You are on page 1of 104

Presenter

Dr. Nishant Shah


M.V.Sc. (Medicine)
Mode of action of poisoning
Broadly classified in 2 major groups
1. Specific action
2. Non-specific action
1. Specific action
Toxicant > alter the functions of specific macromolecules
components (as receptors, ion channels, enzymes & carrier
molecules) > initiate the biochemical and physiological
changes
Eg.: Receptors - Strychnine, Morphine, Atropine
: Ion channels - Barbiturates, Chlorinated hydrocarbon,
Insecticides
: Enzymes - Cholinesterase enzyme
: Carrier molecules - Proteins
Mode of action of poisoning…
2. Non-specific action
a. Physical toxicant. Eg. Heavy metal, dust, asbestos,etc.
b. Direct chemical injury. Eg. Acid, base, formaldehyde, etc.
c. Impairment of oxygen transport. (Eg. Cobalt)
d. Injury to blood and vascular system. (Eg. Warfarin)
e. Altered Ca homeostasis. (Eg. Peroxides)
f. Immunomodulation. (Eg. Mycotoxins, inseticides, heavy
metals)
g. Developmental defect.s (Eg. Heavy metals, quinine)
h. Carcinogenesis. (Eg. DDT)
i. Interference with body metabolism or synthesis:
 Uncoupling of oxidative phosphorylation. (Eg. Fugicides, Arsenates)
 Inhibition of nucleic acid & protein. (Eg. Alfatoxins)
Factors affecting toxicity
(1)Dose: High level of exposure cause more intense toxicity
depending on the dose, use and toxicity etc.
(2)Physico-chemical properties: Toxicity depends on the physical
state of the compounds, solubility etc. A solid toxic compound
is less toxic than powder form. Finely powdered form is more
toxic to course powder and gaseous form is more toxic than
solid or liquid form.
(3)Chemical nature of compounds: e.g.: CO2, CO, BaSO4, etc
(4)Nature of exposure: Intensity of poisoning depends on
multiples single or repeated dose. Several low doses of
poisons will be more effective in producing toxicity than a
single moderate dose.
(5)Route of exposure: It determines the rate and extends of
absorption.
(6)Age: Very young and old are more susceptible to toxic effect.
The mechanism of detoxification and rate of elimination is not
fully developed in young animals.
Factors affecting toxicity….
(7)Sex: Generally females are more susceptible than male.
(8)Species: Toxicological effect varies greatly qualitatively
and quantitatively from species to species.
(9)Pathological condition: Biotransformation and
elimination process are greatly alter during disease
condition.
(10)Concurrent exposure: If the animals are simultaneously
exposed to other drugs the toxic effect may be increased.
Enzyme causes the quantitative and qualitative changes of
toxic effects.
(11)Dietary factors: A high protein factors usually increases
biotransformation of Xenobiotics.
(12)Sources: Chances of poisoning may be enhanced or
reduced based on its nature and sources.
Treatment of poisoning
1. To decrease the absorption of toxicant.
2. To decrease the distribution of toxicant.
3. To increase the threshold level of toxicity.
4. To increase the elimination of absorbed
toxicant.
5. To increase the metabolic conversion of
absorbed toxicant
6. Management of poisoning.
1. To decrease the absorption of toxicant
1. To decrease the absorption of toxicant
Can be done by-
A. Specific Rx
B. Non-specific Rx
A. Specific Rx
B. Non-specific Rx
Emesis
Gastric lavage
Adsorption therapy
Purgation/catharsis
Enema
Cleansing of eyes
Gastrotomy or rumenotomy
Dilution
Cleansing of skin or hair
Material to be used:
 Emesis:
Locally acting - 3% H2O2, 1% CuSO4 soln, 1% ZnSO4
soln, 25% NaCl
Centrally acting - Apomorphine HCl, Xylazine
 Gastric lavage: KMnO4 soln (1:2000), Tincture
iodine (1:250 of 5% soln), Tannic acid soln,
NaHCO3
 Adsorption therapy: Activated charcoal
 Purgation/catharsis: NaSO4, MgSO4,Sorbitol
(70%),
 Enema: Warm water , Soap soln
 Dilution: Water or milk + Egg white
2. To decrease the distribution of toxicant
Can be done by-
A. Specific Rx
B. Non-specific Rx
A. Specific Rx

A. Non-specific Rx
Ion-trapping - (Urinary acidifier: NH4Cl,
alkaliniser: NaHCO3 )
Alternate binding sites: Albumin infusion
3. To increase the threshold level of toxicity
3. To increase the threshold level of toxicity
Can be done by-
A. Specific Rx
B. Non-specific Rx
A. Specific Rx
B. Non-specific Rx
i. Rx of respiratory depression:
 Mechanical ventilation or oxygen given
 Respiratory stimiulants as doxapram
ii. Cardiac disturbances monitoring by cardiac
arrhythymic drugs
iii. Shock control by fluid therapy, blood transfusion
iv. Control of acid-base disturbance and electrolyte
imbalance by NaHCO3, Na-lactate
v. Rx of CNS dysfunctions by diazepam and
phenobarbitone
vi. Rx of hypothermia & hyperthermia
vii. Uresis maintenance by osmotic diuretics as mannitol
4. To increase the elimination of absorbed toxicant
4. To increase the elimination of
absorbed toxicant
Can be done by-
A. Specific Rx
B. Non-specific Rx
A. Specific Rx
B. Non-specific Rx
i. Ion-trapping:
 Urinary acidifier as NH4Cl, Ascorbic acid
 Urinary alkaliniser as NaHCO3
ii. Dialysis:
 Haemodialysis
 Peritoneal dialysis
 Haemoperfusion

iii. Diuresis by mannitol (20-25%), frusemide


5. To increase the metabolic conversion of
absorbed toxicant
6. Management of poisoning
Toxicity caused by Metals
& Non-metals
Arsenic
Lead
Mercury
Copper
Molybdenum
Iron
Iodine
Zinc
Selenium
Nitrate & nitrite
Phosphorus
Arsenic poisoning
Source:-
• Na and K arsenite and thioarsenite. They are frequently
used as insecticides, wood preservatives, and
weedicide.
• Contaminated herbage due to the use of lead (Pb)
arsenite and calcium arsenite.
• Household paint containing lead arsenite or arsenic
trioxide.
• Arsenic contaminated drinking water.
• Arsenic compounds used as poultry feed additives.
• Industrial contaminated pasture land.
• Ingestion of arsenic rat-bait.
• Over dose of arsenic medicinal compounds. (Acetarsol,
Arsphenamide etc.)
Toxic dose:-
Cattle:-
• 1-4gm Na-arsenite and
• 15-45gm arsenic trioxide is lethal.

Horse:-
• 1-5gm Na arsenite and 10-45gm arsenic trioxide is lethal.

Sheep and goat:-


• 0.5gm Na-arsenite and 1-3 gm arsenic trioxide is lethal.

Poultry:-
• 0.01-0.1gm Na-arsenite and 0.05-0.3gm arsenic trioxide is
lethal.
Mechanism of action:-
The mechanism of action may be summarized by
the following 3 ways:-
• Arsenic gives the irritation to the gastro-
intestinal mucous lining.
• Arsenic increases the capillary permeability and
simultaneously causes the dilatation of blood
vessels, which brings the lower blood pressures.
As a result, in per acute cases, animal may die
suddenly without showing any clinical sign.
• Arsenic binds the pyruvic oxidase enzymes and its
co-factor as a result TCA cycle and oxidative
phosphorylation process is disrupted.
Acute symptoms:- • Chronic symptoms:-
• Hemorrhagic diarrhoea. • Dermatitis.
• Severe colic. • Alopacia.
• Excessive thirst • Indigestion.
• Vomition and salivation. • No change in body
• Staggering gait. temperature.
• Paralysis of • Cold extremities.
hindquarters.
• Circulatory shock.
Post mortem lesion:- Diagnosis:-
• Intense rose-red inflamed – Case history.
stomach or intestinal tract. – Clinical signs.
• Extravasations of blood in – Post mortem
lesions.
the alimentary canal.
• Soft and yellowish
discoloration of liver.
• Edematous, swollen and
congested lungs.
• Hemorrhagic lesions in
heart and spleen.
Treatment:-
• Egg albumin, activated charcoal and 0.9%
saline should be administrated to prevent
further absorption. 3-5mg Dimercaprol or BAL
per Kg body weight intramuscularly for first
two days at four hours intervals.
• Then from 3rd days six hours interval and 12
hours interval until recovery. Here,
Dimercaprol acts as chelating agents.
• Na-thiosulphate may be used which replaces
the thio groups.
Lead poisoning
Source:-
• Licking of lead paint containing objects.
• Ingestion of lead pencil or lead batteries.
• Lad contaminated pastureland.
• Use of lead containing insecticide.
• Water supply through lead pipe.
Factors affecting the lead toxicity:-
• Age:- Young animals are considerably more sensitively
than older one.
• Species variation;- Goat, swine, and chickens are more
resistant than others.
• General body condition:- Poorly nourished, debilitated
and parasitized animals are more susceptible.
• Pregnancy:- Pregnancy is more susceptible than non
pregnant one.
• Forms of lead:- Soluble salts are readily absorbed.
• Presence of ingesta in intestine or stomach may delay
or reduce the rate of absorption.
• Previous exposure may reduce or delay the toxic effect.
• Intravenous route of administration is more effective
than others.
Toxic dose or toxicity:-
• 50-400-mg/Kg-body weight in lethal dose for all
animals.

Mechanism of action:-
• Lead particularly inhibits the conversion of heme
precursor D-amino lavaevulinic acid resulting the
inhibition of heme synthesis. Due to the
inhibition of heme synthesis anemia starts to
develop.
• Interfere with GABA & dopamine uptake which
ultimately inhibits neurotransmission.
Acute Symptoms :- Chronic Symptoms :-
• Gastro-intestinal disorders:-
• Gastrointestinal disorders:- Anorexia, lack of appetite,
Diarrhoea, abdominal pain, black color faeces, transient
salivation, vomition. constipation followed by
diarrhoea, abdominal pain
• Nervous sign:- Bellowing, (lead pain or lead colic).
jaw champing, rolling of • Neuro-muscular symptoms:-
eyes, twitching of ears, – Wrist drop
aimless jumping or – Foot drop.
jumping over the wall or – In co-ordination.
any objects. Head is – Muscular weakness.
pushed against the wall or – Paralysis.
objects; excitement, • CNS symptoms:-
blindness, staggering gait, – Disturbance of vision.
muscular spasm, titanic – Vertigo/feeling dizziness.
convulsion and death. – Insomnia.
• Restlessness
Diagnosis:-
• History.
• Clinical signs.
• PM lesions.
• Distribution of lead in serum.

Treatment:-
• Use of saline purgatives, emetics, gastric-lavage to prevent
further absorption.
• Use of sedatives to release from excitement and
convulsion.
• Use of atropine sulphate during salivation.
• Use of dextrose in case of dehydration.
• Use of Na-Ca additives/ Ca-EDTA may be used as chelating
agents to form a soluble non-ionized complex and is
excreted from the body through the urine or may be
deposited in gall bladder.
Mercury poisoning
Source:-
• Mercurous chloride commonly called “calomel”
which is used as purgatives.
• Mercuric chloride used as antiseptics.
• Mercuric oxide used as eye ointments.
• Mercuric iodide used as counter irritant and
fungicides.
• Mercurochrome used as eye lotion.
• Mersalyl used as diuretics.
• Phenyl mercury acetate, methyl mercury acetate,
chloride and hydroxide are used in seed dressing
or fungicides.
Mode of action:-
The mechanism of action may be summarized by
the following 3 ways:-
• Mercury gives the irritation to the gastro-
intestinal mucous lining.
• Mercury increases the capillary permeability and
simultaneously causes the dilatation of blood
vessels, which brings the lower blood pressures.
As a result, in per acute cases, animal may die
suddenly without showing any clinical sign.
• Mercury binds the pyruvic oxidase enzymes and
its co-factor as a result TCA cycle and oxidative
phosphorylation process is disrupted.
Toxic signs:-
• Bloody diarrhoea.
• Violet gastro-enteritis.
• Severe colic.
• Sub normal temperature.
• Dyspnea.
• Circulatory shock, collapse and death.
Treatment:-
• Egg albumin, activated charcoal and 0.9%
saline should be administrated to prevent
further absorption. 3-5mg Dimercaprol or BAL
per Kg body weight intramuscularly for first
two days at four hours intervals.
• Then from 3rd days six hours interval and 12
hours interval until recovery. Here,
Dimercaprol acts as chelating agents.
• Na-thiosulphate may be used which replaces
the thio groups.
Copper poisoning
Sources:-
• Cu salts are extensively use in the veterinary practice.
CuSo4 is frequently used as fungicide, destroying of
intermediate host specially snail; treatment of foot rot.
• Cu naphthenate is used as wood preservations.
• Cu carbonates used as seed dressing.

Mechanism of action:-
• It causes the inhibition of dihydropolydehydrogenase
enzyme which causes the inhibition of pyruvic acid and
alpha keto gluterate dehydrogenase. As a result, TCA
cycle and enzymes systems are disrupted.
Symptoms:-
Acute case:- Chronic case:-
• Severe abdominal • Hemoglobinurea.
pain. • Jaundice.
• Vomition etc. • Anorexia.
• Depression.

Treatment:-
•Ammonium molydate 50-500mg/ Kg body weight orally.
•NaSO4 300 mg/ Kg body weight orally.
Molybdenum poisoning
Sources:-
• When molybdenum is present in excessive amount in soil it
may be taken up by the plants and grasses to makes them
toxic to the animals.
Mechanism of action:-
• Molybdenum is deposited in the bone and kidney. In the
bone, it moves the phosphorus from the bone. It also
interferes on some enzymes, which is necessary for bone
formation and development.
Symptoms:-
• Weak bone, Loss of body weight, Loss of libido.
• Persistent severe scouring of faeces.
• Dyspigmentation of hair, Stiffness back and legs.
Treatment: - Symptomatic.
Iron poisoning
Mechanism of action:-
Selenium poisoning
Sources:-
• Selenium may be found in the soil in the form of organic or
inorganic compounds.
• The plants or grasses grown on selenium-contaminated soil
are the usual sources of selenium poisoning.

Toxicity;-
• 3-10mg per Kg body weight is lethal for large animals.

Mode of action;-
• It decreases the ATP production.
• It causes the inhibition of enzymes concerned with tissue
respiration.
• It replaces the sulphur molecules of essential amino acids.
Acute symptoms:- Sub-acute symptoms :-
• Rapid and weak pulse • Loss of body weight.
rate. • Loss of appetite.
• Prostration. • Moves in cyclic order.
• Cyanosis. • Partial blindness, Lacrimation.
• Dyspnea. • Lower head and ears.
• Polyuria. • Blood tinged frothy nasal
• Death. discharge.
• Coma and death.

Chronic symptoms :-
• The disease in chronic cases is
termed as blind staggers.
Treatment:-
• Strychnine sulphate 2-5mg/Kg Bd. Wt. Of I/M
or S/C.
• Sodium arsenite / Arsenic trioxide: 0.2-0.5
mg/Kg Bd. Wt. Orally.
• High protein diet can prevent selenium
poisoning.
• Use of saline purgatives.
Nitrate or nitrite poisoning
Sources of nitrate or nitrite poisoning:-
a) Plant source:-
• Halencha, Moyna, Shama, Sorghum, Napier, Para, lotus, cucumber
etc.
b) Chemical source:-
• Artificial manure containing Na, K and ammonium nitrate.
• Well water containing excess nitrogen.
• Use of herbicides.
• Therapeutics uses of nitrate in the treatment of cyanide poisoning.
c) Sources from soil materials:-
• Animal wastes.
• Sewerage.
• Decaying organic matter.
Factors altering the toxicity:-
• Use of nitrogenous fertilizer.
• Use of 2,4 dichlorophenoxy acetic acid weedicide.
• Rainfall following prolonged drought.
• Low land ensilage.
• Root of certain plants.
• Active stages of growth of plants.
• Empty stomach condition of the animal.

Factors decreasing the toxicity:-


• Washing of nitrate or nitrite containing feed materials.
• Addition of concentration in feed.
• Mixture of molasses in feed which can reduce the
absorption.
Mode of action of nitrate or nitrite poisoning:-
• Accumulate in the alimentary tract or in the rumen. Accumulated
nitrate causes irritation in the stomach or intestinal wall resulting
hemorrhage, diarrhoea, restlessness etc.
• Nitrate is converted into nitrite, which are the main toxic substances
in nitrate poisoning. Nitrite is ten times more toxic than nitrate.
• Normally ferrous hemoglobin binds with oxygen, which can cause
the easy transportation and releasing of oxygen to the body tissues
depending on their demand. After comes in contact with nitrite
ferrous hemoglobin causes the oxidation of ferrous hemoglobin to
ferric hemoglobin. This ferric hemoglobin cannot transportation
oxygen to the body tissues. As a result animals suffer from lack of
oxygen and finally animals may die from anoxia.
• In addition to this nitrite causes the relaxation of smooth muscle
resulting the vasodilatation and gradual loss of blood pressure. This
also accelerates the anoxic condition.
Symptoms of nitrate poisoning:-
• Restlessness
• Abdominal pain.
• Diarrhoea.
• Abortion in pregnant cases.
• Decrease milk yield.
• Open mouth breathing.
• Dyspnea.
• Death may occur due anoxia.

Diagnosis nitrate or nitrite poisoning:-


• From history and clinical signs.
• Chocolate brown color or dark red color of blood is the
main diagnostic tool for nitrite poisoning in living condition.
• Analysis of suspected materials.
Treatment of nitrate/nitrite poisoning:-
• 1% methylene blue at the rate of 5-9mg/Kg
body weight intravenously.
• Ascorbic acid at the rate of 5-10mg/Kg Body
weight subcutaneously.
• Saline purgatives, e.g.- NaCl, MgSo4.
• Drinking of cold water to inhibit the rate of
conversion of nitrate to nitrite.
• Oral administration of broad-spectrum
antibiotics.
• Oxygen therapy.
• Blood transmission.
Phosphorus poisoning
• Phosphorus is an essential mineral element.
Phosphorus homeostasis in the body is
controlled by hormonal and renal control
systems.
• Toxic exposures have been reported to occur
from its industrial use or from suicidal ingestion
of phosphorus-containing materials.
 There are three allotropic forms of elemental
phosphorus: white, red, and black phosphorus.
 The commercial product is 99.9% pure and may
have a slightly yellow color.
Sources of poisoning
 Phosphorus poisoning is of rare occurrence in
farm animals because of lack of exposure.
 Accidental ingestion of fertilizers, or immediately
from clumps of fertilizers on cultivated land,
fireworks, baits containing lumps of white
phophorus for pets, rats kept on the pastures
 Grazing of animals on the battlefield where
certain explosives have been used.
 finely divided phosphorus is mixed with fats and
oils to promote their absorption and over
consumption of such fats and oils results in
phosphorus poisoning.
Toxic levels of phosphorus in animals

• Vary greatly depending on in which state the


phosphorus is ingested.
• White phosphorus in finely divided form
causes toxicity in animals.
• Horses and oxen= 0.5 – 2 gms
• Pigs= 0.05 – 0.3 gms
• Dogs=0.05 – 0.1 gm
• Fowl= 0.02 gm
Mechanism of Toxicity
• Phosphorus can be absorbed into the systemic
circulation from the skin, lungs, and intestinal tract. For
all practical purposes, white and yellow phosphorus
are readily absorbed while red phosphorus is not. The
target organs of toxicity include the gastrointestinal
tract, liver, kidney, bone, and the cardiovascular and
central nervous systems.
• High mortality rates seen following white phosphorus
burns can be due to its absorption from the burned
surface, which may result in multi-organ failure (mainly
liver and kidneys), hyperphosphatemia, hypocalcemia,
and electrocardiogram (ECG) abnormalities.
Clinical signs
• Per-acute toxicity:
Death after showing intense abdominal pain, violent
convulsions, severe CNS depression, and coma.
• Acute toxicity
Salivation, nausea, vomition, severe diarrhoea with
mild abdominal pain, fever, polydypsia, polyuria.
The garlic-like odor is also detected in the vomitus.
Most exhibit symptoms of jaundice, hematuria,
oliguria followed by delirium, convulsions, coma and
death.
Signs of gastroenteitis appear in 1-2 hours and cause
of illness is 3-5 days depending on severity of toxicity.
• Chronic toxicity
Found rarely.
Post mortem lesions
 If death occurs within l-3 days, no significant
changes are seen, but garlic-odour of GIT
contents, is noticed.
 Liver is enlarged, pale and yellowish.
 Spleen is small and atrophied.
 Congestion and hemorrhagic inflammation of GIT.
 In birds, visible fumes of phosphorus can be
appreciated opening the gizzard.
 The effect of phosphorus damage is evident by
the extreme fatty changes seen on many organs; a
yellowish liver with marked fatty degeneration,
and severe jaundice are usually present.
Diagnosis

• History
• Clinical symptoms particularly acute
gastroenteritis.
• Garlic odour of the vomitus and intestinal
contents.
• Postmortem lesions.
• Estimation of phosphorus in the blood,
vomitus, intestinal contents and faeces.
Treatment
 No specific antidote is available
 Copper sulphate is a very effective to treat white
phosphorus burns, topical application of copper sulphate
to the burnt surface.
 Only tap water irrigations were found to be effective in
preventing death after white phosphorus burns.
 Activated charcoal, emetics or purgatives are used for
removal of the agent.
• Having good lipid solublity, oily purgatives must be
prevented from used, and hence only saline purgatives
should be used.
• Supportive treatment should be provided with fluid
therapy.
Toxicity caused by pesticide or
agro-chemicals

Pesticides are the chemical agents, which are


used to kill the insect and pests. Pesticide is a
general term and insecticide is a class of
pesticide.
Classification of pesticide or agro-chemicals
A. Insecticides
1) Organophosphorus 2) Organochloronated compounds.
compound. a) DDT.
b) BHC
a) Malathion.
c) Endrin.
b) Sumithion. d) Dialdrin.
c) Diazinon. e) Aldrine.
f) Chlordane.
d) Parathion. g) Toxaphane.
e) Dimecron. h) Lindane.
i) Heptachlore.
f) Paraxon.
j) Methoxychlore.
g) Nagos. k) Enosulfan.
l) Mynex.
Classification of pesticide or agro-chemicals…

A. Insecticides…

3) Organocarbamate 4) Synthetic pyrethroid


compounds. compounds.
a) Furadan. a) Cypermethrin.
b) Sevin. b) Flumethrin.
c) Pyralan. c) Permithrin.
d) Zectran. d) Althrin.
Classification of pesticide or agro-chemicals…
B. Rhodenticides. D. Herbicides.
1) ANTU (Alpha 1) 2.4. Dichlorophenoxy
nephthal thio urea) acetate.
2) Warfarin. 2)4.5. Trichlorophenoxy
3) Red squill. acetate.
4) Sodium fluroacetate. E. Fumigates.
C. Fungicide. 1) CCl4.
1) Captan. 2) Hydrocyanic acid.
2) Folfet. 3) SO2.
3) Penta chlorophenol.
Sources of pesticides poisoning:-
A) Accidental exposure:-
1. Drinking of water from pesticide contained crop
field.
2. Ingestion of contaminated concentrate use of
animals.
3. Watering of animals in pesticides containing
container.
4. Spraying of walls with insecticides.
5. Keeping of insecticide with in the reach of animals.
6. Improper and indiscriminate use of insecticide and
its container.
7. Contamination of ponds, lake, river or water from
other sources due to the discharge of insecticides
industries.
Sources of pesticides poisoning…
B) Intentional exposure:-
1. Residues of pesticides on grains, pulses, vegetables.
2. Residues of pesticides from animal products like meat,
milk and eggs.
3. Consumption of pesticides from suicidal commitment.

C) Occupational exposure.
1. Workers in pesticides industries.
2. Faulty spraying of insecticides by unskilled workers or
defective equipments.
3. Dipping of animals.
4. Industrials contaminations.
5. Excess use of pesticides.
6. Excess access use of pesticide.
A. Insecticides

Organophosphorus (OP) poisoning


Mechanism of action
• Organophosphorus directly inhibit acetyl
cholinesterase enzyme by binding and
phosphorylation process. Due to the binding of
enzyme acetylcholine cannot be hydrolyzed. The
excessive accumulated acetylcholine causes the
excessive stimulation on muscarinic and nicotinic
cholenergic receptor and cholenergic synapses in
the CNS. The ultimate effect of accumulated
acetylcholine develops increase parasympathetic
action or parasympathomymetic action.
Symptoms:-
A. Muscarinic symptoms:- B. Nicotinic symptoms:-
• Profuse salivation. • Muscular tremor.
• Bradycardia. • Muscular twitching.
• Lacrimation. • Muscular spasm.
• Pupillary constriction. • Ataxia.
• Urination. C. CNS symptoms:-
• Conjuctivitis. • Hyper excitability.
• Diarrhoea. • Restlessness.
• Anxiety.
• Convulsions.
• Comma followed by
death.
Treatment:-
A. Atropine sulphate @ 0.2-0.5 mg/kg body weight. 1/4th
should be given by I/V and remaining dose should be given
I/M or S/C. The dose can be repeated after 4-5 hours if
needed.
Atropine sulphate prevents acetylcholine to accumulate in the
nerve endings.

B. Liquid paraffin can be administered in case of oral route of


poisoning.

C. Wash with detergents and running water in case of body


surface contamination.

D. Animal should be kept in quite and comfortable places.

E. Use of dextrose saline.


A. Insecticides..

Organochloronated poisoning
Mechanism of action:-
A) Organochloronated compounds cause the ionic
imbalance of Na and K.
B) It increases the cell membrane permeability.
C) It interferes the calcium metabolism.

• It normally deposited in adipose tissue and


excreted through milk that is why butter, cheese,
cream and ghee become public hazard.
• Females are more susceptible than male, young
animals are more susceptible than adult. Skin
wounds enhance the toxicity.
Symptoms:-
A. Acute cases:- ** Locomotion changes:-
** Changes in the behaviour:- • Walks on top toe.
• Excitement. • Staggering gait.
• Aimless movement or jumping. • Moves in a circle.
• Try to climb up the wall or objects. ** Miscellaneous:-
• Abnormal pasture. • High-rise of body
• Sternum on the ground. temperature.
** Neurological changes:-
• Twitching of eyelids. B. Chronic case:-
• Hypersensitivity to external stimuli. • Loss of body weight.
• Muscular tremor. • High level of blood
glucose.
• Convulsions.
• Developmental
** Autonomous changes:- anomalies.
• Mydriasis. • Thin egg shell in
• Involuntary urination. poultry.
• Salivation, vomition, diarrhoea.
Treatment:-
Dog:- Pentobarbital sodium @ 10-14 mg/Kg
body weight intravenously.
Large animals:- 10% chloral hydrate solution
intravenously.
Cat:- Thiobarbiturates @ 10-15 mg/Kg body
weight intravenously.
– Cold water bath.
– Washing of skin by detergents.
– Use of saline purgatives.
– Use of dextrose saline.
– Use of calcium borogluconate.
A. Insecticides..

Organocarbamate poisoning

Mechanism of action
• Organocarbamate are reversible inhibitors of
choline esterase enzyme.
Excretion
• They are rapidly metabolized and 80% is
eliminated through urine.
Symptoms:-
A. Acute case:- B. Chronic cases:-
• Profuse salivation. • In co-ordination.
• Vomition. • Ataxia, Prostration.
• Muscular tremor. • Recumbency, Anorexia.
• Depression. • Dyspnea, Cyanosis.

Post mortem changes:-


•Congested and edematous lungs, liver and kidney.
•Petechial hemorrhage of gastric mucosal lining.
Treatment:-
Same as organophosphorus (OP).
B. Rhodenticides

ANTU (Alphanephthalthiourea)

Mechanism of action
• It causes the dilation of the pulmonary
capillaries leadings to pulmonary edema and
increases the permeability of the pulmonary
membrane, resulting the excessive
accumulations of the fluid in the lung alveoli.
Symptoms:- PM lesions:-
• Pulmonary edema. • Edematous fluid in
• Circulatory distress. the lungs.
• Respiratory distress. • Swelling of the lungs.
• Accelerate pulse rate. • Hydrothorax.
• Increased heart beat.
• Watery diarrhoea. Treatment:-
• White foamy fluid Oxygen therapy.
discharge from the
nostrils and mouth.
• Salivations.
• Vomitions.
B. Rhodenticides..

Warfarin poisoning
Mechanism of action
• It is a member of anticoagulant developed as
rhodenticides. It is a coumarin derivatives. Rat
baits are usually made up by mixing one part of
commercial preparation containing 0.5-1.0%
warfarin with 10 parts of rat meal or other
diluent.
• It inhibits the synthesis of prothrombin in the
liver resulting the delayed blood clotting
mechanism and damages the capillary wall.
Symptoms:-
• Bloody diarrhoea due to the internal
hemorrhage.
• Blood comes out through urine and vomitous
and natural opening.

Treatment:-
• Vitamins K @ 0.5-2mg/ Kg body weight.
• Blood transfusion.
• Use of dextrose saline.
B. Rhodenticides..
Fluroacetate poisoning
Mechanism of action
Mycotoxin
• Mycotoxin are the secondary metabolites of toxigenic
fungi which are generally not essential to the normal
growth and reproduction of fungus but on consumption
cause illness or death in other species.
• Some of the important genera of fungi or moulds
producing toxins are as follows :-
– Aspergillus
– Penicillin.
– Fusarium.
– Claviceps.
Classification of mycotoxins
Aflatoxin
• Aspergillus flavus and A. parasiticus well on
sufficient moisture (more than 15%). Relative
humidity 90-95% and ambient temperature
24-250C.
• Aflatoxins are produced in a variety of grains
like maize, soyabean meal, oil cake, cotton
seed meal, wheat, berley, rice or other cereal
products.
Mechanism of action
• Inhibit or impaired protein synthesis.
• Defective enzyme synthesis which
ultimately affect the energy and fat
metabolism.
• Directly affect the endocrine system
causing hormonal imbalance.
• Also cause chromosomal aberration and
DNA breakage causing mutagenic effects.
3. Chronic toxicity:-
Clinical signs:-
A. In poultry:-
1. Acute toxicity:-
• Reduced egg production and
• Sudden death with in 72 hours sizes of eggs.
due to hepatic insufficiency
from exposure sufficient • Increases susceptibility to IBD,
quantities. Coccidiosis, Marek’s disease,
Salmonellosis, Pasteurellosis etc.
• Laboured breathing.
• Reduced weight gain and flock
• High-rise of temperature. performances.
• Bile stained urine in some • Ascitis.
cases.
B. In cattle:-
• Blood and mucous contain
diarrhoea. • Photosensitive dermatitis.
• Convulsions, vomitions. • Keratoconjunctivities.
2. Sub-acute toxicity:- • Circling movement.
• Internal hemorrhage due to • Frothing of mouth.
hypo-prothrombonenia. • Grinding of teeth.
• Hematoma. • Twitching of ear.
• Ataxia, Recumbency.
• Anal prolapse, Death.
PM lesions:-
• Liver is pale yellowish discoloration, Liver is fragile.
• Kidneys are yellowish and surrounded by fat in some cases in
calves.
• Serous exudates in body cavities.
• Eversion of rectum in cattle.
• Muscular hemorrhage, Catarrhal enteritis.

Treatment:-
• Withdraw of aflatoxin-contaminated feed.
• Provide easily digestible containing low fat and high protein
diet.
• Use of multivitamins, steroids, antibiotics activated charcoal
and liver tonic.
• Avoid stress.
• Use of 0.5% hydrated Na, Ca aminosilicate at feed additives.
Radiation hazard and toxicity
Types of radiation toxicity:-
1. Acute radiation toxicity.
2. Sub-acute toxicity.
3. Chronic radiation toxicity.
4. Local radiation toxicity.
Source of radiation:-
1. Natural: Cosmic rays, radioactive elements
disintegration, solar radiation
2. Nuclear weapon: Nuclear explosion
3. Nuclear power plants: Radioisotopes used in
industry, radioactive wastes, etc.
Mechanism of action
Can be explained by two ways:
1. Direct effects
2. Indirect effects
1. Direct effects:
 Direct transfer of radiation energy to molecules of
cells (esp. DNA) causing ionization and breakage of
linkage. Eg. Beta rays, alpha rays, gama rays,
neutrons
2. Indirect effects:
 Formation of free radicals which react with
macromolecule (nucleic acids, amino acids,
proteins. Lipids, CHO) and cause variety of genetic
and non genetic damage. Eg. H20 > H2+ & OH-
(highly reactive) which react and produce H2O2
(react with macromolecule).
Symptoms
1. Acute radiation toxicity:- 2. Sub-acute radiation
• Acute irritation of alimentary toxicity:-
tract resulting intense and • Anorexia.
refractory diarrhoea. • Vomition.
• Redness of skin. • Depression
• Excessive thirst, Weakness. • Swelling of legs.
• Recumbency, Laboured • Diarrhoea.
breathing.
• Profuse nasal discharge • Dysentry , Anemia.
containing blood. • Laboured breathing
• Impaired blood clotting and • Alopecia, Sterility.
antibody production. • Ulceration of skin.
• Gradual loss of hair. • Hyper irritability
• Ulceration of skin. • Embryonic death.
• Cataract, Genetic mutation. • Newborn mortality
• Death within 1-4 week • Stunted grown
Symptoms… PM lesions:-
3. Chronic radiation • Hemorrhagic & Ulcerative
toxicity:- gastro-enteritis.
• Alopacia • Ulceration of physiological
• Sterility mucosa.
• Genetic mutation. • Pulmonary edema.
• Leukemia • Extra-vasation of fluid.
• Tumors of thyroid, • Fibrinous pneumonia.
lungs and breast. • Pericarditis.
• Stunted growth. • Changes of color of bone
• Embryonic death. marrow.

You might also like