CASE NOTES
VERTEBRAL ABSCESSES CAUSING HIND LIMB PARESIS IN LAMBS
Bruce Watt, Tablelands Livestock Health and Pest Authority
Posted Flock & Herd October 2010
Introduction
Vertebral osteomyelitis causing hind limb paresis is occasionally encountered in lambs and it is generally assumed to be an ascending infection post tail docking and/or mulesing. However, vertebral osteomyelitis of haematogenous origin is recorded in other livestock species.
History
A producer running about 300 Merino ewes called because one of 61 Merino lambs and one of 71 crossbred lambs from separate mobs developed hind limb paresis three days previously. In conversation with a neighbour, she found that they also had lost about four weaned lambs recently and had other showing the same symptoms. The lambs from the first property were September-October drop and were marked in early December. The lambs were also vaccinated with 5:1 and the Merino portion was mulesed and vaccinated with Gudair. They were not yet weaned.
The lambs from the second property were from a mob of 1500 August-September drop Merino lambs that were marked and mulesed in late September when they were also vaccinated with 5-in-1, Scabigard and Gudair. At weaning at the end of November, the lambs were drenched with Cydectin LA and treated with Clik. The owners only found one lamb with hind limb paresis although another four had died recently.
Clinical examination
The two lambs from property 1, examined on 21 January 2009, were bright and alert and in fat score 2.0 and were both weak in the hindquarters. They both appeared to have normal forelimb strength and could stand and walk if assisted to their feet. The lamb from property 2, shown below and also examined on 21 January 2009, was paralysed in the hindquarters but could bear weight on the front legs. Pain perception or patella reflexes were not assessed.
The owner of the lambs on property 1 chose to attempt antibiotic treatment on her two lambs while the owner of the lamb from property 2 elected for euthanasia and post-mortem.
Affected lamb from property 2 showing hind limb paralysis with normal strength in the forelimbs
Post-mortem findings
The only abnormality detected in the affected lamb from property 2 was a fluctuant swelling including and bulging below the tenth thoracic vertebrae. When incised this swelling exuded thin yellow pus as shown below. When this vertebrae was cut longitudinally, purulent osteomyelitis of the vertebrae with bone lysis was apparent. Culture of the exudate was considered unjustified.
Pus draining from vertebral abscess with osteomyelitis
Osteomyelitis with bone lysis and a presumed pathological fracture
Discussion
Vertebral osteomyelitis in sheep is usually assumed to be due to an ascending infection post-tail docking (or mulesing). However vertebral osteomyelitis in young calves (presumably subsequent to surgical or husbandry procedures) most commonly occur in the thoracolumbar vertebrae and is presumed to be haematogenous in origin (Radostits, et al. 2007). Vertebral osteomyelitis is also reported to be a common cause of sudden onset hind limb paralysis in kids a few months of age (Thompson, 2003). Again, the infection is presumed to be secondary to a neonatal bacteraemia with E coli, Streptococcus and Fusobacterium necrophorum most commonly implicated. As with kids and calves, paresis or paralysis can develop slowly as the abscess compressed the cord or rapidly as bone destruction eventually causes a pathological fracture. In my experience, this case is unusual for sheep in that the lesion is in the thoracic vertebrae making an ascending infection less likely. While the lambs from property 1 were not proven to have vertebral osteomyelitis, the similarity of their symptoms and their proximity is striking.
References
- Radostits OM, Gay CC, Hinchcliff KW and Constable PD (2007) Veterinary Medicine, 10th Edition, p 616
- Thompson, K (2003) Chapter 12 Goats, in Gross Pathology of Ruminants, Proc No 350 of Post-Graduate Foundation, Elizabeth Macarthur Agricultural Institute, Camden NSW, 9-11 April 2003, p 269