Abstract
Four outbreaks of leukoencephalomyelopathy in colonies of SPF cats on a long‐term diet of irradiated dry cat food were observed in the Netherlands between 1989 and 2001. As a primary defect in myelin formation was suspected to be the cause of the disease and myelin consists mainly of lipids and their fatty acids, we investigated the fatty acid composition of the white matter of the spinal cord of affected and control cats and of irradiated and non‐irradiated food. The irradiated food had low levels of alpha‐linolenic acid compared to linoleic acid as well as a high total omega‐6:omega‐3 ratio of 7:1 in the irradiated and of 2:1 in the non‐irradiated food. The white matter of the spinal cord showed low levels of linoleic acid and absence of alpha‐linolenic acid in affected cats as well as absence of lignoceric and nervonic acid in both affected and control cats. These abnormalities in fatty acid composition of the white matter of the spinal cord may reflect an increased need for alpha‐linolenic acid as a substrate for longer chain omega‐3 fatty acids to compose myelin and thus indicate a particular species sensitivity to dietary deficiency in omega‐3 polyunsaturated fatty acids, particularly alpha‐linolenic acid in cats. Our findings indicate that abnormalities in fatty acid metabolism in myelin play an essential role in the pathogenesis of this acquired form of leukoencephalomyelopathy in cats.
Highlights
Leukoencephalomyelopathy has first been described in young cats suffering from a progressive form of ataxia between 1969 and 1980
The present paper describes the pathomorphological findings in four outbreaks of leukoencephalomyelopathy in colonies of specific pathogen‐free (SPF) cats fed irradiated dry cat food in the Netherlands between 1989 and 2001
A fourth outbreak with similar symptoms was observed in September– October 2000, in a different breeding colony consisting of 20 females and three males, and affecting 80% of the animals, as well as in January 2001 in a group of eight cats transferred from this colony to a research laboratory for a behavioural study
Summary
Leukoencephalomyelopathy has first been described in young cats suffering from a progressive form of ataxia between 1969 and 1980. Because a definite cause for the disease has not been estab‐ lished until now, and the demyelinating lesions and their distribution throughout the white matter of the central nervous system in these cats show resemblance to primary demyelination due to defective or improper myelin formation as in Canavan's disease and adreno‐ myelopathy in man and associated experimental mouse models (Baumann & Pham‐Dinii, 2001); polyunsaturated fatty acids, includ‐ ing essential fatty acids (EFA), are highly vulnerable to irradiation due to an increase in lipid peroxide formation (Hammer & Wills, 1979), reflected by higher thiobarbituric acid reactive substances (TBARS) and nuclear magnetic resonance (NMR) values after irradiation (De. Oliveira Silva, Mársico, Oliveira de Jesus, Guimarães, & Sloboda Cortez, 2011) mostly affecting polyunsaturated fatty acids result‐ ing in more saturated fatty acids (Javan & Motallebi, 2015), and increased formation of trans fatty acids (Yilmaz & Geçgel, 2007); nervous tissue concentrates omega‐3 polyunsaturated fatty acids in myelin (Lenox, 2015); lipid composition and fatty acid profiles of myelin of rat brain vary in response to the consumption of differ‐ ent fats (Bourre et al, 1984; Srinivasarao, Vajreswari, Rupalatha, & Narayanareddy, 1997); and induction of EFA deficiency in rats re‐ sulted in both a decrease of EFA in myelin and vacuolation/my‐ elin splitting in the optic nerve (Trapp, 1977), we hypothesized that abnormalities in fatty acid metabolism in myelin might play an essen‐ tial role in the pathogenesis of this acquired form of leukoencephalo‐ myelopathy in cats. We investigated in addition the fatty acid profile of the white matter of the spinal cord of affected cats and control animals, and of irradiated and non‐irradiated food
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