:Weaner,Pigs:Growing-finishing pig||Diagnosis|
|General Signs / Orbital, periorbital, periocular, conjunctival swelling, eyeball mass||Pigs:Piglet||Diagnosis|
|General Signs / Pale mucous membranes or skin, anemia||Pigs:All Stages||Sign|
|General Signs / Paraparesis, weakness, paralysis both hind limbs||Pigs:Piglet||Diagnosis|
|General Signs / Petechiae or ecchymoses, bruises, ecchymosis||Pigs:Gilt,Pigs:Sow||Sign|
|General Signs / Reluctant to move, refusal to move||Pigs:Piglet,Pigs:Weaner,Pigs:Growing-finishing pig||Sign|
|General Signs / Sudden death, found dead||Pigs:Piglet,Pigs:Weaner,Pigs:Growing-finishing pig||Diagnosis|
|General Signs / Tetraparesis, weakness, paralysis all four limbs||Pigs:Piglet||Diagnosis|
|General Signs / Trembling, shivering, fasciculations, chilling||Pigs:Piglet||Sign|
|General Signs / Underweight, poor condition, thin, emaciated, unthriftiness, ill thrift||Pigs:Piglet,Pigs:Weaner,Pigs:Growing-finishing pig||Diagnosis|
|General Signs / Weight loss||Sign|
|Nervous Signs / Coma, stupor||Pigs:Piglet,Pigs:Weaner||Diagnosis|
|Nervous Signs / Dullness, depression, lethargy, depressed, lethargic, listless||Pigs:All Stages||Diagnosis|
|Nervous Signs / Excessive or decreased sleeping||Pigs:Piglet,Pigs:Weaner||Sign|
|Nervous Signs / Excitement, delirium, mania||Sign|
|Nervous Signs / Hyperesthesia, irritable, hyperactive||Sign|
|Nervous Signs / Propulsion, aimless wandering||Pigs:Piglet,Pigs:Weaner||Sign|
|Nervous Signs / Seizures or syncope, convulsions, fits, collapse||Pigs:Piglet,Pigs:Weaner||Sign|
|Nervous Signs / Tremor||Pigs:Piglet,Pigs:Weaner||Diagnosis|
|Ophthalmology Signs / Chemosis, conjunctival, scleral edema, swelling||Sign|
|Ophthalmology Signs / Conjunctival, scleral, injection, abnormal vasculature||Sign|
|Ophthalmology Signs / Conjunctival, scleral, redness||Sign|
|Reproductive Signs / Abortion or weak newborns, stillbirth||Pigs:Gilt,Pigs:Sow||Diagnosis|
|Reproductive Signs / Agalactia, decreased, absent milk production||Sign|
|Reproductive Signs / Anestrus, absence of reproductive cycle, no visible estrus||Pigs:Gilt,Pigs:Sow||Sign|
|Reproductive Signs / Female infertility, repeat breeder||Pigs:Gilt,Pigs:Sow||Sign|
|Reproductive Signs / Lack of libido or erection||Sign|
|Reproductive Signs / Male infertility||Pigs:Boar||Sign|
|Reproductive Signs / Mummy, mummified fetus||Sign|
|Reproductive Signs / Small litter size||Pigs:Sow||Sign|
|Respiratory Signs / Abnormal lung or pleural sounds, rales, crackles, wheezes, friction rubs||Pigs:All Stages||Sign|
|Respiratory Signs / Coughing, coughs||Pigs:All Stages||Sign|
|Respiratory Signs / Decreased, muffled, lung sounds, absent respiratory sounds||Pigs:All Stages||Sign|
|Respiratory Signs / Dyspnea, difficult, open mouth breathing, grunt, gasping||Pigs:Piglet,Pigs:Weaner,Pigs:Growing-finishing pig||Diagnosis|
|Respiratory Signs / Increased respiratory rate, polypnea, tachypnea, hyperpnea||Pigs:All Stages||Diagnosis|
|Respiratory Signs / Mucoid nasal discharge, serous, watery||Sign|
|Respiratory Signs / Purulent nasal discharge||Sign|
|Respiratory Signs / Sneezing, sneeze||Sign|
|Skin / Integumentary Signs / Hyperkeratosis, thick skin||Sign|
|Skin / Integumentary Signs / Pruritus, itching skin||Sign|
|Skin / Integumentary Signs / Rough hair coat, dull, standing on end||Sign|
|Skin / Integumentary Signs / Skin erythema, inflammation, redness||Sign|
|Skin / Integumentary Signs / Skin papules||Sign|
Disease CourseTop of page
Pigs can become infected with PRRSV by contact or by aerosol exposure. The virus can be isolated from lung, plasma, serum and blood cells for up to 8 weeks after infection, despite high titres of antibody (Edwards et al., 1992). PRRSV may be similar to other RNA viruses in being able to change rapidly in the presence of antibodies, and hence is able to survive in the circulation for long periods (Carlton, 1993).
In experimental infections with the Lelystad strain of PRRSV, interstitial pneumonia and splenic macrophage changes developed from day 2 onwards and the virus could be isolated from lung tissue for as long as 2 months after infection (Pol et al., 1991). Viral antigens were detected by immunohistochemistry in bronchiolar epithelium, alveolar cells and spleen cells. The virus could be isolated from lung, serum, plasma and blood cells up to 6 weeks after infection. In experimental infections of 3-week-old pigs with a US virus strain, PRRSV antigen was seen primarily within the cytoplasm of sloughed cells (probably pneumocytes) and macrophages in the alveolar spaces and within cellular debris in terminal airway lumina. Lesser intensity of staining was observed in mononuclear cells within alveolar septa and, rarely, in hypertrophied type 2 pneumocytes. Antigen could not be detected in bronchiolar epithelium.
PRRSV can cross the placenta. Antibodies can be found in pre-colostral blood and ascitic fluid of stillborn or weak piglets. Transplacental infection by PRRSV following intranasal inoculation of sows on day 93 of pregnancy has been demonstrated (Christianson et al., 1992). When sows were inoculated intranasally with virus on day 45-50 of gestation, lymphocyte and macrophage levels in blood were decreased by day 3 but returned to normal by day 14. PRRSV infection decreased CD4+ T lymphocytes as well as CD8+ T lymphocytes. Virus was recovered from the blood of infected sows but foetuses from sows killed at days 7-21 after infection appeared normal and virus could not be isolated from them.
In individual pigs an incubation period is from the time of infection to the first appearance of symptoms. A herd of pigs will show a lag period from the time infection arrives on the farm until herd performance (incidence of illness, abortions etc.) is obviously affected. One-week-old gnotobiotic pigs can become ill 4-5 days after infection with PRRSV (Edwards et al., 1992). SPF pigs of 6 months of age developed illness within 2 days of contact with infected sows (Wensvoort et al., 1991). Pregnant sows became ill 4-8 days after intranasal aerosol exposure to Lelystad virus (Plana et al., 1992a; Plana et al., 1992b) or VR-2332 (Christianson et al., 1992). Reproductive effects take rather longer to manifest themselves (e.g. 25 days from infection). These experimental findings contrast with field reports that the appearance of clinical effects in a pig herd may take anything from 1-10 weeks from the introduction of infected animals. It may be that early symptoms in a few individual animals do not attract attention.
In the UK epidemic, the interval from introduction of infected stock to the first obvious inappetence of sows ranged from 14 to 37 days (Robertson, 1991). In the Belgian epidemic this interval was 10-18 days (Varewyck, 1991) and in a USA survey the interval was 3-24 days (Dee, 1992).
PRRSV infection of a pig herd is sometimes subclinical in that pigs may become seropositive without any detectable clinical signs or any obvious deterioration in herd performance or in health parameters (Done and Paton, 1995). Field reports suggest that infection tends to be subclinical in herds that are well managed and already have a good health status. In herds that do develop clinical effects, the incubation/detection period for acute PRRS varies greatly, but is typically about 2-5 weeks from contact with infected animals to initial detection of sick pigs. Where pigs are housed in close proximity, the disease usually spreads around within a matter of days. Typically the farm will experience an acute disease episode of 1-3 months (usually 2 months) of obvious illness, increased stillbirths and increased pre-weaning mortality. After this, on most farms, the production and health gradually return to normal. It is widely assumed that most pigs develop immunity after infection, although scientific understanding of this is limited. A German study found that in 86.2% of affected sows, the next pregnancy was normal (Busse et al., 1992).
Field reports suggest that PRRS tends to be milder in extensive (outdoor) herds and that infection spreads more slowly. Only part of the herd may become infected. Premature farrowings are less obvious because of the absence of service dates. PRRS infection may disappear more readily from outdoor herds (White, 1995).
There have been many reports of a more chronic form of PRRS and occasional reports of farms apparently becoming ‘re-infected’ with the disease some months or years after an initial outbreak. An apparent ‘second wave’ of the disease on Dutch farms as indicated by numbers born alive and average length of gestation was observed by Jong et al. (1991). Investigators in the USA and the Netherlands have described persistent PRRSV infection in growing and breeding pigs many months after acute outbreaks of disease (Thacker, 1992). Dutch researchers found that, in one herd, infected litters were born up to 10 weeks after an acute outbreak of PRRS, while in another herd an infected litter was born (to a sow seronegative after the outbreak) 5 months after the initial disease outbreak (Terpstra et al., 1992). Reports are growing that the virus is involved in continuing respiratory disease problems in weaners and there are suspicions of continuing minor effects on litter size and service success rate. In the USA, PRRSV has been isolated from herds with respiratory disease in weaners and growing pigs 2 years after they had suffered acute outbreaks of clinically typical PRRS (Keffaber et al., 1992). In one report a farm that had a 3 month epidemic of PRRS in 1989 was found to have endemic infection of 8-week-old pigs with PRRSV 2.5 years later (Stevenson et al., 1994). Reproductive performance had been within acceptable limits since the original epidemic, but nursery (weaner) mortality had occasionally exceeded 25%. Septicaemic salmonellosis lesions had consistently been seen in dead pigs and Salmonella choleraesuis var. kuzendorf and PRRSV had been isolated. Weaners were housed in one of four interconnected, controlled environment buildings. Each building had slatted floors over a deep pit. Rooms had interconnecting doors that were often left open. The 'nursery' was continuously occupied and new pigs were added at weekly intervals. From the nursery, pigs were moved, at 10 weeks of age, to a connected, adjacent building divided into a growing room and a finishing room. Transfer to the finishing room was at 17 to 20 weeks of age. Replacement breeding females were selected from market-weight gilts and moved directly to a breeding and gestation building. The farrowing rooms were in the same building as the weaners. PRRSV was isolated from the serum of 3-12-week-old pigs. Sows and piglets were seronegative (IFA test) during the 3-4 week period of lactation. By 10 weeks of age, surviving piglets had been viraemic and seroconverted. Titres peaked at 13-14 weeks of age and ranged from 1:640 to at least 1:2560. Of this group, 22% were seronegative by 21 weeks of age, but immunity could be much more durable than this. In sows, the seroprevalence of IFA antibodies over all parities was 15%. Weaner and grower pigs were the major reservoir for PRRSV. They became infected by contact with older pigs in the ‘nursery’ (weaner housing). There was minimal spread of virus in finishers or breeding pigs.
Possible long-term outcomes of PRRS infection of breeding stock (White, 1995)
Loss of infection
This is especially likely in small herds and extensive (outdoor) herds, and particularly in herds where the weaners are kept some distance from the sows.
Persistent infection without clinical disease
This is particularly reported in herds with high health standards, where the initial infection produced little or no disease.
Persistent infection with occasional effects
Recrudescent PRRS outbreaks are never as severe as the initial outbreak. When there are recurrent reproductive effects, typically no more than 1 month's services are affected, with increased returns to oestrus, 'not in pig' cases, small litters, weak piglets and increased piglet mortality. These episodes have been attributed to loss of immunity in sows or to introduction of non-immune gilts which have not contracted infection before breeding (gilts acquired from infected source herds are not necessarily immune already).
EpidemiologyTop of page
Outbreaks of PRRS usually occur in the winter months. On a national and international basis this observation is supported by the experience of the European Community during 1991-92, when extensive data was collected on new outbreaks of PRRS. In interpreting the data it is important to be aware that a delay of a few weeks often occurred between the start of a herd outbreak and official recording of the diagnosis.
Risk factors increasing probability of herd infection by PRRSV:
- large herd size (>50 sows)
- housing in one building
- introduction of new animals
- housing on slatted floors
- storage of slurry under floors
- exposure to transport vehicles
- lack of disinfection procedures
- totally indoor housing
- fumonisin mycotoxin in feed
- rodent problems
Spread within herdsPRRS can spread rapidly within an infected farm where pigs are housed close together but may take some weeks or months for the disease spread in outdoor herds. The exact route of pig-to-pig spread is still somewhat uncertain. Initially, airborne spread was believed to be the most important.
After infection with PRRSV, pigs can shed virus for up to 157 days (Wills et al., 1997a). During this period, pigs may shed PRRSV in blood (e.g. from wounds), faeces, milk, saliva, semen and urine (Wills et al., 1997a, b; Wagstrom et al., 1998). It is likely that the virus can also be present in expired air and coughed or sneezed secretions, because it can be identified in the mouth and respiratory tract of infected pigs. Sows infected during pregnancy can give birth to infected baby pigs that are infectious to other pigs for up to 11 weeks (Dee and Philips, 1998). While infected pigs are alive, PRRSV can be widespread in their blood and body tissues (a hazard when there is fighting and whenever surgical procedures are undertaken). Even in freshly dead pigs, virus particles can be found in blood, brain, heart, liver, lung, sex organs and spleen (Shin et al., 1996).
PRRSV does not survive long on non-liquid materials. On fomites like lucerne, wood shavings, straw, plastic, boot rubber and stainless steel, the virus survives less than 24 hours (Pirtle and Beran, 1996). In water PRRSV can survive 4-11 days, so contamination of drinking water or lagoons could be a significant source of infection for other pigs. In saliva, urine, faecal slurry, pig feed or denim cloth, survival is less than 24 hours.
The virus can be recovered sporadically from nasal swabs of infected pigs for up to 8 weeks after infection (Edwards et al., 1992) and intranasal inoculation has been widely used to reproduce the disease experimentally.
Experimentally infected weaners became infected when placed in contact with others infected 2 or 8 weeks previously (Terpstra et al., 1992). Surprisingly, however, infection did not spread from weaners infected 4 or 6 weeks previously, even when they were treated with prednisolone to simulate stress.
Spread between herds
Rather more is known about how PRRSV can spread from one pig farm to another, the wind and pig movements (movements of weaners for finishing and of replacement breeding stock) being the principal factors. Six of the first 10 herd cases of PRRS in the UK received gilts from a breeding herd in Humberside (Edwards et al., 1992). Subsequent movement of the disease outside the initial infected area in Humberside was to herds that had received breeding stock from one breeding herd.
In the UK epidemic at least nine herds were believed to have been infected by supplies of semen (Robertson, 1992). Infected boars shed virus in their semen from as early as day 3 after infection, continuing until at least day 21 (Boeckman, 1993).
In Europe, during the winter of 1990/91, PRRS appeared to spread mainly by the airborne route in Germany, across the Netherlands and into Belgium (Komijn et al., 1991). Low temperatures, low sunlight and high humidity may have facilitated the airborne spread. Epidemiological studies have suggested that the disease can spread in air for distances of at least 20 km, although in the UK epidemic, neighbourhood spread (presumed windborne) did not exceed 3 km (Robertson, 1992). Apparent ‘jumps’ of more than 3 km were found to involve subclinical infection of intermediary pig units. In Belgium, 90% of recognized cases of local spread occurred over distances of up to 2 km.
Epidemiological investigations in Belgium (Varewyck, 1991) have attributed 69% of herd infections to local (neighbourhood) spread, 9% to purchase of infected pigs, 4% to other contact, while in 18% of cases the source of infection could not be identified. In the USA. (Dee, 1992), eight out of 10 clinical PRRS outbreaks were attributable to pig movements from a particular breeding company.
In the UK primary infection occurred at the premises of a multiplying unit of a major breeding company and replacement gilts were widely distributed to other farms before the disease was recognized (Robertson, 1992). The disease is also reported to have spread from Germany to Spain by movement of infected pigs. It appears that major geographical jumps of the disease are principally by movement or by cross-contamination during transport with local spread from these foci of infection primarily being airborne.
There are anecdotal reports of people carrying infection to pigs (Dee, 1992), while other field reports mention people moving between infected and uninfected stock without transmitting disease. In experimental studies conducted at the Federal Research Centre for Virus Diseases in Germany, piglets became infected when placed in contaminated stables up to 4 weeks after the removal of infected animals (Albina et al., 1992b).
Factors affecting the spread of disease, see Meredith (1995)
- Movement of pigs
- Local spread within 3 km (airborne)
- Infected buildings
- Urine and faeces
- Rodents (as mechanical vectors)
- Birds (Mallards), insects
- Needles, tattooing instruments
Increased spread in winter?
- Low sunlight
- Low temperatures
- High humidity (>60% RH)
- Wind speed increase
- Fewer thermal air currents
Risk factors increasing probability of herd infection by PRRSV (Fiedler, 1991; Vogel et al., 1991; Edwards et al., 1992).
- Large herd size (>50 or 100 sows)
- Housing in one building
- Introduction of new animals
- Housing on slatted floors
- Storage of slurry under floors
- Exposure to transport vehicles
- Lack of disinfection procedures
- Lack of quarantine facilities
- Totally indoor housing
- Fumonisin mycotoxin in feed
- Rodent problems
- Ignorance of staff about PRRS
- Winter months
There has been no indication of pigmeat or pigmeat products spreading PRRS. Freshly killed meat could be infected, but would not be a favourable medium for viral survival. The survival time in meat under various conditions is not yet known, nor is it clear how infectious the virus is by the oral as opposed to nasal/respiratory route. Theoretically, there is a very slight possibility of spread by this means (ESAVS, 1992), but feeding of uncooked meat waste to pigs is banned in many countries.
Persistence of infection
The UK State Veterinary Service carried out a detailed epidemiological study (Robertson, 1992) including the monitoring of serological changes in healthy ‘sentinel’ pigs placed on farms that had experienced disease. Herds remained infected for at least 2 months after obvious clinical effects had ended. Individual sows can still be infectious 99 days after infection with the ISU-P PRRSV (Zimmerman et al., 1992).
Vectors and intermediate hosts
There are no known vectors. However, birds could theoretically be involved in spreading PRRSV (Zimmerman et al., 1993). After experimental oral infection, virus has been recovered from the faeces of guinea fowl, chickens and mallards. No clinical effects were seen in the infected birds, but long-term shedding of virus occurred in the mallards.
Impact: EconomicTop of page
In clinical cases, the respiratory and/or reproductive systems are primarily involved, but there is also enhanced susceptibility to other disease agents, which can result in illness and, especially in suckling pigs, death. In acute PRRS outbreaks in breeding herds, the most serious effects are on pregnant sows (illness, abortion, premature farrowing, stillbirths, mummifications) and on sucking piglets (illness and death). In herds where there are no breeding stock or in breeding herds where the disease has become enzootic the most serious effect is usually respiratory disease in young growing pigs. Most pigs, particularly older ones, recover from PRRS, but some die from secondary infections. PRRSV does not seem to be truly immunosuppressive, but can impair non-specific defence mechanisms, particularly by damaging macrophages in the lungs. In severe outbreaks, affected farms can lose about 10% of a year's output of pigs, primarily through abortions, stillbirths and neonatal deaths. Deaths in older pigs are less common, but can arise from secondary infections. The effect of these viruses on individual pig herds is extremely variable, ranging from about 50% of animals being affected at one extreme, to no obvious effects at the other extreme. PRRSV tends to persist in infected pig populations if they are large, densely-stocked and constantly contain non-immune individuals. In this situation it can give rise to continuing problems in both growing pigs and breeding stock.
A breeding herd suffering an acute outbreak of PRRS will typically lose about 10% of its annual production of weaners (20% of gross margin). Losses from the disease are extremely variable from farm to farm and seasonal or weather factors also seem to have an influence (White, 1992). In addition to on-farm losses, there may be loss of sales of breeding stock to consider. Potential customers with herds that are not infected may be lost permanently. Statutory control measures may also carry financial penalties arising from restriction of free trade in pigs.
German epidemiologists have studied the breeding records of 200 sows from nine breeding herds experiencing acute PRRS outbreaks from January to April 1991 (Beilage and Beilage, 1992). The mean total loss of piglets from these sows was 22.3% for their litters born before PRRS. During the outbreak they lost 67% of piglets born. In their litters born after PRRS the losses fell again, to 20.3%. Breeding performance after the disease was similar to performance before, in terms of litter size, stillbirth rate and percentage of pregnant sows that had conceived at first oestrus. The culling rate was similar before and after PRRS.
In the USA, direct losses from the disease have ranged from US$50-250 (£29-143) per sow in the herd. The loss of potential profit was an additional US$50-314 per sow. In the UK, economic effects of the disease in six severely affected (2.7 pigs lost/sow/year) herds represented a cash flow loss of £5320 (US$9310) per 100 breeding sows, plus £2600 (US$4550) in lost feed conversion efficiency (Muirhead, 1992). For a ‘farrow to finish’ herd this represented £79 (US$139) per sow or £3.96 (US$6.93) per pig produced. In mildly affected herds losses were less than one pig per sow per year (£1.50/US$2.63 per pig produced).
In finishing units, the economic effects are typically reduced growth rate (up to 7 days increase in average time to reach slaughter weight), decreased food conversion efficiency, increased medication costs, down-grading of carcasses and increased mortality.
On a regional basis the financial losses from this disease have been estimated as 38 million DM in North Rhine Westphalia and 40 million DM in Lower Saxony. Many herd outbreaks of PRRS undoubtedly do not get diagnosed. This is particularly likely in herds that do not contain breeding pigs i.e. finishing herds and ‘grow-out’ units. Because of unreported cases, national losses are extremely difficult to estimate but unofficial figures of 2 million pigs lost in Germany and two million pigs lost in the Netherlands seem to be credible.
After the initial acute period of losses it typically takes 2 or 3 months to return to usual performance, but there may be continuing problems, particularly in growing pigs, for months or even years subsequent to an acute outbreak. Respiratory disease problems in weaners and growers and sub-optimal breeding performance of sows and boars have been linked with continuing PRRSV infection of herds.
The most serious long-term consequence of herd infection is respiratory disease in the post-weaning period (White, 1995). Growth to 95 kg live-weight may be slowed by up to 30 days and mortality from weaning to slaughter increased to 10% (occasionally to more than 15%).
The expense of preventing and treating secondary bacterial infections can also be significant.
Zoonoses and Food SafetyTop of page
Pigs that are incubating the disease, recovering from it, subclinically or only mildly affected can be sent to slaughter and be expected to pass both ante-mortem and post-mortem inspection procedures. It is highly likely that infected animals have been entering the food chains for a long time in countries that have this disease. PRRSV has been isolated from the lungs, blood and other organs of infected animals, so it is highly likely that some pig carcasses and offals contain or can be contaminated by these viruses. However, there are no reports of any adverse effects on humans.
Laboratory personnel working with the disease did not produce detectable antibodies (Done et al., 1992). Are the viruses likely to survive in pigmeat, offals and canned products, such that imports might be a risk to uninfected countries? Theoretically, there is a small risk from freshly killed meat (ESAVS, 1992). Investigations are being undertaken currently and new information is likely to become available soon.
Epidemiological studies in Germany found no evidence that slaughter pigs or meat were implicated in the spread of the disease (Fiedler, 1991). Many countries ban the feeding of uncooked meat products to pigs.
Disease TreatmentTop of page
There is no specific treatment for this disease. Pigs suffering from the influenza-like illness can be given supportive measures, such as raising environmental temperature, improving air quality, ensuring comfort and minimising stresses such as draughts, overcrowding or mixing. For dry sows, the house temperature can be raised to at least 21°C and the farrowing house temperature should be maintained at 21-24°C.
High palatability, high energy (15 MJ DE/kg) diets, or increased rations of normal diets, can be given to minimize loss of condition during the period of illness/inappetence. Alternatively, feed intake can be increased by 0.5-1kg per day for 3 weeks for dry sows.
Antibiotics can be given by injection or in feed or water to control secondary infections. Tetracycline feed medication might be given for 4 weeks for dry sows, a top-dressing of furazolidone pre-mix for lactating pigs, injection of litters with long-acting antibiotics at 3, 6 and 9 days, and for growing pigs 3-4 weeks of tetracyclines, sulphonamides or tylosin. Antibiotic medication is likely to be related to the herd history of probable secondary bacterial infections.
Anti-inflammatory drugs such as aspirin (acetylsalicylic acid), salicylates, flunixin and dipyrone have also been used (Gordon, 1992; White, 1992), but good scientific evidence of their efficacy is not yet available and there are possibilities of side-effects. Acetylsalicylic acid has been used at a dose rate of 8 g/sow/day (sprinkled on top of sows' feed) for a period of 7-10 days. Salicylates can be teratogenic if used in early pregnancy.
Little can be done to prevent abortions and stillbirths although salicylates and other drugs with anti-prostaglandin effects have been tried on a speculative basis. Foetal losses seem to be worse when sows become infected in late gestation (Christianson et al., 1992) indicating that every effort should be made to prevent infection spreading to sows that are at this most vulnerable stage of breeding. It may be helpful to move sows to the farrowing quarters 2 weeks before they are due, in case they farrow prematurely.
Attempts are usually made to reduce neonatal mortality by extra assistance with sucking and by electrolyte, glucose and colostrum (natural or artificial) medication. Success is not usually marked. Farrowing pens and creep areas should be well-bedded (preferably with deep straw). PRRSV antibodies have been detected in the colostrum of recovered sows and there is some indication that fostering sick piglets onto a recovered sow can be helpful.
There have been attempts to use serum from slaughtered recovered pigs to passively immunise sick or ‘at risk’ animals, with limited success. However, there is a danger of such serum containing live virus. Efforts have been made to stimulate immune response in stricken herds with a variety of medications (e.g. ‘Baypamun’ (CPD virus derived), levamisole). In the USA, the use of vitamin E has been suggested (Loula, 1991).
It has been suggested that, in order to reduce stress on infected newborn piglets, iron injections can usefully be delayed until 3 days of age and tail docking, where practised, can be delayed until 5 days of age (White, 1992). It was also suggested that teeth clipping should be omitted, or delayed, for weak piglets. Umbilical cords should be clamped at birth and cross-fostering and induction of farrowing should probably be abandoned during the acute phase of the disease. Kavanagh (1992) has suggested delaying iron injections until 14 days of age and suspending heat lamps on both sides of the rear of sows to improve the neonatal environment.
There are many reports from the field that the effects of the disease appear to be less marked when the housing and climatic environment of the pigs is good and stocking density is low (White, 1992). An acute outbreak of PRRS in a breeding herd can play havoc with breeding programmes, greatly disrupting pig ‘flow’. To minimise this, sows that have lost their litters are usually left unserved until the normal time of weaning. This also reduces the problem of low fertility at the first oestrus after abortion or premature farrowing.
It is also common practice to minimise culling and increase weekly services by 10-15% to maintain weekly farrowings despite a probable drop in service success rate during a disease outbreak. The consequences of boar infertility and low libido can be minimised by use of AI (preferably) or by using multiple sires on each sow. Boar fertility might be impaired for up to 6 weeks after illness. Boar semen may contain virus during the period that they are viraemic, which may be a reason to avoid using them. In equine viral arteritis infection, sexual rest may be important in reducing the likelihood of a stallion becoming a chronic carrier.
Replacement gilts can be vaccinated or exposed to infection before breeding. Sow culling could be minimised in order to increase weekly services during a period of reduced fertility. Pregnancy failures (returns or early abortions) need to be detected promptly, so there is an indication for increased pregnancy testing. Problems in growing pigs during an acute outbreak may be reduced by ‘all-in, all-out’ (AIAO) housing and medicated early weaning (Boeckman, 1993).
Coping with an acute disease outbreak can have deleterious effects on staff morale. Extra workload, severe losses, treatment failures and being regarded as an infection hazard by other people in the industry can all take their toll. Encouragement and support are important and the maintenance as far as possible of normal work routines can be helpful.
- ?? = speculative treatment
- Young pigs: electrolytes; colostrum (natural or artificial); antibiotics (oral, systemic); raise room temperature.
- Adults: vitamins; high-energy diet.
- Acetylsalicylic acid (aspirin)??; sodium salicylate??; dipyrone??; altrenogest??
- Baypamun (CPD virus derived)??; levamisole??
Acute disease management checklists
- Sucking Piglets: avoid cross-fostering; ensure colostrum at birth and at 4 hours; delay iron injections/tail removal; omit teeth clipping if weak; assist suckling; deeper bedding may avoid hypothermia (but avoid restricting mobility of piglets).
- Growing/Finishing Pigs: vigilance for secondary diseases; antibiotic feed medication.
- Gilts: vaccination; exposure to infection before breeding.
- Sows: stop farrowing induction; litterless sows, usual weaning time; allow sows to keep small litters; abortions <70 days, re-serve early; abortions >70 days, serve after 3 weeks; high energy/palatable diet for ill sows; increase pregnancy status checks; AI to avoid boar infertility; minimise culling.
- All pigs: thermal comfort; air quality; hygiene.
- Staff: encouragement and support.
McREBEL is a programme of management measures designed to reduce the spread of PRRSV within young pigs. The name is an acronym for: Management changes to Reduce Exposure to Bacteria to Eliminate Losses. The McREBEL protocol has been particularly useful in herds experiencing acute outbreaks of PRRS. It is low cost and the main features are:
- Strictly NO cross-fostering unless absolutely essential:
- NOT beyond 24 hours after birth,
- NOT to even up piglet body sizes,
- NOT to save weak pigs.
- NO transferring of pigs between farrowing rooms.
- STOP use of nurse sows for weak or runt piglets.
- Minimise all handling of piglets.
- Euthanase ill pigs IMMEDIATELY if unlikely to recover.
- Avoid stressful procedures on litters or weaner (nursery) pigs.
- STOP holding back weak or small piglets in farrowing rooms.
- STOP all feedback of stillborn or aborted fetuses.
- Use AIAO in weaner (nursery) rooms.
- Allow 2-3 days between weaner batches for cleaning/disinfection.
Persistently Infected Herds
Recurrent illness and secondary infections in weaner and growing pigs can be a continuing problem long after an acute disease episode has ended. Some herds have re-populated with PRRSV-free stock for this reason. Re-stocking is only a valid option if the risk of re-infection is low.
Reduction of stocking density, ‘all-in, all-out’ (AIAO) and age-segregation policies such as ‘split-site’ production have appeared to be helpful in persistently infected herds (Keffaber et al., 1992; White, 1995). The theory of split-site production is that separating breeding, nursery (weaners) and finishing pigs onto separate sites reduces the usual spread of infectious agents from older to younger animals. This strategy is showing early promise in control of PRRSV and associated bacterial and viral agents (White, 1995). A possible side-effect of age segregation techniques may be that there is reduced exposure of sows to organisms generated during active infections in susceptible growing pigs. This could reduce both adult and colostral immunity, leaving the breeding herd vulnerable to disease.
Producers with herds that are infected with PRRSV often prefer to purchase replacement breeding stock from farms that are also infected. The hope is that these pigs will already have immunity. Such pigs are not necessarily either seropositive or immune, particularly if it is some time since the source herd experienced obvious disease. They are also a potential source of re-infection. Opinion remains divided over whether it is better to purchase seropositive or seronegative animals as replacements in this situation.
Prevention and ControlTop of page Farm-Level Control
Pig farmers are usually advised to increase precautions against PRRSV entering by quarantining and serological testing of incoming pigs, restricting visitors, changing clothes, keeping vehicles at the perimeter of the farm, etc. These precautions seem to be sensible and may have contributed to the low amount of spread from infected herds in the Belgian and UK epidemic. In other countries, particularly the Netherlands, precautions of this nature have not prevented the disease entering premises. Even high-security minimal disease units with showering and complete change facilities for visitors have succumbed to the disease, presumably because of airborne spread, in pig-dense regions, under favourable atmospheric conditions.
Reducing risk of local spread: For new pig units, siting away from other pigs, particularly away from large, intensively housed populations must be regarded as a high priority for reducing the risk of infection by many types of airborne, rodent and fly-borne infectious agents. Risk of infection by local spread will reduce with increasing distance; distances of less than 3 km seem to be particularly risky.
Reducing this risk for existing herds is more difficult. Some possibilities are:
- re-locating to a less risky area;
- purchasing the neighbouring herd;
- negotiating an agreement for neighbours not to keep pigs;
- entering into a joint ‘disease security’ arrangement (e.g. regarding sources of purchased pigs).
Can a source of purchased pigs be guaranteed free of infection? Many herd infections have originated from purchased weaners or breeding stock. Gilts of 6-7 months of age from an enzootically infected herd can be viraemic (Dee et al., 1993). If a source herd is in a geographical area known to be free of disease, the risk of infection could be very low, but this risk would be increased if any movements into that area from areas of infected or unknown status are occurring, or if the area is at risk of airborne infection (it is suspected that the south of Denmark became infected by airborne spread from Germany).
As PRRSV becomes increasingly widespread in the world, it becomes increasingly difficult to guarantee that any region is free of infection. Lack of reporting of PRRS is no guarantee of virus absence.
Serological survey of a source herd, before the purchase of pigs, to demonstrate freedom from infection, may not be reliable because a substantial proportion of an infected herd can be seronegative, particularly where infection has been enzootic for some time or where the pigs are not housed closely together (Collins et al., 1990; Christianson et al., 1991). There is also the risk that a herd might be incubating infection at the time of a serological survey, or become infected (e.g. by airborne route) after survey. A survey undertaken both before and after removal of the pigs to be traded would be more reliable, particularly if combined with testing of the traded pigs. Appropriate choice of serological test(s) is vital in view of antigenic variation in the PRRSV.
Can purchased pigs be guaranteed free of infection? Current knowledge indicates that individual animals cannot be certified free of infection on a single test, but repeated tests, during a period of isolation from any risk of new infection, would make the risk of infection negligible. Testing a group of pigs in close contact with each other is likely to be a more sensitive test of virus presence than testing a single individual, given the highly infectious nature of PRRSV. It would be of some value, in reducing the risk of importing infection, to test a group of bought-in pigs on a single occasion to ensure that all are seronegative. Ideally this should be after a period of isolation (e.g. 3 weeks) from any risk of new infection, because pigs that are incubating infection can be seronegative. If some of the group were found to be seropositive, it would not be possible to assess the risk of virus still being present on the results of a single sample per animal; seropositive pigs may be recovered and free of virus or they may still be infected.
Paired samples (e.g. taken at an interval of 3 weeks) from each pig are necessary in a situation where some pigs are seropositive. Virus activity in the group would be indicated by seroconversion or rising antibody titres in some of the paired blood samples.
Seronegative pigs have not been known to be infected or infectious, except if incubating disease (i.e. up to 2 weeks after an initial infection). It thus seems likely that the infection risk will be negligible if a batch of pigs remains seronegative after an isolation period of at least 3 weeks. The only note of caution would be that the serological test must be sensitive to antibodies relating to the particular PRRS strain involved. The isolation location would also have to be free of risk of airborne infection.
Semen, embryos and hysterectomy-derived piglets
Reports indicate that there is a slight risk of boar semen being infected when boars have recently been infected. The advantage of using semen for introducing genes is that, if frozen, it can be kept in storage during a period of continued monitoring of the source pigs, to ensure that infection was not being incubated at the time of collection. Unfortunately, it is not yet commercially possible to freeze pig embryos. It is now possible to test semen for the presence of PRRSV.
Spread of PRRSV by embryos and hysterectomy-derived foetuses is a possibility, because of possible viraemia of the sow. Transplacental infection might occur unless the donor sows are known to be seronegative both before, and also 3 weeks after, providing offspring. Can immune, non-carrier sows be used as a source? There is a field report of hysterectomy being used successfully to obtain PRRSV-free offspring from second parity, seropositive sows. Because PRRSV crosses the placenta, hysterectomy is not reliable as a method of obtaining virus-free piglets from an infected herd. It would be necessary to keep such piglets quarantined until serologically checked for absence of infection. Where pigs or semen are introduced to an un-infected pig population, serological screening in conjunction with ‘double quarantine’ (i.e. of the source premises before despatch, and then again after arrival) could greatly reduce the risk of introducing PRRSV.
As with all stock importations, the risk of introducing an infectious agent increases with the number of occasions on which import occurs. Infrequent large imports of animals are generally less risky than many small imports. Similarly, the risk of introducing infection increases with the number of sources that pigs are taken from. Vulnerable sentinel pigs (e.g. pregnant sows) could be kept in close contact with imported animals and monitored clinically and serologically for evidence of infection. This might be particularly useful if there is any risk of a virus strain for which the serological test available is not sensitive.
The latest knowledge of PRRSV indicates that disinfectants effective against classical swine fever (hog cholera) are also likely to be effective against PRRSV strains. Detergents are also likely to have some action against the virus. The Central Veterinary Laboratory, UK, has specifically tested two disinfectants for efficacy against the British strain of PRRSV. A blend of peroxygen compounds, surfactant, organic acids and an inorganic buffer system was effective at a dilution of 1:700, while a blend of organic acids, surfactants and biocides was effective at a dilution of 1:900. Minimal clinical effects of PRRSV in growing pigs in one experiment were attributed to regular disinfection (Plana et al., 1992a; Plana et al., 1992b).
Immunization and Vaccines
There have been many reports from the field indicating that herds with a high health and hygiene status are less severely affected by PRRS when infection with PRRSV occurs (Blaha, 1992, 1993). Secondary infections with enzootic herd pathogens seem to be important determinants of morbidity and mortality. It would therefore seem advisable to improve the existing disease situation and to improve non-specific factors in disease spread and disease resistance (e.g. stocking density, air quality, stress). If a herd is already on antibiotic medication, there is less scope for providing this additional support when PRRS infection occurs.
The first commercial PRRSV vaccine (an inactivated vaccine called ‘Cyblue’) was launched by Cyanamid in Spain in late 1993. There have been difficulties in introducing this vaccine to other countries because it contains virus grown in primary pig alveolar macrophage culture, which could risk contamination with other pig infectious agents.
The USA Department of Agriculture awarded the first Federal Licence for a commercial PRRS vaccine, in June 1994, to Boehringer Ingelheim Animal Health Inc. (BIAHI) of St. Joseph, Missouri. This was the first modified live vaccine in the world against PRRSV infection. It was marketed in the USA by Nobl Laboratories Inc. under the name RespPRRS. In Canada the vaccine was marketed by Boehringer Ingelheim (Canada) Ltd. under the name Ingelvac RespPRRS. In the first year of being on the market, more than 16 million doses of the vaccine were sold in these two countries. Elsewhere in the world, this modified live vaccine was marketed as Ingelvac PRRS MLV by Boehringer Ingelheim Vetmedica [P.O. Box 200, D-55216 Ingelheim/Rhein, Germany]. The vaccine was developed by Boehringer Ingelheim scientists in the USA and Germany, working closely with researchers at the ID-DLO, Lelystad, and the University of Minnesota.
In experimental and field studies, the vaccine was found to be safe and effective in preventing clinical signs, viraemia and leucopaenia associated with the respiratory form of PRRS in growing pigs. It also significantly increased weight gain and reduced the number of treatments required after natural PRRSV challenge. Pigs are vaccinated once intramuscularly at 3-18 weeks of age. Although developed from the US PRRSV strain, ATCC VR-2332, some cross-protection against the 'Lelystad' European strain has been demonstrated (Gorcyca et al., 1995).
There are a number of vaccines on the market including PROGRESSIS (Merial, see www.merial.com) designed for use in sows and gilts. In developing and applying vaccines there is concern regarding their efficacy against the variety of PRRSV strains that can occur. Only time will tell if this is a real limitation or not. In considering the cost-effectiveness of vaccination, it is important to weigh the likely benefits of vaccinating against the costs of vaccinating and the other options for controlling infection. For example, in an enzootic area particularly, most breeders are likely to opt for vaccination of replacement breeding stock. The decision to vaccinate young slaughter pigs may require more careful consideration because rapid generation turnover results in high vaccination costs. These costs might be justified where there is endemic 'nursery' infection, where pigs from several sources are mixed or where there is a significant danger of local spread from other farms.
Where vaccines are in use it is important to interpret diagnostic tests carefully to ensure that vaccine antibodies are not mistaken for natural infection antibodies.
In countries where vaccine is not available, it is advisable, on infected farms, to expose replacement breeding stock to infection prior to breeding. A UK pig specialist has suggested the following programme (White, 1995):
- gilts enter the breeding herd at 95-100 kg, 175 days of age;
- after 2 weeks to 'settle in', put gilts in direct contact with 6-10-week-old weaners (and offer their faeces to the gilts twice weekly) for a period of 3 weeks;
- allow 2 further weeks 'for immunity to develop';
- serve at a minimum of 125 kg live-weight, 220 days of age.
Vaccination with Unidirectional pig flow
This strategy aims to reduce pig-to-pig horizontal spread of PRRSV in segregated finishing herds, for example those that are part of multi-site production systems. All pigs are vaccinated twice, over 1 month, while no new animals are introduced for a period of 2 months. It differs from partial depopulation in that it avoids immediate depopulation of the unit; the premises are gradually emptied as pigs are sent off for slaughter. As rooms become empty, they are washed, disinfected and given 2 days in which to dry.
Depopulation and restocking: Some herds have eradicated PRRS by adopting a total de-population programme, followed by re-stocking from a PRRS-free source. In an US study (Dee et al., 1993), an infected farm was depopulated and pressure-washed with water at >94°C, disinfected with formaldehyde three times, and left empty for 14 days. Slurry pits were emptied between each washing. Re-introduced pigs remained seronegative. It is important to ensure that the risk of re-infection (particularly airborne re-infection from a neighbouring herd) is minimal before adopting such a course.
Segregated early weaning: The theory of segregated early weaning is that separating breeding, nursery (weaners) and finishing pigs onto separate sites reduces the usual spread of infectious agents from older to younger animals. An American group has reported on attempts to eradicate PRRS using multi-site production and modified medicated early weaning (MMEW) techniques (Dee et al., 1993). Depopulation was ruled out because of the high genetic value of the herd, while the high percentage of seropositive pigs ruled out any possibility of a ‘test and removal’ programme. A MMEW programme was also appropriate for dealing with other herd pathogens that were present.
Many health management schemes currently being developed involve early weaning of pigs at 10-14 days of age (Loula, 1995). This early removal from the farrowing facility, at a time when they still have maternally-derived antibodies, reduces the chance of contacting pathogens (PRRSV and secondary pathogens) carried by the sows. Transferring them to an empty, clean, isolated nursery (weaner house) should help ensure that they remain healthy when their maternal protection diminishes.
An 'all-in, all-out' (AIAO) housing policy is an important component of success. Excluding air movement between rooms is as important as preventing animal contact. Rooms must be well cleaned and disinfected between groups and the pigs in a group must arrive and leave together and be of similar age.
Even greater protection is obtained when the nursery is located away from the sow herd and away from the finishing pigs. Ideally, the age range on each site is strictly limited; in true 'multi-site production' there might only be a single week's production phase at each location at one time.
Segregated early weaning usually involves separate sites for the sows, nursery and grow/finish phases of production with AIAO movements. There should be a preliminary survey (by serology, nasal swabs and swabs of post-mortem and abattoir specimens) of pathogens in the herd. This allows specific health control goals to be set. Weaning age is determined by the disease threats that have been identified, because maternal immunity decreases at different rates for different pathogens. For example, prevention of PRRSV or Streptococcus suis transmission requires weaning at 10 days or less. This becomes 12 days or less for Salmonella, 14 days for Pasteurella and Mycoplasma and 21 days for Aujeszky's disease (pseudorabies) and Actinobacillus.
Appropriate vaccines should be given to the sows before farrowing, to boost their immunity (an initial dose 4-6 weeks before farrowing and second dose 2-3 weeks before). Sows should also be treated for internal and external parasites before farrowing. After farrowing ensure good colostrum intake. Check udders and arrange split suckling if necessary. In split suckling, large piglets are removed for a couple of hours so that smaller ones can suck. It is not usual now to routinely medicate the piglets.
Ideally the nursery accommodation will be on a separate site, but it must at least be well segregated. Physical barriers and consideration of the prevailing wind are important. When piglets are loaded and unloaded during transportation, the system must be closed. Transportation must avoid chilling or overheating stress and needs contingency planning for breakdowns.
Monitoring the performance of an early weaning programme is essential. Problems can then be identified and the programme changed in accordance with the herd profiles and goals.
A possible side-effect of age segregation techniques may be that there is reduced exposure of sows to organisms generated during active infections in susceptible growing pigs. This could reduce both adult and colostral immunity, leaving the breeding herd vulnerable to disease.
National and International Control
Past attempts to control spread of PRRSV have been largely unsuccessful, other than in slowing the rate of spread. Slowing spread may have been quite advantageous in reducing the severity of disease by reducing the quantity of virus challenge (particularly by air contamination in pig-dense areas) and providing time for research and education.
As diagnostic tests have become more widely available, the prospects for limiting PRRSV spread are improving because uninfected herds and countries have more opportunity to screen incoming animals and semen. However there remain difficulties arising from antigenic variation of PRRSV (probably none of the existing tests detects all strains of these viruses) (Wensvoort et al., 1992), plus the opportunities for local (particularly airborne) spread in areas of high pig density.
In countries where the disease was made notifiable, this was usually based on the reporting of marked clinical signs in breeding herds. Consequently many herd infections did not get reported because they involved clinically mild, atypical or finishing herd infections.
The movement restrictions imposed in the UK were the most stringent applied anywhere, but were insufficient to totally control spread of the disease, although they undoubtedly did greatly slow down the PRRS epidemic. Movement restrictions alone are unlikely to halt spread of the disease because pig farms can remain infected for many months after clinical signs (and restrictions) have ended. The other difficulties in controlling the disease by this means have been the lack of obvious disease signs in some herds, the occurrence of windborne spread and the limited availability, specialised laboratory requirements and sometimes the high cost of diagnostic tests.
The Commission of the European Communities (EC, now European Union or EU) attempted to restrict spread of the disease (from March 1991 to October 1992) by requiring member states to report municipalities in which the disease occurred. Exports from these areas were banned until the affected farms were declared free (i.e. a period of 8 weeks had elapsed since the end of clinical symptoms). In addition there were regulations concerning hygiene and disinfection. Several EU countries have become infected despite these expensive and trade-restrictive measures. However, restriction of trade no doubt did slow down spread of PRRSV and brought a lot of attention to this health problem.
Many countries have implemented import control policies for PRRS. Early controls have been documented by Annelli (1992). Mexico imposed a complete ban on pig imports in December 1991 and 1 month later accepted a certification statement that a herd of origin had been free of clinical signs for 2 years prior to shipment. Japan, in October 1991, began requiring a certification statement that there had been no introduction of pigs from clinically affected premises 30 days prior to shipment. It later emerged that the country was already infected. South Korea totally banned imports from affected countries, but still became infected.
In May 1992, PRRS was put on list B of diseases scheduled by the International Office of Epizootics (OIE) for reporting by member countries. This means that each country must report its PRRS status and control measures at the end of each calendar year. However, PRRS is not a notifiable disease in many countries, which limits the information about its occurrence.
The past experiences of the UK and Malta are particularly daunting. PRRSV entered these aquatically isolated countries despite substantial controls over live pig and pigmeat imports. The routes of entry have still not been ascertained. However, now that much more is known about the virus, and diagnostic tests are widely available, it is possible for countries to accept live pig and semen imports, with negligible risk, if precautions of testing and quarantine are undertaken.
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