16.1 CNS Infections Beyond Bacterial Meningitis: Encephalitis, Brain Abscess & Epidural Abscess

Viral Encephalitis

Encephalitis is parenchymal brain inflammation, so altered consciousness, seizures, and focal deficits dominate, in contrast to the meningeal signs of meningitis. Many patients have features of both.

Herpes Simplex Virus (HSV-1)

• The most common sporadic cause of fatal encephalitis in adults.
• Features: fever, confusion progressing over days, personality change, aphasia, olfactory or gustatory hallucinations, and temporal lobe seizures.
• Imaging: MRI shows temporal and inferior frontal lobe signal change, often hemorrhagic; CT is frequently normal early.
• CSF: lymphocytic pleocytosis, elevated protein, normal glucose, and often red blood cells. EEG may show periodic lateralized epileptiform discharges over a temporal lobe.
• Diagnosis: CSF HSV PCR has high sensitivity, but can be falsely negative in the first 72 hours. Repeat it if the clinical picture fits.
• Treatment: acyclovir 10 mg/kg IV every 8 hours for 14 to 21 days, started empirically. Each hour of delay worsens outcome. Maintain hydration, because acyclovir causes crystal nephropathy, and adjust the dose for kidney function. Neurotoxicity (confusion, myoclonus) occurs with excessive levels.

Other Important Causes

Autoimmune Encephalitis

Suspect it in younger patients with subacute psychiatric symptoms, memory loss, seizures, orofacial dyskinesias, and autonomic instability.

• Anti-NMDA receptor encephalitis is associated with ovarian teratoma and with preceding HSV encephalitis.
• Diagnosis: serum and CSF autoantibody panels, MRI, EEG (an "extreme delta brush" pattern in some cases), and tumor screening.
• Treatment: corticosteroids plus IVIG or plasma exchange, then rituximab or cyclophosphamide; remove the tumor. ICU care often involves prolonged ventilation, status epilepticus, and dysautonomia.

Brain Abscess

• Routes: contiguous spread (otitis, sinusitis, dental infection), hematogenous seeding (endocarditis, lung abscess, right-to-left shunt), and direct inoculation (trauma, surgery).
• Organisms: streptococci (including the Streptococcus anginosus group) and anaerobes, often polymicrobial; S. aureus after trauma or surgery; Nocardia, Toxoplasma, and fungi in immunocompromised hosts; Listeria in cell-mediated immune deficiency.
• Presentation: headache (the most common symptom), fever in only about half, focal deficits, and seizures. Classic meningitis signs are often absent.
• Imaging: a ring-enhancing lesion with central restricted diffusion on MRI, which helps distinguish abscess from tumor.
• Management:
  • Aspiration or excision for lesions larger than about 2.5 cm, for diagnosis, or when there is mass effect. Stereotactic aspiration gives microbiologic diagnosis with low morbidity.
  • Empiric antibiotics: a third-generation cephalosporin plus metronidazole, adding vancomycin after trauma or surgery, for 6 to 8 weeks with imaging follow-up.
  • Avoid lumbar puncture when there is a mass lesion with mass effect.
  • Corticosteroids are reserved for significant edema and mass effect, because they impair capsule formation and antibiotic penetration.
  • Antiepileptic drugs for seizures; search for and treat the source, including a patent foramen ovale or pulmonary arteriovenous malformation in cryptogenic cases.

Spinal Epidural Abscess

• Risk factors: injection drug use, diabetes, bacteremia, spinal instrumentation or injection, and epidural catheters.
• Classic triad: back pain, fever, and neurologic deficit, but the complete triad is uncommon at presentation. Pain is usually severe and focal, with percussion tenderness.
• Progression: back pain, then radicular pain, then weakness and bladder dysfunction, then paralysis. Once paralysis is established, recovery is poor, so the window is early.
• Diagnosis: MRI with contrast of the whole spine (skip lesions occur), blood cultures, ESR and CRP. S. aureus causes most cases.
• Treatment: urgent surgical decompression and drainage plus 6 weeks or more of antibiotics (vancomycin plus a third- or fourth-generation cephalosporin empirically). Medical management alone is considered only for patients without deficits, with an identified organism and close monitoring.

Cryptococcal Meningitis

• Host: advanced HIV (CD4 below 100 cells/µL), transplant recipients, cirrhosis, and sometimes apparently normal hosts (C. gattii).
• Presentation: subacute headache, fever, and cranial neuropathies. Raised intracranial pressure drives morbidity.
• Diagnosis: cryptococcal antigen in serum and CSF, India ink, and fungal culture. Measure and record the opening pressure at lumbar puncture.
• Treatment:
  • Induction: liposomal amphotericin B plus flucytosine (a single high dose of liposomal amphotericin B with 14 days of flucytosine and fluconazole is an accepted regimen in resource-limited settings), followed by consolidation and maintenance fluconazole.
  • Pressure control is as important as the antifungal: repeat large-volume lumbar punctures daily while opening pressure is above 25 cmH2O, with a lumbar drain or shunt for refractory pressure.
  • Corticosteroids are harmful in HIV-associated cryptococcal meningitis (a trial showed more adverse events and disability).
  • Delay or carefully time antiretroviral therapy (usually after about 4 to 6 weeks) to reduce immune reconstitution inflammatory syndrome.

Tuberculous Meningitis

• Presentation: subacute headache, fever, and cranial nerve palsies (especially cranial nerve VI), with basal meningeal enhancement, hydrocephalus, and infarcts from vasculitis.
• CSF: lymphocytic pleocytosis, very high protein, low glucose. Acid-fast smear has low yield; nucleic acid amplification (Xpert MTB/RIF Ultra) and large-volume culture improve detection.
• Treatment: standard four-drug therapy with adjunctive dexamethasone, which improves survival. Treat for 9 to 12 months, watch for drug-induced hepatitis, and manage hydrocephalus with CSF diversion.