Alimentary Diseases

Salmonellosis in growers

Salmonellosis was diagnosed by Bury St Edmunds as the cause of scour and malaise on a large nursery-finisher unit on which approximately 30 per cent of pigs were affected and 20 had died. Coughing and occasional meningitis cases were also reported. Three dead pigs in poor body condition were submitted with necrotic gastroenteritis and diarrhoea. Salmonella Typhimurium phage type 193 was isolated confirming salmonellosis and was considered the most significant finding. In addition, Actinobacillus suis and Streptococcus suis type 3 were isolated from the meninges of one pig and probably relate to the observed cases of meningitis. It was not possible to investigate further by histopathology as the tissues were too autolysed.

Suspected clostridial enterotoxaemia in neonatal pigs

Clostridial enterotoxaemia, most likely due to Clostridium perfringens type A was suspected on the basis of clinical history and pathological findings in diarrhoeic neonatal pigs. The diarrhoea was starting from two to six days old with around 12 per cent of litters affected per farrowing batch on an indoor unit. Some response to antimicrobial treatment was reported. Gammaglobulin estimation suggested that colostral antibody uptake was satisfactory, the piglets had fluid large intestinal contents with no mucosal lesions, there was a mild acute enterocolitis associated with clostridia-like bacteria although no clostridial toxins were detected.

Chronic problems due to concurrent enteric infections

Long-standing post weaning ill thrift and diarrhoea were investigated in a herd by Luddington. Twenty percent morbidity was reported in a group of 130 6-week-old pigs with five deaths. Post mortem examination of two culled pigs and faecal samples found evidence of concurrent Lawsonia intracellularis, Brachyspira pilicosi and Group B Salmonella infections.

Rectal stricture possibly following salmonellosis

A mixed breed 200 sow unit, part outdoors, weaning at 8 weeks old reported an increasing number of weaners with illthrift. Cases were sporadic and distributed across pens. Post mortem investigation of a 16-week-old fatality found evidence of megacolon associated with chronic rectal stricture. This condition is almost always a sequel to an earlier enteric infection, particularly salmonellosis, and further herd investigation was recommended.

Porcine circovirus 2-associated disease (PCVAD) causing diarrhoea

Up to 30 per cent of a group of eight-week-old pigs developed diarrhoea to varying degrees. One malaised pig was euthanased and submitted to the RVC/AHVLA Surveillance centre for post mortem examination. The mesentery was very oedematous and the colon was filled with watery fluid. There were multi-focal areas of mucosal necrosis filled with diphtheritic material throughout the colon. These findings were suspicious of salmonellosis but no Salmonella spp. were isolated and histopathology identified involvement of PCVAD in the enteritis.

E. coli diarrhoea at weaning

Three live four-week old pigs were submitted to Thirsk to investigate sudden onset diarrhoea causing wasting and 3-5 per cent mortality in weaners on a 250 sow farrow to finish indoor unit. E coli (Abbotstown strain) was found in septicaemic distribution from all three pigs. Histopathology confirmed moderate enterocolitis attributable to the E. coli and also detected marked crypt hyperplasia and some villus atrophy and bridging. The villus atrophy was speculated to be due to a pre-weaning insult with coccidiosis and rotaviral enteritis being possibilities. Disease responded well to in-water antimicrobial treatment and, in the longer term, pre- and peri-weaning management is to be reviewed.

Enteritis of unknown aetiology in pigs with illthrift

Two thin nine-week-old piglets were submitted to Winchester with a history of poor growth since weaning at five-weeks of age. There was marked thickening of the mucosa of the ileum in both pigs suspicious of porcine intestinal adenomatosis (PIA). There was also impaction of the large intestine, caecum and rectum with pale yellow fibrous material. Histopathology confirmed a mild to moderate plasma lymphocytic and eosinophilic enteritis with proliferative mucoid colitis. However, no specific aetiology could be attributed to these changes and they were not typical of PIA. These piglets were bedded on straw with free access to feed and the cause of the large quantity of fibrous material throughout the digestive tract remains unclear.

Respiratory Diseases

Coughing and sudden deaths due to Glässer’s disease

Glässer’s disease was diagnosed in eight-week-old pigs as the cause of coughing, malaise and sudden deaths on an indoor nursery unit on which 50 of 800 growers had died since entry to the unit five weeks earlier. Three dead pigs were submitted in all of which there was significant fibrinous polyserositis and Haemophilus parasuis was isolated from a joint confirming the diagnosis; no viral involvement was detected at the time of submission.

Gastric ulceration contributing to mortality in pigs with PRRS

Finisher pigs were submitted to investigate sudden deaths of good pigs, pallor and coughing on a 1900 pig rearing unit. Twenty percent of pigs were coughing and showing poor response to antimicrobial treatment. There had been significant disease problems earlier in rear with meningitis and suspected Glässer’s disease and, by the time of submission, mortality was around 5 per cent. Four dead pigs were submitted, three of which had severe gastric ulceration, sufficiently severe in one pig to have been the cause of death. In the other pigs with gastric ulceration, the degree of anaemia would have exacerbated the clinical effects of reduced respiratory function due to necrotising pneumonia and focal pleurisy present. One pig also had a fibrinous polyarthritis. Pasteurella multocida was isolated from the lungs, likely secondary to the Porcine Reproductive Respiratory Syndrome virus (PRRSv) which was detected in the spleens. Interruption of the usual feeding pattern is a recognised risk factor for gastric ulceration and inappetance due to PRRS and the pneumonia it causes could have been involved in the ulceration observed in these pigs.

Concurrent infection with PRRSv and pandemic H1N1 2009 swine influenza

An increase in wasting, respiratory disease and mortality in four to six week old pigs prompted the submission of three pigs to Bury St Edmunds for investigation. There were severe and extensive pneumonias (EP-like scores of 45-50), pleurisy and pericarditis from which only Pasteurella multocida was isolated although findings were suggestive of Glässer’s disease. Significantly, dual infection with PRRSv and pandemic H1N1 2009 swine influenza was detected by PCR and was considered likely to be underlying the clinical problem.

PRRS and bacterial infections causing respiratory disease with increased mortality

A finishing unit of 1500 pigs submitted two pigs aged 14 and 17 weeks to Preston to investigate an increase in mortality to 7 per cent. Signs of respiratory illness affecting 60 per cent of the pigs developed within 3 weeks of arrival on the unit. The older pig had severe peritonitis, pleuritis and perihepatitis and Actinobacillus pleuropneumoniae was isolated from the lung. In the younger pig there was a subacute bronchointerstitial pneumonia, Pasteurella multocida was isolated from the lung and PRRS virus was detected. In this pig, there was a necrotising and suppurative bronchointerstitial pneumonia consistent with PRRSv and secondary bacterial infection.

Ampicillin resistant Actinobacillus pleuropneumoniae

Three pig carcases were examined at Thirsk to investigate high mortality in a fully slatted finisher shed on an indoor 250 sow farrow-to-finish unit. After moving to the finisher barn, ten of 350 pigs died in one week. A severe pleuropneumonia due to Actinobacillus pleuropneumoniae (APP) was diagnosed, with this organism grown in a septicaemic distribution from one pig. The APP isolate was resistant to apramycin, trimethoprim/sulphamethoxazole, ampicillin and tetracycline. Ampicillin resistance in APP has been detected by AHVLA in the past but is comparatively rare in England. It is of concern as penicillin/penicillin derivatives are the drugs of choice for the control of APP outbreaks. Plasmidencoded beta-lactamase production has been reported elsewhere in the world in APP and if the resistance in GB APP isolates is plasmid-encoded, the resistance gene could transfer to other coinfecting bacteria such as Pasteurella multocida and Haemophilus parasuis. Improving pig flow and ventilation and avoiding other predisposing factors such as viral disease and stresses are important in controlling disease due to APP and reducing reliance on antimicrobial treatment. Treatment with in-water amoxycillin had been attempted but did not result in the expected clinical response.

Systemic and Miscellaneous Diseases

Iron deficiency in indoor-born piglets on a smallholding and in weaned pigs

Iron deficiency was confirmed in two, three-week-old piglets presented for post mortem examination to Carmarthen. They were from a litter of 11 piglets on a smallholding that kept two sows indoors and farrowed on a concrete floor. The piglets were severely anaemic with watery blood, pale musculature and fluid accumulations in the thorax and abdomen. Both piglets had enlarged ‘flabby’ hearts, which is a feature of iron deficiency in piglets. Iron content of the liver for each piglet was just over 2900 µmol per kilogram dry matter (reference range 5000-120,000 µmol/kg DM). Advice was given on iron supplementation for piglets born indoors with no access to soil as a source of iron.

Examination of a 6 week old piglet from a 50-sow herd at Shrewsbury identified pallor, watery blood and poor body condition with the pig weighing only 4.2 kg. Analysis of the liver confirmed iron deficiency (1588 µmol/kg DM). The farmer reported intermittent problems with diarrhoea and illthrift in piglets.

PRRS underlying streptococcal disease

PRRS was believed to be underlying streptococcal disease with malaise and mortality in growing pigs on an indoor breeder-finisher unit. Pigs were reported to be ill for 48 hours with blue discolouration of the ears and showed poor response to antimicrobial treatment. Six deaths were reported from a group of 550 six-week-old pigs. Rearing pigs were vaccinated for PCV-2 and Mycoplasma hyopneumoniae. One pig was submitted with necrosis of the distal 2-3 cm on the ear pinnae and blotchy red discolouration of the skin of the ventral body. There was fibrin stranding and excess fluid in body cavities suggestive of a septicaemia. PRRSv was detected by PCR and Streptococcus suis 2 was detected in the meninges by FAT although the organism was not isolated, possibly due to antimicrobial treatment.

Thrombocytopenia in neonatal piglets

Figure 1: Piglet with skin haemorrhages associated with areas of trauma due to thrombocytopenia

Bury St Edmunds diagnosed a case of thrombocytopenia in neonatal pigs on an indoor breeder-finisher on which half of one litter in each of the previous three farrowing batches developed subcutaneous haemorrhages and half of these affected pigs then faded and died. The farmer had seen alloimmune thrombocytopenia purpura previously and considered these piglets to be clinically similar but was concerned because piglets showed signs within 24 hours of birth and one was from a gilt litter. Piglets were reported to be unaffected at birth, strong and sucking well. Two live piglets were submitted in good body condition born the previous day, one was bright and active, the other less active, both had subcutaneous haemorrhages distributed according to likely local skin trauma as illustrated in Figure 1 suggestive of a coagulopathy, with no other significant gross lesions. Haematology confirmed thrombocytopenia and anaemia. Further investigation revealed that the gilt had returned to service five to seven weeks after her initial service and was believed to have been pregnant, this duration of pregnancy would be sufficient from thrombocytes to have developed in the foetus and, as the same boar was used to serve the gilt, thrombocytopenia purpura was possible though unusual quite so soon after birth. Gammaglobulin concentrations indicated that both piglets had received good quantities of colostral antibody.

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