Epidemic cerebrospinal meningitis (meningococcal infection)

In the world, 3-10 cases of meningococcal meningitis per 100 000 population are registered.

[1], [2], [3], [4], [5], [6], [7]

Causes and pathogenesis of epidemic cerebrospinal meningitis

Epidemic cerebrospinal meningitis is caused by gram-negative diplococcus - meningococcal Weixelbaum. The disease is transmitted by airborne droplets. Entrance gates are the mucous membrane of throat and nasopharynx. Meningococci penetrate into the nervous system by hematogenous way. The source of infection are not only sick, but also healthy carriers. The most common cases of meningitis are in winter and spring. Sporadic diseases are noted at any time of the year.

[8], [9], [10],

Symptoms of epidemic cerebrospinal meningitis

The incubation period of epidemic cerebrospinal meningitis is on the average 1-5 days. The disease develops sharply: a strong chill, the body temperature rises to 39-40 ° C. Appears and rapidly builds up an intense headache with nausea or multiple vomiting. There may be nonsense, psychomotor agitation, convulsions, impaired consciousness. In the first hours, shell-like symptoms are revealed (stiff neck muscles, Kernig symptom), which increase to the 2-3rd day of the disease. Deep reflexes are animated, the ventral ones are lowered. In severe cases, lesions of the cranial nerves are possible, especially III and VI (ptosis, anisocoria, strabismus, diplopia), less often VII and VIII. On the 2-5th day of the disease, there are often herpetic eruptions on the lips. When a variety of skin rashes (often in children) of a hemorrhagic nature, meningococcemia is recorded. Liquor muddy, purulent, flows under increased pressure. Detect neutrophilic pleocytosis (up to several tens of thousands of cells per 1 μl), increased protein (up to 1-3 g / l), reduced glucose and chloride content. In a thick drop of blood under an ordinary microscope, meningococci are seen in the form of diplococci ("coffee beans"). Meningococcus can also be isolated from mucus taken from the nasopharynx. In the blood - leukocytosis (up to 30x10 ⁹ / l), pronounced shift of the leukocyte formula to the left before myelocytes and an increase in ESR.

According to the severity of clinical symptoms, light, moderate and severe forms of flow are isolated. Along with the damage to the shells of the brain, the brain substance is involved in the process, which has been clinically manifested since the first days of the illness by a violation of consciousness, convulsions, paresis, with a mild meningeal syndrome. Possible visual and auditory hallucinations, and in the future - disorders of memory and behavior. There are hyperkinesis. Increased muscle tone, sleep disorders, ataxia, nystagmus and other symptoms of brainstem lesions. In such cases, meningoencephalitis diagnosed with a severe course and poor prognosis is diagnosed, especially when signs of ependymatitis (ventriculitis) develop. Ependymatitis is characterized by a peculiar posture, in which extensor contractures of the legs and flexion - arms, seizures like the type of hormometry, edema of the optic nerve tracts, the increase in the amount of protein in the cerebrospinal fluid and xanthochromic staining develop.

Meningococcal meningitis can be both an independent clinical form and an integral part of the generalized form of meningococcal infection, which also includes meningococcemia.

Early complications of meningococcal meningitis include cerebral edema with secondary stem syndrome and acute adrenal insufficiency (Waterhouse-Frideriksen syndrome). Acute cerebral edema can occur with lightning fastness or on the 2-3rd day of the disease. The main signs are a violation of consciousness, vomiting, motor anxiety, convulsions, respiratory and cardiovascular disorders, increased arterial and liquor pressure.

With meningococcal meningitis taking place with meningococcemia, acute adrenal insufficiency is possible, manifested by the development of septic shock. They note a certain phase in the development of the processes occurring, corresponding to different degrees of shock.

• Septic shock I degree (phase of warm normotonia) - the patient's condition is heavy, his face pink, but the skin is pale, his limbs are cold. Part of the patients - profuse sweating, in other cases, the skin is dry, warm. Chills, central hyperthermia 38,5-40,5 ° С. Moderate tachycardia, tachypnea, hyperpnoea, normal or elevated blood pressure, central venous pressure is normal or decreased. Urinary excretion is satisfactory or somewhat decreased. Excitation, anxiety with conserved consciousness, general hyperreflexia, in infants often convulsive readiness. Compensated metabolic acidosis due to respiratory alkalosis, DIC-I syndrome (hypercoagulability).
• Septic shock II degree (phase of warm hypotension) - the patient's condition is very severe, the face and skin are pale, with a grayish tinge; acrocyanosis, the skin is often cold, wet, body temperature is normal or subnormal. Expressed tachycardia, tachypnea, pulse weak, heart sounds deaf. Arterial (up to 70-60 mm Hg) and central venous pressure are reduced. The cardiac output decreases. Oliguria. The patient is braked, languid, the consciousness is darkened. Metabolic acidosis. Syndrome ICE of the II degree.
• Septic shock of the third degree (the phase of cold hypotension) is a very severe condition, the consciousness in most cases is absent. Peripheral vasoconstriction. Skin cyanotic-gray color, total cyanosis with multiple hemorrhagic-necrotic elements, venous stasis as a corpse stain. The extremities are cold, moist. Pulse is threadlike or not determined, sudden shortness of breath, tachycardia, blood pressure is very low or zero, does not respond to an increase in the volume of circulating blood. Hypertension of muscles, hyperreflexia, stop pathological reflexes, pupils narrowed, reaction to light is weakened, strabismus, convulsions are possible. Anuria. Metabolic acidosis. DIC-type III syndrome with predominance of fibrinolysis. Possible development of edema of the lungs, toxic edema of the brain, metabolic myocarditis and endocarditis.
• Septic shock IV degree (terminal, or agonal, condition). Consciousness is absent, muscle atony, tendon areflexia, pupils dilated, do not respond to light, tonic convulsions. Expressed a violation of breathing and cardiovascular activity, progressive pulmonary edema and brain. Complete unfolding of blood with diffuse bleeding (nasal, gastric, uterine, etc.).

Swelling-swelling of the brain develops extremely sharply, characterized by extremely severe course. At the forefront are headache and vomiting, and then - frustration, there is psychomotor agitation or general tonic-clonic convulsions. Hyperthermia. The face is hyperemic, then cyanotic, the pupils narrowed, with a sluggish reaction to light. Pulse becomes rare, later the bradycardia can be replaced by tachycardia. Appears shortness of breath, arrhythmia of the breathing, a possible edema of the lungs. Death occurs as a result of stopping breathing; heart activity can continue for another 10-15 minutes.

The course of epidemic cerebrospinal meningitis

There are lightning, acute, abortive and recurrent variants of the course of meningococcal meningitis. The acute and lightning course is most characteristic for children and young people. Recurrent current is rare.

Diagnosis of epidemic cerebrospinal meningitis

Diagnosis is based on clinical data and the results of a CSF study.

Differential diagnosis is carried out with meningitis of another etiology, meningism with common infections and subarachnoid hemorrhage.

[11], [12], [13], [14]

Prevention of epidemic cerebrospinal meningitis

Isolate the patient, ventilate the room in which he was, within 30 minutes. Contacts with him are examined for carriage, they are followed by medical observation 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 the centers of meningococcal infection both during the epidemic upturn and in the inter-epidemic period (emergency prevention) to prevent secondary diseases. The procedure for conducting preventive vaccinations against meningococcal infection, the definition of population groups and the timing of preventive vaccinations are determined by the bodies that carry out state sanitary and epidemiological surveillance.

For emergency prevention of meningococcal infection, chemo-prophylactic 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 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 ME 2 receiving 1.5 million IU for 12 hours); ciprofloxacin orally (adults - 500 mg 1 time); ceftriaxone intramuscularly (adult - 250 mg 1 time).

Forecast

The prognosis is favorable in many cases provided timely treatment. In the residual period of the disease, asthenic syndrome is noted, a headache due to liquorodynamic disorders, children may have mental retardation, mild neurological focal disorders, paroxysmal disorders of consciousness. Severe consequences in the form of hydrocephalus, dementia, amaurosis have become a rarity.

[15], [16], [17], [18], [19],