Veterinary Services

BVD virus was detected in samples of pleural fluid from young piglets in a herd with high postnatal mortality rates of approximately 20 per cent over a four month period. The herd has a high health status, being free from porcine reproductive and respiratory syndrome (PRRS) virus infection, swine influenza virus, Mycoplasma hyopneumonaie and other major pathogens. The breeding herd showed good fertility rates, piglet numbers born, and piglets were of good birth weight. However, a proportion of pigs in most litters appeared to lack vigour and failed to suckle as well as expected. These piglets faded despite the stockmens’ best efforts to care for them. Most affected piglets died during the first week of life. Some remained viable but had poor weights at weaning. Other piglets in the litters performed as expected. Sows and gilts were all in good bodily condition and had ample milk supplies. Seven piglets from different litters were submitted for postmortem examination. There were slight excesses in pleural and peritoneal fluid but otherwise no macroscopic findings of note. Comprehensive bacteriology and histopathology testing was carried out. The only notable finding was reduced cellularity of bone marrow (Fig 5 - see top right-hand side). As part of further virological investigation, pleural fluid samples were tested in two pools for BVD virus by PCR. Both pools were positive. Thereafter, the individual pleural fluid samples were tested by BVD antigen ELISA and six of the seven were positive. No other pathogens were detected during the investigation. The findings suggest a causal role for BVD virus and possible control measures are under consideration.

Losses due to Streptococcus suis serotype 2 were confirmed on several different units. This included polyserositis, septicaemia and meningitis in a 16-week-old boar, one of 16 deaths that occurred on the unit since they arrived five weeks previously. There was intense generalised meningeal congestion.  Meningitis was also confirmed in a 13-week-old boar from a unit where stiffness and clinical signs suggestive of meningitis were observed three days previously. The same diagnosis was made in a 15-week-old gilt. There were seven, mostly sudden, deaths since the pigs moved onto the unit five weeks previously. S.suis serotype 2 was isolated in culture from the brain in all three cases. S. suis serotype 2 infections were diagnosed in nine-week-old pigs from a unit reporting nervous signs. The pigs had fibrinous reaction overlying the cerebellum. Streptococcus suis serotype 2 was isolated in cultures from the brains of three pigs, from the lungs of two pigs and in systemic distribution from one of these.

Glasser’s disease was diagnosed in two 10-week-old boars submitted for postmortem examination. This followed the sudden deaths of 21 pigs over the previous three days. There were no prior clinical signs but pigs in the affected pen varied in size, with evidence of some loss of condition. One pig, in thin to moderate body condition, had polyserositis, with an excess of cloudy peritoneal fluid containing strands and pieces of fibrin. Colonic contents were liquid and yellowish brown in colour and there were foci of friable material adherent to the colonic mucosa.  A profuse growth of Haemophilus parasuis was isolated in culture from the lung confirming Glasser's disease. Salmonella Typhimurium phage type 193 was also isolated in culture from the large intestinal contents.

Alimentary tract conditions

Two pigs of about six weeks of age were submitted to investigate the cause of ill thrift and diarrhoea. Pigs in the batch were very uneven in size and blood was present in diarrhoeic faeces despite being on medicated feed. There were five deaths in the previous week. Salmonella Typhimurium phage type 120 was isolated in culture from the large intestinal contents of both pigs.

An acute necrotising enteropathy associated with adherent bacteria was identified on histopathology of the intestines from four-day-old scouring piglets. A beta haemolytic E coli, which was poly A negative and poly B positive was isolated from the intestinal contents. On histopathology, the intestines showed acute enteropathy with abundant bacterial attachment to villi in the mid-jejunum and ileum. Many of the villi were undergoing necrosis and epithelial loss. None of the sections showed any evidence of colostrum in lacteals.

Respiratory tract conditions

Pandemic (H1N1) 2009 virus was detected in the lung of a six-week-old weaner. Coughing was reported in two pens of pigs which were on the unit for seven days. The morbidity was 25 per cent with zero mortality. There was deep purple consolidation of the apical and middle lobes of the lungs. The pleural surfaces of the diaphragmatic lobes of the lungs were petechiated and the lungs were moderately congested.

Pneumonia due to Pasteurella multocida was diagnosed in two 20-week-old finishers reported to have acute onset, severe respiratory signs. In one pig the lungs had severe generalised congestion and oedema, with widespread yellow fibrin exudates over the diaphragmatic surfaces and margins of the lobes. There was hepatisation of the apical, cardiac and intermediate lobes.  There were severe ecchymotic haemorrhages on the external surface of the pericardium. The lung pathology in the second pig was very similar to that seen in a case of swine influenza due to pandemic H1N1 (2009 virus). However no influenza A RNA was detected by PCR from the lungs from either pig. Profuse growths of Pasteurella multocida were obtained from the lungs of both pigs.

Locomotor diseases

Two 13-week-old gilts were submitted to investigate the cause of lameness affecting about five per cent of the pigs. One gilt had excess bloody synovial fluid in both stifles and in the right hock. The synoviae of the stifles were hyperaemic. Mycoplasma hyosynoviae was detected in the synovial fluid from this case. The other pig had excess bloody synovial fluid in both stifles but only Mycoplasma flocculare was detected in its joints.

Gross pathological changes suggestive of osteochondrosis were suspected as the cause of lameness in 35-week-old gilts. There was thinning, and in some cases distortion, of the articular cartilage of the joints in fore and hind limbs of one gilt. The hip, stifle, hock and elbow joints were particularly affected. In most cases there were minimal associated changes in the periarticular tissues. However, in the case of the hock joints, the synovial membranes were thickened and there was excess bloody synovial fluid. A second gilt had similar, but milder, gross changes with less obvious thinning of articular cartilages and no periarticular reactions or synovitis. No bacteria or Mycoplasma species were isolated in cultures. Histopathology confirmed articular-epiphyseal cartilage changes consistent with osteochondrosis.