8-month-old male black and white Micro Pig (Sus scofra).Wilber presented with dyspnea from potential aspiration. He has had CNS deficits for 2 months, since overeating at Thanksgiving. Recently, he was treated for a facial abscess. Profound hypoglycemia, hypokalemia, depression, bradycardia and hypothermia were recorded. He seizured and went into cardiac arrest.
Mild pneumonia was detected in this emaciated, 2.3kg pig. Animal had hydrocephalus.
A section of the thinned cerebral cortex is presented. A laminar pattern of neuronal necrosis and loss is seen. Remaining is a neuropil of gliosis with astrocytes activated microglia and scattered oligodendroglia. Gitter cells are scattered and also form nests about aciculate cholesterol clefts. Foci of calcified debris and cells and arterioles with a rim of calcium at the medial/intimal interface are noted. Scattered mononuclear cells infiltrate with a few neutrophils and thin cuffs of mononuclear cells are noted. Remaining neuropil is often rarified or has microcavitation (edema) with rare spheroids.
Chronic encephalopathy with laminar cortical necrosis; hydrocephalus ex vaccuo.
Cause: Potato chip binging, salt intoxication.
Salt intoxication d/t potato chip toxicity ;)
Micro pigs are one of a recent proliferation of pocket pets to appear on the market. Sometimes called teacup pigs because when born they can fit in a teacup, they grow to be the height of a medium-sized dog and weigh as much as 65 pounds.
This is a unique lesion and becomes intriguing when you are told that little Wilber loved potato chips, and at Thanksgiving was waylaid by a bag of Lays. He survived the salt intoxication with deficits for 2 months. The gross images of his brain demonstrate injected cerebral vessels and cortex collapse. On cross section, the laminar necrosis is seen nicely. While the morphologic can be followed by a chain of descriptors, this is an encephalopathy. Calcification of neuropil necrosis is common, but the pattern of vessel calcification is interesting. The nests of Gitter cells with cholesterol clefts are reminiscent of lipogranulomas. The mononuclear cells are mostly macrophages like is seen in cases of chronic polioencephalopathy and many infarcts; therefore, encephalitis is probably not a valid morphologic. I am not aware of a similar case being described although a comment on similar chronic lesions is in texts.(5) One must wonder if seizures have a role in developing some of the cortical necrosis.
Salt poisoning of young pigs is well known in its acute form and occurs when high salt diets are given when inadequate water is available.(2,5) Upon the later consumption of water, the salt in the cortical tissues cannot be cleared before water enters to cause the laminar necrosis. Evidence of presumed previous eosinophil cuffing is nowhere to be seen at this time. It is thought that eosinophil cuffs are associated/induced by sodium excess in tissues but may not be seen and cuffs are not present several days after survival.(2,5) Laminar necrosis in cases of salt intoxication does not fluoresce (JFE).
Swine are considered the most sensitive species to salt intoxication.(3) Potato chips have been reported before in this disease in pigs and survivors with CNS deficits are reported.(2,4) It has been shown that diets high in salt lead to increased salt in the pig brain with the highest concentrations being in the cerebral and cerebellar hemispheres.(1,6)
1. Brain, cerebrum: Necrosis, cortical, laminar, with multifocal cholesterol clefts and spongiosis, Micro Pig, porcine.
2. Brain, cerebrum, arteries and veins: Mineralization, diffuse, moderate, with multifocal fibrinoid necrosis.
Conference participants found the proposed etiology in this case of great interest, especially since there was no report of concurrent water deprivation. Although in the face of water deprivation, salt toxicity can occur in pigs with the intake of normal salt amounts (0.25-1%), much higher salt levels (up to 13%) can be tolerated as long as water intake is adequate.(4) It would be interesting to know if Wilber did in fact have a reduced water intake in conjunction with his potato chip binge. Additionally, some participants noted the absence of eosinophils that are often observed in swine salt toxicity; however, as the contributor states, although eosinophilic cuffs around vessels in the cerebral cortex usually develop within 48 hours, they tend to no longer be present after three to four days.(6) Conference participants found the mural mineralization and occasional fibrinoid necrosis of the vessels (not visible on all slides) interesting, but could not determine the cause.
For an acute case of salt toxicity in a pig, participants are urged to review conference 22, case #1 from the 2008-2009 WSC.
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2. Fountaine JH, Gashe DG, Oehme FW. Experimental salt poisoning (water deprivation syndrome) in swine. Vet Toxicol. 1975;17:5-8.
3. Heydarpour F, Derakhshandeh J, Fekri A, Heydarpour P. Salt poisoning blindness in wistar rat, rabbit, and pig. Toxicol & Environmental Chemistry. 2008;90:1035-42.
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5. Summers BA, Cummings JF, de Lahunta A. Veterinary Neuropathology. 1995;254-5.
6. Wells GAH, Lewis G, Hawkins SAC, Don PL. Evaluation of brain chloride determinations in the diagnosis of water deprivation salt intoxication in pigs. Vet Rec. 1984;114:631-635.