Indirect salt toxicosis in swine
Josepha DeLay, Murray Hazlett, Margaret Stalker, Andrew Vince
Samples from nursery and finisher pigs from 3 farms with suspected salt toxicosis were submitted to the AHL in April and May 2017. In herd 1, seizures and apparent blindness were noted in 50% of pigs following a period of water deprivation, and indirect salt toxicosis was suspected clinically. Sudden-onset neurologic signs in herd 2 included seizures, head pressing, and star-gazing. High mortality was noted in herd 3, without mention of specific neurologic signs. Salt toxicosis was listed as a clinical differential diagnosis in herds 2 and 3, although water deprivation was not noted.
Grossly in cerebral cortex of some pigs, there was distinct separation along necrotic laminae. Variably severe laminar cortical necrosis was also evident microscopically (Fig. 1, p. 14). Blood vessels in meninges and cerebral cortex were surrounded by variable numbers of eosinophils mixed with fewer lymphocytes and plasma cells (Fig. 2, p. 14).
Pathologic findings of eosinophilic meningoencephalitis and concurrent laminar cerebral cortical necrosis are virtually pathognomonic for “salt toxicosis” in pigs. The clinical syndrome in pigs is actually one of “indirect salt poisoning” which is a more accurate name for the condition. This is most often due to inadequate water availability and intake, sometimes but not necessarily with a concurrent increase in dietary salt levels. The condition has also been linked to whey feeding. High serum, tissue, and CSF sodium levels precipitate cerebral anoxia, with sudden access to water likely causing an osmotically induced cerebral edema and necrosis.
Since 2007, 10 cases of salt toxicosis have been diagnosed by pathologists at the AHL. The occurrence of the 3 recent cases over a < 2 mo time span is unusual.