Poisoning by ingestion of excessive amounts of salt most commonly occurs in poultry and pigs but it may also occur in ruminants. The main factor determining whether toxicity occurs or not is the availability of drinking water at the time the salt is ingested. When unlimited fresh water is available, poisoning by salt is highly unlikely. In fact the salt poisoning syndrome is frequently referred to as water deprivation/salt poisoning.
The feeding of white whey from dairy factories without free access to water has caused salt poisoning in pigs. White whey is the liquid expressed from butter after the salt is added and it contains a high percentage of salt (4 7%).
Access to other salted food with limited or no water; for example feeding of household scraps. Pieces of corned beef, bacon and beans preserved in salt have all been incriminated in such cases. In one case reported (Wallaceville documents), a pot of porridge into which the contents of a salt container had fallen were fed to fowls with disastrous results. Improper mixing of poultry mashes and other proprietary feeds for pigs and poultry have also been incriminated. Another example was where meat meal from a boiling down works contained salted sheep skins.
Fitch have been poisoned by feeding salted tuna fish which had been steeped in brine. Sheep have also been poisoned by eating salt lick blocks to which they had not had previous access. They were also denied water. Dogs are usually considered to be fairly resistant to salt poisoning but in New Zealand several confirmed cases have been reported. For example dogs have been poisoned from eating salty meat and even drinking large amounts of seawater. The latter case involved a drover's dog moving cattle along a beach in hot weather.
Normal or high salt intake may occur when animals are turned onto a new pasture with a strange water supply (which they don't use) or a sudden change from fresh to more saline water may cause poisoning especially if animals are thirsty when first allowed to drink the water. Water in troughs, (as in Australia) may undergo evaporation in hot weather and lead to the concentration of salt with consequent poisoning of stock.
Frozen water supplies may lead to water deprivation. This form of salt poisoning is most commonly recorded in pigs 8-12 weeks of age but is also recorded in North America in feed lot cattle systems.
In countries where salt (NaCl or CaCl2) is used to melt snow on roads, there have been serious losses among wild animals drinking from slush at the roadside.
All species can be affected, but toxicity is mainly recorded in poultry, pigs and cattle. It has been reported in sheep and cattle grazing tidal areas in NZ.
Tissue and diet levels of sodium (salt) for Cattle, Pigs, Poultry & Dogs (% of feed, mEq/L serum).
| Pigs | Cattle | Poultry | Dogs | |||||
|---|---|---|---|---|---|---|---|---|
| *Feed | +Serum | Feed | Serum | Feed | Serum | Feed | Serum | |
| Normal | 0.09-0.18 | 140-150 | 0.18-0.67 | 135-150 | 0.15-0.3 | 122-160 | 1 | 140-148 |
| High | 2 | 150-180 | 3-5 | >150 | 0.4-0.7 | |||
| Toxic | 4-7 | 180-200 | >5 | >150 | 0.8-4 | >160 | >15 | >150 |
Failure of automatic waterers has led to poultry being poisoned and pigs unused to automatic drinking cups may be at risk because of water deprivation until such time as they learn to operate the water supply system.
Sodium is found in plasma at a concentration of 135-155 mEq/L while its level in cerebrospinal fluid (CSF) is usually 130-150 mEq/L. A passive transfer of sodium ions from plasma to CSF takes place, but the transfer is energy dependent. With prolonged water deprivation, the animal becomes dehydrated and haemoconcentration occurs so that the sodium concentration in the plasma rises to levels as high as 190 mEq/L. Passive transfer of sodium to the CSF may then take place and the sodium ion levels in this fluid also rise to maybe 185 mEq/L. High sodium ion concentration tends to inhibit anaerobic glycolysis at the blood brain barrier, the process from which the energy is derived which is needed for the return of the sodium in CSF to the plasma. The elevated sodium ion levels in the CSF and brain then tend to be retained in these tissues.
Excess plasma sodium can be excreted in the urine and this happens when the animal has access to water. But with the high levels of sodium in the brain and the CSF, water is drawn into these tissues causing oedema. The sodium cannot be returned to the plasma because of the dysfunction of the blood brain barrier. The persistent brain oedema causes the characteristic neurological syndrome seen in all species.
The clinical signs are most likely to occur when after high salt ingestion animals have sudden access to water which promotes rehydration and brain oedema.
There is loss of appetite, thirst, salivation, diarrhoea, shivering and abnormal gait. Pigs often walk backwards with head held almost vertically and assume a sitting position. They may circle, have apparent blindness, normal temperature but ears and skin feel cold. Death takes place usually within 24 72 hours after onset of signs, but is preceded by violent paddling and running convulsions. In "chronic salt poisoning" there may be an initial pruritis or development of the "vegetable" pig, (such animals are just recumbent and semi comatose).
The possibility of birds dying from salt intoxication depends to a large extent on the form in which the salt has been ingested i.e. whether dry, moist or in solution. Birds appear to be susceptible to relatively small doses of salt in their drinking water; concentrations as low as 0.54% causing severe mortality in day old chicks. Salt given in wet mash is more dangerous than if given dry particularly to chicks. Adult birds are less susceptible and can tolerate up to 20% in the ration if they have access to water. Ducks are very susceptible to the toxic action of salt the addition of 2% to feed will depress growth and lower fertility. There are three main reasons for the frequency of salt intoxication in young chicks:
The main clinical signs shown are excessive thirst, diarrhoea, nervousness, convulsions, leg paralysis and weakness.
There are also fluid discharges from the back, and wet faeces are seen. Respiratory distress is also a feature.
Salt poisoning in cattle and sheep is characterised by hyperexcitability, and frequently apparent blindness. Incoordination and knuckling over at the fetlocks is a feature as is walking in circles and standing motionless with their backs arched.
Head pressing is seen in some animals and dragging the dorsum of the fetlocks on the ground is frequently seen.
They show thirst, salivation and frequently diarrhoea with abdominal pain. Death usually appears within 24 hours of the onset of clinical signs.
Salt poisoning is much less common in the dog than in other species. Poisoned dogs show signs of ataxia, blindness, convulsions and these terminate with death in 24 hours.
Gastroenteritis may be evident in some pigs poisoned with large doses of salt but in chronic poisoning there are no consistent gross lesions. Histologically the lesions of chronic poisoning in the pig are characteristic: there is acute cerebral oedema andmeningoencephalitis with eosinophilia of the meninges and perivascular spaces around the blood vessels of the brain.
In pigs that survive the acute stages there may be a residual cerebro cortical mid laminar necrosis with vacuolation.
There may be haemorrhage in the digestive tract and deposits of uric acid in the kidneys, ureters and droppings. Other dominant features include hydropericardium, a non fibrinous ascites, lung congestion and oedema.
There is congestion of the mucosae of the omasum and abomasum and may be oedema of the skeletal muscles and hydropericardium. Brain lesions similar to those of pigs are also seen but eosinophilic menigo encephalitis is not a feature.
Cerebral oedema, gastritis, liver and kidney congestion, lungs collapsed and full of blood are all reported.
Food and water if available may be sent for sodium assay.
In all species, serum sodium levels in live animals or sodium levels in the fresh brain and aqueous humor, may be helpful.
The treatment of affected animals is usually unsuccessful, however the following actions can be taken.
Drinking water for all classes of livestock should not contain more than 0.5% NaCl or total salts. Water should always be available. The standard recommendation for prepared feeds is 2% salt.
Clarke, E.G.C. and Clarke, M.L. (1975). Veterinary Toxicology. Bailliere Tindall. London. 50 52.
Howell, J. (1992). Salt poisoning in broiler chickens. N Z vet J. 40:36.
Howell, J. and Gumbrell, R.E. (1992). Salt poisoning in broiler chickens. N Z vet J. 40:85.
Khanna C. Boermans H.J. (1997) Fatal hypernatremia in a dog from salt ingestion. J of Am Anim Hosp Assoc. 33 (2):113 7.
Paewai, R.H. (1977). Water intoxication/salt poisoning in dogs N Z vet J. 25:195.
Puls, R. (1988). Mineral Levels in Animal Health. Sherpa International, P.O. Box 2256, Clearbrook, British Columbia, V2T 4X2 Canada. 55 60.
Seawright, A.A. (1982). Animal Health in Australia 2: Chemical & Plant Poisons. Australian Bureau of Animal Health. 177 179.
Smith, B. and Fyfe, B.H. (1971). Suspected acute salt poisoning in sheep. N Z vet J. 19:220 221.
Surveillance1974, 1(1): 7.Ingestion of saltwater by cattle.
Surveillance 1974 1(2): 22. Salt poisoning.
Surveillance 1976 3(3): 6. Salt poisoning of cattle and dogs.
Surveillance 1977 4(3): 24. Weekend scare (salt poisoning of pigs).
Surveillance 1978 5(3):Salt poisoning of pigs.
Surveillance 1978 5(4): 23. Salt intoxication syndrome.
Surveillance 1980 7(3): 20. Salt poisoning of dogs.
Surveillance 1980 7(4): 10. Salt poisoning of ducklings.
Surveillance 1982 9(1): 23. Sheepskins cause salt poisoning of fowls.
Surveillance 1982 9(4): 21. Salt poisoning of sheep.
Surveillance 1982 9(4): 22. Salt poisoning of cattle.
Surveillance 1999 26(2):17. Salt poisoning of cattle.