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This article was published in 2005
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Significance of porcine circovirus in outbreak of peracute coughing in pigs
Julie Bolam, SRAHM, Central Slopes, NSW DPI
Porcine circovirus has been generating quite a lot of interest in recent months in Australia and throughout the world. I would like to briefly present an unusual case of peracute coughing in a high health piggery. And then discuss the implications (if any) of porcine circovirus 2 (PCV2) being isolated from the spleen of one of the pigs submitted for autopsy.
Background:
• High health status 1100 sow piggery. Progressively de-stocked and repopulated 18 months previously to exclude both APP (Actinobacillus pleuropneumonia) and enzootic pneumonia (Mycoplasma hyopneumoniae).
• Divided into 3 units
1 Unit 1 which houses all breeding sows (1100) and 1/3 of all weaners, growers and finishers (~600 each of weaners, growers and finishers)
2. Eco Weaner which receives 2/3 weaners with weaners arriving every week (~3400) and
3. Unit 2 which is a grower/finisher unit which receives 2/3 of the pigs produced (total of 3 sheds make up unit 2)
• Isolated Boar Quarantine station on the properly with strict biosecurity measures in place associated with semen collection
• Gilt selection: gilts were selected from the grower/finishers at unit 1. They were then moved to a shed 50m away from unit 1 until they reached an adequate size, were cycling before being introduced back into unit 1 (mating pens) as required.
History & clinical progression
• November 2004, sudden onset coughing selected gilts in unit 1 (mating pens). Six gilts affected. Two of the gilts were euthanased and a post-mortem conducted (first by staff and the 2nd by a private practitioner)
• The other gilts recovered well following administration of the antibiotic excenel®
• No older sows or weaners/growers/finishers in unit 1 were affected
• December 2004 Unit 2 grower/finishers sudden onset coughing, majority pigs affected, no increase in mortality rates
• 7-10 days later Eco-weaner unit also affected - similar picture
• Transient clinical signs throughout all sheds in Eco-weaner and unit 2
• 'every pen in every shed had coughing pigs'
Summary of clinical findings and laboratory results
• Rapid spread, peracute cough, bright other wise, respiratory rate only mild to moderately increased - not noticeably dyspnoeic
• 3 day duration in individual pigs, approximately 10 day duration of clinical signs in each unit
• Low mortalities, but majority of pigs clinically affected
• No drop in feed conversion ratio or feed consumption
• No drop in reproductive performance
• Variable PCR results for M. hyopneumonia & A. pleuropneumonia - lung lesions and clinical syndrome not consistent with either.
• Routine bacterial culture no growth with exception of Arcanobacterium pyogenes in first gilt post-mortemed (considered secondary invader)
• Gross & Histopathology: pulmonary congestion & oedema, petechial haemorrhage lungs, ** severe ulcerative tracheitis, multifocal haemorrhages in skeletal muscle
• Virus isolation was set up on lung, spleen, lymph node & tonsil from the last grower post-mortemed. Circovirus was isolated from the spleen. Testing of the spleen by PCR for both porcine circovirus 1 and 2 demonstrated the presence of both viruses. Immunoperoxidase staining of fixed tissue for PCV2 was negative.
• Note: laboratory samples taken from 3 pigs in total — need to consider whether the animals selected for post-mortem were representative of the observed clinical syndrome
Differential Diagnosis
| Degenerative | •nil |
| Anomaly | •nil |
| Metabolic | •nil |
| Neoplastic | •nil |
| Trauma | • Unlikely |
| Environmental | • Dust negligible. Wet-dry self feeders. Good ventilation. Ammonia levels unlikely to be a problem |
| Toxins | • ? Feed for Unit 1 and Eco-shed Weaners mixed and supplied from home farm. Unit 2 (grower/finisher) sourced off farm |
| Parasitic | • Low likelihood. Well run indoor piggery. Regular FEC conducted in Weaner Eco-shed. No gross lesions in liver or lungs suggestive of parasites |
| Infectious/Inflammatory | |
| • Mycoplasma hyopneumonia | • Status of piggery. post-mortem results and clinical syndrome not consistent • Mixed PCR and culture results. No relapses or indication of slowing FCR or feed intake • Refer to (Buddle and O'hara 2005) for relevant discussion on diagnostic challenges |
| • Actinobacillus pleuropneumonia | • Status of piggery, post-mortem results and clinical syndrome not consistent |
| • Haemophilus parasuis, Tuberculosis, Pasturella | • negative culture, lung lesions not consistent, clinical progression of disease not match a bacterial cause |
| • Porcine respiratory coronavirus (?) | • (Unlikely) not previously recorded in Australia. A mutant strain on transmissible gastroenteritis virus (TGE) which is also exotic to Australia |
| • Porcine circovirus 2 (PCV2) (?) | • Associated with porcine respiratory disease complex (PRDC) overseas, multi-factorial aetiologies, usually expect prolonged & unusually severe clinical disease |
| • An uncharacterised virus (?) | • rapid transmission through 2/3 units, indicative of a virus of low pathogenicity causing transitory infection |
| • Swine influenza virus (SIV) (exotic) | • lack of rapid spread, expect 100% involvement of susceptible animals, high health status piggery |
| • Swine Fever (exotic) | • no mortalities; no GIT signs, not sick enough |
| • Aujezsky (exotic) | • nil nervous signs |
| • PRRS (exotic) porcine reproductive and respiratory syndrome | • no other signs consistent |
Brief update on porcine circovirus
The porcine circoviruses (PCV) are members of the genus Circovirus, which are the smallest non-enveloped, single-stranded, circular DNA viruses. Two types of PCV have been characterised. PCV1 and PCV2. PCV1 is a persistent contaminant of the porcine kidney cell lines and is thought to be non-pathogenic. In contrast, PCV2 is considered to be a virulent porcine pathogen (Chae 2005).
Currently, porcine circovirus 2 (PCV2) is considered to be an important emerging pathogen world-wide associated with a number of different syndromes and diseases in pigs including:
o Post-weaning multi-systemic wasting syndrome (PMWS)
o Porcine dermatitis and nephropathy syndrome (PDNS)
o Reproductive failure
o Porcine respiratory disease complex (PRDC)
o Granulomatous enteritis
o Necrotising lymphadenitis
o Possibly exudative epidermitis
The extent of the involvement of PCV2 in diseases other than PMWS is poorly understood. (Chae 2005). Note that these diseases are almost without exception considered to be due to the interaction of multifactorial aetiologies.
Virologists have questioned why PCV2-associated diseases have suddenly emerged around the world in the last few years. Studies on archived tissues and sera from pigs have confirmed that PCV2 is not so much a new virus, rather newly discovered. PCV2-associated diseases have been present in pigs for at least 15 years in some parts of the world, (Allan et al. 2003)
A western Australian group tested serum and tissues from a range of pigs sourced from WA, NSW, SA and QLD to determine if PCV type 1 and PCV type 2 were present. Both PCV1 and PCV2 are present in Australia and the viruses present appear similar to those in countries with PMWS. They suggested that the absence of PCV2-associated PMWS in Australia may be due to absence of essential secondary factors required for PCV2 to produce PMWS. It is important to remember that PCV2 has been widely detected in clinically normal pigs (Raye et al. 2005)
According to (Kim, Chung and Chae 2003) porcine respiratory disease complex (PRDC) is characterised clinically by slow growth, decreased feed efficiency, lethargy, anorexia, fever, cough, and dyspnoea in growing and finishing pigs typically around 16-22 weeks of age. (Harms, Halbur and Sorden 2002) highlighted that cases of PRDC presented at the Iowa State University Diagnostic Laboratory in 2000 were commonly multiple viral infections, with PRRSV present in 42% of cases, PCV2 present in 22%, SIV present in 19%, and Mycoplasma hyopneumonia present in 22% of cases.
Discussion
This outbreak of peracute coughing affected approaching the entire unit 2 and eco-weaner units. Interestingly only gilts being re-introduced to unit 1 showed clinical symptoms. The remaining older sows and 113 weaners and grower/finishers in unit 1 did not show any signs. One possible explanation is that as a result of selected gilt management, naive gilts came into contact with a virus present in unit 1, and developed clinical signs. The remainder of other pigs in unit 1 were already immune to the agent responsible. However the agent (presumed virus) spread to unit 2 and the eco-weaner unit which were similarly naive and clinical signs developed and spread rapidly.
From the list of possible diagnoses I believe the most likely possibilities are:
1. An uncharacterised virus or
2. Possible PCV2 involvement as part of a more complex aetiology
PCV2 has been documented overseas as a significant part of porcine respiratory disease complex (PRDC). To keep things in context PRRSV and SIV are exotic to Australia and are included with PCV2 and Mycoplasma hyopneumonia as the most common viral aetiological agents.
If PCV2 is involved in this coughing outbreak it does not fit with the clinical signs reported for PRDC. Eight months after this peracute outbreak of coughing there has been no reoccurrence of any problems at this site.
Conclusions
This case study illustrates some of the problems when trying to reach a diagnosis. Generally the tests that we have for viruses are limited. In this situation virus isolation is probably the best option when you don't have a clear idea of what you are looking for. The difficulty exists when a virus is isolated but its significance is unknown. In retrospect submitting multiple fresh samples from the respiratory tract of pigs in early stages of coughing would be beneficial. The fact that most pigs affected were still bright and eating limited material available for laboratory investigation.
It is my conclusion that the most likely diagnosis is the presence of an uncharacterised virus which caused clinical signs in naive pigs (selected gilts) and then was transferred to similarly naive weaners, growers and finishers in two other units. Management of selected gilts and the previous progressive depopulation of units to achieve a high health status also contributed to this sporadic event.
Take Home Messages
• Respiratory disease in pigs is inevitably complex with multi-aetiologies involved
• There is a need to attempt to confirm diagnoses wherever possible
• Possibility of a previously unrecognised disease should always be considered
• The isolation of a virus is not synonymous with a 'causal agent'
• Animals selected for post-mortem may not always be representative of disease
References
- Allan, G, McNeilly, F, Krakowa, S & Ellis, J 2003, 'Pcv-2 infection in swine; more than just postweaning multisystemic wasting syndrome', The Veterinary Journal, vol. 166, no. 3, pp. 222-223
- Buddle, J & O'hara, A 2005, 'Enzootic pneumonia of pigs - a diagnostic dilemma', Australian Veterinary Journal, vol. 83, no. 3, pp. 134-139
- Chae, C 2005, 'A review of porcine circovirus 2-associated syndromes and diseases', The Veterinary Journal, vol. 169, no. 1, pp. 326-336
- Harms, P, Halbur, P & Sorden, S 2002, 'Three cases of porcine respiratory disease complex associated with porcine circovirus type 2 infection', Journal of Swine Health and Production, vol. 10, no. 1, pp. 27-30
- Kim, J, Chung, K & Chae, C 2003, 'Association of porcine circovirus 2 with porcine respiratory disease complex', The Veterinary Journal, vol. 166, no. 1, pp. 251-256
- Raye, W, Muhling, J, Warfe, L, Buddle, J, Palmer, C & Wilcox, G 2005, 'The detection of porcine circovirus in the Australian pig herd', Australian Veterinary Journal, vol. 83, no. 5, pp. 300-303