Animal Anatomy

Student name: Alam Adol Mathiang Student ID: s1210708 Unit name: ALM211 Animal Anatomy and Physiology Due date: Wednesday, 24th July 2013, 5 PM Unit coordinator: Lesley Hawson

Grass tetany (hypomagnesaemia) Introduction Grass tetany (hypomagnesaemia) is also known as winter tetany, grass staggers, lactation tetany and wheat pasture poisoning. It is a very serious metabolic disorder that occurs to cattle grazing on small ryegrass, grain and young forage. Its main cause is magnesium inadequacy and imbalance in blood serum. This disorder occurs to any cattle but mostly confined to lactating cows. Klingerman (2007) explains that grass tetany occurs in cattle during cool and rainy weather. Certain pastures and forages are prone to cause this disease. These pastures are tall fescue, bromegrass, orchardgrass, perennial ryegrass and timothy grass. In addition, small grains such as oats, rye, wheat and barley are also prone to causing grass tetany. Klingerman (2007) also reports that grass tetany can also be caused by grazing cattle on low Magnesium grass hay. Cattle which is rotated to winter pasture paddocks, just after frost, suffers nutritional stress that causes grass tetany as well. The magnesium deficiencies are not problem of the cattle but the forage they eat. The farmers that allow the pasture or forage to mature reduce the likelihood of this problem within their cattle. It is a disease that is easy to prevent but hard to treat. So preventing it is to always increase Magnesium levels in forage and in feed supplements. Grass tetany has a physiological process, clinical signs, and differential diagnosis, diagnosis, and treatment and prevention strategies. The physiology process of Grass tetany As previously mentioned, magnesium deficiency in the blood serum causes the grass tetany. Schweigel and Martens??™ (2000) regard Magnesium as a vital mineral that includes many biochemical and physiological functions. The hormonal feedback

system does not control magnesium homeostasis, but it functions simply by inflow and outflow of Magnesium. Marten??™s (2000) examination records that any excess (inflow greater than the outflow) is excreted through urine. Schweigel and Martens (2000) explain that hypomagnesaemia occurs if the outflow is greater than the inflow because hormonal mechanisms of homeostasis will be lacking. The need for insufficient inflow is a decreased absorption of Magnesium from the fore stomach. Schweigel and Martens??™ (2000) studies suggest a common transport model for Magnesium transportation across the rumen epithelium. This transport model contains two uptake mechanisms across the luminal membrane. These two uptake mechanisms are PD-dependent and PD-independent (what PD stand for isn??™t shown by Schweigel and Martens, 2000). The role of these models among other things is to explain any negative interaction between Magnesium absorption and ruminal K concentration (Schweigel and Martens, 2000).The magnesium deficiencies are not problem of the cattle but the forage they eat. Klingerman (2007) considers levels of Magnesium in the blood to be normal at around 2 mg/100 ml of plasma. 2 mg/100 ml is reduced to be below 1mg/ 100ml if the animal has developed grass tetany (Klingerman, 2007). The reduction of Mg in the blood happens to cattle grazed on pasture if Mg is on a low concentration of less than 0.2% DM in the forage. Nitrogen level will be greater than 4.0% DM and potassium level becomes greater than 3.0% DM if the affected forage Magnesium is low. Forage that is not or at risk of developing grass tetany can be figured out by calculating the tetany ratio. To calculate tetany ratio, producers do not use percentage or PPM but they rather base their calculations on forage weight and account basis for each element??™s molecular weight. (% DM of K ? 39) ? (% DM of Ca ? 20) + (% DM of Mg ? 12.1) is the best way the producers calculate forage that is at

risk and not at risk of causing grass tetany (Filley, 2005). Cows that are up to two plus months of post calving are more susceptible to hypomagnesaemia because they require more excess minerals to replace those lost during milk production, in which ten litres consists approximately 1.2% of Magnesium (Klingerman, 2007). Clinical signs of grass tetany Champness (2007) reports death of the affected animals in the paddock as the first clinical sign. Champness (2007) explains that animals found dead are usually with froth in their mouth and nose. The ground is rubbed due to the animal??™s struggle before death. Champness (2007) considers cow??™s nervous signs such as gallop madly, walking stiffly, exaggerated response to touch or sound, begin convulsing, kicking, rolling of the eye balls, muscle spasms (tetany), frothing at the mouth and nose, and head arched back when being yarded. All those signs indicate possible death within hours. Champness (2007) shows mild clinical signs to be unsteady leg movements and wild facial expression before more severe signs develop or before recovering. Elliott (2007) records that the affected cow does not like being driven and will also have its tail pointing upwards and may appear blind. Differential diagnosis of grass tetany CVVS (2010) considers differential diagnoses to be Irritable, uncoordinated cattle (Ketosis/Acetonaemia) which usually occur during pre-calving or immediately after calving. Phalaris staggers happens to cattle affected. Other toxins include access to toxic weeds, fermented grain, vineyard waste etc. CVVS (2010) also mentions Entertoxaemia/pulpy kidney and Bloating as other diagnosis. It is estimated that herders lose 1-6 adult cows every year. It is always a good to check if there is rapid decomposition, bloating after death, blood stained foam. This can be avoided by

annual vaccination with 5 in 1. Bloating occurs in cattle grazing on high legumes. Bloating only recedes after the cow is dead (CVVS, 2010). Diagnosis of grass tetany A Klingerman (2007) show there is always a difficulty to diagnose grass tetany because the animals usually die before any attempts to treat the disease are made. Magnesium levels in the blood serum become low just before clinical signs are noticed. Measurement of urinary Magnesium is considered to be a better diagnostic method as kidneys will start storing Magnesium if ever it becomes insufficient (Klingerman, 2007). Mistaking grass tetany for other metabolic diseases in cattle is very common. Treatment of grass tetany Klingerman (2007) advises that the affected animal be removed from the pasture (paddock) and allocate it where levels of Magnesium in the blood serum are increased. Champness (2007) explains that Australian farmers should only treat affected cows by injection. Oral treatment with 100 gm Causmag or Epsom salts should also be provided because relapses can occur after a few hours (Champness, 2007). Champness (2007) urges the farmers to feed the affected cows with hay and Causmag soon after recovery to improve magnesium absorption from the rumen. Calcium-magnesium gluconate is another treatment method recommended (Champness, 2007). This sort of treatment in intravenously injected into the animal before treatment to make sure it is calm (Klingerman, 2007). These intravenous injections are advised to be given slowly to avoid cardiac arrest. It is also important to closely monitor respiratory and heart rates of the animal during treatment

(Klingerman, 2007). After fully increasing the levels of Mg in blood serum, the animal is kept on a diet high in Magnesium to avoid relapse (Klingerman, 2007). Prevention of Grass tetany Klingerman (2007) reports that analysis of the forage should always be carried out if there is grass tetany history on the pasture and avoiding fertilisers that are high in potassium or nitrogen makes prevention of this disease easier. Forage high in potassium and nitrogen produces big amounts of ammonia in cow??™s rumen and this causes the conversion of dietary Magnesium into an insoluble hydroxide form. It simply reduces Mg level in the blood serum (Klingerman, 2007). Dolomitic and high Magnesium limestone with 12-13 % of actual Magnesium can be applied as fertiliser to increase Magnesium levels of the soil (Klingerman, 2007). Dolomitic is most needed when the soil pH is low. Adding magnesium to pasture is not mandatory since it can be supplied directly in a cow??™s diet and in the form of Magnesium oxide (Klingerman, 2007). Magnesium oxide diluted in 300 g/l of water and then added to hay and fed at the rate of 1 bale/ 10 cows is very effective (Klingerman, 2007). It is also effective to mix Magnesium oxide with salt and feed the cow directly with it (Klingerman, 2007). The reason for this is that the salt growth high levels of palatability of MgO and sodium in the blood. A mixture is required to be 75% salt with 25% MgO (Klingerman, 2007). To easily prevent grass tetany, lactating and affected cows can be grazed on high legume pastures and hay (Klingerman, 2007).

Conclusion Grass tetany is caused by very low levels of Magnesium in the blood serum. It is not only a preventable disease at best but also a deadly disease at worst. Cows affected with the acute form are likely to die within hours if clinical signs are detected late in which treatment becomes difficult. It is a lot easier to prevent the disease than treat it because it kills the affected animal within a short period of time. Prevention involves increasing Magnesium in the forage and in feeding Magnesium supplements. If the management program and forage testing are properly managed and monitored, this disease is then prevented.

References Champness.D. 2007.Grass Tetany (Hypomagnesemia) in Beef Cattle accessed on 20th July 2013. Clare Valley Veterinary Services.2010. GRASS TETANY ??“ HYPOMAGNESAEMIA ndDiseaseInformation/GrassTetanyGrassStaggers/tabid/2193/Default.aspx accessed on 18th July 2013 Elliot, Mac. 2007. Grass tetany in cattle. NSW Department of Primary Industries. Primefacts. Primefact 420. accessed on 18th July 2013 Filley, Shelby. 2005. Grass tetany??¦Fast growing grass can mean problems. Extension Service Douglas County. Douglas County Circular. L&F:104. accessed on 24th August 2013 Klingerman, M. 2007. Grass Tetany in Cattle??“An Examination of its Causes, Clinical Signs and Cures. accessed on 18th July 2013

Martens H, Schweigel M. Pathophysiology of grass tetany and other hypomagnesemias implications for clinical management. Vet Clin North Am Food Anim Pract 2000; 16:339??“368 accessed on 19th July 2013