CASE NOTES
Selenium deficiency in weaned Hereford calves
Bruce Watt, Tablelands Livestock Health and Pest Authority
Posted Flock & Herd March 2011
History
In April 2010, the owner of a mob of 120 August-September 2009 calves called because he noticed that a marked 'tail' had developed in both the weaned heifer and steer mobs. The affected calves, grazing on granite country in the Bathurst area, were lethargic, with diarrhoea, poor body condition and a rough hair coat. The calves had been yard weaned at the end of January 2010, treated with long acting moxidectin by injection into the base of the ear and vaccinated with 5 in1 clostridial vaccine. The dams of these calves had been vaccinated against pestivirus for the previous 2-3 years.
The owner had previously called the manufacturer of the moxidectin, believing that the product had failed to control internal parasites. A representative of the company visited the property and submitted faecal samples. These were negative for internal parasites and fluke.
The owner also commented that during weaning the yards became flooded as result of a broken pipe. Subsequently 5-6 calves developed foot abscess. In two of these, abscesses developed in the stifle region. An additional steer calf developed hind limb paresis and was subsequently euthanased when it became recumbent in a dam.
Two weeks after weaning, the heifers were run on a paddock of phalaris and cocksfoot while the steers were moved to another property and run on a paddock of abundant native and naturalised plant pasture.
CLINICAL EXAMINATION
The heifer portion of the mob was examined on 12 April 2010. Approximately 20% of the mob appeared lethargic, with diarrhoea, poor body condition and a rough hair coat. Blood samples were taken from three affected heifers.
The steer portion of the mob was examined on 21 April 2010. Again, a marked 'tail' was noted with 12 of 64 calves poorly grown with rough hair coats and diarrhoea.
Image 1: Selenium deficient weaner cattle
LABORATORY FINDINGS
Serology Results (heifer calves)
Three samples were reported as <30 for fluke ELISA indicating no evidence of exposure to liver fluke.
Biochemistry Results (heifer calves)
| SAMPLE | Ref | Value Units | 1 | 2 | 3 |
|---|---|---|---|---|---|
| GGT | 0-35 | U/L | 4 | 0 | 2 |
| GLDH | 0-30 | U/L | 12 | 9 | 8 |
| AST | 0-120 | U/L | 155 H | 92 | 94 |
| BIL | 0.0-24.0 | umol/L | 5.7 | 11.5 | 9.9 |
| CK | 0-300 | U/L | 277 | 412 H | 172 |
| PROTEIN | 60.0-85.0 | g/L | 61.8 | 68.9 | 65.1 |
| ALBUMIN | 25.0-38.0 | g/L | 26.7 | 34.8 | 28.2 |
| GLOB | 30.0-45.0 | g/L | 35.1 | 34.1 | 36.9 |
| ALB/GLOB | 0.7-1.1 | 0.8 | 1.0 | 0.8 | |
| GSH PX | 40-300 | U/gHb | 5 L | 10 L | 10 L |
| COPPER | 9.0-20.0 | umol/L | 17.1 | 17.9 | 18.8 |
| VIT.B12 | 130-500 | pmol/L | 220 | 282 | 170 |
Haematology Result (single heifer calf)
| PROT-RTS | 40-75 | g/L | 73 |
| FIBRIN. | 1-5 | g/L | 4 |
| PR/FI | 15-100 | 17 | |
| PCV | 20-50 | % | 33 |
| RBC | 5.00-12.0 | 10^12/L | 6.95 |
| HB | 6.0-15.0 | g/dL | 10.9 |
| MCV | 32-55 | fL | 47 |
| MCHC | 26-36 | g/dL | 33 |
| MCH | 10-17 | pg | 16 |
| WBC | 2.6-15.0 | 10^9 /L | 8.3 |
| BAND | N. 0.00-0.50 | 10^9 /L | 0.00 |
| NEUTRO. | 0.60-12.0 | 10^9 /L | 1.08 |
| BAND/N | 0.00-0.20 | 0.00 | |
| LYMPHO. | 0.50-11.0 | 10^9 /L | 7.14 |
| MONO. | 0.00-1.20 | 10^9 /L | 0.08 |
| EOSINO. | 0.00-0.70 | 10^9 /L | 0.00 |
| BASO. | 10^9/L | 0.00 |
Serology and Biochemistry Results (steer calves)
Samples were collected from three steers to confirm the liver fluke and selenium status of this mob. Fluke ELISA levels were all <30. GSHPx levels were again exceptionally low ranging from 3 to 5 units.
Discussion
Our surveys indicate that approximately half the cattle in the eastern tablelands are likely to have GSHPx levels indicative of selenium deficiency and yet most cattle appear to be healthy with normal growth rates. In the face of low GSHPx levels it is tempting to diagnose clinical selenium deficiency. The challenge is to support this diagnosis. I consider that a diagnosis of selenium deficiency is only warranted if the clinical signs are consistent with those reported for selenium deficiency, if laboratory findings and in particular low GSHPx levels support the diagnosis and if other causes of poor growth in weaned cattle in this district (under nutrition, gastrointestinal parasitism, cobalt or copper deficiency, chronic phalaris poisoning, liver fluke, pestivirus, chronic liver or kidney disease) have been eliminated.
In this case, I consider that a diagnosis of selenium deficiency is warranted because the most common alternate causes of ill thrift in young cattle were ruled out, GSHPx levels were exceptionally low and the owner considered that they responded to selenium treatment. Nonetheless, in the absence of a response trial (difficult to sell when these cattle urgently needed treatment) I am guarded about the diagnosis of primary selenium deficiency.