CASE NOTES
A case of suspected post-weaning multisystemic wasting syndrome
Phillip Kemsley, DV Casino RLPB
Posted Flock & Herd August 2008
Introduction
Post Weaning Mult- Systemic Wasting Syndrome (PMWS) is scheduled as a disease of livestock considered to be exotic by Proclamation under the Stock Diseases Act. From May 2006 I undertook investigations into a piggery in the Casino district into a suspected case of PMWS. This sparked a surveillance plan developed by the NSW DPI, which required weekly visits over several months.
REVIEW OF THE SYNDROME
PMWS is a Porcine Circovirus 2 (PCV2) related disease. It was first recognized in Canada in 1991 and is has been reported from the USA, Asia, Europe and New Zealand.
PCV2 is a necessary causal agent, but several other factors are believed to be involved in the expression of the syndrome. The virus is widespread in the Australian pig population, but the syndrome has not been diagnosed.
Several other diseases are associated with PCV2, including Porcine Dermatitis and Nephropathy Syndrome (PDNS) which is not considered exotic to Australia.
Official diagnosis of PMWS has three requirements; fulfilling the Australian case definition for signs of the disease, typical histopathology and the presence of virus in tissues.
The syndrome affects weaner pigs causing wasting, lymphoid depletion, respiratory signs and increased mortality. Prior to the advent of vaccines, the only effective control measures used overseas were improvement in management; hygiene, pig flow, and pig environment and controlling concurrent disease.
History and findings
A disease complex in weaner and early grower pigs 7-11 weeks age, first presented in January 2005. A variety of clinical signs was observed, including diarrhoea, upper and lower respiratory signs, sudden death and weight loss followed by death. Losses were in the order of 15 - 20%.About one third of affected pigs recovered.
Pigs sent to the local Regional Veterinary Laboratory showed histopathological changes typical of PCV2 in lymph nodes and the virus was abundant in tissues. To complete an official diagnosis required clinical evidence of disease that was consistent with the Australian case definition. This triggered the development of a surveillance plan and intense veterinary involvement spanning several months. When one includes initial investigations, the weekly surveillance strategy, involvement with consultants and supporting their recommendations and follow up, my involvement with the piggery spanned about 9 months.
Each week mortality and farm records were collected, assessments made of each age group, autopsies undertaken, photographs taken and a report prepared for DPI. An assessment would also be made of the most recent recommendation or therapy being implemented.
Generally the condition was unresponsive to therapy, including Haemophilus vaccine, and a variety of antimicrobials. There were several underlying management issues, largely associated with early (3 week) weaning.
THE PIGGERY
The piggery was a 750 sow unit, a long established family enterprise, run by 3 brothers. Most of the sheds were old, however the weaner shed was modern; insulated, gas heated and controlled environment with automatic ventilation.
The weaner shed
Reproductive and preweaning performance was good, with an average of 2.2 litters a year and 10 piglets weaned per sow. Genetics were good and both AI and natural mating were practiced. Piglets arrived in the weaner shed generally in good condition and with a good start in life. There was some cross fostering in the first few days of life. Weaning was done once a week and the weaners averaged 21 days age (range 18-24). The few piglets that did not meet target weaning weight were fostered for a further 7 days for the next weeks weaning.
Once in the weaner shed several factors contributed to maladaption post weaning.
The only subdivision in the weaner rooms were down the middle, males on one side and females on the other. With an average of 320 pigs weaned each week, this meant 160 weaners in each pen. Stress, fighting, and competition for feed and water were an issue in the first week, leading to starve outs and runts appearing in the second week. Many piglets were simply not learning to feed, or became “lost in the crowd.” The water pressure in the drinkers was also far too high for the piglets to operate.
Fighting triggered an ongoing problem with Greasy Pig disease. To treat this, the pigs were sprayed with disinfectant by a petrol powered backpack daily from the day 1 of weaning. The noise, panic and wetting further added to the stress that the piglets were already experiencing post weaning. By the end of the second week the piglets would mass surge in panic when disturbed.
E.coli and Brachyspira scours and Haemophilus parasuis were problems post-weaning. In the warmer weather there was a low level of Swine Pox. There were sporadic losses from Streptococcus suis.
Summer infertility created some seasonal variation in piglets weaned during the winter, with an initial drop in numbers, tempting management to very early wean (down to as young as 16 days in some batches).This would be followed by a few weeks of overcrowding in the weaner shed, with the rebound in sow fertility.
The herd was both Actinobacillus pleuropneumoniae (APP) and Mycoplasma hyopneumoniae free, following a total depopulation and repopulation several years previously. Temperature, air flow and air quality were generally good as were feed and water quality. Apart from the unevenness and being below industry daily weight gains the piglets were generally healthy from 5 to 7 weeks of age.
In summary it could be said that pig flow and the disease situation in the herd was satisfactory prior to the arrival of this problem.
Clinical findings
At 7 weeks of age a pattern of disease started that remained until the pigs were transferred from the weaner to the grower shed when they were 10 weeks old. From time to time there were new clinical cases in the first week or two in the grower shed.
Initially, the affected pigs go off feed with a watery eye discharge They also held their ears back, had rapid breathing and a deep cough. They would be febrile and in some, peripheral lymph nodes were palpably enlarged. Some pigs in good condition would die suddenly at this stage.
The fever would then subside, but the dyspnoea and cough continued. Within days the pig's condition fell away dramatically and they became gaunt and hairy. Most pigs then became weak and would either die or be euthanased. About one third of affected pigs survived. Most took weeks to regain condition, but some remained poor performers.
These 8 weeks old pigs are in the hospital pen. They are all sick, anorexic and have marked dyspnoea (note the extended neck). The large pig is in the first day of the disease, has a temperature of 41.5 and swollen lymph nodes. The thinner pigs have been sick for up to a week and are now afebrile. The weight range is 9 to 20kg.
Extreme emaciation was a common finding. Typical appearance of affected pigs.
Background
Over the months, I autopsied a large number of pigs and the findings are listed below. A yellow stained pleural effusion that clotted on exposure to air and lungs that were wet and glassy were the most consistent pattern found on post-mortem.
| Lesion | Number | Percentage |
|---|---|---|
| Cranio-ventral lung consolidation (bronchopneumonia) | 68 | 53% |
| Pulmonary oedema | 64 | 50% |
| Pleural/pericardial effusion | 61 | 48% |
| Emaciated/Poor | 23 | 18% |
| Loss of condition | 22 | 17% |
| Mediastinal LN enlargement | 22 | 17% |
| Superficial LN enlargement | 19 | 15% |
| Polyserositis (esp. pleural, pericardial, peritoneal cavities) |
18 | 14% |
| Mesenteric LN enlargement | 17 | 13% |
| Meso-colonic oedema | 16 | 13% |
| Skin lesions | 10 | 8% |
| Watery intestinal contents | 9 | 7% |
| Swollen joints | 9 | 7% |
| SI mucosal corrugation/"furriness"/thickening | 9 | 7% |
| Intestinal necrosis | 7 | 5% |
| Neurologic signs | 5 | 4% |
| Perirenal oedema | 5 | 4% |
| Jaundice | 3 | 2% |
| Non-collapsing lungs | 2 | 2% |
| Pallor | 1 | 1% |
Typical glassy appearance of the lungs. Oedema of the interlobular septa was a common finding.
On exposure to air the thoracic effusion clotted
Some had enlarged lymph nodes, some had normal, in others the nodes were atrophic
ASSESSMENT
Over the course of 12 months several consultants were called in and a wide range of issues investigated. With each new consultant old ground would be ploughed over and the net cast wider.
These included:
Evaluation of general management.
Assessment records and herd performance.
Nutritional assessment.
Mycotoxin analysis of feed.
Assessment of air quality, ventilation and temperature variation.
Water quality testing.
Background and historical disease assessment.
Biochemistry.
Bacterial isolates from lungs and other tissues, including Haemophilus typing.
ATTEMPTS AT TREATMENT AND PREVENTION
With the exception of one strategy, the condition was generally refractory to both prevention and treatment. Generally it was unresponsive to antimicrobials. Mass medication with Tilmicosin Phosphate (Pulmotil®) would delay the onset of the condition by about a week, only to have the pigs die at a heavier (and therefore more expensive) weight. Amoxycillin seemed to have some, but not dramatic, influence on the outcome of clinically affected pigs. Other strategies tried with little success included; Mycotoxin binders, Haemophilus vaccination and diet modification, including Vitamin E supplementation.
MY ROLE ON THE FARM INCLUDED
Collecting and recording information, including performance and mortality data.
Weekly visual assessment of each age group.
Tagging and sometimes weighing pigs.
Conducting an enormous number of clinical assessments and autopsies.
Assessing concurrent disease.
Collecting an enormous number of samples for an equally enormous amount of histopathology and virology.
Assessing the success or otherwise of the latest therapy or intervention.
The occasional red herring, such as rat autopsies and sampling (for some reason their numbers had fallen at the time).
Trying to support the management and staff as they went through the various stages of denial, anger, frustration, depression and finally acceptance that the business would fold.
WHAT WORKED
A thorough overview of preweaning and postweaning management identified a variety of physical, psychological and social stressors. Overseas experience has been that these stressors are believed to play a part in the expression of PCV2, probably from the effects of stress on the immune system. A decision was made to totally review how the piglets were handled, particularly in the first week postweaning.
Weaning later at 28 days may have eased some of the weaning maladaption issues. However, this was not considered an option as this would require a huge increase in available farrowing space, or a reduction in the number of sows. When the herd was depopulated at a later date, there was a window of opportunity for 28 day weaning and this was in fact found to reduce the impact of the disease complex.
A novel technique in weaner management was instituted. It incorporated aspects of both pig social behaviour and nutrition. The basis for the technique is the feeding behaviour of pigs. The trigger for piglets to suckle from the sow is not primarily hunger as one would expect, but rather that the sow has called them up to feed. An early weaned piglet finds its self without this stimulus after being removed from the sow. To replicate this when first weaned the piglets are given no free access to feed, but are called up to feed by a member of staff, often by them being woken from sleep. Piglets that do not respond are identified and shepherded onto feed. Very slow individuals may even need catching and their noses placed in the trough. However, the piglets quickly learn to make the association.
The technique also makes use of feeding gruel in troughs, as a transition from a liquid to a solid diet. This is gradually changed to full solid feed over a period of three days. It is important to prolong this period of transition, and create a “double wean” effect. During this period the interval between feeding is increased and the piglets introduced to dry feed, scattering it onto mats and into feed bins. The socialisation also quietens the piglets, greatly reduces their fear of humans and minimises fighting down to the usual tussles associated with forming a new social group. As one would expect, women are usually much better at this technique than men (as they with the rearing of all young animals). The female staff member on this piggery perfected the technique very quickly.
Day 1 50/50 Starter/ Piggy Milk every 1 ½ hours
Day 2 am 60/40 every 2 hours
pm 70/30
Day 3 am 70/30 every 3 hours
pm 80/20
Day 4 Check that all feed on gruel in am then Starter only
Needless to say, the spraying with Virkon S ® for Greasy Pig Disease was stopped and this disease almost disappeared in the first batch of piglets.
There was still the occasional non starter and starve out and the odd fight wound, but numbers were dramatically reduced. Within a few batches it was noted that the level of the “syndrome” at 7 weeks declined into single figures. However, it never totally disappeared.
Weaners called onto feed
Graph courtesy of Barbara Moloney
THE OUTCOME
The combined effects of the syndrome, high grain prices and the dissolution of the family partnership saw the last pig born in early 2007 and the piggery closed at the end of that year.The weaner shed is now used as a grow out for a local integrated rabbit farm.