Pug dogs in United States, Australia, New Zealand, Japan, and Europe have been documented to develop a unique, chronic, nonsuppurative meningoencephalitis that is different from granulomatous meningoencephalitis. Histopathology shows meningoencephalitis characterized by wide distribution of degenerated neurons with glial satellitosis and neuronophagia and prominent perivascular cuffing with lymphoid cells.

The cause of pug encephalitis is unknown. Theories have included infectious, immune mediated, and familial causes. It has been documented to occur in families of pug dogs and therefore may have an inherited tendency.

Disease description in this species:
Pug dog encephalitis can affect pugs as early as 6 months and as late as 7 years of age. Inflammation of the forebrain often results in generalized or partial seizures, circling, postural deficits, or visual deficits. Some cases present in status epilepticus from which they do not recover. Cranial nerves and the cerebellum may be affected in some cases. Clinical signs progress over days to months to years. Some cases progress rapidly; others have been known to live several years with anticonvulsant medication.

A tentative diagnosis is based on signalment and progressive neurological signs. One report has described MRI changes consisting of dilated cerebral ventricles and inflammatory lesions in the whole cortex of the bilateral cerebral hemispheres as well as the lower left parietal and the middle right temporal lobes.

Definitive diagnosis is based on histopathology of the brain. There is no treatment except for supportive management.

A similar disease has been also documented in Maltese terriers.9 Seizures, spinal fluid pleocytosis, and nonsuppurative inflammation of the cerebral gray and white matter are similar between these diseases. A 4 year old Pekingese has also been reported with similar clinical and histopathologic findings. 11 An older Yorkshire terrier has been described with similar signs but the histopathology was different enough to suggest that it was another disease process.10

Etiology:
Congenital
Idiopathic, unknown
Immune mediated
Breed predilection:
Maltese
Pekingese
Pug
Yorkshire terrier
Age predilection:
Juvenile
Young adult
Clinical findings:
AFEBRILE
ANOREXIA, HYPOREXIA
BEHAVIOR CHANGE
BLINDNESS
Blindness partial
Cachexia, weight loss
Case fatality rate high
CENTRAL NERVOUS SYSTEM (CNS) SIGNS
Cervical rigidity
Circling
CONVULSIONS, SEIZURES, FITS
Dementia
Disoriented
ENCEPHALITIS, ENCEPHALOPATHY
FEVER
Head pressing
Malaise
Screaming intermittently
Status epilepticus
TACHYCARDIA
ZZZ INDEX ZZZ
Diagnostic procedures: Diagnostic results:
Brain CT or MRI scan Abnormal brain scan by CT or MRI

Cerebrospinal fluid (CSF) analysis Cerebrospinal fluid (CSF) lymphocytic pleocytosis
Cerebrospinal fluid (CSF) mononuclear pleocytosis
CEREBROSPINAL FLUID (CSF) PLEOCYTOSIS
Cerebrospinal fluid (CSF) protein increased

Biopsy and histopathology of muscle, neural tissue Nonsuppurative encephalomyelitis

Biopsy and histopathology of brain Cerebral perivascular mononuclear infiltrate
White matter degeneration

Necropsy Encephalomyelitis

Treatment/Management/Prevention:
SPECIFIC
1) None

SUPPORTIVE
1) Anticonvulsants if seizures are a clinical sign.
2) The use of cortiosteroids has not shown to be of any great benefit.

Preventive Measures:
Avoid breeding parents of affected offspring.

Differential Diagnosis:
Encephalitis due to other causes
Intracranial neoplasia
Toxins
Metabolic encephalopathies