Blocked Goats

Urolithiasis (Urinary Stones)
Wethers are at a high risk of urinary tract blockage due to “stones” (urinary calculi).  The most common types of stones are calcium phosphate and struvite (magnesium phosphate).  Mineral imbalances in feed are the most common inciting cause of stones and commonly occurs in diets that are rich in phosphorus and poor in calcium.  High grain and/or alfalfa diets are most often implicated in predisposing wethers to developing stones.  Calculi usually have the appearance of either sand or a BB (small, hard and smooth). The castrated male urethra is narrower than the urethra of females or intact males and stones have a tendency of lodging themselves in the vermiform appendage (at the very tip of the penis), the sigmoid flexure or the ischial arch (at the pelvis).
Clinical Signs
The blocked goat will be uncomfortable and will strain and act depressed. Often the presenting complaint is constipation. If observed carefully, the producer may notice frequent dribbling of small amounts of urine which may be blood tinged. If not sure if the goat is urinating, place in an unbedded, cement pen by himself for several hours. Prepucial hairs may have dried crystals on the end. If not noticed and blockage is total, the bladder ruptures in 24 to 36 hrs. After rupture, the abdomen swells with urine and the goat appears more depressed. He may live another few days before succumbing to the toxins in his system. Occasionally the urethra ruptures and the urine pools under the skin. This condition is called “water belly”.
In bucks, the penis can be exposed and the urethral process examined. Sand or stones, discoloration and swelling may be evident. A normal appearing process may mean the blockage is higher. In wethers, often the prepuce is adherent to the penis and it is difficult to expose the end. Veterinarians may “tap” the abdomen to detect urine in cases of suspected bladder rupture. Catheterization of the urethra is difficult and should only be attempted by a vet. It isn’t possible to catheterize into the bladder as there is a diverticulum at the pelvis that the catheter cannot get past.
If the blockage is at the urethral process, then it can be snipped off. If urine is voided after this “surgery” then the prognosis, while not good, has some hope. Oral therapy with ammonium chloride which dissolves the remaining stones is highly recommended. If the blockage is higher, then there are two options, both with major problems. A perineal urethrostomy, in which the penis is exposed and cut in its location below the rectum and the urethra exposed, often results in failure if the blockage is higher. In addition, even if immediately successful, it is a salvage procedure as the hole heals up in a few weeks and the goat re-blocks. Therefore it is not a suitable option for breeding bucks or pets. The second option is very expensive and few practitioners will undertake the surgery. The abdomen is opened and the bladder opened. A catheter is introduced from the bladder into the urethra and the stones flushed down the penis. If successful, all stones are removed and the buck is still capable of breeding. Often the stones are firmly lodged, there is tissue damage from the stones and recovery is very prolonged. Only valuable bucks or valued pets are recommended for this option.
As usual, this is a condition better prevented than treated. The diet should have a calcium:phosphorus ratio of 1.5 to 2:1. Salt should be included at 1% of total dry matter intake. Plenty of fresh, palatable water should always be available. Diets high in potassium should be avoided. Vitamin A requirements should be met (good quality green hay and pasture will do this). For herds with previous problems, it is sometimes recommended to include ammonium chloride in the ration at ½ % of dry matter intake. This is particularly true with kids on creep grain. Other diseases such as coccidiosis, pneumonia, etc. which might cause decreased water consumption or increased needs may spark an “outbreak” of urolithiasis so these diseases should be managed as well.
Dr. Paula I. Menzies – Ruminant Health Management Group, Ontario Canada

Copper Toxicity

How does chronic copper poisoning (CCP) occur?
Sheep are the domestic animal most prone to CCP. They absorb copper from the diet in proportion to the amount of copper offered, not to the body’s need as with the absorption of other minerals. Any excess absorbed copper is stored in the cells of the liver, eventually reaching toxic levels. Levels in the liver above 500 ppm dry weight are usually considered toxic. This storage in the liver can take months or even years to reach a toxic level. The elimination of copper from the body through the kidneys is slow.
Even then, it needs a stress to release the copper. This stress can be weather, poor nutrition, transportation or handling. The liver cells rupture, releasing copper into the blood stream. There are suggestions that excess liver copper can cause death and rupture of liver cells. Once the copper is in the blood stream in sufficient concentration, it causes haemolysis, a breakdown of the red blood cells (RBC). Up to 60% of the RBC’s circulating in the blood can be damaged. Their haemoglobin is released into the blood serum to be converted to methaemoglobin, a form of haemoglobin that cannot carry oxygen to the tissues. A sheep at this point is anemic, with very pale mucous membranes and lethargic. The visible membranes rapidly yellow as jaundice (icterus) sets in throughout the body. At post mortem all the tissues of a CCP sheep are pale to dark yellow. The kidneys are very dark, and the urine a bloody color. If the haemolysis is massive, sheep can die without showing any sign of jaundice.
Once the diagnosis is confirmed, the question is “how did it happen?” Often by mistake, extra copper was added to the feed at mixing; orphan lambs were fed calf creep feed which contains copper. Then there are the less obvious sources. One recent case in Ontario was through the sharing of a custom mineral mix on two operations. This mineral had been fortified with copper because of a diagnosis of swayback, copper deficiency, in newborn lambs on the original operation. A neighbor thought that such a mix would help his flock, and proceeded to order the same mix from the mill. Luckily, the sheep advisor spotted the extra copper on the mineral bag “tag”, and had the mineral mix withdrawn before any symptoms appeared. As the stored liver copper has to be removed, the concentrate pellets now contain extra molybdenum to slow the uptake of copper from the gut, and allow the elimination of the body’s excess copper.
The uptake of copper from the herbage is a complex interaction between the copper, molybdenum, sulfate, possibly other mineral and the herbage plants themselves. The normal level of copper in a plant is 10-20 ppm dry weight. If the molybdenum level is greater than 1 ppm, copper is not absorbed at toxic levels. High sulfate levels in the soil reduce the availability of molybdenum by tying it up as molybdenum sulfate. In a recent case where the diagnosis was CCP, the copper level in the herbage was 8 ppm but the molybdenum was only 0.5 ppm. Young growing plants tend to be lower in molybdenum than the mature.
In one reported case, the source of the high herbage copper was traced to the spraying of pig manure to fertilize a sheep pasture. The pig slurry contained 85 ppm copper, from the normal dietary copper levels in pig feed. Both the soil and the herbage had high copper levels, which translated to the unexplained death of a number of ewes over the seven years when this slurry had been used.
What should you do if you suspect CCP?
First, get the diagnosis confirmed by your local veterinarian or diagnostic laboratory. Look for all the obvious sources of copper. Analyze the copper levels in all prepared feeds; ask yourself if a feeding mistake has been made, especially in a mixed cattle sheep operation. Have the copper and molybdenum levels checked in your pasture plants and hays. Try to avoid spreading pig manure on sheep pastures or hay.
Usually, only a few animals die, but the survivors need immediate treatment. Getting molybdenum into them over an extended time will curtail the uptake of copper from the gut and allow the slow elimination of the body’s stored copper. Your veterinarian will be able to advise you on the dose and the preferred route of treatment for your flock. The RBC count soon returns to normal as new cells are produced in the bone marrow.
Finding the source of copper in a CCP case can often be a very frustrating and protracted investigation. Getting an accurate diagnosis, and starting treatment are the first essentials. Once the sheep are receiving extra molybdenum they are protected against excess copper absorption, then you can search for the source.
Dr. S. John Martin – Veterinary Scientist, Sheep, Goat and Swine/OMAF
N.B.  Sheep that have had sublethal copper poisoning will generally be very susceptible to further stresses and poisonings.  As Dr. George once said “Copper Toxicity Sheep are like ticking time bombs!”


   Infection with Eimeria (a type of Coccidial or gastrointestinal parasite related to Giardia) is one of the most economically important diseases of sheep. Historically, some Eimeria spp were thought to be infectious and transmissible between sheep and goats, but the parasites are now considered host-specific. Lambs and calves from 1-6 months old are most commonly infected and affected.  Older animals are often unaffected carriers and may serve as a source of infection for the young.

Clinical Signs may include bloody, mucusy diarrhea, fever, dehydration, inappetence, weight loss, anemia, and death.  Fly strike and secondary bacterial infections may accompany coccidiosis. Coccidiosis may be diagnosed through clinical signs and/or a fecal examination.

Treatment:  There are a number of sulfa based drugs that may be effective in treating a coccidial infection.  Please contact your veterinarian for more information.