This document summarizes arsenic and lead poisoning in animals. It discusses sources of exposure, factors affecting toxicity, absorption and distribution in the body, mechanisms of toxicity, clinical signs, post-mortem findings, diagnosis, and treatment for both arsenic and lead poisoning. For arsenic, common sources of exposure include improper use of drugs, contaminated water or herbage, and overdose of feed additives. Clinical signs can be acute, subacute, or chronic and include gastrointestinal issues, neurological effects, and poor condition. Treatment involves chelating agents like Dimercaprol. For lead, sources include contaminated grass or foods, and exposure increases toxicity. Clinical signs vary by species but include neurological, gastrointestinal, and hematological

1. Arsenic and Lead Poisoning in
animals

2. Arsenic

3. Sources:
 Indiscriminate use of drug as a drug
for control of ectoparasites, blood
parasites and skin tonics
 Water, herbage contamination
 Animals licking wood preserved in
arsenical preparations
 Overdose of arsenical feed additives

4. Factors Affecting Toxicity:
 Species:
Herbivores>Dog,cats>fowl,swine
 Oxidation state: organic arsenicals<
Arsenate<Arsenite<Arsine
 Solubility/Form: Finely divided &
soluble-more toxic
 Status of animals: Dehydrated,weak,ill
and poor body condition- more
susceptible
 Tolerance: constant exposure-

5. Toxicokinetics:
 Absorption- Readily absorbed from all body
surfaces
 Distribution- Throughout the body
 High concentration in liver,kidney,heart & lungs
 High concentration in nails & hair because of
high sulphydryl contents
 Cross placental barrier
• Partly methylated in liver
• Excreted in urine, feces, bile,milk,saliva & sweat
• Lethal oral dose of sodium arsenite in most
species 1–25 mg/kg. Cats more sensitive. In
livestock, arsenates are 5–10 times less toxic
than arsenites.

6. Mechanism of Toxicity:
A. Trivalent Arsenic
Trivalent As
Binds with two sulphydryl groups of Lipoic acid
Stable six-membered ring
(As-Lipoic acid complex)
Inhibition of Glycolysis and TCA cycle
 Lipoic acid is a sulphydryl containing cofactor for the
enzymatic decarboxylation of ketoacids-pyruvate,
ketoglutarate

8. Mechanism of Toxicity:
B. Pentavalent Inorganic Arsenic:
Blocks Mitochondrial Oxidative
Phosphorylation
No ATP Production

9. C. Pentavalent Organic Arenicals:
 MOA-not clearly understood
 Pentavalent Organic Arenicals:
Interference with Vit.B
Demyelination and Axonal
Degeneration

10. D. Arsine gas:
 MOA-not clearly understood
 Arsine + Hb
React with O2
Hemolysis
Pulmonary Edema

11. Clinical signs:
 Acute , subacute or chronic
 Acute:
High morbidity & mortality
GI pain,colic
Diarrhoea,vomiting, Ruminal
atony,etc.
 Subacute:
Watery bloody diarrhoea
Depression,dehydration
Anuria

12.  Chronic:
Poor condition
Excessive thirst
Weak regular pulse
Nervous derrangement like ataxia,
incoordination and blindness

14. PM findings:
 GIT inflammation
 Rupture of blood vessel
 Liver- diffuse inflammation
 Kidneys-pale swollen

15. Diagnosis:
 Clinical signs
 PM findings
 Urinalysis

16. Treatment:
A. Dimercaprol / British Anti-Lewisite (BAL):
Large animals-3 mg/kg i.v. until recovery
Small animals- 2.5 mg/kg i.v. until recovery
B. Thiocitric acid
50 mg/kg b.w i/m tid (cattle)
C. Sodium Thiosulphate:
Horse & cattle: 20-30 mg; PO + 300 ml water
8-10 g i.v in 10% solution
 Emetics, Gastric Lavage
 Rehydration Therapy
 High protein diet

18. Sources:
 Grass near busy streets
 Licking of discarded batteries, paints,
etc.
 Milk secreted from lead-poisoned
animals
 Agricultural use of fertilizers,
fungicides, herbicides
 Drinking water from old lead pipes
 Lead parasiticide sprays particularly
those containing lead arsenate

19. Factors influencing Toxicity:
 Age: Young animals more susceptible
 Species: Goats, swine, chicken are more
resistant
 Reproductive state: Pregnant ewe more
susceptible than nonpregnant
 Rate of ingestion: large amount within short
time is more toxic
 Undernutrition and presence of other
debilitating factors
 Presence of food or ingesta in stomach or
intestine delays absorption and thereby
reduces toxicity

20. Absorption and Fate:
 Almost lead enters through ingestion
 Absorption from gut (only 1 or 2 %)
 85-90% binds to Hb in erythrocyte
 Remainder bind to serum albumin
 Less than 1% actually free

21.  Distribution of unbound fraction to various parts of body
 Mainly sink in bone (90-98%)
 Via portal circulation reaches to liver and then to
duodenum via bile
 Excretion via milk, urine and feces.
 Can cross Blood Brain Barrier and Placental Barrier
 Concentrations of lead in the blood at 0.35 ppm, liver at
10 ppm, or kidney cortex at 10 ppm in most species
 lead concentrations in blood >0.05–0.10 ppm to be a
notifiable disease in food-producing animals

22. Mechanism Of Toxicty:
 Toxicity mainly by inhibiting sulfhydryl
groups of essential enzymes of
cellular metabolism

23. A. Neurotoxic mechanism:
lead
Enter into brain cells
Disturbs the function of cellular calcium
Damage to capillary endothelium
Inactivates BBB
Cerebral edema & hemorrhages

24. B. Gastro-Intestinal toxicity:
 Specific mechanism-not understood
 Could be secondary to neurological
mechanisms
 Lead
Contraction of smooth m/s of intestinal wall
-gastroenteritis
-anorexia
-Vomition
-Colic

25.  C. Haematopoietic toxicity:
 Inhibition of Heme synthesis by
inhibiting key enzymes involved in
synthesis eg. ∂-ALAS,∂-ALAD, HS
Inhibits Na+/K+ ATPase pump
Attach to RBC membrane
Lysis of RBC

26. D. Immunotoxicity:
 Decreased production of Antibodies
E. Nephrotoxicity:
 Inhibition of cellular respiration
Generalized dysfunction of renal tubular & energy
dependent function
F. Endocrine toxicity:
o Decreased release of GH & insulin growth factors
G. Reproductive toxicity:
 Gametotoxocity (both male and female)

27. Clinical Symptoms:
 Acute or Chronic
 Acute:
 common in cattle
 Bellowing, rolling eyes and frothy mouth
 Excitation followed by quiscient phase
 Muscular spasm, tetany and death
 Chronic:
 Anorexia, constipation, recumbency and death
(cattle and sheep)
 Paralysis of limbs, anorexia, jaundice, nasal
discharge, Roaring due to laryngeal muscle
paralysis (Horse)

28.  Pigs- considerably resistant
 Dog- i) Gastrointestinal symptoms
(anorexia, vomiting, colic, diarrhoea)
ii) Nervous symptoms (anxiety,
hysterical barking, salivation,
convulsions)
 Cats- not very common
 Birds- anorexia, ataxia, excitement,
loss of condition;decrease in fertility,
hatchability and egg production; High

29. Post-Mortem Lesions:
 No observable gross lesions
 Stomach and intestine may present
ingested lead
 Brain edema, gastritis, hyperemia and
petechiae on various organs

30. Diagnosis:
 History, Clinical signs, PM lesions,
lead content in body inclusions
 Measurement of ALA dehyratase in
blood
 Urine ALA is increased
 Level of lead >4 ppm in liver , 0.2 ppm
in whole blood indicates lead
poisoning

31. Differential Diagnosis:
 Hypomagnesemic tetany
 Tetanus
 Vit.A deficiency
 Listeriosis
 Barley poisoning
 Encephalitis
 Acute pancreatitis
 Hepatitis
 Encephalits Dog
 Rabies
 Distemper

32. Treatment:
 Calcium Ethylenediamine tetra acetate (EDTA) as an
antidote
 Cattle and horses:110 mg/kg i/v or s/c two doses @
6hrs. Interval every other day for three treatments
 Dogs: 110 mg/kg s/c as 1% solution diluted with
0.9%saline divided into four doses every other day for
three treatments
 BAL increases lead excretion in urine
 Intestinal lavage or a cathartic to eliminate the
unabsorbed lead
 Vit.D and Ca-borogluconate give additional support
 MagSulf will prevent further absorption of lead by
reducing lead solubilty
 Cerebral oedema can be controlled using
dexamethasone and mannitol
 Broad spectrum antibiotics to control secondary
bacterial infection

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