Classification
Based on the nature of inflammation and changes in the cerebrospinal fluid (CSF), meningitis is divided into two major groups:
- Purulent (bacterial). Occurs due to infection with Neisseria meningitidis, Streptococcus pneumoniae, or Haemophilus influenzae. Staphylococci, streptococci, or gram-negative bacteria such as Escherichia coli are less common causes.
- Serous. Most commonly viral in origin (Coxsackie and ECHO enteroviruses, less frequently herpes viruses, Epstein-Barr virus, HIV). Can also be caused by Mycobacterium tuberculosis or spirochetes.
According to the mechanism of development, they are classified as:
- Primary — the disease occurs independently, without a preceding infectious focus in the body.
- Secondary — inflammation of the meninges is a complication of another infection (e.g., pneumococcal meningitis following otitis media or sinusitis).
Clinical presentation
The disease manifests with general systemic symptoms: fever, tachycardia or bradycardia, facial flushing, and tachypnea.
In neurological status, the foreground features are:
- Headache — constant, bursting, diffuse. Usually accompanied by vomiting.
- Meningeal signs — nuchal rigidity, Kernig's and Brudzinski's signs.
- Signs of intracranial hypertension and brain edema — ranging from psychomotor agitation or drowsiness to deep coma. Generalized epileptic seizures frequently occur in infants.
In rare cases, cranial nerve involvement is possible, most commonly the oculomotor and abducens nerves.
Diagnostics and CSF findings
Meningitis can be suspected based on clinical presentation, but the diagnosis is always confirmed by lumbar puncture. Without it, etiotropic therapy cannot be prescribed.
| Parameter | Purulent meningitis |
|---|---|
| Appearance | Turbid, yellow-green fluid |
| Pressure | Elevated (200–400 mm H₂O) |
| Cells (cytosis) | Neutrophilic pleocytosis (100–10,000 per 1 mm³) |
| Protein and glucose | Moderate protein elevation, marked decrease in glucose (<40 mg/dL) |
To identify the pathogen, CSF is Gram-stained and cultured on nutrient media. Additionally, blood cultures and a nasopharyngeal swab are performed. Instrumental methods (chest X-ray, brain CT or MRI) are needed to locate the primary focus or rule out complications.
Complications and treatment
As purulent meningitis progresses, blood vessels and brain tissue become involved in the pathological process. Bacterial toxins penetrate the meninges, causing superficial non-inflammatory necrosis. Cerebral arteritis, thrombosis, brain infarction, and hydrocephalus may develop.
Treatment is initiated immediately — a delay in antibiotic therapy sharply increases the risk of death or severe neurological deficit.
Empiric regimens pending bacteriological results are based on high-dose benzylpenicillin (18–24 million IU daily intravenously or intramuscularly; up to 80 million IU in coma). Once the pathogen is identified, treatment is continued with penicillin (for meningococcal and pneumococcal infections) or ampicillin 12–15 g/day (for Haemophilus influenzae).
Briefly: answers to topical questions
What CSF changes are characteristic of serous viral meningitis?
Serous viral meningitis is characterized by clear CSF and lymphocytic pleocytosis.
Key cerebrospinal fluid findings:
- Appearance — clear or slightly turbid.
- Cytosis — lymphocytic pleocytosis (up to 100 or more cells per 1 mm³, up to several thousand mononuclear cells, including activated B lymphocytes).
- Biochemistry — positive Pandy's test, elevated albumin quotient up to 20 × 10⁻³, lactate level 20 × 10⁻³, glucose decreased to less than 50% of the plasma level.
- Immunology — elevated IgG and IgA levels.
What antibiotics are used for modern empiric therapy of purulent meningitis?
For empiric therapy of purulent meningitis with an unidentified pathogen, benzylpenicillin is used; if generalized meningococcal infection is suspected, ceftriaxone is used.
- Benzylpenicillin — administered intravenously or intramuscularly every 3–4 hours. The standard dose is 18–24 million IU/day. In severe cases or lack of response, the dose is increased to 48 million IU, and in comatose states to 64–80 million IU.
- Ceftriaxone — used empirically intravenously until bacteriological results are obtained when generalized meningococcal infection is suspected.
What are the absolute contraindications to lumbar puncture in suspected meningitis?
Absolute contraindications to lumbar puncture are conditions that threaten the patient's life or distort diagnostic results.
These include:
- Progressive cerebral edema — due to the high risk of herniation syndrome (cerebellar tonsillar herniation into the foramen magnum).
- Herniation syndrome — presence of clinical or instrumental signs of herniation.
- Increased bleeding tendencies — hemorrhagic syndrome or a high risk thereof creates a risk of traumatic tap and red blood cells in the CSF, distorting the diagnostic picture.
Class and exam questions
What is the difference between primary and secondary meningitis?
Primary meningitis develops without an infectious focus in other organs (e.g., meningococcal). Secondary is always a consequence of another infection, such as pneumococcal meningitis secondary to otitis media or sinusitis.
Why does CSF glucose decrease in purulent meningitis?
Glucose is actively consumed by replicating bacteria and leukocytes (neutrophils) that have migrated to the site of inflammation. A similar decrease is characteristic of tuberculous and fungal meningitis.
What type of rash is typical for meningococcal meningitis?
Characterized by a hemorrhagic rash presenting as firm, palpable «starry» lesions of varying size and shape.
What else to study on this topic
- Pathogenesis of non-inflammatory cortical necrosis induced by endotoxins
- Differences in CSF between serous and purulent meningitis
- Mechanism of cell-protein dissociation development
- Clinical features of Haemophilus meningitis in newborns
- Specific complications: subdural effusion and sensorineural hearing loss
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