Webinar by Dr. Abdul Samad on Common Poisonings in Ruminants
toxin-poisoning-webinar_compressed
Read: Poisoning Questions and their Answers
Respected Sir,
Hello, Hope you are well! I was very happy to hear your zoom lecture- on Common poisonings in ruminants (advances)- for the first time after graduation. Sir, I am currently posted in Kinwat, Nanded as LDO. We come across HCN, Pesticide and Oxalate poisoning commonly over here. Out of which HCN and OP/ Carbamate poisonings do recover if treated on time. The only problem is with Oxalates. The cause of oxalate poisoning in this area is probably a wild plant called Anagallis arvensis which is commonly found here (there has been a MVSc thesis on the same by a student of Parbhani Vet College). We are following the treatment protocol advised in your lecture and in addition, we also advise the supernatent of lime water orally. But the prognosis in most cases is still guarded to poor. Sir my question is regarding an anecdotal treatment with Sodium thiosulphate orally which is being advocated by a few practitioners here. They are reporting good success rate after its use. I however have been unable to find any reference regarding use of Sodium thiosulphate as an antidote for oxalate poisoning! I wanted to bring this to your notice and also request your advice as to whether I too should attempt the above anecdotal treatment in addition to the routine treatment protocol?
I shall be very grateful for your advice Sir!
Thank you very much and hope to hear more of your webinars in future.
Warm regards,
Ashwin Jayarajan,
BVC: 2003-08 batch
Reply of Dr. Samad
Dear Ashwin:
Poor prognosis in oxalate poisoning has two sites of adverse effects: (a) rumen- where it binds to calcium and magnesium hence reduces their availability leading to hypocalcaemia and hypomagnesaemia, and (b) the absorbed soluble oxalate will reach blood and bind to serum calcium forming ca oxalate crystals which is deposited in the kidneys causing chronic nephritis (also called calciphylaxis). For the management of oxalate poisoning you have to intervene at both the sites. For taking care of rumen oxalate give enough calcium chloride and magnesium salts (Epsom salt) orally to form an insoluble compound which is then excreted in the faeces. Both calcium and magnesium should not only saturate the oxalate in rumen but the excess should be available for absorption. DCP 100 g orally and around 50-75 g magnesium sulfate orally to be give for 3-5 days. To address the issue of absorbed oxalate causing calciphylaxis, the approach should be to dissolve calcium oxalate crystals, for which alkalinizing agents are used. Sodium thiosulphate is one of the alkalinizing agents used even in human oxalate crystalluria. Other alkalinizing agents such as, sodium bicarbonate, sodium lactate and calcium acetate can also be used.
In chronic nitrate poisoning endemic areas, a cost effective way of monitoring the livestock is to keep an eye on clotting time (it should not exceed 12 minutes) to know how much oxalate is being consumed and absorbed.
Dr. Abdul Samad
Respected Sir,
Thank you very much for sending over the treatment protocol. I shall share it with my colleagues here too and I hope we will be able to improve the prognostic indicators in oxalate poisoning cases. I would like to share an experience of a Gir farm with you Sir. Somebody started a Gir farm in the middle of the forest here with around 60 cows. The animals are left for grazing too and are probably exposed to the previously mentioned Anagallis arvensis plants. These animals were showing uterine prolapse both pre and post mortem. Some were recumbent and succumbed even after calcium therapy. I had collected blood from a few animals and found delayed clotting times (as mentioned by you). I did calcium estimation at Nanded Polyclinic and in a couple of cows the Calcium levels were in the range of 5-6 mg/dl. So I think it may be hypocalcemia secondary to oxalate poisoning. Unfortunately Sir, we are diagnostically challenged over here both in terms of facilities as well as owners paying capacity. Also the animal husbandry department prioritises ‘husbandry/development’ over animal health which is also a drawback. Thank you once again for your interest and advice Sir. Hope to interact more with you on various
media!
Regards,
Ashwin Jayarajan,
BVC: 2003-08 batch
Dear Ashwin:
You are right. Hypocalcemia reduces the tone of smooth muscle due to which there will be hypocalcemia. The problem will be accentuated in recently-calved cows because there is an additional loss of calcium in colostrum. One of the strategies you could adopt here is to start giving oral calcium gel one week prior to calving and a single injection of vitamin D3. Giving high calcium for a longer time in gestation will render the animal more prone to milk fever. Fortunately, animals have enough calcium reservoirs as most forages are rich in calcium but low in phosphorus. The problem however is efficiency in mobilization. In the case of ruminants, calcium absorption is not dependent on vitaminD3 and kidneys do not pay a significant role in calcium homeostasis. There is one more old test called, Sulkowitch test, which is done in the urine. It detects calcium in the urine. The principle is if there is hypocalcemia, calcium will be retained and excretion in milk will stop hence, the Sulkowitch test will be negative. You can prepare this reagent in your laboratory:
Sulkowitch reagent is composed of :
- Oxalic acid: 2.5 g
- Ammonium chloride 2.5 g
- Glacial acetic acid: 5 ml
- Distilled water: 150 ml
Principle: Ca present in urine reacts with sulkowitch reagent, forms precipitates of insoluble calcium oxalate. Procedure: Take 2 test tubes. Take 5 ml of distilled water and 5 ml of urine in one test tube. Then in the second test tube take 5 ml of urine and 5 ml of sulkowitch reagent. Compare the 2 test tubes in transmissible light after 2-10 min. The presence of a white ppt is an indication of a positive test. Indication: Increased calcium (thick or heavy precipitations) is seen after renal osteodystrophy, hyperparathyroidism, hypervitaminosis, and administration of calcium solutions. It decreases in hypothyroidism and osteomalacia.
Dr. Abdul Samad
Dr. Amarpreet Pannu
Thanks, Sir for very informative lecture on poisoning. There are few queries I want to ask .1. can chronic HCN toxicity occur in ruminants? 2. From where can we get strips for testing Nitrate toxicity?. 3. What amount of cabbage or onions safe to be fed to cattle?
Reply of Dr. Samad
Dear Dr. Pannu:
Thanks for the email. Chronic HCN poisoning is common in cattle and it is called cystitis ataxia syndrome. As the name indicates it is a debilitating disease. No test kit is available for nitrate (to check-in the rumen content/plant). The ones available are for aquarium ammonia levels. For nitrate, I rely more on blood tests. Compare the blood colour with the standard.
Dr. Abdul Samad
Sir,
I am Dr. Gouranga Bardhan, from W Bengal.
Last year I got some vetero-legal cases, where it was complain that a group of goats and heifers were poisoned with urea, puffed rice and mollases with water. I performed P M exam after more than 24 hr of the incident. No ammonia like smell but ruminal layer found putrefied. What should be my ideal approach to find the truth? I did sent ruminal content, intestinal content piece of liver, lungs, kidney, spleen to state forensic lab through police but don’t know the result yet. There was controversy about the medium in which it would be sent, finally sent in formalin. (As ice pack is not possible). I think you are the right person to get my answer. So that in future I can establish the fact.
Yours truly
Dr Gouranga Bardha.
9163837025
Reply of Dr. Samad:
Dear Dr. Bardhan:
Thanks for the email. The puffed rice is starchy and molasses is high in soluble fermentable carbohydrate. Both will produce severe rumen acidosis and bloat. In case acidosis is severe, it may also lead to systemic acidosis. The signs of acidosis, like depression, head pressing, and bloating would indicate that. Urea poisoning is usually acute and deaths would happen faster. Since the amount and type of toxicants is not known the forensic confirmation is always required. As a general rule, if you are interested in estimating the content of any chemical, it is not advisable to add any chemical as a preservative. Freeze the sample and send the same on ice. The same is the case for bacteria and toxins. In case of rumen, the problem is microflora, as these will continue to function even after death for quite some time. Except for histopathology or histochemistry, adding formalin is not recommended as a preservative.
In future, try to observe an animal that is showing signs if any. If it is a common-source poisoning in feed, other flock mates should also show signs or carry some amount of toxin. If it is a large flock, sacrificing one live poisoned animal might be a good idea to collect the samples. If the cold chin is not feasible, then collect samples in formalin for histopathology and toxico-pathology.
Dr. A. Samad