On two occasions approximately six months apart merino wether lambs brought over long distances to a property within the Riverina Rural Lands Protection District suffered an epidemic of haemorrhagic enteritis. Attack rates were high and mortalities were 13.7% and 20.7%. Gross pathological changes were similar. No causative organism was identified although histology suggested that one incident was associated with bacteria and the other associated with coccidia.
On 19th November 2004 483 merino wether lambs were trucked from Hay to Deniliquin. On 24th and 25th November, they were vaccinated against Clostridia and jetted to prevent flystrike, mixed with another mob of lambs and run on irrigated lucerne. By 8th December an estimated 40% of the mob was scouring and 19 had died.
There was haemorrhagic enteritis, sometimes with clear demarcation at the pylorus and with particular involvement of the caecum and colon. The mucosa of the caecum and colon was thickened and haemorrhagic with frank blood in the lumen.
Microscopically there was severe diffuse vascular congestion, necrosis and ulceration of the mucosa associated with masses of rod-shaped bacteria, extensive submucosal oedema with fibrupurulent exudate and diffuse serosal oedema. A presumptive diagnosis of salmonellosis was made and the mob was treated with an injection of long-acting oxytetracycline.
The lambs from Hay were drafted from the other lambs in the paddock. These lambs were not treated and none of them were affected.
By 17th December the incident had passed with most of the mob grazing normally except for about 20 that had loose faeces and were not moving freely. Sixty eight of the original 483 in the mob died.
On 4th June 2005 579 merino wether lambs arrived at the property from Quilpie, Qld. They were in poor condition and were held near the yards and fed good quality clover hay. On 19th June 4 died. On 20th June an estimated 25% were tucked up and scouring and another 4 were dead. Gross pathology was identical to the earlier incident
The mob was treated with long-acting oxytetracycline and moved to a fresh paddock. Mortalities stopped on 30th June with 119 dead.
Microscopically the mucosa was haemorrhagic and necrotic with masses of coccidia in the epithelium. There was a profuse growth of Campylobacter jejuni and Clostridium perfringens from the caecum.
The similarities in the history, clinical course and pathology leave little doubt that these incidents were the same syndrome. The daily death rates are shown in Figure 1
At no stage were any of the discrete intestinal lesions usually associated with coccidiosis of lambs observed.
That plus the lack of coccidia in sections from the first incident suggest that the incidents were not a straightforward coccidiosis but a mixed infection. The profuse growth of Campylobacter and, to a lesser extent, Clostridia would also reinforce that assumption.
In both cases the owners of the properties of origin reported that they had seen no similar incident. This combines with the absence of spread to the in-contact lambs in the first incident indicates that the stress associated with the transport was a significant predisposing cause. The timing of each incident makes identification of the source of any infection problematical.
In both incidents the first deaths occurred 15 days arrival indicating that is probably the incubation period, but the rapid increase in the death rate hints of the likelihood that a substantial amount of infective material was available very soon after the lambs arrived on the property. For the second incident to be a result of the first, any infectious agent would have to survive for six months, including several months of a hot, dry summer.
In retrospect a combination of anticoccidial and antibacterial therapies may have been more effective.