CASE NOTES


Possible haemonshosis in grazing camels (Camelus dromedarius)

FJA Neilson, District Veterinarian

Posted Flock & Herd August 2007

Background

I had just started working with the Tweed Lismore RLPB in December 2001 when within a couple of days I was asked to look at a recumbent young camel. Despite my protestations that I knew nothing about camels I was asked to examine this camel.

It was a 4month old female camel and as it was feeding on its mother I was more concerned about the mother attacking me. The camel had been recumbent for 2 days had what appeared to be a rapid heart rate (90/minute) with a normal temperature (38.40C). Samples confirmed anaemia as the PCV was 0.17L/L (racing camels race best at 0.27 - 0.33L/L) with hypoproteinaemia (48g/l compared with a normal of 54 - 75). The samples confirmed normal levels of Ca, P, Mg, Cu & Se. I suggested the likely cause of the recumbency was haemonchosis.

History

In December 2007 I was again contacted the camel lady as a referral from the local practitioner. Prior to my visit she emailed me a history of all the problems plus and including a huge list a substances that she was feeding to the camels. She was following a Pat Coleby diet for horses and goats.

A summary of the history indicated that the camels had difficulty gaining weight, recurrent diarrhoea, oedema of the pedestal and limbs, eating dirt, difficulty arising from a crouched position and at times looked anaemic. Skin problems were common and there seemed to be a history of swollen heads like big head in horses and shifting leg lameness. There was a history of fenbendazole and ivermectin anthelmintic usage.

Laboratory findings

Four camels named Nebo, Sheba, Solomon and Lawrence were examined. I found it difficult to estimate anaemia as the gums seemed to have a black pigment. Faecal eggs counts for the 4 camels were 400, 1600, 2360 and 6420epg and a larval differentiation on pooled samples revealed 42% Haemonchus and 58% Trichostrongylus. No stomach or liver fluke eggs were seen.

One of the camels was dosed with I think about 180mls of ivermectin liquid for sheep while I was present and the other 3 the next day. I explained that I thought it unlikely fenbendazole would be effective. The sheep dose rate is 2.5ml/10kg. If these camels weighed 500kg this dose is nearly 1.5 times the sheep dose. The camel lady was adamant that you had to give camels higher doses of anthelmintics. Faecal samples were collected 10 & 11 days later for a FECRT. All the FECs were zero indicating both worms were susceptible to ivermectin i.e. >95% reduction in the faecal egg count.

I began by trying to bleed the camels from the tail but quickly reverted to jugular bleeding. All 4 camels were anaemic with PCVs of 8, 14, 14 & 25%. As previously stated racing camels should have a PCV of at least 27%. As 'Surra' was suspected in a shipment of Indian camels that entered Australia in 1907 samples were checked and negative for Trypanosoma species including I presume Trypanosoma evansi.

The owner was feeding one tablespoon of copper sulphate per day per camel plus the camels had access to a lick containing copper. My memories of CuSO4 are that horses, which are less susceptible to copper poisoning, should only receive about 1/10th of a teaspoon per day. The serum copper levels were 9.9, 12, 17.8 and 18.2 mol/L with normal levels of 6 - 15 mol/L. This indicates copper poisoning.

It appeared to be at an early stage as all the liver function tests (GGT, GLDH & AST) were normal but bilirubin were elevated in 3 of the 4 camels with levels of 2.7, 3.8, 6.8 & 8.32 mol/L; normal levels are 0.1 - 3.2 mol/L. Bilirubin is derived from haemoglobin so presumably the excess copper was causing intravascular haemolysis.

The owner stopped copper sulphate supplementation at the time of my visit.

Serum protein levels were below normal in 2/4 camels and this was reflected in 3 of 4 camels having hypoalbuminaemia with levels of 17.9, 19.1 & 24.4g/l with normal levels from 25 - 45g/L. Internal parasites are the likely cause of this.

A number of analyses were requested to try and explain why the camels were eating dirt. Initially I thought the pica may have been associated with a deficiency of salt or phosphorus. The camels also had access to seaweed meal. The serum levels of P, Se, Mg, Na, K, Cl & the anion gap were normal but 3 of 4 samples had low serum calcium with levels of 1.62, 1.69 & 1.72 mol/L compared with normal levels of 1.9 - 2.7 mol/L. This is despite the fact that the camels were supplemented with dolomite.

The camels have access to good kikuyu and paspalum pasture. I recommended Kynofos supplementation as there is a suggested history of osteomalacia. Interestingly pica has been reported associated with osteomalacia.

Acknowledgements

As always, I am grateful for the advice and assistance from Graeme Fraser Veterinary Pathologist from DPI NSW Regional Veterinary Laboratory at Wollongbar.

 


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