Alimentary Disease

Swine dysentery in a breeding herd

Swine dysentery was diagnosed by Starcross in a breeding pig herd of 170, in which a small number of a group of 90 pigs had diarrhoea. Brachyspira hyodysenteriae was identified in pooled faeces from two pens by both FAT and culture. Advice was provided on swine dysentery control, emphasising the risk that swine dysentery-infected units pose to uninfected ones.

Enteric colibacillosis confirmed in preweaned pigs

Four live pigs were submitted to Thirsk from a unit with a history of watery scour two to three weeks post weaning. Pigs were reported to also lose condition, become sunken eyed and most affected pigs died.

Post mortem examination of the submitted pigs which were in the early stages of disease revealed
mucoid colitis from which E. coli 0149:K91, K88 ac (Abbotstown) was isolated. No porcine epidemic
diarrhoea virus was detected by PCR.

Brachyspira pilosicoli colitis

Faeces were submitted to investigate generalised looseness in 14-week-old housed finishers which were otherwise healthy. Brachyspira pilosicoli was identified by PCR; there was no evidence of Salmonella infection and Lawsonia intracellularis DNA was not detected. Brachyspira pilosicoli is the cause of porcine intestinal spirochaetosis and can cause a mild to moderate colitis.

Combined coccidiosis and salmonellosis in recently arrived replacement gilts

Combined coccidiosis and salmonellosis was diagnosed at Bury St Edmunds as the cause of malaise
and diarrhoea in five of 49 16-week-old replacement breeding gilts which had arrived on an outdoor
breeding unit one week prior to disease developing. A monophasic Salmonella Typhimurium-like isolate, phage type 193, was isolated by direct culture and 69,750 coccidial oocysts per gram faeces were also detected (58% Eimeria polita, 38% Eimeria debliecki). Similar outbreaks of salmonellosis have been diagnosed in the past, with and without concurrent coccidiosis, where replacement breeding pigs from indoor units are introduced into contaminated paddocks, with disease usually developing within one to two weeks of arrival.

Respiratory Diseases

Actinobacillus pleuropneumoniae in finishers

Two fresh plucks were submitted to Bury St Edmunds from pigs close to finishing in which on-going
respiratory disease was reported with a cumulative postweaning mortality of 10%. Pigs were vaccinated for PCV2, Mycoplasma hyopneumoniae and PRRS and approximately 30% of 1,600 pigs were reported to have been affected. Severe bronchopneumonias were present in the submitted lungs, with Pasteurella multocida isolated from both and Actinobacillus pleuropneumoniae isolated from one which had typical multifocal consolidated lesions. The Actinobacillus pleuropneumoniae was identified as serotype 3, 6, 8. These serotypes can show a high degree of cross-reactivity. No viral involvement was identified.

Porcine circovirus 2-associated respiratory disease with concurrent swine influenza

Complex viral disease involving both swine influenza and PCV2 was diagnosed at Bury St Edmunds in
nine-week-old pigs submitted to investigate a problem of increased mortality of 1% in the five weeks since weaning, with some respiratory disease and coughing. Some fading pigs and sudden deaths were also being seen. The pigs were from two sources and were vaccinated for Mycoplasma hyopneumoniae at weaning and for PCV2 10 days later. Losses had been from both sources. One pig had severe interlobular pulmonary oedema and a massive pleural effusion (Figure 1), which was suggestive of the acute pulmonary oedema presentation that porcine circovirus 2-associated disease can produce.

Differentials include other causes of acute heart failure (eg septicaemia, bracken poisoning, mulberry heart disease) or fumonisin (a Fusarium species mycotoxin) toxicity. Histopathology and
immunohistochemistry confirmed PCV2-associated disease in this pig. In another pig submitted, the
gross lesions were consistent with a severe bronchointerstitial pneumonia and Streptococcus suis type 2 was isolated from the lung. This pig also had PCV2-associated disease confirmed by histopathology and immunohistochemistry and active swine influenza virus infection was detected by PCR. The delay of PCV2 vaccination to 10 days postweaning was considered to be a potential factor in PCV2-associated disease occurring in the pigs.

Porcine circovirus 2-associated disease in unvaccinated smallholder pigs

The carcase of a four-month-old pig was submitted to Sutton Bonington to investigate refractory
diarrhoea in a group of eight pigs purchased by a smallholder. The pigs had been treated for suspected swine dysentery but had failed to thrive and, following the death of one, diagnostic postmortem examination was requested. Gross examination showed enlarged liver and kidneys and pneumonia. An untypable Streptococcus suis was isolated but histopathology revealed a lymphohistiocytic, bronchointerstitial pneumonia and immunohistochemistry confirmed extensive labelling throughout the lung tissue for PCV2 virus. It was suspected that the PCVAD diagnosed had resulted in immunosuppression culminating in a terminal bacterial septicaemia. Advice on vaccination for PCV2 was provided.

Porcine reproductive and respiratory syndrome involved in pneumonias in late finishers

Four pens comprising 160 pigs of 900 19-week-old finishers were reported to be showing inappetence, malaise and respiratory disease. Three of them were euthanased for submission to Bury St Edmunds.

The pigs were on an indoor batch-finisher and were vaccinated for PCV-2 and Mycoplasma
hyopneumonia at weaning and for PRRS at 40kg bodyweight. Patchy cranioventral pulmonary
consolidation affecting cranial and middle lung lobes was present in all three pigs, with a widespread thin coating of fibrin on lungs and thoracic wall. Thoracic lymph nodes were enlarged and pale. Pasteurella multocida was isolated from the lungs of all the pigs and also from the liver of one. No Haemophilus parasuis was isolated by selective culture, but PRRS genotype 1 (European strain), was detected by PCV in the spleens of two of the pigs and further investigation by immunohistochemistry on lung detected PRRSv indicating involvement of the virus in the pneumonia.

Systemic Disease

PRRS virus detected in serum of finishers with loss of condition

Ten percent of 2000 17-week-old housed finishers were reported to be losing condition, with occasional dyspnoeic pigs and 20 deaths over a two week period. The pigs were vaccinated for PCV2, Mycoplasma hyopneumoniae and PRRS at weaning. Pooled serum was tested for PRRS virus by PCR, and genotype 1 (European strain) was detected. At 17-weeks-old, this probably indicated challenge with field virus; sequencing is in progress to investigate further. To determine whether the PRRS virus was responsible for the clinical disease would require submission of typically affected pigs for post mortem examination and testing, rather than serum.

Acute Glässer’s disease in finishing pigs

Three finisher pigs were submitted to Thirsk to investigate six deaths from a group of 500 at 22-weeks old. Most pigs were just found dead but a few affected individuals behaved as if they had meningitis then went off their hind legs and died soon afterwards. Post mortem examination revealed fibrinous polyserositis typical of Glässer’s disease and Haemophilus parasuis was isolated from pleura, meninges and joints confirming the diagnosis. No underlying PRRS or swine influenza viruses were detected.

Nervous Disease

Typical nervous disease and sudden deaths due to Streptococcus suis type 2

Meningitis and septicaemia due to Streptococcus suis type 2 infection was diagnosed as the cause of sudden deaths and meningitis-like signs in 10-week-old pigs on an indoor nursery-finisher unit with 1,900 pigs. Nine pigs had been found dead in the 24 hours prior to submission of three dead pigs. Septicaemia/meningitis and fibrinous peritonitis and polyarthritis were found.

Porcine sapelovirus outbreak in pigs with active PRRSv infection

An unusual outbreak of nervous disease due to porcine sapelovirus (PSV, formerly known as porcine
enterovirus 8) was diagnosed in finishers by Bury St Edmunds. The outbreak caused an upsurge in
meningitis-like signs (lateral recumbency and paddling) and sudden deaths in 12-week-old pigs on an indoor nursery-finisher site receiving pigs from two sources. Only one source of 1,000 pigs was affected and around 50 pigs died over a three-week-period, with remaining pigs on the unit growing well.

Histopathology revealed a non-suppurative polioencephalomyelitis, typical of neurotropic viral infection. Immunohistochemistry confirmed involvement of PSV, and no labelling to porcine teschovirus was detected. Porcine sapelovirus is an uncommon diagnosis and in this outbreak, clinical signs closely resembled those of streptococcal meningitis but, not surprisingly, disease did not respond to antimicrobial treatment. Porcine sapelovirus outbreaks previously investigated by AHVLA have tended to show neurological disease characterised by progressive ataxia and paraparesis, with pigs staying alert.

In this outbreak, clinical signs and pathology were more severe, and concurrent PRRS virus infection was detected which may have exacerbated clinical disease. Subsequent batches of pigs weaned from the same breeding source have not, to date, shown similar signs.