Canine Meningitis Study Guide

Overview and Clinical Importance

Meningitis refers to inflammation of the meninges, the protective membranes covering the brain and spinal cord. In dogs, meningitis represents an important category of neurological disease frequently tested on the NAVLE. Understanding the classification, clinical presentation, and management of different meningitis types is essential for veterinary practice.

Meningitis in dogs can be broadly categorized into infectious and non-infectious (immune-mediated) causes. Critically, non-infectious causes comprise approximately 80% of meningitis cases in dogs in Europe and the USA, with steroid-responsive meningitis-arteritis (SRMA) being the most common type overall.

Classification of Canine Meningitis

Steroid-Responsive Meningitis-Arteritis (SRMA)

SRMA is the most common cause of meningitis in dogs. It is an immune-mediated inflammatory disease affecting the leptomeninges and associated arteries, characterized by marked neutrophilic pleocytosis in the CSF and excellent response to corticosteroid therapy.

Signalment and Breed Predisposition

Age: Typically 6-18 months (range: 3 months to 9 years)

Sex: No significant predisposition; some studies suggest slight male predilection

Predisposed breeds: Beagles, Bernese Mountain Dogs, Boxers, Weimaraners, Border Collies, English Springer Spaniels, Jack Russell Terriers, Nova Scotia Duck Tolling Retrievers, Golden Retrievers, Wirehaired Pointing Griffons, German Shorthaired Pointers

Clinical Signs

SRMA presents in two forms: acute and chronic.

Diagnostic Findings

Clinicopathologic Abnormalities

• CBC: Inflammatory leukogram with neutrophilia (often marked), possible left shift
• Serum biochemistry: Hypoalbuminemia, hyperglobulinemia
• C-reactive protein (CRP): Markedly elevated; useful for monitoring treatment response
• IgA levels: Elevated in serum and CSF; supports diagnosis

CSF Analysis (Key Diagnostic Test)

Advanced Imaging

MRI findings: Often normal or shows mild meningeal contrast enhancement. MRI is primarily used to rule out other conditions (disc disease, neoplasia, GME). In classic SRMA presentations with characteristic signalment and CSF findings, MRI may not be necessary.

Treatment of SRMA

The cornerstone of SRMA treatment is immunosuppressive corticosteroid therapy. Treatment typically continues for a minimum of 6 months.

Adjunctive Immunosuppressants

Second-line agents may be added for refractory cases or steroid-sparing:

• Cyclosporine: 5 mg/kg/day PO
• Azathioprine: 2 mg/kg/day PO initially, then every other day
• Mycophenolate: 10 mg/kg PO BID

Prognosis and Monitoring

• Overall prognosis: Good to excellent for acute SRMA with proper treatment
• Relapse rate: 16-60% of cases; relapses are treatable
• Mortality: 5-8% overall
• Monitoring: Serial CRP measurements; repeat CSF if relapse suspected

Meningoencephalitis of Unknown Origin (MUO)

MUO is an umbrella term for non-infectious inflammatory CNS diseases where definitive histopathologic diagnosis is unavailable. It encompasses GME, NME, and NLE. These conditions are presumed immune-mediated and require immunosuppressive therapy.

Granulomatous Meningoencephalomyelitis (GME)

GME is characterized by perivascular granulomatous inflammation within the CNS white matter. It can affect the brain, spinal cord, or optic nerves and accounts for up to 25% of all canine CNS disorders.

Signalment

• Age: Young to middle-aged (4-8 years typical)
• Sex: Female predisposition reported
• Breed: Toy and terrier breeds overrepresented (Poodles, Chihuahuas, Maltese, Yorkshire Terriers)

Clinical Forms of GME

Diagnostic Findings in GME

• CSF: Mononuclear to mixed pleocytosis (variable severity); elevated protein; 16-22% may have normal CSF
• MRI: Multifocal hyperintense lesions on T2/FLAIR; variable contrast enhancement; may mimic neoplasia in focal form
• Definitive diagnosis: Histopathology (brain biopsy or necropsy)

Treatment of GME

Prognosis for GME

• 15-25% of dogs die or are euthanized within first week of diagnosis
• Dogs surviving past 1 month may live months to over 1 year with treatment
• Focal form has better prognosis than disseminated
• Seizures and mental status changes associated with shorter survival

Necrotizing Meningoencephalitis (NME) - Pug Dog Encephalitis

NME is a rapidly progressive, fatal inflammatory brain disorder characterized by extensive cerebral necrosis. It has strong breed associations and accounts for 69-81% of all intracranial conditions in Pugs.

Breed Predisposition

• Pug (most common - hence "Pug Dog Encephalitis")
• Maltese
• Chihuahua
• Pekingese, Shih Tzu, Papillon, Brussels Griffon

Age of onset: Typically less than 6 years; median 1.5-2.5 years

Genetic Component

NME in Pugs is associated with genetic risk loci within the dog leukocyte antigen (DLA) MHC class II complex on chromosome 12. Genetic testing is available to determine risk status. Disease incidence is approximately 1-2% in Pugs.

Clinical Signs of NME

• Seizures (most common presenting sign)
• Behavioral changes, circling
• Visual deficits, blindness
• Vestibular signs, ataxia
• Lethargy, obtundation
• Rapid progression typical

Diagnostic Findings

• CSF: Lymphocytic/mononuclear pleocytosis (66% lymphocytic); mean 120 cells/microliter; elevated protein
• MRI: Loss of gray/white matter distinction; asymmetric cerebral lesions; cortical necrosis; may show brain herniation

Necrotizing Leukoencephalitis (NLE)

NLE primarily affects the cerebral white matter and brainstem, with relative sparing of gray matter. It is considered a variant of necrotizing encephalitis with distinct breed associations.

Breed Predisposition

• Yorkshire Terrier (most common)
• French Bulldog

Clinical signs and prognosis similar to NME; vestibular and brainstem signs may predominate.

Bacterial Meningitis

Bacterial meningitis is relatively rare in dogs compared to SRMA and MUO. It typically occurs secondary to extension from adjacent infections or hematogenous spread.

Routes of Infection

• Extension from adjacent focus: Otitis media/interna (most common source), sinusitis, dental disease
• Hematogenous spread: Bacteremia, endocarditis, distant abscess
• Direct inoculation: Bite wounds, trauma, surgical/iatrogenic
• Foreign body migration

Clinical Presentation

The classic triad in human bacterial meningitis is pyrexia, neck stiffness, and altered mental status. In dogs, only 8-17% present with all three signs. Common findings include:

• Cervical hyperesthesia and pain
• Neurological deficits (75% of cases) - differs from SRMA
• Vestibular signs (42%), especially with otogenic origin
• Altered mentation, cranial nerve deficits
• Fever (less common than expected - only 13% at referral)

Diagnostic Findings in Bacterial Meningitis

Treatment of Bacterial Meningitis

• Empirical antibiotics: Start broad-spectrum pending culture; CNS penetration essential
• First-line options: Doxycycline (10 mg/kg PO BID), Clindamycin (10-20 mg/kg PO TID), Fluoroquinolones
• Duration: Prolonged (median 8 weeks; range 2-16 weeks)
• Surgery: TECA-LBO for otogenic infections
• Prognosis: 83% survive to discharge with aggressive treatment

CSF Interpretation Summary