Ram Diseases

Ram Diseases (Pre and Post Sale)

As a consequence of high concentrate feeding often in preparation for sale, rams are prone to several conditions including urethral obstructions (calculi), copper poisoning and acidosis (grain overload, barley poisoning). All rams should be fully vaccinated against clostridial diseases.

Urolithiasis (partial or complete urethral obstruction)

·         This disease is not uncommon in intensively-reared rams. The disease is caused by a blockage of the narrow tube (urethra) connecting the bladder and the exterior, via the penis. Irreversible kidney damage can quickly result from excessive urinary back pressure; so early diagnosis is important.

·         The most common cause of urolithiasis is a crystal composed of magnesium ammonium phosphate hexahydrate (struvite), resulting from feeding concentrate rations high in phosphate (>0.6%), usually from grain based rations and magnesium (>0.2%) typically found in ewe rations. Calculi may lodge within the urethra at a level just above the scrotal/sigmoid flexure or within the vermiform appendix (“worm”) at the tip of the penis.

·         Early clinical signs of urinary tract obstruction include discomfort, teeth grinding and separation from the group. Also seen, is a wide stance and tail switching more than normal.

·         Affected sheep do not feed and there is frequent straining and teeth grinding. Only a few drops of blood-tinged urine are voided rather than a clear continuous flow of urine. Rupture of the urethra/penis may occur in neglected sheep after a few days, with resultant extensive swelling extending from the scrotum towards the prepuce.

·         Diagnosis requires prompt vet examination. The penis is extruded and the calculi can be felt within the vermiform appendix in most cases. Diagnosis confirmation follows excision of the vermiform appendix with production of free flow of urine once the ram stands.

·         To treat this disease, if excision of the vermiform appendix is not helpful, euthanasia is the more economic and sensible choice. As further surgery, requiring methods to correct the sigmoid flexure, leaves the ram unsuitable for breeding and is costly.

·         Prevention is achieved by feeding appropriately mineralised rations. Urine acidifiers, such as ammonium chloride (NH₄Cl) are commonly added to rations. Salt (NaCl) may be added to rations to promote water intake.

Copper Poisoning

As well as being susceptible to copper deficiency, sheep are also prone to copper accumulation and toxicity.

·         There is considerable breed variation with Texel and Suffolk two of the most susceptible breeds.

·         Chronic copper toxicity results from ingestion of relatively high levels of copper over a prolonged period. ‘Relatively high levels’ is used in this term because levels of molybdenum and sulphur exert considerable influences on copper availability.

·         During periods of high copper intake, the liver can store this copper up to a certain limit, after this limit is reached, the critical levels are exceeded resulting in the liver suddenly releasing massive amounts of copper into circulation; this will cause destruction of erythrocytes, jaundice and liver and kidney damage. This crisis may be encouraged by numerous stressors. The stressors are often: pregnancy, adverse weather, transportation, sale and housing. The adverse effects of chronic copper toxicity may occur some days to weeks after the removal of the copper source.

·         Care is needed when formulating ration for rams receiving high levels of concentrate feeding both before sale and after purchase.

·         Sheep with copper poisoning are weak, very dull and depressed and separate themselves. They have a poor appetite and often foetid diarrhoea. There is evidence of dehydration and obvious yellowing of the eyes.

·         Prevention/Control: when cattle and sheep are grazed together, this can be an important cause of disease in sheep. As cattle feed contains too much copper for the sheep to cope with.

Acidosis

·         This disease results from the sudden unaccustomed ingestion of large quantities of carbohydrate-rich feeds, typically grain or concentrates but may also occasionally result from a sudden change or interruption in feeding, usually following sale.

·         The severity of the disease depends on the amount of grain ingested, whether the grain is rolled or whole, and the rate of introduction of the dietary change. There may be no diarrhoea for the first 12 – 24 hours after carb ingestion, thereafter is profuse foetid diarrhoea which may contain whole grains. Affected sheep do not graze and spend long periods lying down.

·         Treatment: intravenous multivitamin injection and intramuscular penicillin to counter bacteria crossing the compromised gut wall. Diluted oral rehydration can be given by stomach tube.

·         Prevention/Control: grain or concentrate feeding must be done gradually over a minimum of two weeks. If all sheep are not coming to the feed troughs, the total allocated amount must be reduced accordingly. Good quality roughage must be available at all times.