Prognosis and possible consequences
The prognosis in generalized meningococcal infection (MI) directly depends on its clinical form. For isolated meningococcal meningitis (provided there is no coma or focal neurological symptoms), the prognosis is considered relatively favorable: the case fatality rate does not exceed 1–5%.
The situation deteriorates sharply when complicated by meningococcemia (sepsis). In this case, the average case fatality rate increases to 10–15%, with death most frequently occurring within the first 24–48 hours after hospitalization. In fulminant forms of meningococcemia, the prognosis is extremely unfavorable — from 40% to 80% of patients die, even if etiotropic and pathogenetic therapy is initiated in a timely manner and administered absolutely correctly. A specific feature of MI is the risk of rapid death in a healthy individual within hours of infection.
Complications and outcomes:
- Significant complications: pneumonia, nephritis and pyelitis, aortitis, thrombophlebitis, uveitis.
- Permanent sequelae: hearing impairment or complete hearing loss, epilepsy, ataxia, CSF hypertension, endocrinopathies, as well as cognitive and behavioral impairments.
- Relapses: are recorded extremely rarely and are usually associated with the patient's genetic predisposition.
Laboratory diagnostics
Physicians of all specialties and mid-level medical personnel at all stages of care are required to identify patients with the generalized form of MI. The diagnosis is based on clinical and epidemiological data (seasonality, contact with an infected person), but definitive confirmation requires instrumental and laboratory facilities.
Complete blood count (CBC) findings: Neutrophilic leukocytosis with a left shift, elevated ESR, thrombocytopenia. In meningococcemia, hyperleukocytosis and a left shift are markedly pronounced.
Cerebrospinal fluid (CSF) analysis: This is a key stage in the diagnosis of meningitis, requiring a lumbar puncture.
- Macroscopy: the CSF is turbid, whitish, and escapes under increased pressure.
- Cytology: pronounced neutrophilic pleocytosis (500–1000 cells/µL or more, with neutrophils accounting for 60–100%).
- Biochemistry: protein levels increase up to 2–8 g/L (cell-protein dissociation develops — the cell count increases faster than the protein level), and glucose concentration decreases.
- Bacterioscopy: gram-negative diplococci (intra- and extracellular) are found in the smear.
Additional methods:
- Bacteriological culture (CSF, blood, mucus) with determination of saccharolytic activity and antibiotic susceptibility.
- Rapid immunological methods (latex agglutination, CIE) detect antigens in the CSF from the first hours of the disease.
- PCR (polymerase chain reaction) detects N. meningitidis DNA. Its diagnostic yield is highly informative and, unlike culture, does not drop during ongoing antimicrobial therapy.
- Serology (IHA) is used starting from the 2nd week to detect a rising antibody titer.
Differential diagnosis of CNS lesions
Distinguishing meningococcal meningitis from similar conditions is performed solely on the basis of laboratory data, primarily CSF analysis.
Purulent meningitis of other etiology (pneumococcal, Haemophilus influenzae, etc.) Clinically also presents with high intoxication and meningeal syndrome; CSF shows neutrophilic pleocytosis. They can be differentiated only by isolating the specific pathogen (bacterioscopy, culture, PCR, ELISA).
Serous meningitis (viral, tuberculous) Characterized by moderate intoxication (or gradual onset in tuberculosis). Blood tests more often show leukopenia with lymphocytosis (in viral cases). CSF shows lymphocytic pleocytosis, with moderately elevated protein (up to 2 g/L).
Meningism A condition associated with severe infections or poisonings. Meningeal symptoms are present, CSF pressure is elevated, but there are no inflammatory changes in the CSF (cytosis, protein, and electrolytes are normal).
Subarachnoid hemorrhage Begins hyperacutely (thunderclap headache). Meningeal signs appear later (after 6 hours). CSF escapes under pressure and has a reddish color (erythrocytic pleocytosis). 12 hours after centrifugation, the supernatant becomes xanthochromic.
Brain abscess Develops gradually. Characterized by focal neurological symptoms and papilledema on the affected side. CSF reveals mixed pleocytosis (10–200 cells) and significantly elevated protein (protein-cell dissociation). The diagnosis is confirmed by CT, MRI, or Echo-EG.
Briefly: answers to topical questions
What classic meningeal signs must be checked during a physical examination of the patient?
During a physical examination of the patient to detect meningeal syndrome, muscle tonus signs, hyperesthesia, and reactive pain signs are checked. The examination must include:
- Nuchal rigidity
- Kernig's sign
- Brudzinski's signs — upper and lower.
- Hyperesthesia — photophobia, hyperacusis, increased tactile sensitivity.
- Mendel's sign — tenderness upon pressure from within on the anterior wall of the external auditory canal.
- Bechterew's sign — tenderness upon percussion of the zygomatic arch.
- Pulatov's craniofacial reflex — painful grimace upon percussion of the cranium.
What antibacterial agents are used for the etiotropic therapy of meningococcal meningitis?
For the etiotropic antibacterial therapy of meningococcal meningitis, first-line and reserve drugs from several pharmacological groups are used. These include:
- Chloramphenicol — at a dose of 80–100 mg/kg of body weight per day.
- Ciprofloxacin — 0.8–1.2 g/day.
- Carbapenems (meropenem).
- Ampicillin.
- 3rd-generation cephalosporins (ceftriaxone) — used for primary purulent meningitis of unknown etiology, including meningococcal meningitis.
The duration of the antibiotic course for meningitis is 5–10 days.
How to remember CSF findings in meningococcal meningitis: the "4M" rule (in Russian). Turbid fluid (Mutnaya), Many neutrophils/pleocytosis (Mnogo), Low glucose (Malo), Meningococcus/diplococcus in the smear.
Class and exam questions
Is it possible to differentiate meningococcal meningitis from pneumococcal meningitis based on symptoms alone?
No, the clinical presentation of purulent meningitis cases is similar. The exact etiology is established exclusively based on the results of microscopy, bacterial culture, or CSF PCR.
What is the difference in CSF between meningism and true meningitis?
In meningism, cerebrospinal fluid pressure is elevated due to toxic edema, but the cellular composition (cytosis) and protein level remain completely normal.
Why is PCR preferred over bacteriological culture in delayed diagnosis?
The diagnostic yield of PCR does not depend on how much time has passed since the onset of the disease or whether antibiotics have already been administered, because the method detects the genetic material (DNA) of the pathogen rather than live bacteria.
What else to study on this topic
- Features of the differential diagnosis of meningococcemia with typhus (Rosenberg's enanthema, Chiari-Avtsyn spots)
- Clinical presentation and differential diagnosis of meningococcal infection with severe forms of influenza
- Fulminant forms of meningococcemia: pathogenesis of infectious-toxic shock development
- Instrumental diagnostics of brain abscesses (MRI, CT, Echo-EG)
- Assessment of saccharolytic activity and antibiotic susceptibility testing of the isolated N. meningitidis culture
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