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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
Horse:-
• 1-5gm Na arsenite and 10-45gm 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.
• 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
A. Insecticides…
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
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.
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.
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.