Meningococcal infection

Etiology and pathogenesis

The causative agent of the disease is the meningococcus—a Gram-negative diplococcus belonging to the genus Neisseria. To date, 11 serotypes of this microorganism are known, but types A, B, and C are of the greatest clinical and epidemiological significance. The microbe possesses pronounced pathogenicity factors, as it is capable of producing both endotoxin and exotoxin. In the external environment, the bacterium is extremely labile and dies rapidly.

The infection is transmitted via the aerogenic (airborne droplet) route. The port of entry is the mucous membranes of the nasopharynx. If the patient has developed an adequate local immune response, the process remains limited to local inflammation. However, due to the antigenic similarity between bacterial structures and host tissues, lymphocytes may fail to recognize the pathogen as a foreign agent. As a result, the meningococcus penetrates unhindered into the systemic bloodstream.

Massive bacterial destruction occurs in the blood, accompanied by the release of huge amounts of toxins. The resulting toxinemia triggers a cascade of coagulopathic reactions, leading to the development of disseminated intravascular coagulation (DIC). Clinically, this process manifests as meningococcemia. In cases of critically massive toxinemia, infectious-toxic shock develops. In addition, bacteria circulating in the bloodstream are capable of crossing the blood-brain barrier (BBB). This risk is particularly high in infants due to the physiological vulnerability of the barrier, leading to the development of purulent meningitis.

Clinical forms: from local to generalized

The disease is characterized by several variants of the clinical course.

Nasopharyngitis (localized form):

• Pronounced intoxication syndrome and severe headache.
• Local symptoms: sore throat, abundant purulent discharge from the nasal passages.

Meningococcemia (generalized form, septicemia): The disease begins in an extremely acute manner. Body temperature rises to febrile levels (38–40 °C), and general well-being deteriorates sharply. A specific sign is a hemorrhagic rash that appears rapidly—within a few hours (less frequently up to 1–2 days) from the onset of fever.

Characteristics of the rash in meningococcemia:

• Localized predominantly on the lower half of the body (buttocks, thighs, shins); the trunk, arms, and face are affected less frequently.
• Presents as solitary hemorrhagic elements of irregular "stellate" shape, ranging from 3 to 7 mm in size (visually described as a " starry sky" picture).
• The elements are slightly elevated above the skin surface and do not fade upon pressure (diascopy).
• Over time, the hemorrhages coalesce, forming areas of skin necrosis.

Additionally, epistaxis (nosebleeds), hemorrhages into the sclera and mucous membranes are possible. The cardiovascular and respiratory systems (dyspnea, tachycardia, arterial hypotension), joints, and eyes may be involved (synovitis, iridocyclitis). With timely treatment, these systemic changes are reversible.

Fulminant form (Waterhouse-Friderichsen syndrome): Occurs in 6–20% of affected children. Characterized by a hyperacute onset with high fever and rapid spread of the rash. The leading pathogenetic mechanism is infectious-toxic shock (ITS), manifested by a drop in blood pressure, thready pulse, vomiting, depressed consciousness, the appearance of cyanotic spots, and pronounced meningeal syndrome. The prognosis is extremely unfavorable: without emergency care, death occurs within 6–48 hours.

Nervous system involvement and diagnostics

In CNS involvement, the incubation period is short, lasting 1–4 days. Meningitis begins abruptly: temperature elevation, severe headache, vomiting, and psychomotor agitation are noted. By days 1–2, meningeal syndrome develops: nuchal rigidity, positive Kernig's and Brudzinski's signs. In infants under one year of age, bulging and tension of the anterior fontanelle are typical, as well as a positive suspension sign (Les萨ge sign / Lessage's sign).

The appearance of focal neurological symptoms (profound disturbance of consciousness, clinic-tonic seizures, pareses, oculomotor disorders) is atypical for uncomplicated meningitis and indicates involvement of the brain parenchyma—transition to meningoencephalitis. When the process spreads to the brainstem, bulbar disorders (impaired swallowing and speech), tachypnea, and bradyarrhythmia occur. Increasing edema poses a threat of brainstem herniation through the foramen magnum, leading to a fatal outcome.

Diagnostic principles:

1. The diagnosis of localized forms (nasopharyngitis) is usually established based on epidemiological data (identification of contact in an infection focus).
2. In generalized forms, despite vivid clinical presentation, the gold standard of verification is performing a lumbar puncture.
3. Obtaining purulent cerebrospinal fluid confirms the bacterial nature of the inflammation.
4. In children aged 2 months to 12 years, differential diagnosis must be performed with purulent meningitis caused by Haemophilus influenzae type b and Streptococcus pneumoniae.

Class and exam questions

What else to study on this topic

• Pathophysiology of DIC and infectious-toxic shock in meningococcemia.
• Features of lumbar puncture and interpretation of cerebrospinal fluid analyses.
• Differential diagnosis with infections caused by Haemophilus influenzae and Streptococcus pneumoniae.
• Mechanisms of development and clinical signs of brainstem herniation.

Other topics from the section «Chapter 12. Infectious and parasitic diseases»

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