Epidemic cerebrospinal meningitis (meningococcal infection)

Worldwide, 3-10 cases of meningococcal meningitis are registered per 100,000 population.

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Causes and pathogenesis of epidemic cerebrospinal meningitis

Epidemic cerebrospinal meningitis is caused by a gram-negative diplococcus - Weichselbaum meningococcus. The disease is transmitted by airborne droplets. The entry points are the mucous membrane of the pharynx and nasopharynx. Meningococci penetrate the nervous system by the hematogenous route. The source of infection is not only sick people, but also healthy carriers. Meningitis most often occurs in winter and spring. Sporadic diseases are noted at any time of the year.

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Symptoms of epidemic cerebrospinal meningitis

The incubation period of epidemic cerebrospinal meningitis is on average 1-5 days. The disease develops acutely: severe chills, body temperature rises to 39-40 °C. Intense headache with nausea or repeated vomiting appears and quickly increases. Delirium, psychomotor agitation, convulsions, and impaired consciousness are possible. In the first hours, meningeal symptoms (rigidity of the occipital muscles, Kernig's sign) are detected, increasing by the 2nd-3rd day of the disease. Deep reflexes are brisk, abdominal reflexes are reduced. In severe cases, cranial nerves are affected, especially III and VI (ptosis, anisocoria, strabismus, diplopia), less often VII and VIII. On the 2nd-5th day of the disease, herpetic eruptions on the lips often appear. With the appearance of various skin rashes (more often in children) of a hemorrhagic nature, meningococcemia is recorded. The cerebrospinal fluid is cloudy, purulent, and flows out under increased pressure. Neutrophilic pleocytosis (up to several tens of thousands of cells in 1 μl), increased protein content (up to 1-3 g/l), and decreased glucose and chloride content are detected. Meningococci in the form of diplococci ("coffee beans") are visible in a thick drop of blood under a regular microscope. Meningococci can also be isolated from mucus taken from the nasopharynx. In the blood, leukocytosis (up to 30x10 ⁹ /l), a pronounced shift in the leukocyte formula to the left to myelocytes, and an increase in ESR.

According to the severity of clinical symptoms, mild, moderate and severe forms of the disease are distinguished. Along with the damage to the meninges, the brain matter is also involved in the process, which is clinically manifested from the first days of the disease by impaired consciousness, seizures, paresis with a weak expression of the meningeal syndrome. Visual and auditory hallucinations are possible, and later - memory and behavior disorders. Hyperkinesis, increased muscle tone, sleep disorders, ataxia, nystagmus and other symptoms of damage to the brain stem occur. In such cases, meningoencephalitis is diagnosed, which is characterized by a severe course and a poor prognosis, especially when signs of ependymatitis (ventriculitis) appear. Ependymatitis is characterized by a peculiar posture, in which extension contractures of the legs and flexion contractures of the arms, hormetonia-type cramps, swelling of the optic discs, an increase in the amount of protein in the cerebrospinal fluid and its xanthochromic staining develop.

Meningococcal meningitis can be either an independent clinical form or a component of a generalized form of meningococcal infection, which also includes meningococcemia.

Early complications of meningococcal meningitis include cerebral edema with secondary brainstem syndrome and acute adrenal insufficiency (Waterhouse-Friderichsen syndrome). Acute cerebral edema may occur with a fulminant course or on the 2nd-3rd day of the disease. The main symptoms are impaired consciousness, vomiting, motor restlessness, convulsions, respiratory and cardiovascular disorders, increased arterial and cerebrospinal fluid pressure.

In meningococcal meningitis, occurring with meningococcemia, acute adrenal insufficiency is possible, manifested by the development of septic shock. A certain phase in the development of the processes occurring is noted, corresponding to different degrees of shock.

• Septic shock stage I (phase of warm normotension) - the patient's condition is severe, the face is pink, but the skin is pale, the extremities are cold. Some patients have profuse sweating, in other cases the skin is dry and warm. Chills, central hyperthermia 38.5-40.5 °C. Moderate tachycardia, tachypnea, hyperpnea, arterial pressure is normal or elevated, central venous pressure is normal or decreased. Urine output is satisfactory or slightly reduced. Agitation, anxiety with preserved consciousness, general hyperreflexia, in infants often convulsive readiness. Compensated metabolic acidosis due to respiratory alkalosis, DIC syndrome stage I (hypercoagulation).
• Septic shock grade II (warm hypotension phase) - the patient's condition is very severe, the face and skin are pale, with a grayish tint; acrocyanosis, the skin is often cold, moist, body temperature is normal or subnormal. Tachycardia, tachypnea are expressed, the pulse is weak, the heart sounds are muffled. Arterial (up to 70-60 mm Hg) and central venous pressure are reduced. Cardiac output decreases. Oliguria. The patient is inhibited, lethargic, consciousness is clouded. Metabolic acidosis. DIC syndrome grade II.
• Septic shock grade III (cold hypotension phase) is an extremely severe condition, consciousness is absent in most cases. Peripheral vasoconstriction. Skin is bluish-gray, total cyanosis with multiple hemorrhagic-necrotic elements, venous stasis like cadaveric spots. Extremities are cold, damp. Pulse is threadlike or not detectable, severe dyspnea, tachycardia, blood pressure is very low or zero, does not respond to an increase in circulating blood volume. Muscle hypertension, hyperreflexia, pathological foot reflexes, pupils are constricted, reaction to light is weakened, strabismus and convulsions are possible. Anuria. Metabolic acidosis. DIC syndrome grade III with prevalence of fibrinolysis. Development of pulmonary edema, toxic cerebral edema, metabolic myocarditis and endocarditis is possible.
• Septic shock stage IV (terminal or agonal state). Consciousness is absent, muscle atony, tendon areflexia, pupils are dilated, do not react to light, tonic convulsions. There is a pronounced impairment of breathing and cardiovascular activity, progressive pulmonary and cerebral edema. Complete incoagulability of blood with diffuse bleeding (nasal, gastric, uterine, etc.).

Edema-swelling of the brain develops extremely acutely, characterized by an extremely severe course. Headache and vomiting come to the fore, followed by a disorder of consciousness, psychomotor agitation or general tonic-clonic seizures. Hyperthermia. The face is hyperemic, then cyanotic, pupils are constricted, with a sluggish reaction to light. The pulse becomes rare, later bradycardia can be replaced by tachycardia. Dyspnea, respiratory arrhythmia appear, pulmonary edema is possible. Death occurs as a result of respiratory arrest; cardiac activity can continue for another 10-15 minutes.

The course of epidemic cerebrospinal meningitis

There are fulminant, acute, abortive and recurrent variants of meningococcal meningitis. Acute and fulminant course is most typical for children and young people. Recurrent course is rare.

Diagnosis of epidemic cerebrospinal meningitis

Diagnosis is based on clinical data and the results of cerebrospinal fluid examination.

Differential diagnosis is carried out with meningitis of other etiologies, meningism in general infections and subarachnoid hemorrhage.

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Prevention of epidemic cerebrospinal meningitis

The sick person is isolated, the room he was in is ventilated for 30 minutes. Those who came into contact with him are examined for carriage, and medical observation is established for them for 10 days with daily thermometry and simultaneous examination of the nasopharynx by an ENT doctor.

Necessary preventive measures include specific prevention of meningococcal infection. Meningococcal polysaccharide group-specific vaccines (A+C, A+C+Y+W135) are used in foci of meningococcal infection both during the period of epidemic rise and in the interepidemic period (emergency prevention) to prevent secondary diseases. The procedure for carrying out preventive vaccinations against meningococcal infection, determining population groups and timing of preventive vaccinations are determined by the bodies implementing state sanitary and epidemiological supervision.

For emergency prevention of meningococcal infection, chemoprophylactic measures are carried out using one of the antibacterial drugs listed in the current sanitary regulations (2006):

• rifampicin orally (adults - 600 mg every 12 hours for 2 days; children - 10 mg/kg body weight every 12 hours for 2 days);
• azithromycin orally (adults - 500 mg once a day for 3 days; children - 5 mg/kg of body weight once a day for 3 days); amoxicillin orally (adults - 250 mg every 8 hours for 3 days; children - children's suspensions in accordance with the instructions for use);
• spiramycin orally (adults - 3 million IU 2 times a day, 1.5 million IU over 12 hours); ciprofloxacin orally (adults - 500 mg once); ceftriaxone intramuscularly (adults - 250 mg once).

Forecast

The prognosis is favorable in many cases, provided that treatment is timely. In the residual period of the disease, asthenic syndrome, headache due to cerebrospinal fluid dynamics disorders are observed; in children, mental retardation, mild focal neurological disorders, and paroxysmal disturbances of consciousness are possible. Severe consequences in the form of hydrocephalus, dementia, and amaurosis have become rare.

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