9-week-old, female, large white pig, porcine (Sus scrofus)At a hog grower operation two sheds had been cleaned out and the water turned off from each shed prior to the introduction of a new batch of pigs. On a Thursday, 400 9-week-old grower pigs were introduced into each shed. It was not realized until the following Saturday that drinking water to each shed had not been turned on. The pigs engorged with water on Saturday and Sunday, and by Monday many of the pigs were paddling and had muscle fasciculation, others were blind, and many were having seizures or were down and non-responsive. To confirm the field diagnosis, the attending veterinarian collected and submitted to the laboratory three entire brains fixed in 10% neutral buffered formalin and three meningeal swabs for bacteriology.
No significant gross pathological lesions were evident in the brain.
Lesions varied in severity in each of the three brains.Â The most consistent findings were as follows: brain, forebrain, in which the leptomeninges, particularly in the sulci are multi-focally and segmentally thickened by increased numbers of well differentiated eosinophils.Â In the cerebral cortical laminar blood vessels, particularly veins and venules, show thick perivascular cuffs of eosinophils(Fig.Â 1-1), 1 to 3 cells deep, rarely there are macrophages.Â Multi-focally blood vessels in the cerebral cortical laminae have prominent and swollen endothelial cells.Â Segmentally along the cerebral cortical laminae, particularly in the sulci, there is a well delineated multi-focal astrogliosis and microgliosis.
Chronic severe multifocal eosinophilic meningoencephalitis
On meningeal swabs from three pigs, no bacteria grew on horse blood agar, and haemolysed blood agar plates incubated aerobically for 72 hours.
This was a case of indirect salt poisoning also known as water deprivation or water intoxication.Â Of the 800 at risk pigs, 600 died or were euthanized.Â Only pigs with the mildest of clinical signs survived.Â It was two weeks before clinical signs ceased in the surviving pigs.Â Interestingly, the farmer said that one or two pigs started to have seizures before the water supply was turned on.Â The attending veterinarian immediately recognized this as a case of indirect salt poisoning (water deprivation) and collected brains for histology to confirm and provide evidence of the clinical diagnosis.Â Bacterial swabs were collect to exclude the possibility of bacterial meningitis.Â The farmer was a contract grower for a parent company.Â The parent company was furious and treated this as a serious breach of animal welfare and a situation that should not have occurred.Â Furthermore the company protocol for pigs that have been deprived of water is to turn the overhead sprinklers on and gradually re-introduce water allowing pigs to lick water off the floor.Â The contributor has only seen one previous case of indirect salt poisoning and that was in pigs delayed in road transport that when they finally arrived engorged on water.
In domestic animals direct salt poisoning occurs in cattle, horses, sheep and pigs with the ingestion of excessive amounts of sodium chloride.Â Direct salt poisoning can occur in pigs where bore water is used for livestock drinking or diets with excessive salt including salted fish waste, salt whey from cheese factories and excessive salt in baker's bread dough.(2) Indirect salt poisoning involves a normal intake of sodium chloride, but with limited water intake.(4) The latter is also termed water deprivation or water intoxication.Â Indirect salt poisoning has only been proven to occur in pigs, with circumstantial evidence in cattle and sheep.(1) Pigs are particularly susceptible to indirect salt poisoning because of the relatively high salt diets.Â Restriction of water intake to pigs, 4 to 12 weeks of age, fed prepared diets containing 2% salt can result in clinical disease.(2) Poisoning occurs when the animals again have access to unlimited water.
Indirect salt poisoning with decreased water intake, but normal sodium chloride intake results in an accumulation of sodium ions in the brain and other tissues over several days.Â High sodium accumulation inhibits anaerobic glycolysis, preventing active transport of sodium out of the cerebrospinal fluid.Â When there is access to water again, water migrates to the tissues to re-establish the salt-water balance.Â Acute cerebral edema develops and increased intracranial pressure results.Â Specific to pigs and of diagnostic significance, is that there is an influx of eosinophils into the meninges.(2,4)
In cases of salt poisoning there are two characteristic changes.(4) The first is eosinophilia of the leptomeninges and Virchow-Robin spaces in the cerebral cortex.Â The second, develops with increased duration of the lesion, is cerebral cortical necrosis and with advanced lesions cavitating areas of malacia.(1) A mixture of both reactions is most common, but either alone may be encountered.(4)
The differential diagnosis for CNS signs in young pigs includes viral encephalomyelitis, Aujeszky's disease, edema disease, Streptococcal meningitis, Glasser's disease, toxicosis, nutritional deficiencies and Mulberry heart disease.(3) Meningeal and perivascular infiltrates can occur in the brains of pigs with leukomalacia of Mulberry heart disease and other causes of encephalitis.(1) However, the combination of laminar cortical cerebral necrosis and cerebral eosinophilia is pathognomonic for direct or indirect salt poisoning.(1) Histologically, eosinophilic meningoencephalitis can also occur with parasitic infections.Â In Australia parasitic encephalitis is rare.Â In dogs Angiostrongylus cantonensis occurs infrequently, but has not been observed in pigs.Â
The importance of this report is that direct or indirect salt poisoning cases often affect many animals and mortalities can be high.Â In cases of indirect salt poisoning veterinary pathologists should recognize that a restricted water intake is often the cause and this may be due to an underlying animal welfare issue.Â Veterinary pathologists should recognize that they play an important role in recognizing or confirming animal welfare associated diseases.
Brain, cerebrum: Meningoencephalitis, eosinophilic, acute, multifocal, moderate with neuronal necrosis(Fig.Â 1-2)
The lesion in this brain had a striking eosinophilic component.Â Other causes of eosinophilic meningoencephalitis in domestic species include parasitic nematodes and protozoans.(1)
Idiopathic eosinophilic meningoencephalitis has also been reported in dogs and one cat.Â Severe neurologic signs including recumbency and loss of consciousness have been reported with this syndrome.Â Eosinophilia and CSF pleocytosis with a predominance of eosinophils are common clinical pathologic findings.Â Grossly, the meninges often have a green tinge because of the eosinophilic inflammatory infiltrate.Â Histologic changes include eosinophilic and granulomatous meningitis of cerebrum and cerebellum with eosinophilic perivascular cuffing.Â In dogs, Golden Retrievers and Rottweilers are the most commonly affected breeds.(1)
In pigs, salt toxicity can cause laminar cortical necrosis.Â Several of the submitted slides did have very good examples of neuronal necrosis, while other slides had a dearth of necrotic neurons.Â Slides submitted for this case were from three different pigs, so that may be the reason for slide variation.Â In ruminants, differentials for laminar cortical necrosis include lead poisoning, salt toxicity, sulfur toxicity, hypoxia, and thiamine deficiency.(1)
1.Â Maxie MG, Youssef S: Nervous system.Â In: Jubb, Kennedy and Palmers Pathology of Domestic Animals, ed.Â Maxie MG, 5th ed., vol 1, pp.351-358 445.Â Elsevier Limited, Philadelphia, PA, 2007
2.Â Radostits OM, Gay CC, Hinchcliff KW, Constable PD: Diseases associated with inorganic and farm chemicals.Â In Veterinary Medicine.Â A textbook of the diseases of cattle, horses, sheep, pigs and goats.Â 10th ed.Â pp 1824 - 1826, Saunders Elsevier, Edinburgh, Scotland, 2007
3.Â Straw BE, Dewey CE, Wilson MR: Differiential diagnosis of swine disease.Â In Diseases of Swine 8th ed.Â Straw BE D'Allaire S, Mengeling WL, Taylor DJ.Â pp.Â 62-65, Blackwell Science, London, UK, 1999
4.Â Summers BA, Cummings JF, de Lahunta A: Degenerative Diseases of the Central Nervous System.Â In Veterinary Neuropathology.Â pp254-255.Â Mosby, St Louis, MO, 1995