Foodborne Poisoning in Animals: Causes and Diagnosis
Dr. Anushri Tiwari1, Dr. Madhu Swami1, Dr. Yamini Verma1, Dr. Amita Dubey1,
Dr. Prateek Mishra2
Department of Veterinary Pathology1
Department of Veterinary Pharmacology & Toxicology2
College Of Veterinary Science and Animal Husbandry College Jabalpur (M.P.)
INTRODUCTION
Due to the maximum expenditure on food in the animal husbandry business, balanced diet is of special importance. Due to the supply of nutrients at the lowest rate in green fodder, they have been considered as the best animal feed, but due to the severe famine situation at present, their availability has become very less. After sowing of fodder crops, due to lack of water, the growth of the crops stops and the fodder starts drying up due to which toxic elements are produced in the undeveloped and withered fodder, due to which the food poisoning occurs in the animals.
In the absence of green fodder during famine, to supply nutrients and other dry fibrous fodders are fed with urea treatment. Inadvertently or inadvertently by consuming more quantity of urea treated fodder while preparing dry fodder treated with distance. Food poisoning can occur due to many reasons, which are not controlled by the animal owners, but some poisonings which often occur due to the lack of knowledge of the animal husbandry, the animal owners can take some precautions on them and keep their animals away from their effects.
- cyanide poisoning,
- nitrate poisoning
- Urea poisoning
- CYANIDE TOXICITY
Plants Contains cyanogenic glucosides. These glucosides have enzymes present in the feed or rumen. In cyanide poisoning, oxygen-carrying enzymes are affected, resulting in a lack of oxygen to the body’s tissues, leading to the death of the animal by suffocation. Although there are many plants/fodders whose consumption can cause cyanide poisoning, but the amount of cyanide in these varies in different seasons and different parts of the plant. mainly tides,Bajra, Chari, etc., sometimes some special have sodium nitrite 3 grams and cyanogenic glucoside in sodium conditions due to high thiosulfate 15 grams, 200 ml of water, animals die due to their consumption.
The amount of poison in the fodder, its state, the presence of nitrogen in the soil, do not allow the farmer to eat the sorghum and chari crops at the time of sowing. The amount of urea or other fertilizer given for the growth of fodder depends on factors like water scarcity etc. Especially the plants whose growth and development have stopped due to lack of water, the leaves dry up and turn yellow, Cyanide quantity increases in such feed. In the absence of green fodder, hungry animals see this fodder and eat it out of greed. In the absence of information, the livestock owners also start giving withered and underdeveloped jowar, millet and chari in the absence of green fodder, due to which the animal dies.
SYMPTOMS
- Symptoms of poisoning in the animal begin to appear within 10 to 15 minutes after a sudden overdose of feed containing cyanide. The animal becomes restless, with saliva pouring out of its mouth.
- It seems There is difficulty in breathing and the animal breathes by opening its mouth, mainly due to the consumption of such four.
- There is spasm and pain in the muscles, due to extreme weakness, the animal staggers on the ground and hydrocyanic acid is formed which becomes toxic and falls.
- The mouth smells like bitter almonds. The color of the blood becomes bright red.
- There is groaning and pain like suffocation at the time of death.
Treatment
- After onset of signs of cyanide toxicity give 3 gram sodium nitrite with 15 gm sodium thiosulphate in 200 milliliters of water by intravenous route
- The amount of poison in the fodder, its state, the presence of nitrogen in the soil, do not allow the farmer to eat the sorghum and chari crops at the time of sowing. The amount of urea or other fertilizer given for the growth of fodder depends on factors like water scarcity etc.
- Especially the plants whose growth and development have stopped due to lack of water, the leaves dry up and turn yellow, the amount of cyanide increases in such fodder. In the absence of green fodder, hungry animals see this fodder and eat it out of greed. In the absence of information, the livestock owners also start giving withered and underdeveloped jowar, millet and chari in the absence of green fodder, due to which the animal dies.
- Give only well irrigated jowar and chari to the animals as green fodder. After two to four rains, feed the standing crop to the animals. Cyanide infested feed can be preserved as ‘Hey’.
- After drying the cyanide affected fodder for some time, mixing molasses in it and feeding it in the form of silage also reduces the effect of the poison. Do not use small wilted, yellow and dried up plants as fodder.
- NITRATE TOXICITY
Nitrate poisoning results from consumption of feed containing high nitrates. The amount of nitrate in fodder is generally not high, but when nitrogen-containing fertilizers are given in excess quantity in the land, then the amount of nitrate increases in the green fodder grown on that land, especially maize, oats, Sudan grass etc.
Sudden overdose of feed/water containing high nitrates results in the conversion of nitrates to nitrites, which are extremely toxic. 5, converts hemoglobin into Met hemoglobin, due to which oxygen does not reach the body’s tissues. Of the four, up to 0.15 percent nitrogen is not harmful on a dry basis, while the amount above 0.45 percent is extremely toxic.
SYMPTOM
In case of nitrate poisoning, the respiratory and pulse rate of the animal increases.
The animal turns its head towards the stomach and keeps its mouth open.
In the acute stage of poisoning, the color of the blood becomes chocolate brown and the animal dies within 1 to 4 hours.
TREATMENT
50 100 ml of 1 percent solution of methylene blue. The dose should be given directly into the vein. Ascorbic acid 5 mg should be given intravenously according to body weight.
- UREA POISONING
One of the most prevalent types of toxicity encountered in ruminants, particularly cattle and buffaloes, is urea poisoning. For more than a century, ruminants have been fed urea and other non-protein nitrogen compounds as a cost-effective alternative for vegetable and animal proteins. Nitrogen is released as ammonia from urea in the rumen and can be utilised by rumen microorganisms to help ruminants synthesise protein. This protein is subsequently made accessible to the animal through regular digestion and absorption processes.
If too much urea is ingested, ammonia is taken into the bloodstream from the rumen. In the liver, ammonia is converted to urea, which is subsequently expelled by the kidneys. When excess ammonia and urea circulate in the blood, this route is readily overloaded, resulting in poisoning. The intentional use of urea in cattle feed has the potential to be lethal and result in significant farm animal loss. As a result, farmers should be well-versed in the dose and manner of urea addition in cattle feed, as well as be cautious in this case.
Causes of urea poisoning:
- Excessive urea intake in supplemented ration.
- Introducing large amounts of urea to animals who haven’t been exposed to it before.
- Low calorie, low protein, and high roughage diets have an improperly mixed or high urea content.
- A urea-based wet supplement.
- After transportation, urea separates from the supplement.
Doses of urea supplement:
It is advised that urea make up no more than 3% of the concentrate ration, or 1% of total feed intake, and that NPN make up no more than one-third of total nitrogen consumption.
In cattle, doses of 0.3-0.5 g/kg/day are poisonous, while doses of 1-1.5 g/kg/day can be deadly.
Signs of urea poisoning:
Clinical signs of urea poisoning included restlessness, abstinence from food and water, suspension of rumination, subnormal rectal temperature (98.5°F), grinding of the teeth, frothy salivation, nasal discharge, increased respiratory rate (60 per minute), dyspnea, coughing, increased heart rate (95 per minute), arrhythmia, muscle tremors, tympany, atony of rumen, fluid filled rumen felt on percussion Animals are frequently discovered dead near the source of the urea supplement.
Diagnosis of urea poisoning:
The history of urea access and the indications displayed by live, afflicted animals are the most effective diagnostic markers. Blood tests in the lab aren’t particularly useful, and post-mortem examinations reveal no identifiable alterations.
Treatment of urea poisoning
Acetic acid was used orally as an antidote. Oral administration of 4 L vinegar is the remedy for a mature cow suffering from ammonia poisoning, and it may need to be repeated every 20-30 minutes until the symptoms diminish. Use of acetic acid after 90 minutes of urea administration does not appear to have significant impact.
To dilute the poisons in the blood, fluid treatment was given. Oedema was treated with diuretics. To increase appetite and digestion, stomachic and live yeast extracts were administered. It’s possible to use cold water as a treatment.
https://www.pashudhanpraharee.com/food-borne-zoonoses-fbzs-control-strategies-in-india/
https://my.clevelandclinic.org/health/diseases/21167-food-poisoning
