~ 1 ~ International Journal of Fauna and Biological Studies 2025; 12(2): 01-03 E-ISSN 2347-2677 P-ISSN 2394-0522 https://www.faunajournal.com IJFBS 2025; 12(2): 01-03 Received: 02-12-2024 Accepted: 07-01-2025 Javaid Ahmad Baba Bcteriologist, Disease Investigation Laboratory Nowshera, Srinagar, Jammu and Kashmir, India Mubashir Ali Rather Senior Epidemiologist, Disease Investigation Laboratory Nowshera, Srinagar, Jammu and Kashmir, India Khalid Bashir Veterinary Assistant Surgeon, Disease Investigation, Laboratory Nowshera, Srinagar, Jammu and Kashmir, India Corresponding Author: Javaid Ahmad Baba Bcteriologist, Disease Investigation Laboratory Nowshera, Srinagar, Jammu and Kashmir, India Urea toxicity in sheep: A case study of improperly adapted animals fed poor-quality feed Javaid Ahmad Baba, Mubashir Ali Rather and Khalid Bashir Abstract Urea poisoning is a significant concern in sheep production, particularly when animals are exposed to high levels of urea without proper adaptation. An outbreak of urea toxicity occurred in a flock of sheep that were fed a pelleted feed containing high levels of urea (9.67%), which contributed 20.98% to an overall crude protein content of 45.94. The feed analysis revealed significant deviations from normal ranges, including high dry matter (94.89%), crude protein (45.94%), crude fat (5.51%), total ash (22.53%), acid-insoluble ash (4.81%), and silica (4.67%) content. Clinical signs included bloat, frothy salivation, and excessive urination. Postmortem examination revealed severe pathological changes, including pulmonary edema and hemorrhages on the epicardium and endocardium. This case highlights the importance of careful feed formulation, balancing proximate principles, and gradual introduction to prevent urea toxicity in small ruminants. Keywords: Urea toxicity, sheep, poor-quality feed, improper adaptation, stress Introduction Urea poisoning occurs when sheep ingest excessive amounts of urea, a common nitrogen-rich feed supplement. Ruminants can leverage Non-protein Nitrogen (NPN) compounds to fulfill their protein nitrogen needs. Specific NPN compounds like urea, ammonium acetate, and ammonium sulfate are frequently incorporated into ruminant diets due to their cost- effectiveness compared to traditional protein sources. Feed-grade urea, CO(NH2)2, stands out as the most affordable, efficient, and widely available nitrogen source (Oruç et al., 2015) [1] . Urea is typically recommended to comprise around 3% of the concentrate portion of the ration, or approximately 1% of the total ration (Oruç et al., 2015) [1] . However, unadapted ruminants can exhibit toxic signs at relatively low doses of 0.2-0.5 g urea/kg body weight [1, 2] . In contrast, adapted animals can tolerate higher doses, up to 1 g urea/kg body weight, without showing adverse effects. All mammalian species are potentially susceptible to non-protein nitrogen (NPN) toxicities through consumption of ammonium-containing feeds, provided the dose is sufficiently high. Sheep and other ruminants are most vulnerable after 50 days of age due to the presence of urease and suitable environment in their rumen, which facilitates the hydrolysis of urea, releasing carbon dioxide and ammonia (Patra and Aschenbach. 2018) [3] . Several factors can increase the likelihood of urea poisoning in ruminants, including inadequate adaptation to high NPN diets, low energy diets, elevated rumen pH, increased body temperature, dehydration, stress, concurrent disease, alterations in rumen microflora, and hepatic insufficiency [4, 5, 6] . Rations with high total digestible nutrients (TDN) or digestible energy (e.g., high grain) facilitate better urea utilization, whereas low-energy rations (e.g., high forage) result in reduced urea utilization [6] . Upon consumption, urea is swiftly broken down into ammonia by bacterial urease in the rumen of adult ruminants. Rumen bacteria then utilize this ammonia, along with soluble carbohydrates, to synthesize amino acids and proteins. Excess ammonia is primarily converted to the ammonium ion, trapping it in the rumen. Prolonged excess ammonia production can elevate rumen pH, potentially leading to ammonia poisoning if significant amounts are absorbed into the bloodstream (Parkes et al., 2011) [7] . Excess ammonia has been shown to disrupt critical metabolic processes, including inhibition of the citric acid cycle, causing lactic acidosis, and interfering with cerebral energy metabolism and the sodium-potassium ATPase pump. The systemic metabolic acidosis is thought to be related to hyperkalemia, ultimately leading to cardiac arrest (Oruç et al., 2015) [1] . The onset of clinical signs in ruminant animals poisoned by toxic levels of urea and other NPN compounds can be extremely rapid, Occurring within 10 minutes to several hours after