Toxicology 2 Course 8: Food Additives and Intoxication in Animals

CONTENTS

• FEED ADDITIVES
• SALT
• UREA
• ORGANIC DERIVATIVES OF ARSENIC
• COPPER

Emanuela Badea
assistant professor | DVM | PhD | MSc
Faculty of Veterinary Medicine of Bucharest
UASVM

IV. FEED ADDITIVES

IV. 1. SALT

Salt is used as a feed additive in combined feed, in proportion of 0.3-0.8 % in pigs, 0.2-0.3 % in
hens, 0.15-0.2 % in turkey poults, 0.2-0.25 % in turkeys, 0.5 % in calves and lambs, 1 % in cattle
and sheep over three years old.
Excess salt causes significant economic damage, especially in the most susceptible species
(pigs and birds), but also in species with a higher tolerance, such as ruminants.

Causes of Salt Intoxication

Intoxication occurs in pigs when feed exceeds 0.8-1 % salt concentration.
In birds, intoxication can appear when salt is administered in the amount of 1-2 g in chickens of
0.5 kg, 5-6 g in chickens of 1 kg, and 10 g in adult birds, under the conditions of water restriction.
In large ruminants, the toxic dose is 1 g/kg, in sheep 250 g/animal, and in lambs 125 g/animal. In
minks and foxes, the toxic concentration is about 3%, but intoxication can also occur at 2% in
the case of water deficiency.
Generally, a diet containing from 0.5-1% salt is normally acceptable, but can become toxic if
water is withheld or water intake is reduced. More than 10% of the diet may be salt if adequate
water is available. Increased urination will occur, but not an intoxication.

Toxicodynamics of Sodium Chloride

The toxicity of sodium chloride is mainly due to excess sodium ion, which is considered a true
tissue purgative.
The sodium ion is involved in neuromuscular physiology and water economy in the body, but, in
excess, it acts in two directions: a special ionic action and a general osmotic action, producing
disorders of nerve physiology and hydro-electrolytic imbalance.
In salt poisoning, during the first 4-6 hours there is a brutal reduction in the water content of the
cells of muscle tissue, the nervous system, and the liver parenchyma, which will subsequently
recover, but without reaching the initial water concentration, with adverse consequences on
metabolism.

Salt Intoxication in Pigs

Causes of Intoxication in Pigs

The causes of intoxication are:
. the incorrect dosing of salt in feed
. the inadequate homogenization of premixes or long-distance transport that can lead to
decantation
· administration of feed intended for other species
2. access to salt blocks destined for other species
. the administration of brine from the industrialization of milk or fish
. restrictions on water supply

Clinical Signs in Pigs

In general, the intoxication evolves acutely. The animal has polydipsia (very severe thirst),
anorexia, tachycardia, tachypnoea, which occur 1-3 hours after feeding.
The following sings are also observed: initially mild hyperthermia then hypothermia, congestion
of the oral mucosa, salivation with empty chewing, vomiturition and vomiting, diarrhoea,
agitation, aggressiveness, tremors, tonic-clonic contractions interrupted by longer and longer
periods of drowsiness, bruxism, myoclonic contraction of the diaphragm, anteropulsion,
retropulsion, circular gait, paraparesis, dog sitting, paralysis of the pharynx, enophthalmia,
amaurosis, and dyspnoea.

Anatomopathological Changes in Pigs

Anatomopathological changes are represented by anaemia, watery blood, catarrhal
gastroenteritis, hepatic dystrophy, congestion and cerebral oedema. Histopathologically,
vacuolization of neuronal nuclei, perineural oedema, vasodilation, hyaline thrombi,
eosinophilic meningoencephalitis (considered pathognomonic) are observed.

Diagnosis of Salt Intoxication in Pigs

The diagnosis is based on the clinical signs, lesions, and feed control (NaCl identification and
dosing).
Differential diagnosis should include Aujeszky's disease, classical swine fever, solanine
intoxication, and organomercurial fungicides intoxication.

Treatment for Salt Intoxication in Pigs

It is recommended to administer water, per os, in small amounts, repeatedly, slow perfusions
with calcium and magnesium gluconate, glucose solutions, gastric protectors, anticonvulsants,
and antidiarrheal drugs.

Salt Intoxication in Poultry

Causes of Intoxication in Poultry

Salt intoxication in poultry generally occurs as a consequence of
· higher salt intake because of overdosing the feed additive, either by mistake or as a
result of technical malfunctions
. lack of homogenization of salt in the combined feed
. long-distance transport (during which decantation can occur)
· confusion with CaCO3
· watering deficiencies
· change of watering system (birds do not consume water for 1-2 days, intoxication
occurring in these situations even at non-toxic doses, salt having cumulative properties)
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Clinical Signs in Poultry

Intoxication evolves acutely or chronically. In the acute form the following signs are found:
polydipsia, anorexia, half-open beak from which a slimy-viscous liquid drips, diarrhoea, and
nervous phenomena represented by ataxia, lateral decubitus, sitting on the hocks, wings
hanging down, progressive paralysis, and death.
In the chronic form, anaemia (pale comb and wattles on a jaundiced background), diarrhoea,
weakening, and decreased egg production is observed.

Anatomopathological Changes in Poultry

Macroscopic lesions are represented by infiltration of subcutaneous connective tissue from the
head and neck region, proventriculitis, duodenitis, typhlitis, cloacitis, and haemorrhages in the
proventriculus. Histopathological lesions include eosinophilic encephalitis and eosinophilic
infiltration in the intestinal submucosa.

Diagnosis of Salt Intoxication in Poultry

The diagnosis is based on the clinical examination and anatomopathological changes, and
examination of feeding and watering conditions.
Differential diagnosis is necessary to rule out avian influenza, Newcastle disease,
encephalomalacia, infectious encephalomyelitis, hypovitaminosis A, intoxication with
organomercurial fungicides.

Salt Intoxication in Cattle

Causes of Intoxication in Cattle

Salt intoxication in cattle occurs especially in the case of insufficient water intake or of salty
water consumption (from regions with salty soils), pica syndrome, or because of mistaking salt
with calcium carbonate.

Clinical Signs in Cattle

The acute form is expressed by polydipsia, excitation phenomena, colic, tremors,
forestomaches' paresis, tachypnoea, and drying of the oral mucosa.
The chronic form evolves with inappetence, weight loss, severe diarrhoea that is non-
responsive to treatment, and decreased milk production.

Anatomopathological Changes in Cattle

Anatomopathological changes are uncharacteristic, represented by gastroenteritis and hepatic
dystrophy.

Diagnosis of Salt Intoxication in Cattle

The diagnosis is based on the anamnesis, clinical signs, and analysis of feeding and watering
conditions.
Differential diagnosis includes rabies, paratuberculosis, grass tetany, arsenic intoxication, and
organochlorine insecticides intoxication.
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IV. 2. UREA

Urea is a synthetic non-protein nitrogen substance, used exclusively in ruminant feeding as a
feed additive, subjected to the processes of conversion to protein in the rumen, under the
action of microbial enzymes.
Recommended doses are 60 g/animal/day in 1-year-old cattle, 90 g/animal/day in 2-3-year
cattle, 120-150 g/animal/day in 3-year-old cattle, and 15 g/animal/day in sheep.

Causes of Urea Intoxication

The cause of intoxication mainly consists of non-compliance with the technology of urea
supplementation in feed. No more than a third of the protein required by the body can be
substituted by urea. Additionally, non-compliance with the accommodation interval of the
ruminal microflora of a minimum of 14 days can cause intoxications.
Typically, urea is homogenized in the factory with dried beet noodles and fixed with stabilizers. If
it is in the form of granules in feeding stuff, decanting during transport can occur.
Other causes of intoxication could be poor homogenization (improvisations, untrained
personnel), stagnation of urea solutions (leading to recrystallization), and increased
concentration in some portions of the feed. Corn silage reduces tolerance to urea.
Administered in solution, urea is much more toxic.

Toxicodynamics of Urea

Urea, in the presence of rumen microbial urease, breaks down into ammonia and carbon
dioxide. Excess ammonia, absorbed into the circulation, is a powerful nervous and respiratory
toxicant, determining tetany and dyspnoea. Being an irritant of all tissues where it is eliminated,
it causes congestion of the mucous membranes (conjunctival, oral, ruminal) and pulmonary
oedema.

Clinical Signs of Urea Intoxication

Intoxication evolves over-acutely or acutely, with clinical signs appearing approximately 20
minutes after feeding. Initially, blepharospasm, frightened gaze, tremors, repeated defecation
and urination, tachypnoea, and bradycardia are observed.
Characteristic are exophthalmia, foamy salivation, colic, groans, retropulsion, lateral decubitus
with opisthotonos, clonic-tonic contractions, hyperexcitability. Cardiac tachyarrhythmia,
dyspnoea with periodic apnoea, tympany, sometimes mydriasis can also be observed.

Anatomopathological Changes in Urea Intoxication

Anatomopathological changes are represented by pulmonary oedema with vicariant
emphysema, subepicardial, subendocardial, and adrenal glands hemorrhages, congestion of
the ruminal walls. The pH of the ruminal juice is alkaline (> 8), and the meat is ammonia-
scented.
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Diagnosis of Urea Intoxication

The diagnosis is based on the clinical signs, i.e., the increased excitability and tendency to
tetany, 15-20 minutes after the consumption of the feed, and confirmation is obtained by dosing
the ammonia from the ruminal juice, especially in the case of forensic expertise.

Treatment for Urea Intoxication

The treatment is effective if instituted immediately, with acetic acid being used as a specific
antidote. For this purpose, vinegar, per os, diluted 1:1 with cold water, or glacial acetic acid 3-
4% can be used, in a dose of 3-5 liters in cattle and 0.2-0.5 L liters in sheep. Alternatively, a
mixture of equal parts of 10% sodium acetate solution and 10% glucose solution is
administered in a dose of 1-2 liters/animal.
Sour milk or whey can also be administered, in a dose of 4-5 L/animal, as well as 100-200 g
granulated glutamic acid in plenty of cold water, as it promotes elimination of ammonia. It is
also recommended to administer broad-spectrum antibiotics, per os, in cold water, to interrupt
the microbial conversion of urea into ammonia, as well as hydro-electrolytic rebalancing.

IV. 3. ORGANIC DERIVATIVES OF ARSENIC

Organic derivatives of arsenic (e.g., arsanilic acid, carbarsone, nitrarsone, roxarsone, etc.) have
been used as feed additives for promoting growth and improving feed efficiency in pigs and
birds.
Organic derivatives of arsenic were also used in the prophylaxis and treatment of enteritis with
unknown etiology (in pigs) and the prevention of infectious entero-hepatitis and histomoniasis.
Arsenic is one of the metals recognized as having carcinogenic effects in humans, therefore in
foodstuffs of animal origin it must have a concentration of 0.

Clinical Signs of Arsenic Derivatives Intoxication

In pigs, they are represented by inappetence, diarrhoea, ataxia, astasia, circular gait, and
amaurosis.
In birds, there is a reduction in growth. After 1-2 weeks, it followed by anorexia, weakness of the
limbs, penguin position, shaking of the head, keeping the eyes closed, avoiding movements,
and paralysis.

Anatomopathological Changes in Arsenic Derivatives Intoxication

In pigs, degenerative changes in the optic tract and nerves are observed, as well as increased
hepatic and renal arsenic concentration.
In birds, degenerative changes in the nervous system are frequently observed.
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