Feed and Water Related Toxicants Flashcards
Sources of NPN/Urea
- Urea > common
- Excess in feed as additive
- Inadequate [ ]’s
- Cotam of feed by urea fertilizer
- NH4+ salts & NH3 tx’d feed
Phys and Chemical properties of NPNs/Urea
- Liberation of NH3
- One part urea -> ~3 parts protein
- Urea by urease (rumen microflora) changes to NH3 & CO2
- NH3 aminates ketoacids (from soluble CHOs) to AAs
- AAs form bacterial protein
- Bacterial protein converted to animal protein
- Alkaline pH enhances hydrolysis of urea by urease (Urea is basic)
Toxicokinetics of NPN/Urea
NH3 produced rumen @ normal pH (5.0-6.5) is in the ionized form (NH4+) & not absorbed
- Too much urea & NH3 -> elevation of the rumen pH (8.0-9.0) & ↑NH3
- NH3 absorbed & converted by L to urea & excreted in U+
- More than the capacity of the L, will produce hyperNH3
- NH3 crosses cell membranes, BBB & placenta
Toxicity of NPN
Ruminants most susceptible
- Eq susceptible
- Urea is the most toxic NPN compounds
-3-6 weeks old tolerant
Feeding managment of Urea
- Usual [urea] is 3% of grain ration & 1% total ration
- Animals preconditioned or adapted to NPN are > tolerant
- Toxic dose in Bv not preconditioned or adapted is ~ 0.45 g/kg; lethal dose in adapted animals is 1-1.5 g/kg
What increases toxicity of urea?
• Fasting, dehydration or ↓H2O intake, feeds rich in urease (soybeans), L insufficiency, & diet low in E & protein but Hi in fiber ↑ tox
MOA of Urea
- NH3 inhibits citric acid cycle -> lack of E &↓cellular resp & tissue damage
- ↑B+ NH3, anaerobic glycolysis, lactate & systemic acidosis, BG, BUN, K+&P+
- ↑ transaminases & PCV
- COD may be ♥ or resp failure
CS/Lesions associated w/ Urea
Rapid OoA (0.5-3 hr)
-CS: restlessness, aggression, muscle tremors, Slv+, teeth
grinding, colic, sternal recumbency while standing on the hind limbs (play bow), bloat, rumen stasis, usually no diarrhea, lots of urination C+ & death w/in 1-2h
-Nothing characteristic
-Main lesions d/t vascular damage
-Congestion & degeneration in L&K
-NH3 odor
-Dead usually very bloated
Analysis and Dx of Urea
-Analysis of feed & NH3 in whole B+, rumen fluid & vitreous fluid
-Freeze specimens (not B+) immediately
-↑rumen pH (7.5 or >)
Dx: B+ chem, Hx of exposure, CS, NH3 odor
Tx/Prognosis of urea
- Tx bloat 1st
- Acetic acid 5% or vinegar to Bv (2-6 L) or Ov & Cp (0.5-1.0 L) then large vol cold H2O
- Repeat tx every 4-5h for 48h
- Normal saline for dehydration
- NaHCO3 IV for acidosis
- Rumenotomy
Ddx of Urea poisoning
DDx: Agents which -> colic i.e., caustics, inorganic arsenic: Generally they cause diarrhea (often B+y) & no CNS signs
- Pb, metaldehyde, & CCH pesticides: No abnormal posturing, jumping over objects & maniacal behavior as in CCH poisoning
- OP: Parasympathomimetic signs, respond to atropine tx
- Grain engorgement, nitrate poisoning, enterotoxemia & cyanide poisoning: DDx by necropsy & lab tests
Uses of Ionophores
- Anti-coccidial
-Growth promoter feed additive
-↓ bloat & rumen acidosis
-Prevent tryptophan-induced atypical Bv pulmonary
Emphysema
-Eq sensitive
Ionophore sources
- Monensin > common
- Eating feeds containing ↑ lvls in Ck, Bv & Pc
- Eating feeds w/added ionophores, in Eq, Ov, & K9s
- Malicious in Eq
- Eq that ingest Bv levels not poisoned
Physical and chemical properties of Ionphores
-Also include lasalocid, salinomycin, narasin, semduramicin
sodium, & laidlomycin propionate K+
-Carboxylic acid derivatives antibiotics
-Slightly soluble in H2O & soluble in organic solvents & oils
-Form lipid-soluble complexes with polar cations (Na+, K+, Ca2+, Mg2+) that are transported across cellular membranes
Toxicokinetics of ionophores
- PO
- Ru absorb ~ 50%, Monos absorb most
- WD
- B+ & tissue lvls relatively ↓
- P-450 rapid metab (except in Eq) excreted mainly in bile
Toxicity of Ionophores
- All susceptible
- Eq > sensitive followed by adult Tk
- Concurrent admin of other Rx↑ toxicosis: ♥ glycosides, Tiamulin (DOC tx mycoplasma in LA, Fluro in SA) Chlor-amphenicol, Erythromycin, Sulfonamides (inhibit microsomal enzymes)
MOA or Ionophores
-Disrupt transmembrane electrochem gradients
-Mitochondria of highly energetic tissues main target (myo♥, SKM, K, GI mucosa)
-Influx of the Na+-ionophore complex ↑ing intracellular Na+& Ca++
-Sequestering of Ca++ by mitochondria & inhibition of mitochondria & ↓ATP & E
-Cell death d/t disrupting homeostatic mechanisms
-Disruption of [ion] in excitable cells (neurons,
myo♥, SKM, SMM) alters their functions
CS of equine ionophore toxicity
Anorexia, profuse sweating, colic, depression, incoordination, HrVent, tachy♥ tachyarrhythmias, prostration, & death
-Mainly ♥muscle lesions (pale ♥muscles, white streaks of necrosis in myo♥) & some SKM
CS of bovine ionophore toxicity
Anorexia, diarrhea, ↓, labored breathing, ataxia, prostration, & death
CS of poulty ionophore toxicity
Anorexia, diarrhea, ataxia, resting on the knees with wings & legs directed outward, & ↓egg production
-Both SKM & ♥muscle lesions in Bv & Av
K9 CS of ionophore toxicity
Ataxia, muscle weakness of hind limbs, resp paralysis, dysuria, constipation, & ↓
-Mainly SKM lesions in Ov, PC & K9s (pale SKM)
Lab Dx of ionophore toxicity
Chem analysis for ionophores • Methods detect ppb levels, FEED, GI contents, L, & feces Clin Path • ↑enzymes of muscle origin (CPK, AST) • Others: ↑(LDH, ALP) • ↑PCV • ↓serum Ca2+ & K+ w/in 12h
Dx of ionophore toxicity
-Hx of feed problem, CS, Lesions, Lab dx
Tx/Prevent ionophore toxicity
-None specific
-Remove source
-↓ing absorption
• AC, Mineral oil, saline cathartics
-Symptomatic Tx
• IV fluid & electrolyte therapy (to correct HoVol & support
♥vascular & renal functions)
•K+ if
