Disease of the Digestive System

Muscular thickening of the small intestine in finishers

Sudden death of two finisher pigs on different units within the same week yielded an unusual diagnosis. The pigs were outdoors and were aged 25 and 18-weeks-old. Both were female and in good body condition, and had died with generalised fibrinous peritonitis as a result of intestinal rupture. There was no torsion associated with the rupture, however in both pigs, there was thickening of the ileal wall, not typical of proliferative enteropathy associated with Lawsonia intracellularis. Histopathology was not suggestive of PIA and the thickening was due to muscular hypertrophy of the ileum. This is a recognised finding in the terminal ileum of unknown underlying aetiology and rupture at the site of muscular hypertrophy can occur in association with feed impaction or development of diverticulae. This muscular hypertrophy is thought to be secondary to functional obstruction of the ileocaecal orifice, no obvious physical obstruction was seen grossly.

Outbreak of gastric ulceration in outdoor sows

A dead sow was submitted to investigate deaths of ten sows over a period of six weeks in farrowing paddocks on an outdoor breeding herd where on-farm post-mortem examinations had revealed gastric ulceration and haemorrhage. The submitted sow had farrowed three weeks earlier. The carcase was pale and this sow had also died due to fatal gastric ulceration with the stomach full of clotted and unclotted blood due to haemorrhage from the ulcerated pars oesophagea. There was no evidence of swine influenza or PRRSV and no other indication of another disease process. The sow was in fair body condition and, as any interruption in feeding or normal feeding pattern predisposes to gastric ulceration, it was recommended that feeding be reviewed.

Salmonellosis cases continue in growers

Several cases of salmonellosis were diagnosed, briefly these affected:

• 27 of 4,000 pigs with seven deaths due to a monophasic Salmonella Typhimurium phage type 193 organism. The pigs were reared in outdoor tents prior to moving indoors for finishing. A post cleaning and disinfection visit revealed a significant rodent population with S.Typhimurium isolated from rat faeces and several environmental samples.
  
  
• Six to nine-week-old rearing pigs on an indoor breeder-finisher with sudden deaths. A similar monophasic S.Typhimurium-like organism was responsible, in this case the phage type was 120. The unit had a history of salmonellosis and an advisory visit had revealed deficiencies in cleaning and disinfection of weaner pens.
  
  
• Eight-week-old pigs causing six deaths over a weekend on a 1,100 pig indoor nursery-finisher. Prior to these deaths, only six pigs had died since entry four weeks earlier. In-water treatment for meningitis had finished just before the outbreak.
  
  
• 35 weaners from a group of 400 pigs with yellow diarrhoea, wasting and four deaths.

Coccidiosis causing poor growth in pre-weaned pigs

A breeding unit reported diarrhoea and poor growth rates from around 10 days of age affecting 30 out of 150 piglets a week. Necropsy of a recently euthanased piglet revealed signs of moderate enteritis. No bacterial pathogens were recovered and there was no evidence of cryptosporidia or rotavirus infection. However histopathology revealed evidence of enteritis with intralesional coccidia consistent with infection with Isospora suis. Reports in the literature indicate that coccidial infection prior to weaning can also adversely affect post-weaning growth rates.

Post-weaning E.coli enteritis

Four Pietrain-cross piglets died approximately one week after weaning from three litters comprising 28 piglets. Two were submitted and post-mortem findings included navel abscessation and enteritis. There was a rich growth of a haemolytic E. coli, which was positive for F4 (formerly K88 antigen), consistent with post-weaning enteric colibacillosis.

Nervous Disease

Streptococcus suis meningitis outbreaks in pigs of widely differing ages

Streptococcal meningitis due to S. suis (untypeable) was diagnosed in a four-week-old piglet from a unit which reported 12-15 piglets with neurological signs in a group of 250 suckling piglets. The clinical presentation included recumbency, tremors, paddling and pallor. The animals responded well to antibiotic treatment with only the submitted pig dying. At necropsy the meningeal vessels were prominent and there was a fibrinous polyarthritis.

Increased mortality in outdoor nine to 10-week-old growing pigs was described with 30 deaths from 2000 pigs. Pigs were described as lethargic with some ataxia prior to death. Non-specific gross lesions were present in the submitted pigs with fibrin stranding in the peritoneal cavity and excess peritoneal and pericardial fluids, three pigs tested had Streptococcus suis 2 identified by FAT on meningeal smears pointing to streptococcal meningitis which was confirmed by isolation of S. suis type 2. In addition there was rupture of the liver in two pigs and epicardial haemorrhages in one pig raising suspicion of mulberry heart disease which was confirmed in the pig with epicardial haemorrhage, but not in those with ruptured livers. Liver rupture and haemorrhage is sometimes seen in submissions of pigs with septicaemias, possibly secondary to trauma from other pigs while the affected pigs are recumbent.

A S. suis type 2 outbreak occurred in 10-week-old pigs on an indoor nursery-finisher on which about 60 deaths had occurred in the six weeks since entry. The organism was isolated from the meninges which were cloudy in one pig and which had prominent blood vessels in all three pigs submitted.

Increased mortality was reported in finishers on an indoor breeder-finisher unit with a background of mild coughing in 5 per cent of 15 to 18-week-old pigs. A dead finisher was submitted which showed superficial evidence of recent fighting, S. suis type 2 septicaemia/meningitis was confirmed and PRRSV was also identified by PCR in the spleen. The unit was aware of past active PRRSV infection during the rearing period and was vaccinating pigs for PRRSV at weaning. The detection of PRRSV in the submitted finisher confirmed the need to continue with PRRSV control measures, including vaccination.

An unusual cluster of deaths likely to be due to Streptococcus suis type 2 occurred on an outdoor breeding unit where a total of nine pigs died (eight gilts and one boar) over seven days in three outdoor paddocks containing approximately 16 gilts and one or two boars in each paddock. The gilts were at the point of service and were vaccinated for Mycoplasma hyopneumoniae, PCV-2, erysipelas, parvovirus, PRRSV and clostridial disease. The gilts were homebred and on land used previously by pigs. No signs were seen prior to the sudden deaths but two lame pigs in the group were treated with penicillin and recovered. A dead gilt submitted was in good body condition, and was dehydrated with non-specific lesions including reddened lymph nodes, red oedematous lungs, epicardial haemorrhages and very prominent meningeal blood vessels. A meningeal smear tested positive for S.suis 2 by FAT, however unusually in an untreated pig, the organism was not isolated. In view of the unusual late presentation of disease and the absence of significant bacterial isolates, histopathology was performed but only revealed severe cerebral congestion, histopathology on other tissues were consistent with septicaemia and, as no further cases occurred following parental antimicrobial treatment, the overall evidence pointed to bacterial septicaemia, likely to be S. suis 2. No involvement of swine influenza or PRRSV was detected.

Characteristic back-dipping in pigs with severe sunburn

A video clip from a mobile phone was submitted of a group of grower pigs, some of which had distinctly dipped backs. This is a characteristic sign seen in cases of severe sunburn. It was confirmed that there was gross evidence of sunburn. Mud wallows and/or shading need to be provided for pigs at risk.

Systemic Disease

Iron deficiency causing weight loss

A five-week-old piglet was presented from one of two litters that had lost condition and scoured in the first weeks of life. The piglets had not been injected with iron at birth but had had access to soil for part of the day and to sods of earth when housed. The majority responded to iron and antibiotics but this animal continued to deteriorate and died. On post mortem examination, classic signs of iron deficiency anaemia were detected, including a pale tan coloured liver and a dilated heart with flabby ventricles containing watery blood. The bone marrow of the sternum was also pale.

PCV2-associated disease in pigs suspected to have missed PCV2 vaccination

Wasting and jaundice due to PCV-2 associated disease was diagnosed in one group of six-week-old pigs in flat decks. 25 of 75 pigs were affected with 11 deaths, the problem began 10 days prior to submission approximately one week after weaning and it was suspected that the affected group had inadvertently not received PCV-2 vaccine. Pigs in an adjacent room which would have been vaccinated at the same time were not affected. Two pigs were submitted; one had died in poor body condition with severe necrotic enteritis, the second in fair body condition had been euthanased and gross findings were generally unremarkable apart from peritoneal fibrin stranding and a navel abscess due to Pasteurella multocida infection. No enteropathogens were detected associated with the necrotic enteritis, however, histopathology revealed severe PCV-2-associated enteritis with typical lymphoid lesions and large numbers of intracytoplasmic amphophilic inclusion bodies in the lymph nodes and Peyer’s patches and also PCV-2-associated hepatitis. Streptococcus suis type 1/2 was isolated from the liver of pig 1 and peritoneal fluid of pig 2, in both cases likely to be superimposed on the pre-existing disease. In the second pig, there was no evidence of PCV-2 associated disease and its poorer weight gain may well have been associated with the navel abscessation.

Typical Glasser’s disease in growing pigs

Nine six-week-old pigs were found dead unexpectedly in a pen of 30. Post-mortem examination of three pigs revealed variations in polyarthritis, pericarditis, pleurisy and peritonitis. Haemophilus parasuis was detected in pure growth from one of the three carcases confirming a diagnosis of Glasser’s disease. H. parasuis is difficult to grow; its isolation is most successful from freshly dead or culled affected pigs which have not been treated or chilled and are submitted promptly to the laboratory.

Clostridium novyi hepatitis in breeding pigs

A single sow from a herd of Gloucester Old Spots died unexpectedly 24 hours after service. She had shown various signs of malaise since weaning six weeks previously. Post mortem examination confirmed an enlarged dark red liver with a distinct area of mottled paler parenchyma. The cut surface of this lesion revealed dry dark gassy parenchyma (‘aero chocolate’). Within the heart there was a large florid 2.5 cm diameter mass on the left atrioventricular valve. Fluorescent antibody testing detected moderate numbers of Clostridium novyi within liver tissue confirming clostridial disease, which probably occurred secondary to the anaerobic conditions induced by the endocarditis. Erysipelothrix rhusiopathiae was cultured from the heart valve lesion.

The carcase of an 18-month-old breeding boar was submitted with a history of having been found dead. There was marked blotching of the skin and reddened conjunctival mucous membranes. There was also subcutaneous emphysema, congestion and gelatinous oedema along the ventral abdominal wall. Examination of abdominal content showed an excess of serosanguinous fluid and the liver had an “aero-chocolate“ appearance due to emphysema. Small sections of liver floated in formol saline fixative. Fluorescent antibody testing of the liver and subcutaneous tissues gave a positive result for the presence of Clostridium novyi.

Colisepticaemia following agalactia

Three Tamworth piglets stated to be three-days-old were submitted for post-mortem examination. They were born to a single sow on a smallholding. The sow reportedly had no milk and six piglets had already died. None of the piglets appeared to have fed, two had retained meconium, and there were umbilical infections; colisepticaemia was confirmed. Lack of colostrum was suspected to have led to the E. coli infection.

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Further Reading

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