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Carbon monoxide
• One of the most common fatal poisonings, occurs by inhalation.
• CO is a colorless, odorless gas that results from incomplete
combustion of hydrocarbons.
Common sources of CO in poisonings:
• House fires and improperly vented automobiles, gas heaters,
furnaces, hot water heaters, wood- or charcoal-burning stoves,
and kerosene heaters.
• Carbon monoxide is produced due to incomplete combustion of
organic matter.
• CO is produced when natural gas (methane or propane) burns.
• Inhaling tobacco smoke results in CO in the blood but not enough
to cause poisoning
• Carbon monoxide has 200 times more affinity than oxygen for
• Carbon monoxide converts haemoglobin to carboxyhaemoglobin
and thus the oxygen carrying capacity is affected.
• Blood is bright red in colour and the mucous membrane is
healthy pink
• This poisoning commonly arises from exhaust fumes when
chicks are being transported by truck or from improper
ventilation in hatchers.
• Mortality may be high unless fresh air is provided immediately
• At necropsy, the beak is cyanotic, and a characteristic bright
pink color is noted throughout the viscera, particularly the
• Diagnosis can be confirmed by a spectroscopic analysis of the
• Patients should be removed from the source of CO and
stabilized as necessary.
• They are given 100% O2 (by nonrebreather mask) and
treated supportively.
• Hyperbaric O2 therapy (in a chamber at 2 to 3
atmospheres of 100% O2) typically should be
considered for patients who have any of the following:
Life-threatening cardiopulmonary complications, Loss
of consciousness (no matter how brief), A
carboxyhemoglobin level > 25%
• (the efficacy of hyperbaric O2 therapy is becoming more
controversial, with some studies suggesting harm)
• Prevention involves checking sources of indoor combustion to
make sure they are correctly installed and vented to the
• Exhaust pipes should be inspected periodically for leaks.
• Cars should never be left running in an enclosed garage (near
• CO detectors should be installed because they provide early
warning that CO is free in a dwelling's atmosphere.
• If CO is suspected in a dwelling, windows should be opened, and
the dwelling should be evacuated and evaluated for the source
of CO
• As a micronutrient (0.1-0.3 ppm), it is added to the diet to
prevent several deficiency disease states of cellular
degeneration and cell mEmbrane damage such as white
muscle disease in cattle and sheep, hepatosis dietetica in
swine and exudative diathesis in chicken.
• Dietary allowance of selenium above the requirements during
pregnancy has been reported to improve selenium status of
the newborn calves
• Enhances calf vitality and immune response; -important
micronutrients in the feed/diet of animals.
Sources of Selenium
• Plants – important source in ruminants
• Parenteral Se products (younger ones)
• Medicated Shampoos( SeS-in pets dermatitis,
• Insect repellants, lubrcicating oils, fungicides
( Se as antioxidant)
Seleniferous plants
• WOODY ASTERS (Xylorrhiza spp.);
• GOLDENWEEDS (Oonopsis spp.);
• Oxytropis spp.);
• Oonopsis spp. (GOLDENWEEDS);
• PRINCESS'S PLUME (Stanleya pinnata)
• Atriplex spp
• Selenium is present in inorganic and organic forms and all
animal species are susceptible to selenium toxicosis.
• Poisoning is, however, more common in forage eating
animals when dietary selenium level exceeds 5 ppm
• Severity of disease depends upon
– the oxidation state of selenium (selenide, selenite or selenate)
– quantity ingested
– Organo-selenium, after absorption in the form of selanomethionine
– May bc oxidize from selenide state to selenite or reduced from
inorganic selenate form to selenite.
– It is the selenite form which (selenium in selenite state may substitute
sulphur in the synthesis of aminoacids and proteins) is responsible for
• Variable amounts (25-70 %) of dietary selenium may be
eliminated within 2 days of ingestion of a large dose
• Gastrointestinal signs and lesions in acute selenium toxicity
are, in part, due to the irritant nature of selenium in large
• The biochemical effects due to
• (i) Replacement of sulphur of aminoacids such as cysteine
and methionine resulting in the synthesis of abnormal
proteins and enzymes.(hoof and hair defects of chronic
• (ii) Inhibition of SH - containing enzymes, such as succinic
and other dehydrogenases, may result in decreased ATP
• As a result of this, oxygen utilisation is decreased in liver,
kidneys and brain.
• Inhibition of cell oxidation-also due to interference with
haeme containing selenoprotein found in muscle tissue of
selenium - treated animals.
Toxicodynamics: ….contd

(iii) Drastic reduction in the tissue glutathione (GSH)

concentration occurring in the affected animals could be
brought about by direct complexion of two molecules of GSH
with every selenite ion.
• There is, perhaps, a competition between selenium and
sulphur in the regeneration or synthesis of GSH, stimulation
of liver and erythrocyte GSH-peroxidase activity (a selenium
containing enzyme) or a combination of the two.
Clinical signs:

Acute selenium poisoning:

• death usually follows within few hours after the consumption
of highly seleniferous feeds/forage.
Ruminants :
• abnormal posture, unsteady gait, peculiar "rooted-to-one
spot" stance with head and ears lowered,
• diarrhoea, polyuria, fever, mydriasis,
• abdominal pain, increased pulse and respiratory rates,
• blood tinged froathy nasal discharge, prostration and death
• Sheep, -depressed and die suddenly without any signs of
 Readily orally absorbed
 Distributed- throught- liver, kidney spleen
 Chronic- in hair and hoof
 Cross placental barrier( in eggs)
 May penetrate abraded skin
 Se after absorption in the form of
Selenomethionine – oxidized from selenide state
to selenite state or selenate – to selenite
 selenite form- toxic(sulphur substitute)
Chronic selenium poisoning:- two types
Blind staggers: Manifested in three stages:
 Animals intend to wander and may walk into objects. Usually,
the body temperature is normal. The vision becomes impaired
and the animal looses its appetite.
 The wandering increases, the front legs become weak and
the vision becomes further impaired.
 Throat and tongue become paralysed, body temperature
becomes subnormal and the animal dies from respiratory
 In sheep, these stages are less clearly differentiated.
Chronic selenium poisoning:- two types…contd
• Cracking of hooves, lameness. Stiffness of joints, d
• Dulness and lack of vitality, emaciation and loss of
• In horses, loss of long hair from the mane and tail
usually is the first clinical sign and is followed by
cracking of the hoof at the coronary band
• New growth of the hoof, dead tissue downward and
causes sloughing.
• In cattle- deformed hooves, 15-18 cm long and
turned upward, may be seen.
• Pigs: breaks in the hoof , In sows, conception rate
decreases and mortality of piglets at birth increases.
• Eggs (> 2.5 ppm of selenium) -low hatchability and
embryos are usually deformed, without beaks and
with ropy feathers.
• Biochemical changes : decreased fibrinogen levels
and prothrombin activity, increased serum alkaline
phosphatase, ALl', AST and succinic dehydrogenase
History, clinical signs
 PM Findings
 Lab confirmation – estimation
 laboratory confirmation in animal's diet
(feed, forage, grains) and blood or tissues
(liver, kidney). Selenium levels > 5 ppm in diet
blood Se- upto25 ppm, ; chronic Se tox. 1-4
ppm. In the hair or urine.
Necropsy findings
 Acute toxicosis- pulmonary congestion and oedema and
degenerative changes in liver and kidneys.

 Blind staggers- necrosis and cirrhosis of liver, enlargement

with localised haemorrhagic areas on the spleen.
 Congestion of renal medulla, epicardial petechiae, hyperaemia and
ulceration of abdomen and small intestine and erosion of the articular
surface (particularly of tibia) are seen at necropsy. Ascites is almost a
common finding.

 Alkali disease. Lesions almost resemble those of blind

staggers, the more pronounced being atrophy of heart and
atrophy and cirrhosis of liver
Differential diagnosis:
• Acute, Blind staggres: Pneumonia, anthrax, infectious
hepatitis, enterotoxaemia and pasteurellosis.
• Alkali disease: - ergotism, molybdenosis, fluorosis
and laminitis.
• The odour of rotton garlic or rotten horseradish in a
carcass is suggestive of acute toxicosis
• but absence of such an odour may not completely
rule out this condition because the volatile selenides
may escape quickly.
Treatment and preventive measures.
• No specific treatment or antidote
• Eliminating the source and exposure.
• Symptomatic and supportive care of affected
animals should be started as early as possible.
• A high protein diet, linseed meal, sulphur, arsenic,
copper and cadmium have been reported to reduce
selenium toxicity in laboratory species, but use of ail
these under field conditions needs confirmation
• Arsenic has been recommended in drinking water (5
ppm of arsenic as sodium arsenite) or arsenic salt
(containing 25 ppm of arsenic) or as arsinilic acid at
0.02% to reduce the incidence of selenium toxicity,