CASE NOTES


WEANER SHEEP COLITIS OF UNCERTAIN AETIOLOGY: A CASE STUDY

Scott Ison, Murray Local Land Services, Deniliquin

Erika Bunker, NSW State Veterinary Diagnostic Laboratory, Menangle

Jim Walsh, Coopers Animal Health, Bendigo

Posted Flock & Herd April 2017

INTRODUCTION

Weaner colitis is a syndrome in sheep with many possible aetiological agents including Campylobacter spp., Coccidia spp., Yersinia spp., E coli, Salmonella spp., Cryptosporidium spp. and Rotavirus (Abbott & Maxwell 2002). Many of these pathogens also present a zoonotic risk to farm workers or cause food poisoning through the food chain (Bailey et.al 2003). This case report describes an investigation of seasonal weaner colitis in a self-replacing fine wool merino flock in southern NSW, carried out over two summers in early 2015 and 2016 with an apparent failure of, or resistance to, antibiotic treatment.

CASE REPORT/SERIES

History

The manager of a self-replacing merino flock near Holbrook, NSW, reported a syndrome that he described as sulphur responsive scours that did not respond to treatment in February 2015. 

Each year, August/September-born lambs are treated with an initial clostridial vaccination at marking. A booster and anthelmintic are given in November at weaning. Scouring in weaners has been observed to coincide with hot weather events in December and January annually. The manager has observed scouring in his weaners each year from 2005 to 2014 and successfully treated them by removing any affected animals and giving them three consecutive daily oral doses of sulfadimidine solution (6.6g CCD Sulfadimidine Sodium Soluble, CCD Animal Health). The first treatment failure was observed in December 2014 with lambs treated again in January 2015 and finally resolving after treatment in February 2015.

Clinical findings

Observations were made on a single visit in February 2015. The manager reported that there had been approximately 200 mortalities since weaning and of 1100 remaining weaners, 250 had been drafted off and treated for scouring. The other 850 weaners had been split on visual size and moved into different paddocks and were not showing clinical signs. The affected weaners were lethargic and in low body condition. Some had signs of chronic scour with dried dags on the breech while others only had fresh breech staining.

The flock was monitored more closely the following year. 500 wether and 484 ewe lambs were weaned on 27 November 2015. They were treated with clostridial vaccine including selenium (Tasvax 5in1 + Selenium Vaccine for Lambs, Coopers), anthelmintic (1.6mL Cydectin Long Acting Injection for Sheep, Virbac) and topical fly treatment (14mL CLIK Spray-on Sheep Blowfly Treatment, Novartis). The ewe lambs were also injected with campylobacter vaccine (Campyvax, Coopers) with a primer at marking and a booster at weaning. The ewes and wethers were run in separate paddocks with similar topography, dam water, phalaris-based pasture and supplementary barley. The manager noted that the ewes did not adjust well to barley supplementation while the wethers did. Qualitative visual assessment of phalaris pasture and supplementary barley was deemed sufficient for growth of these lambs.

Mild scours attributed to grain poisoning occurred in the ewe mob through December. Moderate clinical signs were observed in the wether mob on 19 January 2016 and the entire mob was treated with oral sulfadimidine (dosage as above). 103 were removed to a hospital paddock based on more severe clinical signs and these were treated daily for a total of 3 days. Moderate clinical signs were noticed in the ewe mob on 22 January and the whole mob was treated with oral sulfadimidine for three days. 28 ewe weaners were moved to the hospital mob. Clinical signs were suppressed in all 3 mobs but remained at a low level.

A veterinary visit was performed on 1 February for post mortem examination and sample collection. Approximately 20% of the ewe mob were observed with signs of fresh scouring and a further 10-20% were observed with signs of past scouring. The entire mob appeared to be ill thrifty and although there was not a defined tail to the mob, some of the lighter lambs were very lethargic. The wether mob was not examined as thoroughly but appeared to be affected similarly.

On 5 February 11 ewes and 5 wethers were moved to the hospital mob and treated with parenteral trimethoprim sulfonamide. On 19 February 25 wethers and 50 ewes were moved to the hospital mob and treated with long acting parenteral oxytetracycline. Weaners treated with the two injectable antibiotics responded similarly to treatment as the ones treated with oral sulfadimidine. Clinical signs improved throughout March and by early April 2016 the condition was fully resolved. The sheep from the hospital mob were moved back to their original mobs. A final count of 398 ewes and 365 wethers indicated a mortality rate of 18% (86/484) in the ewe mob and 27% (135/500) in the wether mob.

Post mortem findings

Three sheep were autopsied in February 2015. Temperatures of 40.3°C, 40.5°C and 40.5°C were recorded before euthanasia, however this might have been artificially elevated as the lambs were recumbent and exposed to full sun. Each had mild, erythematous inflammation of the jejunum, moderately enlarged mesenteric lymph nodes and watery faeces present in the colon. Mild oedema was observed in the perirenal area and the kidneys of one sheep.

The two sheep autopsied in February 2016 had similar findings, with perirenal oedema in the smaller lamb much more severe to the point where the perirenal fat had been replaced by a light yellow serous fluid.

Laboratory findings

In February 2015, a range of samples from two affected lambs were submitted to the EMAI for histopathology and bacterial culture. The morphological diagnosis for the intestinal lesions was mild multifocal erosive typhlocolitis with moderate multifocal crypt damage. Weaner colitis caused by campylobacter-like bacteria was suggested as a possible aetiological diagnosis. Routine bacterial culture of kidney and large intestinal contents were negative. Selective culture of lymph nodes for Campylobacter, Salmonella and Yersinia were also negative. Kidney histopathology revealed a moderate multifocal chronic lymphoplasmacytic interstitial nephritis with multifocal tubular degeneration and regeneration and intraluminal crystals, consistent with oxalate nephropathy. There was also a minimal multifocal acute neutrophilic hepatitis. Faecal egg count numbers were negligible.

A similar set of samples was submitted from two affected lambs in February 2016. Intestinal histopathology also revealed a colitis in one of these lambs which was mild, multifocal and neutrophilic, with inflammatory infiltrates in the lamina propria of the deep mucosa but no crypt damage as seen in the 2015 cases. Nephritis was more severe with a large number of intratubular crystals and a Pizzolato stain was performed to confirm that crystals were oxalates. There was also a mild acute suppurative hepatitis. Selective cultures on intestinal contents and lymph nodes were negative for Salmonella and Yersinia. Campylobacter selective culture of colon contents resulted in growth and isolation of campylobacter-like bacteria. These were submitted to 16sRNA sequencing PCR and found to be consistent with Campylobacter jejuni. Lawsonia PCR was negative.

Outcome

After campylobacter was suggested as a potentially significant pathogen within the flock in early 2015, a vaccination program of ewe lambs commenced in November 2015. The vaccinated ewe mob was monitored for a reduction in prevalence or severity of diarrhea but was not noticeably different to the unvaccinated wether mob based on clinical observations. The difference in mortality between the two mobs was attributed to other factors.

The flock was monitored again from weaning in November 2016 to February 2017. A similar colitis syndrome was observed in December and January and again appeared resistant to treatment with oral and parenteral antibiotics but resolved in February.

DISCUSSION

Weaner colitis in sheep was described by Stephens et.al. (1984) with Campylobacter-like bacteria isolated as the causative agent. Jopp and Orr (1980) described a similar syndrome which occurred each year on farms in New Zealand and was characterised by colitis and acute nephropathy. The authors later reviewed this case report and decided that the syndrome likely described disease processes which could be caused by a number of gastroenteric parasites and/or bacteria such as Campylobacter (Orr and Jopp 1989). The kidney lesions may have been caused by acute renal failure due to dehydration or other treatments.

The nephropathy in this case report was caused by calcium oxalate, as confirmed by the Pizzolato staining technique (Pizzolato 1964). Calcium oxalate was not reported in other cases of weaner colitis reviewed for this case report. Oxalate-rich plants are the most likely source of calcium oxalate but no known sources were identified on this farm. Oxalate producing fungi on contaminated feed are a rare cause (James 1972) and there were no signs of significant fungal growth observed in this case. Ruminants have a resistance to oxalate poisoning due to oxalate-degrading bacteria in the rumen (Rahman et.al. 2013). It is plausible that this mechanism has been compromised in these lambs with antibiotic treatments affecting rumen bacterial populations, making them more susceptible to low dietary oxalate levels. Interestingly, in humans, oxalate nephropathy has been associated with colitis; one proposed mechanism is that calcium is consumed by unabsorbed fat, so oxalate is absorbed instead of excreted as insoluble calcium bound complex (Canos et al, 1981); there is no evidence though that this can occur in ruminants. Sulfadiazine has been reported to cause crystal nephropathy (Yarlagadda & Perazella 2008) and is a similar antibiotic to sulfadimidine used in this case but would not be expected to produce oxalate crystals.

While Campylobacter jejuni was isolated from one clinically affected animal on this farm, its presence does not prove causation. It is the author’s opinion that the disease process is multifactorial and could be related to relative numbers of multiple species of pathogenic bacteria and low numbers of non-pathogenic bacteria. Antibiotic resistance also seems to be having a significant effect on this farm with treatments that were previously used on this farm no longer being effective.

As this farm predictably has a disease outbreak each year it is likely to be a good candidate for further monitoring and research.

REFERENCES

  1. Abbott KA, Maxwell WMC. Diseases of the alimentary tract. Sheep Health & Production. Accessed online February 2017: vein.vetsci.usyd.edu.au
  2. Bailey GD, Vanselow BA, Hornitzky MA, Hum SI, Eamens GJ, Gill PA, Walker KH, Cronin JP. A study of the foodborne pathogens: Campylobacter, Listeria and Yersinia, in faeces from slaughter-age cattle and sheep in Australia. Commun Dis Intell Q Rep 2003;27:249-257 
  3. Canos HJ, Hogg GA, Jeffery JR. Oxalate nephropathy due to gastrointestinal disorders Can Med Assoc J 1981;124:729-733
  4. James LF. Oxalate Toxicosis. Clin Toxicol 1972;5:231-243
  5. Jopp A, Orr MB. Enteropathy and nephropathy associated with winter scour in hoggets. N Z Vet J 1980;28:195
  6. Orr MB, Jopp A. Winter scours in sheep – an obsolete term. N Z Vet J 1989;37:38-39
  7. Pizzolato P. Histochemical recognition of calcium oxalate. J Histochem Cytochem 1964;12:333-336
  8. Rahman MM, Abdullah RB, Wan Khadijah WE. A review of oxalate poinsoning in domestic animals: tolerance and performance aspects. J Anim Physiol Anim Nutr (Berl) 2013;97:605-614
  9. Stephens LR, Browning JW, Slee KJ, Hayes J, Tzipori S. Colitis in sheep due to a Campylobacter-like bacterium. Aust Vet J 1984;61:183-187
  10. Yarlagadda SG, Perazella MA. Drug-induced crystal nephropathy: an update. Expert Opin Drug Saf 2008;7:147-158

 


Site contents and design Copyright 2006-17©