Urea poisoning.docx

**Urea Poisoning in Cattle** **Urea poisoning** is one of the more commonly suspected toxicities of cattle in the Top End and it is also called ammonia poisoning. Urea is used as a source of non-protein nitrogen (NPN) in feed supplements. In ruminants, nitrogen from urea is released in the rumen as...

**Urea Poisoning in Cattle** **Urea poisoning** is one of the more commonly suspected toxicities of cattle in the Top End and it is also called ammonia poisoning. Urea is used as a source of non-protein nitrogen (NPN) in feed supplements. In ruminants, nitrogen from urea is released in the rumen as ammonia and can be used by rumen microflora to synthesise protein. This protein then becomes available to the animal through the normal processes of digestion and absorption. However, if more urea is consumed than the rumen organisms can metabolise, the ammonia is absorbed from the rumen into the blood. The ammonia is then converted back to urea in the liver, and is then excreted by the kidneys. This pathway can easily be overwhelmed, when excess ammonia and urea circulate in the blood, causing poisoning. Poisoning can occur rapidly from a few minutes to four hours after consumption. Suspect urea poisoning if cattle are found dead close to the supplement. C**ause of urea poisoning** 1. Excess consumption of urea. 2. Sudden introduction to high quantities of urea. 3. Irregular consumption of urea. 4. Wet supplement containing urea. 5. Urea separating out from the supplement after transport; re-mix prior to feeding. **Signs of urea poisoning** 1. twitching of ears and facial muscles, 2. grinding of the teeth, frothy salivation, 3. bloat, abdominal pain, 4. frequent urination, forced rapid breathing, 5. Weakness, staggering, violent struggling and bellowing, and terminal spasms. Often, animals are found dead near the source of the urea supplement. **Diagnosis**: The most useful diagnostic indicators are the history of access to urea and the signs shown by live, affected animals. **Laboratory tests** of blood samples are not very helpful, and no specific changes are seen at post-mortem examination. The following are general indicators of urea poisoning: · History of access to urea. · **Laboratory testing** of collected blood and rumen fluid immediately after death may indicate urea poisoning. · **Post-mortem** -- bloat; white foam in airways; ammonia odour when the rumen is opened; rumen pH 7.5- 8.0. Often a large pool of rumen fluid is seen on the ground at the nose of the beast. The animals usually suffer severe bloat and the fluid buildup in gases forces the rumen fluid out through the mouth when the animal dies. Keep rumen and reticulum samples in formalin for subsequent diagnosis. Recommended feeding quantities vary according to what other feed is available and whether the cattle are accustomed to urea. **Tolerance** is decreased by starvation and by a low protein, high fibre diet. About **35 g** of urea per day is considered sufficient for a 400 kg cow (i.e. approximately 0.1 g/kg body weight). It is recommended that urea should provide **no more than 3% of the concentrate ration, or 1% of the total feed intake**, and no more than one third of the total nitrogen intake should be NPN. In cattle, 0.3-0.5 g/kg/day (e.g. 120-200 g for a 400 kg cow) is considered to be toxic and 1-1.5 g/kg/day (e.g. 400-600 g for a 400 kg cow) can be fatal. Laboratory testing Blood ammonia levels can be measured, but this is only useful in live, sick animals. Proteins in the blood break down rapidly after death and produce ammonia, so testing blood from dead animals is of no value. For the same reason, the handling and storage of blood after collection is very important. Blood must be taken into lithium heparin or EDTA, placed immediately on ice and the plasma separated within 30 minutes of collection. Plasma may be stored for 2 hours at 4°C before testing, or frozen immediately and kept frozen until ready to test. These restrictions on measuring blood ammonia make it impractical as a diagnostic test in field situations. If it is important to measure blood ammonia levels, then collect blood from animals that appear unaffected, as well as from sick animals, and treat all samples the same way. If all samples show elevated ammonia, then it is likely to be a non-specific elevation (i.e. due to storage). Ammonia levels in rumen fluid can also be measured, but only fluid taken straight after death is likely to be of any value. Again, it must be frozen immediately and kept frozen until tested. Post mortem examination and histopathology Animals decompose rapidly after death from urea poisoning and there are no specific signs of poisoning. Postmortem examination immediately after death can show evidence of bloat, generalised congestion of the carcase, excess fluid in the pericardial sac, pulmonary oedema with excess stable white foam in the large airways and haemorrhages on the heart (epicardial and endocardial). There can be a marked ammonia smell when the rumen is opened. The pH of fresh rumen contents is a useful test that can be done in the field. An alkaline rumen (pH greater than 7.5-8) is suggestive of urea poisoning. There is very little in the literature on histopathological signs, there appear to be inflammatory changes in the rumen, particularly in animals that may survive the initial poisoning but die or are euthanised a day or two later. Inclusion of formalin-fixed sections of rumen and reticulum from animals that die from suspected urea poisoning, will assist diagnosis. **Treatment** is rarely effective. However, if cattle can be handled, a stomach tube can be passed to relieve the bloat and then used to drench the animal with a large volume of cold water: 45 L for an adult cow is suggested, followed by 2-6 L of 5% acetic acid or vinegar. This dilutes rumen contents, reduces rumen temperature and increases rumen acidity, which all help to slow down the production of ammonia. Treatment may need to be repeated within 24 hours, as relapses can occur. Rumenotomy and removal of rumen contents is suggested for valuable animals. **Prevention** Start with pure salt; slowly and then gradually introduce urea supplement -- increasing it slowly and gradually to about 0.1g/kg body weight/day. (35-40 g/day for a 400 kg cow). · Ensure that cattle get regular (daily) access to supplement once supplementation has started. · If cattle unavoidably miss out on urea supplementation for a couple of days, then restart them at a lower intake level. · Prevent over-consumption of supplement mix or blocks (e.g. by using salt to regulate intake). · Feed supplement mixes or blocks under a roof to prevent urea getting wet and dissolving. · Suspect urea poisoning if cattle are found dead close to the supplement. **Bovine spongiform encephalopathy** (**BSE**) commonly known as mad cow disease, is a fatal [neurodegenerative disease](http://en.wikipedia.org/wiki/Neurodegenerative_disease) ([encephalopathy](http://en.wikipedia.org/wiki/Encephalopathy)) in [cattle](http://en.wikipedia.org/wiki/Cattle) that causes a spongy degeneration in the [brain](http://en.wikipedia.org/wiki/Brain) and [spinal cord](http://en.wikipedia.org/wiki/Spinal_cord). BSE has a long [incubation period](http://en.wikipedia.org/wiki/Incubation_period), about 2.5 to 8 years, usually affecting adult cattle at a peak age onset of 4-5 years, all [breeds](http://en.wikipedia.org/wiki/Breed) being equally susceptible. BSE is caused by a **misfolded prion.**  In the [United Kingdom](http://en.wikipedia.org/wiki/United_Kingdom), the country worst affected, more than 180,000 cattle have been infected and 4.4 million slaughtered during the eradication program. The disease may be most easily transmitted to [human beings](http://en.wikipedia.org/wiki/Human_beings) by eating food contaminated with the brain, spinal cord or digestive tract of infected carcasses. However, the infectious agent, although most highly concentrated in nervous tissue, can be found in virtually all tissues throughout the body, including blood. In humans, it is known as new **variant Creutzfeldt--Jakob disease (vCJD or nvCJD)**. A British and Irish inquiry into BSE concluded the [epizootic](http://en.wikipedia.org/wiki/Epizootic) was caused by cattle, which are normally [herbivores](http://en.wikipedia.org/wiki/Herbivore), being fed the remains of other cattle in the form of [meat and bone meal](http://en.wikipedia.org/wiki/Meat_and_bone_meal) (MBM), which caused the infectious agent to spread. The cause of BSE may be from the contamination of MBM from sheep with scrapie that were processed in the same slaughterhouse. The epidemic was probably accelerate by the recycling of infected bovine tissues prior to the recognition of BSE. The origin of the disease itself remains unknown. The infectious agent is distinctive for the high temperatures at which it remains viable, over 600 °C (about 1100 °F). This contributed to the spread of the disease in the [United Kingdom](http://en.wikipedia.org/wiki/United_Kingdom), which had reduced the temperatures used during its [rendering](http://en.wikipedia.org/wiki/Rendering_(food_processing)) process. Another contributory factor was the feeding of infected protein supplements to very young calves. **Cause** The infectious agent in BSE is believed to be a specific type of misfolded [protein](http://en.wikipedia.org/wiki/Protein) called a [prion](http://en.wikipedia.org/wiki/Prion). Prions are not destroyed even if the beef or material containing them is cooked or heat-treated. Prion proteins carry the disease between individuals and cause deterioration of the [brain](http://en.wikipedia.org/wiki/Brain). BSE is a type of [transmissible spongiform encephalopathy](http://en.wikipedia.org/wiki/Transmissible_spongiform_encephalopathy) (TSE). Transmission can occur when healthy animals come in contact with tainted tissues from others with the disease. In the brain, these proteins cause native cellular prion protein to deform into the infectious state, which then goes on to deform further prion protein in an exponential cascade. This results in protein aggregates, which then form dense [plaque](http://en.wikipedia.org/wiki/Senile_plaques) fibers leading to the microscopic appearance of \"holes\" in the brain, degeneration of physical and mental abilities and ultimately death. Different hypotheses exist for the origin of prion proteins in cattle. Two leading hypotheses suggest it may have jumped species from the disease scrapie in sheep or that it evolved from a spontaneous form of \"mad cow disease\" that has been seen occasionally in cattle for many centuries. **Signs** Cows affected by BSE are usually apart from the herd and will show progressively deteriorating behavioural and neurological signs. One notable sign is an increase in aggression. Cattle will react excessively to noise or touch and will slowly become [ataxic](http://en.wikipedia.org/wiki/Ataxia). Systemic signs of disease, such as a drop in milk production, [anorexia](http://en.wikipedia.org/wiki/Anorexia_(symptom)) and lethargy are present. **Diagnosis** Diagnosis of BSE continues to be a practical problem. It has an incubation period of months to years, during which there are no symptoms, though the pathway of converting the normal brain prion protein (PrP) into the toxic, disease-related PrPSc form has started. At present, there is virtually no way to detection except by examining post mortem brain tissue using neuropathological and immunohistochemical methods. The traditional method of diagnosis relies on histopathological examination of the [medulla oblongata](http://en.wikipedia.org/wiki/Medulla_oblongata) of the brain and other tissues, [post mortem](http://en.wikipedia.org/wiki/Post_mortem). [Immunohistochemistry](http://en.wikipedia.org/wiki/Immunohistochemistry) can be used to demonstrate prion protein accumulation. In 2010, a team from New York described detection of PrPSc even when initially present at only one part in a hundred billion (10−11) in brain tissue. The method combines amplification with a novel technology called [Surround Optical Fiber Immunoassay (SOFIA)](http://en.wikipedia.org/wiki/Surround_Optical_Fiber_Immunoassay_(SOFIA)) and some specific antibodies against PrPSc. **Control** A ban on feeding cattle meat and bone meal has resulted in a reduction in cases in countries where the disease was present. In disease-free countries, control relies on import control, feeding regulations and surveillance measures. At the [abattoir](http://en.wikipedia.org/wiki/Slaughterhouse) in the UK, the brain, spinal cord, trigeminal ganglia, intestines, eyes and tonsils from cattle are classified as [specified risk materials](http://en.wikipedia.org/wiki/Specified_risk_material) and must be disposed of appropriately.