Article first published online: 10 JAN 2013
© 2013 Blackwell Publishing Ltd
Volume 18, Issue 1, pages 41–42, January/February 2013
How to Cite
White, M. (2013), Porcine self-assessment. Livestock, 18: 41–42. doi: 10.1111/j.2044-3870.2012.00176.x
- Issue published online: 10 JAN 2013
- Article first published online: 10 JAN 2013
A client who farrows 42 sows every three weeks indoors complains that a batch of pigs weaned onto flat decks two weeks previously are showing signs of running off and scouring. The pigs are weaned at an average of 26 days into washed, disinfected and dried rooms on plastic slats and fed high quality creep diets containing zinc oxide at therapeutic levels for the first two weeks after weaning. The problem began before the pigs came off these diets. Organic acids are also supplied through the water system. They are vaccinated for Mycoplasma and PCV2 prior to weaning and are PRRS free. Prior to cessation of meat juice testing, ZNCP salmonella prevalence had been running at less than 10% at slaughter.
On examination 18 days post weaning, the problem batch of 452 pigs was seen to contain approximately 40 with marked loss of condition and hairy coat some of which had pasty scour spread through all three rooms. Problems were reported to have started around 14 days post weaning and since then three had died after fading. An estimate of 5% of the total batch was scoured.
1. What is your preliminary differential diagnosis:
- a. Post weaning colibaccillosis
- b. Swine dysentery
- c. Ileitis
- d. Salmonella enteritis
- e. PMWS.
2. What would be your first approach to dealing with the problem:
- a. Introduce water medication on a suck and see basis
- b. Introduce feed medication on a suck and see basis
- c. Take rectal swabs and inject all pigs with enrofloxacin
- d. Take blood samples
- e. Sacrifice some affected pigs and subject to post mortem examination.
3. From these gross post mortem findings, how is your differential diagnosis altered:
- a. Salmonella remains the most likely
- b. It confirms E. coli enteritis
- c. Necrotic enteritis as a sequel to ileitis is most likely
- d. This is typical of PCV2 infection
- e. It has raised the spectre of classical swine fever.
4. What is your next step:
- a. Leave the farm and tell the client the pigs will recover without treatment.
- b. Take samples for bacteriology and fixed gut tissue for histopathology
- c. Inform the DVM of your findings.
- d. Medicate the room via water with apramycin and inject affected pigs with enrofloxacin.
- e. Double the organic acid level in the water.
5. Given the diagnosis and the fact that the problem had never been seen before, how can you explain its occurrence:
- a. Likely to have been introduced via feed
- b. Caught it off stockman
- c. Was present all the time but was triggered by management failure
- d. A new strain of Salmonella has recently been introduced into the farm
- e. Bird contamination was to blame.
6. Given the sensitivity pattern described, which of the following lists sets the priority for selecting treatment:
- a. Enrofloxacin, neomycin, ceftiofur, colistin, apramycin
- b. Apramycin, enrofloxacin, neomycin ceftiofur, colistin
- c. Colistin, apramycin, enrofloxacin, neomycin, ceftiofur
- d. Ceftiofur, colistin, apramycin, enrofloxacin, neomycin
- e. Neomycin ceftiofur, colistin, apramycin, enrofloxacin.
1. d. is the most likely, but e is possible if there has been a failure with vaccination. a would tend to occur sooner after weaning and b or c later.
2. e. Without a clearer diagnosis appropriate treatment cannot be selected. In-feed medication would be totally inappropriate in this instance. Blood sampling is of no value. The use of fluoroquinolone treatment without a clearer diagnosis is to be discouraged.
3. a. The gross findings are typical of those seen with necrotic enteritis, caused either by Salmonella or Lawsonia infection. These lesions take some time to develop and would represent extremely early infection with Lawsonia. Such lesions are not seen with E. coli or PCV2 infection and classical swine fever produces more ulcerative enteritis.
4. b. A definitive diagnosis is essential. It is now appropriate to introduce treatment but this must still be speculative. In the circumstances individual treatment with enrofloxacin can be supported, but it is not known at this stage what the cause is and its sensitivity pattern. Care of the use of apramycin in water in conjunction with organic acids is required. There is no reason to suspect notifiable disease that would necessitate notification of the DVM.
In this case histopathology confirmed enterobacteria associated necrotic enteritis; silver staining for Lawsonia was negative and Salmonella typhimurium DT109 was isolated from the gut wall. It was sensitive to apramycin, neomycin, ceftiofur, colistin and enrofloxacin.
5. d. Whilst replacement gilts came from the same supply breeding farm, gilts had been directed through a different grow out unit. Salmonella was later found in gilts on the day of delivery.
It is possible that low-level infection had been present all the time, but ZNCP scores suggest this is less likely.
6. b. Given the sensitivity pattern, from a therapeutic point of view any of the lists are valid. Apramycin, neomycin and colistin are only active in the gut given orally and are appropriate for whole batch medication. Enrofloxacin and ceftiofur are only available for injection.
Neomycin is only available by importation under a Special Import Certificate from the EU. Colistin, enrofloxacin and ceftiofur are considered ‘last resort’ treatments in human medicine and resistance within bacteria presents major problems. Responsible use in animals would suggest only using them with sensitivity testing support and not as a first choice if applicable.