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Why is phosphorus important?

Phosphorus is found in all animal tissues and fluids and is involved in many body functions such as energy transfer reactions. Therefore, it affects every activity in the body, including growth and reproduction.

When should phosphorus be fed?
Phosphorus requirements are related to the animal’s intake of protein and energy. When energy and protein intakes are high and allow rapid growth and production (milk and reproduction), (i.e. during the wet season) the need for phosphorus is also markedly increased. In phosphorus deficient areas it is during this period, the wet season, that phosphorus deficiency is most evident and when additional phosphorus (supplements) is most needed.

Phosphorus is less important in the dry season as protein and energy are more likely to be limiting so intakes will be low and therefore the requirement for phosphorus is also low. Animals will show little if any response to phosphorus supplements during this period. There is even evidence that animal performance can be reduced if phosphorus is fed at high levels when nitrogen is deficient.

How much phosphorus do cattle and sheep require?
Cattle require 5 – 10grams/head/day, depending on the severity of the deficiency. Intakes should be at the lower end of the scale during the dry season and at the higher end of the scale during the wet season.

Sheep have a lower requirement for phosphorus as they efficiently utilize phosphorus because they recycle a large proportion of phosphorus, hence deficiency is not commonly seen.

Symptoms of Phosphorus Deficiencies

• Depraved appetite – animals chew bones, twigs, bark and other strange objects. Bone chewing can also be a habit and be present even if phosphorus is not deficient.
• Poor growth rates – research results indicate 10 -20% reduction in growth rates
• Low reproductive rates – calving rates can be reduced by up to 40% on acutely (severely) deficient country.
• Peg leg – Stiff, proppy gait and arched back.
• Rough, coarse coats and cattle in poor condition, especially lactating breeders. Soft, weak bones.

Ruminants: Vitamin D

Deficiency

Rickets, the primary vitamin D deficiency disease, is a skeletal disorder of young, growing animals generally characterized by decreased concentration of calcium and phosphorus in the organic matrices of cartilage and bone. Vitamin D deficiency results in clinical signs similar to those produced by deficiency of calcium and (or) phosphorus, because all three nutrients are required for proper bone formation. In the adult animal, osteomalacia is the counterpart of rickets. Cartilage growth in the adult has ceased, and thus this condition is characterized by a decreased concentration of calcium and phosphorus in the bone matrix (demineralization). Symptoms of rickets include the following skeletal changes, varying somewhat with species depending on anatomy and severity: (1) weakened long bones, resulting in curvature and deformation; (2) enlarged, painful hock and knee joints; (3) general stiffness of gait, arched back and a tendency to drag hind legs; and (4) beaded ribs and deformed thorax. With osteomalacia, in adults, the progressive demineralization of bones eventually results in fractures and breaks. The disturbance of calcium and phosphorus metabolism produces other symptoms such as reduced performance, hypocalcemia and reproductive failure. Although there appear to be differences among species in the susceptibility of different bones to degenerative changes, as well as differences that probably reflect body conformation (e.g., pigs compared with sheep), there is nevertheless an apparent common pattern in vitamin D deficiency (Maynard et al., 1979). The spongy and cartilaginous parts of individual bones (mainly the bone ends or epiphysis) and bones relatively rich in this tissue, such as the ribcage, are generally the first and most severely affected. As in simple calcium deficiency, the vertebrae and the skull have the greatest degree of demineralization followed by, the scapula, sternum and ribs. The most resistant bones are the metatarsals and shafts of long bones, which would have obvious survival value to the animal. Other clinical signs of vitamin D deficiency in ruminants are decreased appetite and growth rate, digestive disturbances, stiffness of gait, labored breathing, irritability, weakness and occasionally tetany and convulsions. These symptoms may precede the skeletal symptoms (i.e., enlargement of joints, slight arching of the back, bowing of legs, with erosion of joint surface causing difficulty in locomotion) (NRC, 1996). There can be an increase in the birth of dead, weak or deformed calves and lambs. Grazing animals that have normal exposure to direct sunlight are normally protected from vitamin D deficiency. However, under most conditions of commercial livestock production, where animals have limited exposure to direct sunlight and where rates of growth or milk production are high, dietary supplementation with vitamin D is prudent and recommended.

A. Vitamin D Deficiency in Cattle

Vitamin D should be supplied to growing and lactating cattle housed in confinement or with limited sun exposure. In more northern latitudes during winter months, photochemical conversion of provitamin D to its active compound (cholecalciferol) in the skin can be limited because of insufficient ultraviolet radiation. Hidiroglou et al. (1979) reported that 25-(OH)D was higher in plasma of cattle in summer than in winter. Richter et al. (1990) found higher concentrations of 25-(OH)D in blood plasma when bulls were kept outdoors as compared to indoors: 21.1 vs. 14.3 ng per ml, respectively. The normal range of plasma 25-(OH)D in cattle is 20 to 50 ng/ml, and therefore even the bulls exposed to direct sunlight in this experiment appeared to have marginal vitamin D status. Similar relationships have been observed in human populations (Romagnoli et al., 1999), where plasma 25-(OH)D was significantly higher in summer than in winter. During winter 15% of young adults, 32% of postmenopausal women and 71-82% of hospital inpatients exhibited vitamin D deficiency based on plasma levels of 25-(OH)D. Clinical signs of vitamin D deficiency in calves involving the skeleton begin with thickening and swelling of the metacarpal or metatarsal bones (Illus. 1 and 2). As the disease progresses, the forelegs bend forward or sideways. In severe or prolonged vitamin D deficiency, the force exerted by normal muscle tension results in bending and twisting of long bones and the characteristic bone deformity. There is enlargement of bone ends (epiphyses) from deposition of excess cartilage, giving the characteristic “beading” effect along the sternum at the point of attachment of the ribs (NRC, 1996; 1989).

In calves, the mandible becomes thick and soft, and in the worst cases, calves have difficulty eating. In calves so affected, there can be slobbering, inability to close the mouth and protrusion of the tongue (Craig and Davis, 1943). Joints (particularly the knee and hock) become swollen and stiff, the pastern straight and the back arched. In severe cases, synovial fluid accumulates in the joints (NRC, 1989). Posterior paralysis may also occur as the result of fractured vertebrae. The structural weakness of the bones appears to be related to poor mineralization. The advanced stages of the disease are marked by stiffness of gait, dragging of the hind legs, irritability, tetany, labored and rapid breathing, weakness, anorexia and cessation of growth. Calves born to vitamin D-deficient dams may be born dead, weak or deformed (Rupel et al., 1933). In older animals with vitamin D deficiency (osteomalacia), bones become weak and fracture easily, and posterior paralysis may accompany vertebral fractures. For dairy cattle, milk production may be decreased and estrus inhibited by inadequate vitamin D (NRC, 1989). Cows fed a vitamin D-deficient diet and kept out of direct sunlight showed definite signs of vitamin D deficiency within six to 10 months (Wallis, 1944). Functions that deplete vitamin D are high milk production and advancing pregnancy, especially during the last few months before calving. The visible signs of vitamin D deficiency in dairy cows are similar to those of rickets in calves. The animal begins to show stiffness in her limbs and joints, which makes it difficult to walk, lie down and get up. The knees, hocks, and other joints become swollen, tender and stiff. The knees often spring forward, the posterior joints straighten, and the animal is tilted forward on her toes. The hair coat becomes coarse and rough and there is an overall appearance of unthriftiness (Wallis, 1944). As the deficiency advances, the spine and back often become stiff, arched and humped. In deficient herds, calving rates are lower, and calves can be born dead or weak. Hypocalcemia, either milk fever (parturient hypocalcemia) or unexplained lactational hypocalcemia and paresis, may also be observed as a result of chronic vitamin D deficiency in dairy cattle. These signs are also produced by calcium, phosphorus or electrolyte deficiency or imbalances and are therefore not specific to vitamin D deficiency. 1. Milk Fever in Dairy Cattle (Parturient Paresis) Milk fever (parturient paresis) is a metabolic disease characterized by hypocalcemia at or near parturition in dairy cows. Goff et al. (1991b) and Horst et al. (1994) discussed milk fever and calcium metabolism of dairy cattle in detail. In essence, milk fever is a failure of calcium homeostasis in the face of increased metabolic demand for calcium. Causative and risk factors are partly, but not completely, understood (Enevoldsen, 1993; Horst et al., 1994; Liesegang et al., 1998). Milk fever is related to factors such as (a) previous calcium and phosphorus intakes, (b) previous vitamin D intake, (c) previous intakes and dietary ratios of potassium, chloride, magnesium, sulfur and sodium, and (d) age and breed of cow. Cows that develop milk fever are unable to meet the sudden demand for calcium brought about by the initiation of lactation. Milk fever usually occurs within 72 hours after parturition and is manifested by circulatory collapse, generalized paresis, depression and eventually coma and death. The most obvious and consistent clinical sign is acute hypocalcemia in which serum calcium decreases from a normal 8 to 10 mg % to 3 to 7 mg % (average 5 mg %). Initially a cow may exhibit some unsteadiness of gait. More commonly, the cow is observed lying on her sternum with her head turned sharply toward her flank in a characteristic posture. The eyes are dull and staring, and the pupils fixed and dilated. If treatment is delayed, paresis will progress into coma, which becomes progressively deeper, leading to death. Treatment with intravenous calcium boro-gluconate is an extremely effective treatment. Some cows will relapse, sometimes with multiple episodes of paresis that indicate a severe failure of the calcium regulatory system or in some cases, severe depletion of body calcium stores. Oral calcium pastes and gels are also used both prophylactically and as an adjunct to intravenous calcium treatment. Aged cows are at the greatest risk of developing milk fever. Heifers rarely develop milk fever, which is borne out by their superior calcium status at parturition (Shappell et al., 1987). Jersey cattle are generally more susceptible than Holsteins. Older animals have a decreased response to dietary calcium stress due to both decreased production of 1,25-(OH)D and a decreased responsiveness to the 1,25-(OH)2D. In older cows, fewer osteoclasts exist to respond to hormonal stimulation, which delays the bone contribution of calcium to the plasma calcium pool (Goff et al., 1989, 1991b). The aging process is also associated with reduced renal 1-alpha-hydroxylase response to hypocalcemia, therefore, reducing the amount of 1,25-(OH)2D produced from 25-(OH)D (Goff et al., 1991b; Horst et al., 1994). Tissue receptors for 1,25-(OH)2D decline at parturition (Goff et al., 1995), although there was not a significant difference between paretic and nonparetic cows. Osteoblast activity also appears to be decreased during late pregnancy and around parturition (Naito et al., 1990). This may be related to the reduced plasma calcitonin concentrations around parturition and especially in hypocalcemic, aged cows (Shappell et al., 1987). Low magnesium status is also a risk factor for parturient hypocalcemia as well as hypomagnesemia (Van de Braak et al., 1987; Van Mosel et al., 1991). Infection with the common brown stomach worm (Ostertagia) has been strongly implicated as a causative agent of milk fever and displaced abomasum in dairy cows (Axelsson, 1991), apparently due to an anaphylactic reaction at parturition. Parturient paresis can be prevented effectively by feeding a low-calcium and adequate-phosphorus diet for the last several weeks prepartum, followed by a high-calcium diet after calving (Horst et al., 1994). Feeding low-calcium diets prepartum is associated with increased plasma PTH and 1,25-(OH)2D concentrations during the peripartum period (Kichura et al., 1982; Green et al., 1981). Green et al. (1981) suggested that the increased PTH and 1,25-(OH)2D concentrations resulted in “prepared” and effective intestinal absorption and bone resorption of calcium at parturition that prevents parturient paresis. Phosphorus deficiency did not affect plasma concentrations of vitamin D3 or its 25-OH or 1,25-OH active metabolites, but did elevate plasma calcium and appeared to increase 1,25-(OH)2D3 receptor binding in the duodenum of phosphorus- depleted lactating goats (Schroder et al., 1990). Prepartal dietary cation-anion balance (DCAD) influences the degree and incidence of milk fever (Ender et al., 1971; Block, 1984; Gaynor et al., 1989; Oetzel et al., 1988; Enevoldsen, 1993). Dietary excess of cations, especially sodium and potassium, relative to anions, primarily chloride and sulfur, tends to induce milk fever, while anionic diets can prevent milk fever. The cation-anion balance of the diet affects acid-base status of the animal, with cationic diets producing a more alkaline state and anionic diets a more acid state of metabolism. Mild metabolic acidosis in turn promotes calcium mobilization and excretion (Lomba et al., 1978; Fredeen et al., 1988; Won et al., 1996). Anionic diets increase the amount of 1,25-(OH)2D produced per unit increase in parathyroid hormone (Goff et al. 1991a). Debate remains as to the mechanisms of action and the relative importance of individual mineral ions (Enevoldsen, 1993; Horst et al., 1994). Used correctly, anionic diets prepare the cow’s metabolism for a sudden demand for calcium at calving and reduce the incidence of subclinical hypocalcemia and paresis (Horst et al., 1994). Because most legumes and grasses are high in potassium, typical dry cow rations are alkaline. Addition of anions, usually as anionic salts, to the diet for two to four weeks prepartum has been used successfully to reduce the incidence of milk fever. Goff et al. (1991a) concluded that low calcium diets, anionic diets and PTH administration all increase renal 1-alpha hydroxylase activity, resulting in increased production of 1,25-(OH)2D and prevention of milk fever. Increased plasma 1,25-(OH)2D3 concentration in response to feeding acidified diets prepartum was reported by Phillippo et al. (1994). Supplemental vitamin D has been used to prevent parturient paresis in dairy cows for a number of years (Hibbs and Conrad, 1976, 1983; Littledike and Horst, 1982). Feeding or injecting massive doses of vitamin D has been an effective preventive of milk fever, but toxicity symptoms and death have occurred as well. In some cows, milk fever has been induced by the treatment. Due to the toxicity of vitamin D3 in pregnant cows and the low margin of safety between vitamin D3 doses that prevent milk fever and those that induce milk fever, Littledike and Horst (1982) concluded that injecting vitamin D3 prepartum is not a practical solution to milk fever. However, more recent reports from the same laboratory have provided data suggesting that injection of 24-F-1,25-(OH)2D (fluoridation at the 24 position) delivered at seven-day intervals prior to parturition can effectively reduce incidence of parturient paresis (Goff et al., 1988). Hodnett et al. (1992) used a combination of 25-(OH)D3 and 1-alpha-hydroxy D3 to reduce parturient paresis in dairy cows fed high dietary calcium. The incidence of the disease was reduced from 33% to 8%. Feeding high doses of vitamin D has been more successful than parental administration in preventing milk fever without inducing toxicity (Hibbs and Conrad, 1976). Feeding 20 million to 30 million IU of vitamin D2 for three to eight days prepartum prevented 80% of expected milk fever cases in aged, Jersey cows (Hibbs and Conrad, 1976). However, prolonging the treatment to 20 days prepartum has resulted in toxicity. The same authors fed cows 100,000 to 580,000 IU vitamin D2 per day on a continuous, year-round basis and reported a reduction in milk fever in cows with a history of the disease but not in cows without a history of milk fever. The most practical approach to controlling milk fever today appears to be through optimizing macro-mineral levels in the diet and providing continuous supplementation with vitamin D at normal levels.

B. Vitamin D Deficiency in Sheep and Goats

Clinical signs of vitamin D deficiency in sheep and goats are similar to those of cattle, including rickets in young animals and osteomalacia in adults (NRC, 1981; 1985) (Illus. 3). An early report of rickets in Scotland referred to the condition as “bent leg,” which occurred in ram lambs seven to 12 months of age (Elliot and Crichton, 1926). The condition was prevented by administration of small amounts of vitamin D in the form of cod liver oil. Newborn lambs can receive enough vitamin D from their dams to prevent early rickets if the ewes have adequate vitamin D status (Church and Pond, 1974). Newborn kids develop rickets if the doe is fed a diet deficient in vitamin D during pregnancy (NRC, 1981).

Vitamin D deficiency has been observed in young lambs or goat kids kept in complete confinement without access to sun-cured roughage. Hidiroglou et al. (1978) reported the clinical history of a flock of sheep kept in total confinement that showed a high incidence (8%) of an osteodystrophic condition which was vitamin D-responsive. A form of osteodystrophia has also been produced experimentally in goats (NRC, 1981). Parturient paresis occurs in ewes. It is a disturbance of calcium metabolism in pregnant and lactating ewes and is characterized by acute hypocalcemia and the rapid development of hyperexcitability, ataxia, paresis, coma and death. The disease occurs any time from five weeks before to 10 weeks after lambing, principally in overconditioned, older ewes at pasture. The onset is often triggered by abrupt changes in diet, sudden weather changes or periods of stress and fasting imposed by circumstances such as shearing or transportation. The extent of involvement of vitamin D in calcium metabolism in paretic ewes is unclear. Maternal calcium homeostasis is under stress in pregnant ewes (Paulson and Langman, 1990). Sheep differ from all other species studied thus far in that pregnancy does not result in an increase in circulating levels of 1,25-(OH)2D3 (Paulson and Langman, 1990). The signs (e.g., hyperexcitability) and conditions under which this disorder occur (lush pasture, stressful events) suggest that hypomagnesemia is also involved.

Cobalt/vitamin B12 deficiency – The disease

Cobalt is required by the rumen micro-organisms for the synthesis of vitamin B12. A lack of cobalt will therefore cause vitamin B12 deficiency in ruminants. Deficiency causes loss of appetite resulting in poor growth. The disease is therefore often referred to as a starvation or wasting disease even though the animals are usually grazing adequate feed.

Cobalt/vitamin B12 deficiency – Effects on the animal

Cobalt deficiency in soil and/or pasture leads to a lack of vitamin B12 in body tissues. vitamin B12 is essential in energy and protein metabolism.

Under deficient conditions, calves and lambs can thrive and grow normally until they deplete their vitamin B12 reserves in liver and other tissue. They will soon lose appetite and fail to grow. In severe cases anaemia, rapid weight loss and finally death will occur.

Pastures that are marginally cobalt deficient result in low vitamin B12 levels in the dam and can cause birth of weak lambs and calves among which the death rate can be high.

Even a marginal deficiency may cause poor production, particularly poor growth rates in young stock as they are most sensitive to vitamin B12 deficiency.

 

 

Cobalt/vitamin B12 deficiency – The signs

In severe cases, a watery discharge from the eyes may be seen and anaemia, rapid weight loss and finally death may follow this. In sheep, wool may appear white or washy with a reduced growth rate. In cattle, dull harsh coats may be seen. Commonly, impaired weight gain in lambs or calves will be the first sign of deficiency noted.

Cobalt/vitamin B12 deficiency – Lost production and reduced returns

Most animals do not show any outward sign of the disease unless there is a marked deficiency. The health and productivity of affected animals can, however, be severely affected with marked decreases in;

• growth rates in young stock,
• fertility and reproductive performance with more still births and early deaths,
• milk production, and
• fibre production.

Vitamin B12 deficiency affects profitability through production targets not being achieved and reduced returns.

 

Criteria to assess vitamin B12 status

Cobalt deficiency is best diagnosed by measuring serum and/or liver vitamin B12 concentrations.

To assist in determining the need for vitamin B12 supplementation the following criteria provide a guide.

		Serum		Liver
		(pmol/l)		(nmol/kg fresh tissue)
	Low	Marginal	Adequate	Low	Marginal	Adequate
Sheep	< 336	336 to 500	> 500	< 280	280 to 375	> 375
Cattle	< 75			< 75	75 to 220	> 220

Consult your veterinarian as to the response to vitamin B12 supplementation you could expect on your farm.

 

Preventing cobalt/vitamin B12 deficiency

Increasing cobalt intake by application of cobalt in the fertiliser can prevent cobalt deficiency in grazing animals although repeat applications may be required in a season making this a costly method.

The direct treatment of grazing animals with cobalt is difficult and labour intensive as large weekly or fortnightly oral doses are needed. Intraruminal cobalt bullets can be effective if they are not regurgitated or coated with ruminal contents.

Injecting vitamin B12 has been used for many years as a means of protection against Cobalt/vitamin B12 deficiency. While widely used, injections of vitamin B12 preparations at a rate of 0.05 to 0.1 mg vitamin B12/kg liveweight have been shown to only be effective for up to 4 to 6 weeks.

 

What is Colic?

The term “colic” means only “pain in the abdomen” or “pain in the belly”. There are many causes for such pain, ranging from the mild and inconsequential to the life-threatening or fatal. One of the problems with equine colic is that it can be very difficult in the early stages to distinguish the mild from the potentially fatal. This is why all cases of abdominal pain should be taken seriously right from the onset.

 

A tour of the gastro-intestinal tract

A guided tour of the horse’s gastro-intestinal tract (GIT or “guts”) helps to explain why there are so many forms of colic. The horse’s GIT is similar to that of most species but it has a number of specialised design features, some of which predispose it to colic. These are noted by an asterisk (*) below.

Once food has been chewed, it passes down the esophagus (“gullet”) into the stomach. The horse has a fairly small stomach for its size (8-15 litres), a design well suited to an animal which grazes almost continuously in its natural state. After a period of digestion in the stomach, food passes into the small intestine. This part of the gut is approximately 22 m in length, with a diameter of 7-10 cm, and a capacity of 40-50 litres. The majority of the small intestine hangs from a curtain-like membrane called the mesentery*. The messentery is attached to one point in the middle of the abdomen, under the spine. (The small intestine looks like a very long sausage running along the bottom of a thin net curtain, with the top of the curtain all bunched together.)

At the junction of the small and large intestines the equine GIT has a large blind-ended* outpouching over 1 m long with a capacity of 25-30 litres. This is the caecum (the horse’s version of our appendix). Food passes from the small intestine into the caecum before passing into the large intestine. Together, the caecum and large intestine form the horse’s “fermentation chamber”, allowing it to gain nutritional support from the complex carbohydrates contained in grasses and other forage. Three to 4 metres long with a diameter of 20-25 cm along most of its length and a capacity of over 50 litres, the large intestine fills a significant part of the abdomen.

Surprisingly, this large unwieldy structure is tethered to the body wall at only two points*: at its beginning (where it joins the small intestine and caecum) and at its end (where it joins the short, narrow* small colon which leads to the anus). With only two immobile points, the large intestine lies in the abdomen in a neatly-arranged double-U formation, one “U” stacked on top of the other. This arrangement entails the food making it round a number of 180 bends* (known as “flexures”) in the intestine.

Major types of colic

Impaction colic: This is the term used when the intestine becomes blocked by a firm mass of food. Impactions most commonly occur in the large intestine at one of the flexures. This is a fairly common type of colic which usually resolves relatively easily with appropriate treatment. However, an impaction may be just the first obvious sign in a more complicated case.

Gas colic: Sometimes gas builds up in the intestine, most commonly in the large intestine and/or caecum. The gas stretches the intestine, causing pain. Gas colics usually resolve fairly easily with appropriate treatment, although it is essential to ensure that there is no underlying reason for the problem.

Spasmodic colic: Some cases of colic are due to increased intestinal contractions, the abnormal spasms causing the intestines to contract painfully. These cases usually respond fairly well.

Displacement/volvulus/torsion (‘twisted gut”): In a “displacement”, a portion of the intestine has moved to an abnormal position in the abdomen. A “volvulvus” or “torsion” occurs when a piece of the intestine twists. The suspension of the small intestine from the mesentery (the “net curtain”) and the unfixed nature of much of the large intestine predispose horses to intestinal displacements and torsions. Except in rare cases, these types of colic cause a total blockage of the intestine and require immediate surgery if the horse is to survive. In the early stages of a displacement/torsion colic, the signs may be similar to those of a horse with one of the more benign causes of colic. That is why it is important to take all cases of colic seriously, and to seek veterinary advice at an early stage.

Enteritis/colitis: Some cases of abdominal pain are due to inflammation of the small (enteritis) or large (colitis) intestines. These are serious medical cases and require immediate veterinary attention.

Gastric distension/rupture: When a horse gorges itself on grain or, even more seriously, a substance which expands when dampened like dried beet pulp, the contents of the stomach can swell. The horse’s small stomach and its inability to vomit mean that in these circumstances the stomach may burst. Once this has happened death is inevitable. If you suspect that your horse may have gorged itself on concentrate feeds, seek veterinary advice immediately.

“Unknown”: In many cases of colic it is impossible to determine the reason for the pain. Symptomatic treatment, close monitoring and attention to any adverse developments usually lead to resolution of the problem.

Signs of Colic

The signs of colic in horses range from almost imperceptible in mild cases to extremely violent in severe cases. The following list includes the most common signs:

lying down more than usual
getting up and lying down repeatedly
standing stretched out
standing frequently as if to urinate
turning the head towards the flank
repeatedly curling the upper lip
pawing the ground
kicking at the abdomen
rolling

What to do

The severity of the case will dictate what you do when you find your horse showing signs of colic. If he is behaving violently call your veterinarian immediately. Violent behaviour usually equates with great pain which usually equates with a serious case of colic. Time is of the essence here. Not all horses show the same severity of signs with the same type of colic, though, and some horses may become quite violent with a relatively “mild” case. If the signs of pain are less extreme, you can take a few minutes to observe the horse’s appearance and behaviour before calling the veterinarian.

• If possible, take his temperature, pulse and respiration rates.
• Note what his appetite has been like in the past day or so, and the consistency and frequency of defecation.
• Has his water intake been normal?
• Are his gums a normal colour?
• Think about whether he has had access to any unusual feedstuffs in the past day or so, whether any medications have been administered, and whether there have been any changes in management.

Now call your veterinarian. It is important to take all food away from the horse until the veterinarian arrives. If he is nibbling at his bedding, find a way to prevent this. Walking the horse can be a useful way of distracting him from the pain, but he should not be walked to exhaustion. If the horse insists on rolling, there will be little you can do to prevent it. If possible, try to get the horse to an area where he will do himself the least damage when he rolls. But do not get hurt yourself. Do not administer any drugs until your veterinarian has seen the horse, or unless he/she tells you to do so.

Prevention of colic

If you happen to be a horse, colic is probably an unfortunate fact of life. Annual colic incidences of approximately 10% are quite common. Listed below are some of the management factors which are thought to reduce colic incidence. Horses which fall into high-risk categories, such as stabled horses in intense training and fit horses recently injured, should be monitored particularly closely.

allow as much turnout as possible
maintain a regular feeding schedule
ensure constant access to clean water
provide at least 60% of digestible energy from forage
do not feed excessive digestible energy
do not feed moldy hay or grain
feed hay and water before grain
provide access to forage for as much of the day as possible
do not over graze pastures
do not feed or water horses before they have cooled out
maintain a consistent exercise regime
make all changes in diet, exercise level and management slowly
control intestinal parasites and assess efficiency periodically.

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Author Janet Douglas earned her degree in Veterinary Medicine at the University of Cambridge, England. She continued her pursuit of excellence at the Equine Research Centre, Guelph, Ontario, where she focused on equine orthopaedics.

References:

Reeves, M.J. and Salman, M (1993). Risk factors for equine colic identified by means of a multicentered case-control study. Proc. Am. Assoc. Eq. Pract. 39 93.

White, N.A. (1994) Epidemiology of colic. Equine Research Centre’s Farm Management Proceedings. 48 Cohen, N.D., et al (1995). Case control study of the association between various management factors and development of colic in horses. J. Am. Vet. Med. Assoc. 206 (5) 667.

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The following information is taken from a study of a normal, healthy horse population in an effort to identify risk factors associated with colic. An understanding of risk factors can provide practical approaches to preventing colic.

The study, conducted by Dr. Nathaniel White II professor of surgery at Marion DuPont Scott Equine Medical Center in Virginia, profiles 1,443 horse from farms in Virginia and Maryland which had populations of 20 or more horses.

After monitoring the farms for a full year, 100 factors were analyzed to see if a pattern could be identified. The possible risk factors examined were based on the farm’s history, the age, sex and breed of the horse, its use, feeding, parasite burden, the weather, management routines and daily events.

 

Risk Factors Identified in Study	Lower Than Normal Risk	No Effect	Higher Than Normal Risk
sex, breed
crossbred (other than Thoroughbred)
foals, weanlings, yearlings
fed grain before hay at meals
horses in training for racing or eventing
school horses
horses confined to stall more than 12 hours/day

WRITTEN BY: The Equine Research Centre

f you’re not sure which horse wormer to use, check out the horse wormer comparison chart below.

This handy chart compares most Australian brands of horse wormers, including Equimax, Equest Plus Tape, Strategy-T,
Ammo Paste, Valumec, Valumax, Oximinth, Equimec Plus Tape, MecWorma, Equiban, Evolve & more.

Worms are internal parasites which are very common in cats. They may be divided into two types; the roundworm and the tapeworm. Your cat may have worms but not show any signs of a problem; however worms can occasionally cause debility, especially if they are present in large numbers. All cats should be wormed regularly to control these parasites.

Roundworms may be carried by a cat which shows no obvious sign of ill health. However they may sometimes be noticed in a pet’s vomit or in faeces. They are about 5-15 cm long, off-white in colour and are sometimes coiled. In kittens they can cause gastrointestinal problems; this most often manifests as vomiting and diarrhoea. In adult cats they do not seem to cause problems very often. Cats catch roundworms from other cats and infected animals will constantly re-infect themselves when they groom around their bottom and tail.

Tapeworms vary in length but can be up to 30 cm long. Usually the worm itself is not seen but the mobile tapeworm segments may be observed around the cat’s anal region or on its bedding. They are white in colour and look a bit like grains of rice about 1 cm in length. Tapeworms are not passed from one cat to another but are carried by fleas and small prey mammals such as mice. Therefore tapeworms do not tend to affect kittens but are more of a problem for the adult cat. Cats are especially at risk from tapeworms if they have fleas or they are regular hunters. Housecats kept free of fleas are less at risk from tapeworms. If an adult cat has tapeworms they may not cause any noticeable problems but sometimes they may cause irritation around the anus or diarrhoea.

Ideally your adult cat should be wormed regularly whether you see worms or not. There are a wide range of different products available. Wormers commonly come as tablets, powders or pastes, but there are newer spot-on products available as well. Different products control different worms; some products such as Drontal control roundworms and tapeworms, other products may control either roundworms or tapeworms or both; many of the spot-on preparations control fleas as well as worms. Remember that by controlling fleas you will also help to control tapeworms because they are the most common source of tapeworm infection for the cat. In many situations the spot on products are the easiest to use since it can be very difficult to get a cat to take any medication by mouth.

During pregnancy a cat should be wormed every two weeks in the final third of the gestation period, then after the birth until the kittens are weaned. Speak to your vet about products suitable for use during pregnancy. Kittens will often get roundworms from their mother so they should be wormed with a product such as Panacur from around 6 weeks of age. Treat them every 2 weeks until they are 12 weeks old then monthly until they are 6 months old. After this treat them as adults. If you see roundworms in a young kitten it would be advisable to see your vet as they may have a very heavy infestation. As adults, cats who hunt frequently or that often have fleas will need to be wormed more frequently than cats that spend most of their time indoors and don’t suffer from fleas; but as a rough guide the average cat should be wormed every three months. Ask your vet for a product suitable for your cat and worm at an interval suitable for your cat and the product you use.

Worms are internal parasites which may or may not cause debility or disease in dogs. Worming (or treating these parasites) is an important issue in the dog because Toxocara canis is a very common roundworm in these animals and it can be passed to humans, with possibly quite serious consequences. Dogs are affected by many other types of worm including tapeworms, hookworms, whipworms and heartworms.

The most common worms in dogs are the roundworm and the tapeworm. Roundworms are often about 10 cm long, an off white colour and may be coiled. They cause the most severe problems in young puppies: signs include abdominal distension. vomiting, diarrhoea and debility. In adult dogs they cause few problems but will form cysts in the muscles which are activated when a bitch is pregnant to infect new pups. The most common roundworm in dogs is Toxocara canis which is zoonotic and causes Toxocariasis in humans which may result in epilepsy or blindness.

Tapeworms may be up to 30 cm in length. The whole worm is not often seen but the tapeworm segments may be noticed around the anal area or on the bedding. These segments are white in colour and look like grains of rice about 1 cm in length. Tapeworms are passed to dogs by fleas or small prey mammals such as rabbits, they cannot be passed directly from one dog to another. Puppies are not often affected by tapeworms but they are a problem for adult dogs. They may sometimes cause irritation around the anus or diarrhoea in affected animals.

All dogs should be treated for worms regularly whether you see signs of them or not. This is especially important in households with young children who are at most risk of catching worms from their pet! Most dogs should be wormed every three months with a product which ideally treats both types of worm. Speak to your vet about the best product for your pet. Puppies are very likely to be infected with Toxocara when they are born because they have been infected as a foetus from their mum. About 70% of pups will be infected in this way or from their mother’s milk after birth. Worming is therefore essential in puppies and a suitable wormer should be given to puppies every 2 weeks from 4 weeks of age until they are 12 weeks old. After this they should be treated every month until they are 6 months old. They can then be treated every 3 months, the same as an adult dog. If you actually see the roundworms in a puppy then they may have a very severe infestation and it would be wise to seek a veterinary consultation. Pregnant bitches should be wormed with a suitable product to help prevent the transmission of worms to their pups. Speak to your vet about the most suitable product for your pet.

Due to the zoonotic potential of Toxocara and other zoonotic diseases found in dog excrement I believe it is every dog owner’s duty to worm their pet regularly and clean up their faeces when they are out on walks. This is especially important when the dog frequents areas also used by children. All children should be taught to wash their hands after handling a dog. Adults should obviously also take sensible hygienic precautions

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