AHVLA Pig Disease Surveillance Monthly Report: May 201324 September 2013
Among the highlights of this report are continuing salmonellosis in pigs post-weaning, swine influenza outbreaks (two influenza virus strains), pigs with PRRS exacerbated by earlier enteric disease and sudden deaths in finishers caused by Actinobacillus pleuropneumoniae.
Salmonellosis continues to cause diarrhoea and wasting in post-weaned pigs
Several outbreaks of salmonellosis were diagnosed at Bury St Edmunds in postweaned pigs and some typical examples are described below.
Salmonellosis was found to be the cause of diarrhoea and wasting in approximately 10 per cent of 800 eight-week-old housed growing pigs which had been treated with amoxicillin in-water for respiratory disease two weeks prior to signs of salmonellosis commencing.
This history resembles some previous submissions where a suspected predisposing factor for salmonellosis was treatment with an antimicrobial to which the salmonella isolated was resistant.
In this case, Salmonella Typhimurium phage type 32 was isolated.
Salmonellosis was also diagnosed in two pigs submitted to investigate mild coughing, uneven growth and diarrhoea in 45 of 930 six-week-old pigs from which 30 had died in the week prior to submission. On-farm post mortem examinations at the beginning of the problem revealed pigs with suspect Glässer’s disease (fibrinous polyserositis) and amoxicillin treatment was initiated. This gave a good initial response but pig deaths then reoccurred.
In both dead pigs submitted, there was diarrhoea with diphtheresis in the large intestine suggestive of salmonellosis, which was confirmed by isolation of a monophasic Salmonella Typhimurium-like organism (phage type U311). One of the pigs also had a generalised fibrinous polyserositis; Actinobacillus pleuropneumoniae was isolated from pericardium and Streptococcus suis type 1 from lung, rather than Haemophilus parasuis. Importantly, the Streptococcus suis type 1 isolate was found to be penicillin-resistant.
Penicillin resistance in S. suis is unusual in GB pigs; two clinical isolates were found to be resistant in recent years and this is the only other resistant clinical isolate identified by AHVLA since. The streptococcal disease was not considered the primary diagnosis in the pig, and disease attributable to Streptococcus suis was not reported to be persisting on the unit. However, the need to investigate any upsurge in disease on the unit was emphasised.
Another diagnosis of salmonellosis due to monophasic Salmonella Typhimurium-like organisms (phage type 193) was made when dead pigs were submitted from an indoor all-in all-out nursery-finisher unit on which approximately two per cent of 1,200 six-week-old pigs were affected with diarrhoea and 18 had died. The submitted pigs were dehydrated and two had necrotic typhlocolitis suspicious of salmonellosis, which was confirmed by isolation of the monophasic isolate.
Swine influenza diagnosed in weaners and finishers
Several outbreaks of swine influenza were diagnosed as the cause of respiratory disease in the early and late stages of rear, these are outlined below.
Concurrent swine influenza and salmonellosis due to Salmonella Typhimurium phage type U288 were diagnosed at Bury St Edmunds as the cause of mild coughing and ill-thrift of approximately two weeks duration with 15 per cent of pigs estimated to be affected and a few deaths.
The pigs had necrotic enterocolitis and were in poor body condition, most likely due to the salmonellosis with mild cranioventral pulmonary consolidation due to the swine influenza. PCR testing revealed the infecting influenza strain to be the pandemic H1N1 2009.
Nasal swabs were submitted to Bury St Edmunds from five and six-week-old pigs weaned in groups of approximately 150 into flatdecks and showing some sneezing without mortality from approximately four days post-weaning. Swine influenza virus was detected in one of the nasal swabs by PCR and H1N2 virus was isolated: this is one of the predominant strains circulating in GB pigs at present, the other being pandemic H1N1 2009.
Three dead 20-week-old finishers were submitted to Winchester to investigate severe respiratory disease and increased mortality. All three pigs showed severe respiratory tract pathology with bilateral fibrinous pleurisy and bronchopneumonia. Two of the pigs also had a severe fibrinous pericarditis.
Pasteurella multocida was isolated from the lungs and was likely to have contributed to the severity of clinical signs and mortality. However, disease was most likely initiated by swine influenza, which was detected by PCR and serology pointed to H1N2 as the infecting virus strain.
PRRS exacerbated in pigs disadavantaged by enteric disease prior to weaning
Live pigs were submitted to Bury St Edmunds to investigate disease occurring from five to six weeks of age in each batch of weaned pigs over the few months prior to submission, worsening in the most recent month. Approximately 25 per cent of each batch were affected with up to 15 per cent mortality with signs including respiratory disease, ill-thrift and malaise. Pigs were derived from PCV2-vaccinated sows and were vaccinated for Mycoplasma hyopneumoniae.
There was a variable degree of ill-thrift in the submitted pigs. In one pig, there was significant very poorly demarcated cranioventral pneumonia, consolidated lung was pale grey and the right lung was most affected (Figure 1).Pasteurella multocida and Trueperella pyogenes were isolated, PRRS virus was detected by PCR and a PRRS-associated pneumonia was confirmed by immunohistochemistry.
This illustrates the usefulness of full diagnostic investigation into respiratory disease as the appearance of the lungs did not alone indicate the cause, although the more diffuse nature of the pneumonia was somewhat suspicious of a viral cause.
In the other two pigs, gross lesions were limited to slight thickening of the large intestines. No enteropathogens were identified apart from a monophasic Salmonella Typhimurium phage type 193 by enrichment culture only; however, histopathology identified significant villus atrophy in the small intestines and a mild acute enteritis. The aetiology of the villus atrophy was not determined but coccidiosis or rotaviral infection earlier in rear were possible causes.
The three pigs submitted were chosen as being early in the course of disease and the findings indicate that a PRRS virus challenge was occurring early in the post-weaning period and that some pigs were being weaned already disadvantaged by an earlier enteric insult, exacerbating the clinical effects of the PRRS challenge. PRRSv vaccination of breeding sows and interventions in the farrowing houses including treatment for coccidiosis have greatly improved the clinical situation.
Actinobacillus pleuropneumoniae in finishers dying suddenly on two units
A finishing pig was submitted to Sutton Bonington from a 2,000-pig unit that had recorded six similar deaths and respiratory disease in the previous few weeks. There was a cranioventral pneumonia, with 40 per cent of the lung mass affected.
Areas of consolidation were detected in the caudal lobes with severe pleurisy and adhesions to thoracic pleura. Multiple bacterial pathogens were isolated including Actinobacillus pleuropneumoniae, Streptococcus suis type 2 and Pasteurella multocida. Advice was provided with regards to the potential trigger factors for respiratory disease with antimicrobial sensitivity tests assisting appropriate treatment.
Actinobacillus pleuropneumoniae (APP) was isolated from lungs submitted to Thirsk from a unit to investigate the cause of seven sudden deaths from about 2,000 16-week-old finishing pigs. The lungs had numerous firm raised well-demarcated dark-purple lesions throughout the lungs with overlying fibrinous pleuritis. These lesions were considered typical for APP which was isolated, confirming the diagnosis.
Porcine stress syndrome suspected in a pig dying suddenly
A five-month-old Landrace-cross fattening pig was found dead and submitted to Preston to investigate an ongoing problem with respiratory disease on the finishing unit. Approximately three per cent of the 1,800 finishers at this site had died and approximately 40 per cent were showing respiratory signs. The animals were vaccinated against Mycoplasma hypopneumoniae , PCV-2 and erysipelas. Post-mortem revealed very pale wet musculature, evidence of gastric, duodenal and cardiac haemorrhage and a single renal infarct with no evidence of respiratory disease. No significant bacteria were isolated.
Histopathology identified a moderate acute to subacute myonecrosis, slight multifocal myocardial necrosis, a mild to moderate interstitial nephritis and severe pulmonary oedema and congestion. The lesions within the skeletal muscle were non-specific and taken together with the gross changes were suggestive of either porcine stress syndrome or a nutritional myopathy.
Selenium levels in the liver were adequate while the vitamin E concentration was low although serum vitamin is preferable to assess vitamin E status.
Overall, porcine stress syndrome was considered the most likely diagnosis in this case which was not representative of the main clinical problem and swine influenza was subsequently diagnosed by PCR testing of respiratory tissues of another pig submitted.
Endocarditis in unvaccinated outdoor pig
A four-month-old pig was found dead and submitted to the RVC-AHVLA Surveillance Centre. The pig had shown lethargy four weeks earlier and had responded to treatment.
Lesions were consistent with heart failure with a marked serofibrinous pleural effusion, oedematous lungs, marked interstitial emphysema and diffuse lung haemorrhages. Large vegetative endocarditis lesions were found on the bicuspid valves explaining the heart failure.
Further investigation revealed that the outdoor pigs were not vaccinated against erysipelas and vaccination was strongly advised.
Erysipelas endocarditis in finisher pigs
One live 16-week-old finisher pig was submitted to Thirsk to investigate weight loss with some malaise in a group of 100 pigs on a 2,000 pig-place straw-based finisher unit. At the time, only 700 pigs were left on the unit, the rest had gone to slaughter. Usually the unit operates on a wean-to-finish basis but this time, pigs entered at 40kg.
The carcass had multifocal petechiation, marked fibrinous pericarditis and vegetative endocarditis of the mitral valve. Erysipelothrix rhusiopathiae was cultured from the valve lesion.
Subsequent on-farm post-mortem examinations identified more cases of endocarditis in the group. Further investigation revealed that the previous two batches of pigs on the farm had also suffered disease, which might retrospectively have been due to erysipelas. It is not clear why this particular unit should have a higher-than-expected incidence of erysipelas but interventions such as improved hygiene, vaccination or strategic medication are being considered for the next batch.
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