A staggering syndrome with deaths occurred in a flock of cross-bred ewes and lambs on the western edge of the Warrumbungle Mountains near Tooraweenah NSW. The sheep were grazing a lucerne paddock which also contained dry mustard weed and quinine trees. The pasture conditions were dry up until late December. After the December rains, weeds of cultivation emerged including Tribulus micrococcus spp and marshmallow plants.
The ewes had lambed in September 2009, the lambs were marked on 22nd October 2009. The ewes had been drenched with ivermectin.
The first signs of staggering were noticed by the owner in November 2009. The first deaths occurred in December during very hot weather; the sheep’s condition progressed until they were unable to rise and later died. The lambs were affected earlier and in greater numbers than the ewes.
FIRST PROPERTY VISIT – 14TH JANUARY 2010
11 lambs and 1 ewe were yarded. Each showed varying degrees of hindlimb ataxia, progressing to both forelimb and hindlimb paresis and inability to rise.
• Progressive ataxia of hind limbs; knuckling of fetlocks and some lambs appeared to 'bunny hop'.
• More severely affected lambs also had forelimb involvement, could not support their own weight and fell forward or threw themselves forward. These lambs also had muscle tremors and calluses on their carpi.
• When disturbed they became distressed, panted and were tachycardic.
• They lay down and panted after walking short distances.
• Muscle tremors were evident after movement or stress.
• When sitting down, they appeared alert and would nibble at grass.
• One severely affected lamb was pyrexic (41.2°C), had no proprioception, had pain sensation and was able to move its limbs in response to stimuli. It appeared bright, alert and responsive, with no evidence of cranial nerve involvement.
A moribund lamb was euthanased. There were no gross abnormalities however there was generalised pallor of the carcass and Haemonchus worms were found in the abomasum. A second moribund lamb was euthanased and necropsied a week later. Myocardium was flabby and thin walled. The semimembranosis, semitendinosis, neck and dorsal anterior thoracic muscles were pale pink.
Histopathology in both cases revealed moderate, diffuse Wallerian (axonal) degeneration in the spinal cord and cerebellum.
Biochemistry from the first lamb showed elevated creatinine kinase and selenium, azotaemia and abnormally low copper and vitamin E levels. Subcapsular microabscesses were found in the liver .
The second lamb biochemistry showed elevated liver enzymes, suggestive of hepatic damage, azotaemia and low copper levels 1.2 umol/L ( 7.5-20 umol/L). Vitamin E levels were normal. Histopathology revealed liver and kidney changes consistent with a cholangiohepatopathy and subacute non-suppurative interstitial nephritis respectively.
Cu levels in ewes & lambs January 2010
Markedly low blood levels in clinically affected ewe and lambs: range 0.9 – 1.8 umol /L Normal (7.5 – 20) umol/L
2 ex 5 sampled had marginally low Vitamin E = 2 umol/L Normal (>2.3umol/L) range 2-5umol/L
Cu levels ewes and lambs September 2010
The same group of ewes lambed for a second time in the same lucerne paddocks. Blood samples were taken from ewes and lambs at marking time in September. Blood copper levels were again low Lambs ranged 1.0 umol/L to 2.1umol/L. Ewes ranged from 1.6 – 2.3umol/L. At the time of sampling there was no clinical evidence of enzootic ataxia. The owner reported staggering in the younger group of these lambs 1 month later.
• Marshmallow staggers
• Tribulus staggers
• Vitamin E deficiency (some evidence of vitamin E deficiency in lambs tested in January 2010)
• Selenium deficiency
• Polyarthritis : chlamydia or erysipelas
Copper deficiency; causing enzootic ataxia.
One of the first reports of enzootic ataxia in NSW came from the Gulargambone area in 1920. This was reported to have occurred in 2 to 4 month old merino and merino x border Leicester lambs. Tooraweenah district is SE of Gulargambone, and lies in the foothills and plain extending west from the Warrumbungle Ranges. The Warrumbungle range was formed from the Warrumbungle volcano.
Copper deficiency develops due to a complex interplay of many different factors. The deficiency may be primary (i.e. due to a deficiency of copper in the soil) or secondary; which may develop due to many factors such as mineral interactions (as high levels of molybdenum and sulphur can interfere with absorption), decreased copper uptake by plants or increased demand for copper in the animal. Copper deficiency also manifests in certain groups of sheep due to variations in demand for copper, with pregnant, lactating and rapidly growing animals having the highest requirement, and can also vary with season, occurring most commonly in spring (Caple and McDonald, 1983; Radostits et al., 2000; Zachary, 2007).
In this case, the deficiency was determined to be primary, as soil tests revealed that copper levels were low; 0.38mg/kg and 0.43mg/kg in the two paddocks tested, with optimal levels being 0.5–5mg/kg.
The congenital form ‘swayback’, occurs when lambs are born to ewes that are copper deficient in the last two months of pregnancy. The lambs present with a staggering gait at or a few weeks after birth. Lesions are found in the cerebrum, brain stem and spinal cord.
In this case, the lambs were approximately two to three months old when ataxia was first noticed. Lesions were found in the cerebellum and spinal cord. Lambs were determined to have low blood copper levels one month prior to clinical signs developing. Signs of enzootic ataxia can be delayed until six months of age (Zachary, 2007). Some of the ewes developed an ataxia, leading to paralysis and death. Other signs of copper deficiency were not observed in the ewes (Caple and McDonald, 1983; Radostits et al., 2000).
There are a number of treatment options for primary copper deficiency in sheep. These include commercially available injections for cattle (off label use in sheep) and drenches for individual animals, as well as copper-containing salt licks and blocks. The use of copper-containing fertilisers for long-term prevention has been used in the past. Copper deficiency in cattle and sheep is usually managed by treating the animal. Copper toxicity may result with any administration method if the copper status of the animals has not been determined. Pre- existing liver damage would predispose sheep to copper toxicity. Additionally, care must be taken with copper injections as improper administration can lead to abscessation (Caple and McDonald, 1983).