While we try and keep our website as up to date as possible, sometimes prices change before this update can occur. Price can change without notice. If you have placed an order via our website we will try and honour that price, however if we do need to charge extra we will inform you via email and ask if you wish to proceed. If you decide to cancel the order, a full refund will be issued. If you wish to proceed then the diffeerence will then be invoiced and items will be shipped once payment has been made

Webstock Levels

Our Website is not a live site with our point of sale system, therefore some items may be out of stock at the time of purchasing due items being sold at our shop front. The website is updated 3 times a week to try and keep it as up to date as possible.

Customers can call us on 0353492661 for an update on stock if required.

Our new Melbourne metro Shipping is available to Melbourne Vic customers only. All orders over $59.00 will be shipped free of charge. Please note that this is a courier service so no PO Boxes are able to be used. Must be a physical address.

Normal Delivery times will be 3 – 5 business days for this service.

Our new Ballarat Shipping is available to Ballarat Vic customers only. All orders over $59.00 will be shipped free of charge. Please note that this is a courier service so no PO Boxes are able to be used. Must be a physical address.

Please note that this excludes Origin gas deliveries

Normal shipping times for this service is 1 – 2 business day providing we have stock.

Online Store – orders can be made simply by selecting the item(s) you wish to purchase, and clicking on the ‘add to cart’ button located at the bottom of each image. Once you have finalised your purchases you can proceed to the checkout. Orders can be placed by credit card using our secure server SecurePay, or direct bank deposit. An acknowledgement email will be sent to you once the transaction has been completed.

So we are based in Australia, Due to large shipping cost we prefer to only ship to Australian Customers. If you would like to place an order from outside Australia, please email for freight charges before placing an order. If you place an order without freight charges and then cancel the order, then administration cost will be charged to your order to cover the cost of transaction and international banking fees.

Due to Illegal activity from some international customers we only accept payment from Paypal for all international orders. No Order will be shipped internationally without using this service. If payment is made via credit card we will cancel the order and refund all fund, we will then ask that the order be resubmitted using Paypal. This is to protect our customers and ourselves against fraudulant orders

Please Note: that different countries have different rules when it comes to customs, Beaufort Animal Supplies accepts no responsibility once an item has been shipped. It is up to the purchaser to check with local authorities about the items they wish purchase. Beaufort Animal supplies also accepts no responsibilities for lost or damaged goods once it has left our care.

Each product size will either be charged on its cubic weight or dead weight  – whichever is the greater.

Warranty

For Click & collect transactions:

Terms and conditions relevant to the sale will be the Terms and Conditions on which the Beaufort Animal Supplies trades with its customers for any claims or returns,

For products shipped by Beaufort Animal Supplies

All products are covered by statutory warranties, namely we warrant the products we sell to you are free from defects in workmanship and materials; of merchantable quality; fit for the purpose for which they were made and will match the description contained in our online catalogue or any sample provided to you. All products will meet these statutory requirements for at least three months from the date of purchase unless the product is covered by an extended warranty. Statutory and extended warranties (if applicable) will not apply where you have caused the products to become damaged.

Examples of occasions where the warranties and additional promises (if applicable) will not apply are:

Where you have mistreated or abused the products (whether intentionally or unintentionally); or Damaged the products as a result of using them in a way they were not intended to be used.

We recommend that you refer to the packaging instructions for further information about the intended purpose for which a product was made.

We reserve the right to test or assess any product returned to us in order to determine whether a breach of warranty has occurred.

Returning a Product for a Refund

Beaufort Animal Supplies want you to be completely satisfied with every item that you purchase from us.  We understand that there may be times when you will need to return a product that you have purchased from us, and we aim to make this process as easy and hassle free as possible.  Our returns policy has been constructed to comply with the relevant consumer rights and retailer obligations as set out under the Australian Consumer Law (ACL).

When to return a product

You are entitled to a refund, replacement or credit from Beaufort Animal Supplies when an item purchased fails to meet one of the consumer guarantees as per the Australian Consumer Law (ACL), i.e. the product:

Is faulty or of unacceptable quality

Does not match the description or sample

Is unfit for the intended purpose (i.e. does not do what it is meant to do).

Is not delivered in a reasonable time frame

This also includes non-compliance with any applicable warranties or guarantees as set out by the manufacturer (e.g. the palatability guarantee on super premium foods).

Proof of purchase is required for all returns, which can be in the form of your receipt/tax invoice, a debit/credit card statement or online purchase transaction history.

Beaufort Animal Supplies will not accept change of minds returns

How do I return a product purchased online and delivered to me?

Items purchased from our online store can be returned via post to Beaufort Animal Supplies. Please Contact us via beaufortanimals@bigpond.com.au to orgainsie a suitable arrangement for return or call us on 035349266. Please include your name, phone number, the name of the product in question and your reason for return.

Who pays for the return of my purchase?

Beaufort Animal Supplies will cover any associated delivery charges for the return of any products which fail to meet the consumer guarantees as per the Australian Consumer Law (see ‘When to return a product’ above), provided they are returned to us using the recommended shipping method (as discussed with a Beaufort Animal supplies Online customer service team member).  Any return delivery charges will be added to your refund amount once processed.  We will also refund the cost of the original delivery and pay for the delivery of any replacement item.

If the error is caused by Beaufort Animal Supplies by means of a picking error i.e the goods ordered do not match what was delivered, Beaufort Animal Supplies will cover the shipping costs associated with your return.

Repairs under Manufacturer’s Warranties

There may be circumstances where you have a problem with a product however it does not amount to a breach of a statutory warranty provided by us i.e. you are not entitled to a refund from us. In those circumstances, however, the product may have come with a warranty from the manufacturer.

Where your purchase of the product has been sold with a warranty from the product manufacturer, the warranty will typically grant you a right to have the product repaired (rather than entitle you to a refund) if defects arise falling within the scope of the warranty.

Some Manufacturer’s use external Service Agents to repair faulty or damaged products. Where applicable, the item will need to be sent away for repair. Please contact us for manufacturer’s contact details. We recommend you firstly phone the relevant manufacturer if you experience any difficulties operating a product.

Limitation of liability

Any direct, indirect, incidental, special or consequential damages as a result of use or misuse of the website will not be the responsibility of Beaufort Animal Supplies. Beaufort Animal Supplies will also not be liable for the costs resulting in further purchases as a result of the initial purchase, the cost of obtaining substitute products. In addition to these, messages received, transactions entered into through the website or as a result of unauthorised access to your information contained on this website will be in no way the responsibility of Beaufort Animal Supplies.

Where an Act of Parliament suggests any term, condition or warranty in the Terms and Conditions and does not allow for provisions in a contract for exclusion of liability, the liability of Beaufort Animal Supplies will be limited. If the breach relates to a good purchased Beaufort Animal Supplies may choose to replace the goods or supply the equivalent goods, repair the goods, pay the cost of replacing the goods or of acquiring equivalent goods or payment of the repair costs for the goods.

Use of Website

Information on the Website is only general and while we have provided this information in good faith based on what we believe are accurate sources, the information may not be complete or accurate for your purposes. The information provided does not take into anyone’s individual situation. General information should not be relied on instead of professional advice specifically directed to you and your circumstances.

You must not use the Website or its contents:

1. in breach of any law or regulation;
2. to infringe a third party’s rights;

iii. to breach any standards, content requirements or codes promoted by any relevant authority; or

1. in connection with any information or material that may be, or that may encourage conduct that may be unlawful, threatening, abusive, defamatory, obscene, pornographic, profane or indecent.
2. You are responsible for ensuring any equipment, software or service required to use the Website is working properly, and that you know how to use it to access the Website.

All customers who are registered with the Australian Alpaca Association are entitled to a discount of all their orders place through the website. We use the herd code to verify your status with the the Australian Alpaca Association. Once you are verified we update our system with automatically applies the discount at the check out.

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.

 

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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