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Infectious inflammatory disorders

Infectious causes of encephalitis and meningoencepha- and cerebellar cortical gray–white matter interface as
litis include viral, bacterial, mycotic, protozoal, and well as subtle T2 hyperintensity of the pons. Enhancement
parasitic agents. Detailed imaging descriptions are of the frontal and parietal lobe pachymeninges was
sporadic, but features of the more common entities are evident on contrast‐enhanced T1 images. A loss of
3
included here. gray–white matter definition due to demyelination
would likely be a prominent feature on proton density
Viral encephalitis weighted images as well.
Canine distemper encephalitis
The canine distemper virus causes systemic illness in Feline infectious peritonitis
dogs and other species, with central nervous system meningoencephalitis
involvement a common component in both the acute The feline infectious peritonitis (FIP) coronavirus causes
and chronic phases of the disease. Acute distemper systemic illness in domestic cats, with central nervous
encephalomyelitis is characterized by mild mononuclear system involvement being a common component,
inflammation and demyelination and is widely dissemi- particularly in cats with the dry or pyogranulomatous
nated. Chronic encephalitis (“old dog encephalitis”) may form of the disease. FIP infection causes an immune‐
arise from long‐term persistent viral infection and is complex pyogranulomatous vasculitis, and in the central
characterized by nonsuppurative inflammation and nervous system (CNS), it targets the leptomeninges, cho-
demyelination involving primarily the brainstem and roid plexus, ependymal cells, brain parenchyma, and eyes.
cerebral hemispheres. 1 Generalized or regional obstructive hydrocephalus
MR imaging features of acute distemper encephalitis may be present because of ependymal and choroid
include focal or regional T1 hypointense and T2 hyper- inflammation. Cerebrospinal fluid (CSF) may have
intense lesions of the forebrain with little or no mass variable T1 and FLAIR intensity depending on cellular
effect. The temporal lobes may be predisposed, and and macromolecular content. The brain parenchyma
lesions are centered on cortical gray matter and the may appear unremarkable on unenhanced T1 MR
gray–white matter interface. Similar lesions have also images, although cerebellar herniation may be evident
been reported in the brainstem and cerebellum. Contrast in cats with obstructive hydrocephalus. Focal or multifo-
enhancement is inconsistent and minimal when present cal regions of parenchymal hyperintensity may be
(Figure 2.7.1). 2 evident on T2 images, and the meninges may appear
MR imaging features of chronic distemper encephali- thickened and T2 hyperintense. Choroidal, ependymal,
tis have been described in one case report and included and meningeal enhancement may be marked on
T2 hyperintensity and loss of definition of the cerebral contrast‐enhanced T1 images (Figure 2.7.2). 4–7

Atlas of Small Animal CT and MRI, First Edition. Erik R. Wisner and Allison L. Zwingenberger.
© 2015 John Wiley & Sons, Inc. Published 2015 by John Wiley & Sons, Inc.
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