NON-METAL

POISONING
M.PAVITHRA
MVM19034
CHLORATE TOXICOSIS

Source – weedicide, defoliants, dry salt (sodium chlorate)

Chlorate toxicosis has been reported in cows, sheep, horses, chickens, dogs and
humans
species Lethal dose
cattle 1 g/kg
sheep 2 g/kg
Poultry 5 g/kg
Dogs 1.5 – 3.5 g/kg

Cattle are more often poisoned than sheep

MECHANISM OF TOXICITY

• Chlorate – strong oxidizing agent that converts hemoglobin to methemoglobin

• This process is slow when compared to nitrite poisoning
• It increases fragility of red blood cell membranes, which may result in intravascular
hemolysis
• Chlorates also result in formation of low concentration of sulfhaemoglobin
(partially oxidized and denatured) – not life threatening
CLINICAL SIGNS

GI symptoms – vomition, diarrhoea, colic, etc

Hematuria, hemoglobinuria, blood from natural orifices which clots readily
Later respiratory distress
Acute cases – death without any clinical signs

POSTMORTEM LESIONS

Generalized cyanosis
Blood – dark chocolate colour
Brownish discoloration of organs and tissues
Blood from natural orifices
Gastroeneteritis as chlorate is directly irritant to GI tract
DIAGNOSIS

• History
• Clinical symptoms
• Dark color blood and muscle
• Liver almost black and heart is flabby and dark
• Analysis of blood, urine, tissues and ruminal contents for chlorate
• Concentration of met-Hb increases even after death of animal
DIFFERENTIAL DIAGNOSIS

Nitrate poisoning – no blood from orifice

Cyanide poisoning – blood bright red
Hydrogen sulphide – dark color blood
Carbon monoxide – bright red blood
Warfarin poisoning
Poisoning from other hemolytic agents
TREATMENT

Unlike nitrate toxicosis, methylene blue treatment of chlorate toxicosis is often

disappointing because chlorate also denatures glucose-6-phosphate dehydrogenase.
(The antidotal effect of methylene blue depends on NADPH produced by glucose-
6-phosphate dehydrogenase.)

In addition to methylene blue treatment (4 mg/kg in dogs, 10-15 mg/kg in cattle),

treatment should also include gastric lavage and vitamin C (20 mg/kg).
FLOURINE TOXICITY

SOURCE

• Found in combination with many elements

• Fumes or effluents from industries settle on fields, pastures or water reservoirs
• Also gas or smoke from volcanic eruptions also result in contamination
• Animals with a long, productive life span such as dairy cattle are more susceptible.
ACUTE FLOURINE POISONING

• Occurs due to accidental ingestion of large quantities of fluorine containing

salts
• Sodium fluoride – vermifuge
• Sodium fluoroacetate – rodenticide

Pigs commonly affected

Lethal dose
4-5% of sodium fluoride – pigs
Fluorosilicate – 100 mg for equines
200 mg for bovines
MECHANISM OF TOXICITY
Strong irritant produce gastroenteritis
Increases permeability and cause coagulation defects, hemorrhage, edema
particularly in brain
It inhibits number of enzymes – preglycolytic, phosphatases and cholinesterase there
by increasing the sensitivity of body to acetylcholine
CLINICAL SIGNS

Vomition, anorexia, salivation, ruminal stasis, abdominal pain, diarrhoea, weakness,

excitability, muscle tremors, pupillary dilatation, clonic convulsions, coma and death
due to respiratory and cardiac collapse

POSTMORTEM LESIONS

Hemorrhagic gastroenteritis
Congestion of liver and kidney
Bone and dental lesions are absent
TREATMENT

No specific antidote
Symptomatic treatment – GI sedatives
Intravenous infusion of calcium salts and glucose solution
CHRONIC FLOURIDE POISONING – FLUOROSIS

Non fatal syndrome

Due to consumption of contaminated water or fluoride containing feed supplements
It gets deposited in bone and teeth without any signs of toxicity
Bones and teeth – sink , 95 to 96% deposited

Sources of poisoning
Feed, fodder, water, mineral supplements rich in fluorine
Top dressing of pastures with phosphate lime stone
Factors affecting toxicity

• Solubility of the compound – sodium fluoride is more toxic when compared to

calcium fluoride
• Amount ingested
• Duration of exposure
• Rate of excretion
• Age of the animal
• Nutritional status of the animal
• Individual susceptibility and resistance
• Stress factors
• Species variation, etc
dairy cattle > beef cattle > sheep > horses > pig > poultry
MECHANISM OF TOXICIY

Fluoride interferes with excretion of calcium or osteoclast activity

It replaces hydroxyl radicals in apatite crystals resulting in abnormal osteoid – poor
bony matrix and irregular mineralization
Also inhibits enzyme involved in bone and teeth formation
Deposition of fluoride in bone occurs throughout the life but in teeth only during
formative stage (so dental lesions absent in adult even in severe cases)

In bones, deposition is higher in periosteal surface of long bone - exostoses

Also produce degenerative changes in bone marrow, kidney, liver, adrenal glands, heart
muscles and CNS

Two forms of fluorosis

1. dental fluorosis
2. osteofluorosis

DENTAL FLUOROSIS
Lesions are painful
Earliest sign – mottling ( light yellow green, brown or black spots or bands arranged
horizontally) occurs mostly on incisors
Teeth give dull, opaque, white and chalky appearance

Later mottled areas become

pits, teeth become brittle and
break unevenly and
sometimes reduced to the
level of gums
 Worst cases - shedding of teeth
Young ones- delayed eruption, hypoplasia of teeth
with wide gaps

• Due to uneven surface – mastication become

difficult – result in poor growth and acetonaemia
• Affected animals like to drink cold water to avoid
pain
OSTEOFLUOROSIS

Sudden onset of lameness, stiffness, painful gait and posture

Lameness – first in one leg and then to the other leg
Bones become palpably and visibly enlarged and thickened - observed on medial
surface of proximal third of metatarsal bones
Thickening and enlargement of mandible
Deformation of jaw, sternum, metacarpal, ribs, spine
Thickening of periosteal layer of long bones – exostoses
Other bone lesions are hyperostosis, Osteoporosis, enlargement
Bones become more prone for fractures
Other signs are loss of weight, intermittent diarrhoea, polydipsia, polyuria, poorly
concentrated urine, aplastic anaemia, reduction in milk and wool production,
anestrous, etc
Fluoride ions have no toxic effects on fetus

Postmortem lesions
Change of bone color from ivory to chalky white
Surface of bones enlarged, roughened and exostoses of long bones
PM lesions

• Mottling and cavities on teeth

• Bone marrow cavity diminished and show gelatinous degeneration and aplastic
anemia
• Bony trabeculae are thickened
• Degenerative changes in internal organs
• Kidney- degeneration and disintegration of tubular epithelium, thickened
arterioles and fibrosis
Diagnosis
• History
• clinical signs
• Postmortem findings
• X ray examination
• Fluoride assay of feed, water, blood, urine, bone, teeth and faeces

Differential diagnosis
• vitamin D deficiency
• Ca and P deficiency
• Parathyroid disease
TREATMENT

• Prognosis is poor
• No specific antidote
• Remove animals from contaminated pasture
• Correct mineral deficiency in food and rations. Add vitamin A, D to feed
• Symptomatic treatment using steroids, analgesics, antibiotics, fluid therapy
• Addition of aluminium sulphate 30g / day or calcium carbonate to feed. These
helps in absorption of fluorides from intestine
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