Microscopic examination (Quantity and morphological structure of cellular elements)

The number and morphological structure of cellular elements are essential for establishing the nature of inflammatory processes in the brain and its membranes.

Based on the nature of changes in the cerebrospinal fluid, purulent and serous meningitis (meningoencephalitis) are differentiated. Serous include meningitis (meningoencephalitis), in which the cerebrospinal fluid is transparent, sometimes slightly cloudy, and opalescent; the number of cellular elements is increased to 500 - 600 in 1 μl, lymphocytes predominate.

Purulent ones include meningitis (meningoencephalitis), in which the number of leukocytes exceeds 0.5 - 0.6 * 109/l and can reach 20 * 109/l or more. Colorless, transparent or opalescent cerebrospinal fluid should be specially examined to identify a fibrin film (“mesh”) specific to tuberculous meningitis, which can form in a test tube after 12–24 hours.

Very often, tuberculosis bacilli are detected microscopically in such a film.

MICROSCOPIC STUDY OF CSF

With meningitis, meningoencephalitis, septic thrombosis of the cerebral sinuses, changes in the cerebrospinal fluid are inflammatory in nature.

The number of cellular elements (mainly neutrophils) increases to a much greater extent than the protein content increases - cell-protein dissociation.

In pathological processes accompanied by cerebral edema, increased intracranial pressure and leading to blockage of the liquor-conducting pathways, a significant increase in protein content with a slightly increased or normal number of cellular elements (protein-cell dissociation) is more typical.

Such ratios are observed in acutely manifested brain tumors, large epidural and subdural hematomas and some other pathological processes that cause swelling and dislocation of the brain.

As a result of microscopic examination of cerebrospinal fluid smears, it is not always possible to determine the causative agent of meningitis (bacteria, fungi, protozoa, tumor cells) - in 35 - 55% of cases. Thus, the role of microscopy in establishing the etiology of inflammatory lesions of the meninges is limited.

This equally applies to the possibilities of bacteriological diagnosis of the etiology of meningoencephalitis, brain abscesses and septic thrombosis of the cerebral sinuses. The sugar content in the cerebrospinal fluid decreases in many pathological processes due to a decrease in its transport through the blood-brain barrier.

“Emergency conditions in neuropathology”, B.S. Vilensky

Diagnostic research includes the following procedures:

1. Clinical and biochemical blood test.
2. CSF analysis.
3. EEG (electroencephalography).
4. EMG (electromyography).

What kind of liquid is this?

Liquor is the fluid that constantly circulates in the elements of the brain and spinal cord. Normally, it looks like a colorless transparent fluid substance that fills the ventricles of the brain, subarachnoid and subdural spaces.

Cerebrospinal fluid is produced in the ventricles of the brain by the choroid covering these cavities. Liquor contains various chemicals:

• vitamins;
• organic and inorganic compounds;
• hormones.

In addition, the liquor contains substances that process incoming blood and decompose it into useful nutrients. At the same time, a sufficient amount of hormones are produced that affect the endocrine, reproductive and other systems of the body.

Reference! The main function of cerebrospinal fluid is considered to be shock absorption: thanks to it, conditions are created to soften the physical impact when a person makes basic movements, which protects the brain from critical damage during a strong impact.

How is the research conducted?

The procedure performed to collect cerebrospinal fluid is called a lumbar puncture. To carry it out, the patient takes a lying or sitting position. If the subject is sitting, he should be upright, with his back bent so that the vertebrae are located in the same vertical line.

When the patient is lying down, he turns to his side, bending his knees and pulling them to his chest. The injection site is chosen at the level of the spinal column, where there is no risk of damaging the spinal cord.

Lumbar puncture is a procedure that can only be performed by a qualified doctor! The doctor treats the back of the person being examined with alcohol and an iodine-containing solution, after which he feels the puncture site along the intervertebral spaces: in adults at the level of the II and III lumbar vertebrae, and in children - between the IV and V.

The specialist injects an anesthetic there, after which they wait 2-3 minutes to provide tissue anesthesia. Next, the doctor performs a puncture using a Beer needle with a mandrel, moving between the spinous processes and passing the ligaments.

A sign of a needle entering the subarachnoid space is a feeling of failure. If you remove the mandrin after this, liquid will be released if the procedure is performed correctly.

A small amount is taken for research.

Normal values ​​in a healthy person

In the absence of pathology, cerebrospinal fluid has the following composition:

1. Density: 1003-1008.
2. Cellular elements (cytosis): up to 5 in 1 µl.
3. Glucose level: 2.8-3.9 mmol/l.
4. Content of chlorine salts: 120-130 mmol/l.
5. Protein: 0.2-0.45 g/l.
6. Pressure: in a sitting position – 150-200 mm. water Art., and lying down - 100-150 mm. water Art.

Attention! Normal cerebrospinal fluid should be transparent, colorless and not contain any impurities.

Table of the relationship between the form of the disease and the color of the liquid

Composition of the fluid substance

Depending on the causative agent of the infection, cerebrospinal fluid may have a different composition. Let's take a closer look at the cerebrospinal fluid 2 forms of inflammation.

Serous

Characteristics of cerebrospinal fluid:

• Color – colorless, transparent.
• Cytosis: lymphocytic pleocytosis is detected. The level of cellular elements is from 20 to 800 in 1 µl.
• Protein values: increased, up to 1.5 g/l (protein-cell dissociation).
• Glucose and chloride levels were unchanged.

Purulent

Characteristics of cerebrospinal fluid in pathology:

• The color varies depending on the causative agent of meningitis. For example, when it is cloudy, yellow, when it is whitish and bluish in the case of blue-purulent bacillus.
• Cytosis: a huge number of cells (cell-protein dissociation), reaching 1000-5000 cellular elements per 1 μl. Neutrophilic pleocytosis is characteristic.
• Protein content: increased, in the range of 0.7-16.0 g/l.
• Glucose levels are reduced, about 0.84 mmol/l.
• The amount of chlorides is reduced or unchanged.
• The presence of a fibrin film in the cerebrospinal fluid or sediment.

Decoding indicators

Based on the values ​​of the cerebrospinal fluid data, specialists clarify the diagnosis and, in accordance with this, can prescribe adequate therapy.

Number of cells and cytosis

The cells in the cerebrospinal fluid are counted and their predominant type is subsequently determined. An increased content (pleocytosis) indicates the presence of an inflammatory process. Pleocytosis is more pronounced with, in particular, tuberculous inflammation of the meninges.

In other diseases (epilepsy, hydrocephalus, degenerative changes, arachnoiditis), cytosis is normal. Specialists count cellular elements, which are represented in most cases by lymphocytes or neutrophils.

After studying the cytogram, the doctor can draw a conclusion about the nature of the pathology. Thus, lymphocytic pleocytosis indicates serous meningitis or tuberculous meningitis with a chronic course. Neutrophilic leukocytosis – observed during acute infection (bacterial meningitis).

Important! During the analysis of cerebrospinal fluid, it is necessary to evaluate dissociation - the ratio of cellular elements to protein content. Cellular-protein dissociation is characteristic of meningitis, and protein-cellular dissociation is characteristic of serous inflammation of the meninges, as well as stagnation in the cerebrospinal fluid tract (neoplasm, arachnoiditis).

Protein

Glucose

Glucose values ​​should be 2.8-3.9 mmol/L. However, even healthy people may have slight fluctuations in the content of the substance. To correctly assess glucose in the cerebrospinal fluid, it is advisable to determine it in the blood: in the absence of pathology, it will exceed 2 times the values ​​in the cerebrospinal fluid.

Increased levels are observed in diabetes mellitus, cerebrovascular accidents, and acute encephalitis. Reduced glucose levels occur with meningitis, neoplasms, and subarachnoid hemorrhage.

Enzymes

Liquor is characterized by low activity of the enzymes it contains. Changes in the activity of enzymes in the cerebrospinal fluid in various diseases are mainly nonspecific. With tuberculous and purulent meningitis, the content of ALT and AST increases, LDH increases in bacterial inflammation of the meninges, and an increase in total cholinesterase indicates the acute course of meningitis.

Chlorides

Normally, the content of chlorine salts in the CSF is 120-130 mmol/l. A decrease in their level may indicate meningitis of various etiologies and encephalitis. An increase is observed in diseases of the heart, kidneys, degenerative processes and formations in the brain.

Conclusion

The procedure for collecting cerebrospinal fluid must be carried out by a qualified, experienced specialist, and the patient must strictly follow all his instructions. A study of the cerebrospinal fluid allows the doctor to clarify the diagnosis and, based on this data, select the correct treatment.

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Tuberculous meningitis occurs more often in children and adolescents than in adults. As a rule, it is secondary, developing as a complication of tuberculosis of another organ (lungs, bronchial or mesenteric lymph nodes) with subsequent hematogenous dissemination and damage to the meninges.

Clinical picture

The onset of the disease is subacute; there is often a prodromal period with increased fatigue, weakness, headache, anorexia, sweating, sleep inversion, character changes, especially in children - in the form of excessive sensitivity, tearfulness, decreased mental activity, and drowsiness.

Body temperature is subfebrile. Vomiting often occurs as a result of headaches. The prodromal period lasts 2-3 weeks. Then, mild shell symptoms gradually appear (stiff neck, Kernig’s sign, etc.). Sometimes patients complain of blurred vision or weakening of vision. Signs of damage to the III and VI pairs of the CN appear early (slight double vision, slight ptosis of the upper eyelids, strabismus). In the later stages, if the disease is not recognized and specific treatment is not started, paresis of the limbs, aphasia and other symptoms of focal brain damage may occur.

The most typical course of the disease is subacute. In this case, the transition from prodromal phenomena to the period of appearance of ophthalmic symptoms occurs gradually, on average within 4-6 weeks. Acute onset is less common (usually in young children and adolescents). A chronic course is possible in patients who were previously treated with specific drugs for tuberculosis of internal organs.

Diagnostics

The diagnosis is established on the basis of an epidemiological history (contact with tuberculosis patients), data on the presence of tuberculosis of internal organs and the development of neurological symptoms. The Mantoux reaction is not very informative.

The study of the cerebrospinal fluid is decisive. The cerebrospinal fluid pressure is increased. The liquid is clear or slightly opalescent. Lymphocytic pleocytosis is detected up to 600-800x106/l, the protein content is increased to 2-5 g/l (Table 31-5).

Table 31-5. Indicators of cerebrospinal fluid are normal and with meningitis of various etiologies

Often, at the onset of the disease, mixed neutrophilic and lymphocytic pleocytosis is detected in the cerebrospinal fluid. Characterized by a decrease in glucose content to 0.15-0.3 g/l and chlorides to 5 g/l. When the extracted liquor is stored in a test tube for 12-24 hours, a delicate fibrin web-like mesh (film) is formed in it, which starts from the liquid level and resembles an overturned Christmas tree. Mycobacterium tuberculosis is often found in this film during bacterioscopy. An increase in ESR and leukocytosis are determined in the blood.

Differential diagnosis is facilitated by culture and detailed cytological examination of the cerebrospinal fluid. If tuberculous meningitis is suspected clinically, and laboratory data do not confirm this, anti-tuberculosis therapy exjuvantibus is prescribed for health reasons.

Treatment

Various combinations of anti-tuberculosis drugs are used. During the first 2 months and until sensitivity to antibiotics is detected, 4 drugs are prescribed (the first stage of treatment): isoniazid, rifampicin, pyrazinamide and ethambutol or streptomycin. The regimen is adjusted after determining sensitivity to the drugs. After 2-3 months of treatment (the second stage of treatment), they often switch to 2 drugs (usually isoniazid and rifampicin). The minimum duration of treatment is usually 6-12 months. Several drug combinations are used.

Isoniazid 5-10 mg/kg, streptomycin 0.75-1 g/day in the first 2 months. With constant monitoring of the toxic effect on the VIII pair of the CN - ethambutol 15-30 mg/kg per day. When using this triad, the severity of intoxication is relatively low, but the bactericidal effect is not always sufficient.

To enhance the bactericidal effect of isoniazid, rifampicin 600 mg is added along with streptomycin and ethambutol, 600 mg once a day.

In order to maximize the bactericidal effect, pyrazinamide is used at a daily dose of 20-35 mg/kg in combination with isoniazid and rifampicin. However, when these drugs are combined, the risk of hepatotoxicity increases significantly.

The following combination of drugs is also used: para-aminosalicylic acid up to 12 g/day (0.2 g per 1 kg of body weight in fractional doses 20-30 minutes after meals, washed down with alkaline water), streptomycin and phthivazid in a daily dose of 40-50 mg/kg (0.5 g 3-4 times a day).

The first 60 days of the disease are critical in treatment. In the early stages of the disease (within 1-2 months), it is advisable to use glucocorticoids orally to prevent adhesive pachymeningitis and associated complications.

Treatment in a hospital should be long-term (about 6 months), combined with general strengthening measures, enhanced nutrition and subsequent stay in a specialized sanatorium. Then the patient continues to take isoniazid for several months. The total duration of treatment is 12-18 months.

To prevent neuropathies, pyridoxine (25-50 mg/day), thioctic acid, and multivitamins are used. Monitoring of patients is necessary to prevent drug intoxication in the form of liver damage, peripheral neuropathies, including damage to the optic nerves, as well as to prevent complications in the form of cicatricial adhesions and open hydrocephalus.

Forecast

Before the use of anti-tuberculosis drugs, meningitis ended in death on the 20-25th day of the disease. Currently, with timely and long-term treatment, a favorable outcome occurs in 90-95% of patients. If diagnosis is delayed (after 18-20 days of illness), the prognosis is poor. Sometimes relapses and complications occur in the form of epileptic seizures, hydrocephalus, and neuroendocrine disorders.

For quotation: Dekonenko E.P., Karetkina G.N. Viral and bacterial meningitis // RMZh. 2000. No. 13. P. 548

Institute of Poliomyelitis and Viral Encephalitis named after M.P. Chumakov RAMS, Moscow

MGMSU named after N.A. Semashko

Meningitis is a group of diseases characterized by damage to the meninges and inflammatory changes in the cerebrospinal fluid.

Normal number of cells in cerebrospinal fluid (CSF) is no more than 5 in 1 µl, the amount of protein is no more than 0.45 mg/l, sugar is no less than 2.2 mg/l. Cells in normal cerebrospinal fluid are represented by lymphocytes.

According to the composition of formed elements in the cerebrospinal fluid and etiology, meningitis is divided into purulent (bacterial) with a predominance of neutrophilic leukocytes and serous (usually viral) with predominantly lymphocytic pleocytosis. Some bacterial meningitis is characterized by a predominance of the lymphocytic (serous) composition of the cerebrospinal fluid (tuberculosis, syphilitic, Lyme borreliosis, etc.). Meningitis may be primary or secondary(develops against the background of an existing general or local infectious process); according to the nature of the flow - sharp, chronic, sometimes lightning fast.

In pathogenesis Meningitis is played by a complex of factors: first of all, the properties of the pathogen, the reaction of the host organism and the background against which the contact of the micro- and macroorganism occurs. The virulence of the pathogen, its neurotropism and other features are of great importance. In the host’s reaction, a significant role is played by age, nutrition, social factors, previous injuries and diseases, the nature of previous treatment, immune status, etc. Environmental conditions include exposure to physical factors of cooling, overheating, insolation; contacts with animals, vectors and sources of infection, etc.

Certain individuals have an increased risk of developing infections of the nervous system. These include people with certain concomitant diseases and chronic infections, such as skull injuries, consequences of neurosurgical interventions and shunting of the cerebrospinal fluid system, chronic purulent processes in the chest cavity, septic endocarditis, lymphoma, blood diseases, diabetes, chronic diseases of the paranasal sinuses, alcoholism, long-term therapy with immunosuppressants, etc. The high-risk group also includes patients with congenital and acquired immune defects, pregnant women, patients with unrecognized diabetes, etc. In such individuals, due to a defect in immune defense, there is an increased risk of viral infections that they have already encountered in early childhood. This primarily includes diseases caused by the herpes group: cytomegalovirus, Epstein-Barr virus, varicella-zoster virus.

The pathogen can penetrate into the meninges in various ways: hematogenous, lymphogenous, perineural or contact (in the presence of a purulent focus in direct contact with the meninges - otitis media, sinusitis, brain abscess).

Overproduction of CSF, disruption of intracranial hemodynamics, and the direct toxic effect of the pathogen on the brain substance are essential in the pathogenesis of meningitis. The permeability of the blood-brain barrier increases, the endothelium of the brain capillaries is damaged, microcirculation is disrupted, and metabolic disorders develop, aggravating brain hypoxia. The result is cerebral edema, the progression of which can lead to brain dislocation and death from respiratory and cardiac arrest.

Viral meningitis

The etiological classification of viral meningitis most fully meets epidemiological and practical requirements. Most authors consider enteroviral meningitis to be one of the most common types of viral meningitis. The genus of enteroviruses (family Picornaviridae) includes poliovirus types 1-3, Coxsackie viruses A (types 1-24) and B (types 1-6), ECHO viruses (types 1-34), enteroviruses 68 -71st types. All representatives of enteroviruses cause meningitis, but most often the Coxsackie and ECHO viruses. Often the causes of viral meningitis are also paramyxoviruses (mumps, parainfluenza, respiratory syncytial), viruses of the herpes family (herpes simplex type 2, varicella-zoster, Epstein-Barr, herpes virus type 6), arboviruses (tick-borne encephalitis) , lymphocytic choriomeningitis, etc.

Clinic

Meningitis, including viral, characterized by an acute onset with high fever, headache, nausea and vomiting, general malaise and weakness . Typical for meningitis is the presence of meningeal symptoms, indicating irritation of the meninges. The meningeal symptom complex includes, in addition to headache, stiff neck, Kernig and Brudzinski symptoms, photophobia, and hyperesthesia of the skin. In young children, bulging and tension of the fontanelle, tympanitis when tapping the skull, and a symptom of “suspension” (Lessage) are observed.

With some types of pathogens, a blurred clinical picture is observed with low-grade fever and moderate headache, absence of vomiting, meningeal monosymptoms or reduced symptoms.

General cerebral symptoms in the form of disturbances of consciousness, convulsions and signs of focal lesion nervous system absent with meningitis, and their presence indicates encephalitis, but some authors assume their short-term presence at the onset of the disease as a manifestation of cerebral edema.

The main criterion for meningitis is an increase in the number of cells in the CSF. With viral meningitis there is lymphocyte composition of CSF. Cytosis is represented by a two to three-digit number, usually no more than 1000 in 1 μl. The percentage of lymphocytes is 60-70% of the total number of cells in the cerebrospinal fluid. Protein and sugar levels are within normal limits. In the presence of meningeal signs, but in the absence of inflammatory changes in the cerebrospinal fluid, they speak of meningism. In some meningitis, signs of a general viral infection are observed (Table 1).

The duration of viral meningitis is 2-3 weeks. In 70% of cases the disease ends in recovery , but in 10% the course is longer and may be accompanied by complications.

Features depending on the pathogen

Although in most cases of viral meningitis there is no clear clinical correlation with a specific pathogen, some features may be observed. Yes, often Coxsackievirus group B cause diseases that occur with severe myalgic syndrome (so-called epidemic pleurodynia or Bornholm disease); Diarrhea may occur. Both groups of Coxsackieviruses can cause pericarditis and myocarditis .

Adenoviral meningitis accompanied by an inflammatory reaction from the upper respiratory tract, conjunctivitis and keratoconjunctivitis .

Mumps leaks often with damage to the parotid glands , abdominal pain and increased levels of amylase and diastase (pancreatitis), orchitis and oophoritis. At the onset of the disease, the composition of the CSF may be neutrophilic with low sugar levels. Often the disease becomes protracted with a delay in the sanitation of the cerebrospinal fluid.

A protracted course can take and lymphocytic choriomeningitis, and meningitis caused herpes simplex virus type 2. With these types of disease, at the onset of the disease, the sugar level in the CSF may be below normal, which forces them to be differentiated from tuberculous meningitis.

Herpetic meningitis often observed against the background of a primary genital infection - in 36% of women and 13% of men. In most patients, herpetic rashes precede the signs of meningitis an average of a week. Herpetic meningitis can cause complications in the form of sensory disturbances, radicular pain, etc. In 18-30% of cases, relapses of the disease are described.

Meningitis with herpes zoster in some cases it occurs with minimal meningeal syndrome or asymptomatically. As a rule, it is not a monosyndromic lesion of the nervous system, but develops against the background of concomitant radicular phenomena, sensory disturbances, etc.

Meningitis with tick-borne encephalitis observed in almost half of the sick. The onset is acute, accompanied by high fever, intoxication, pain in muscles and joints. Characterized by hyperemia of the face and upper body, severe headache, and repeated vomiting. In 20-40% of cases, a two-wave fever is observed with a period of apyrexia of 2-6 days. In the first days of the disease, neutrophilic leukocytes may predominate in the cerebrospinal fluid, the preponderance of which may persist for several days. Inflammatory changes in the CSF last a relatively long time - from 3 weeks to several months, accompanied by poor health. At the same time, diffuse neurological symptoms may be observed. Asthenic syndrome after illness, characteristic of tick-borne encephalitis, is observed in approximately 40% of those who have recovered from the disease and persists from 1-3 months to 1 year. In 2-6%, a transition to a progressive form of the disease may subsequently occur.

Diagnosis

The diagnosis of viral meningitis is difficult, especially in cases of sporadic disease. For some viral meningitis, a history or associated organ involvement may be helpful (Table 1). But the main focus is on laboratory diagnostics: isolation of the virus from the CSF and determination of a 4-fold increase in specific antibodies in the dynamics of the disease . Currently used in large treatment centers polymerase chain reaction(PCR), which has high sensitivity and specificity.

Treatment of the vast majority of viral meningitis symptomatic . In the acute period it is prescribed detoxification therapy : solutions of glucose, Ringer, dextrans, polyvinyl lyrrolidone, etc. Moderate dehydration is used: acetazolamide, furosemide). Symptomatic drugs (analgesics, vitamins A, C, E, group B, antiplatelet agents, etc.).

For meningitis caused by herpes simplex virus type 2, intravenous administration is recommended acyclovir 10-15 mg per 1 kg per day for 10 days, based on 3-fold administration.

Bacterial meningitis

The causative agents can be meningococci, pneumococci, Haemophilus influenzae, staphylococci, salmonella, listeria, tubercle bacilli, spirochetes, etc. The inflammatory process that develops in the meninges is usually purulent. In recent years, the etiological structure of purulent bacterial meningitis (PBM) has changed significantly. In adults, in more than 30% of cases the causative agent is Streptococcus pneumoniae, in people over 50 years old - S.pneumoniae and gram-negative bacteria of the intestinal group (E.coli, Klebsiella pneumoniae, etc.), in children under 5 years of age in more than 30% of GBM caused by Haemophilus influenzae type B. However, according to the forecast of epidemiologists, another increase in the incidence of meningococcal infection is expected in a few years.

Clinically GBM is characterized by a more acute onset of the disease, more severe intoxication and high fever, compared to viral meningitis, and a more severe course . CSF in GBM is turbid, with high neutrophilic pleocytosis, increased protein content; sugar levels are reduced.

Meningococcal meningitis

Meningococcal meningitis occurs mainly in children and young people. In almost half of the patients it is preceded by nasopharyngitis, which is often mistakenly diagnosed as ARVI. Against this background or in the midst of complete health, meningitis begins acutely - with chills, an increase in body temperature to 39-39.50 C, a headache, the intensity of which increases with every hour. On the very first day, vomiting, photophobia, hyperacusis, skin hyperesthesia, and meningeal symptoms appear. There is a revival or suppression of tendon reflexes and their asymmetry. A little later, signs of increasing cerebral edema may appear: attacks of psychomotor agitation, followed by drowsiness, then coma. Focal symptoms are also possible: diplopia, ptosis, anisokaria, strabismus, etc. When often combined with meningococcemia, a characteristic hemorrhagic rash appears on the skin, the appearance of which usually precedes the symptoms of meningitis.

Possible atypical forms, especially in patients receiving antibacterial drugs. The course of meningitis in these cases is subacute, the body temperature is subfebrile or normal, the headache is moderate, there is no vomiting, meningeal symptoms appear late and are mild, but encephalitis, ventriculitis subsequently develops and death can occur.

In infants The onset of meningitis, including meningococcal, is manifested by general anxiety, crying, screaming, refusal to suck, sudden agitation from the slightest touch, and convulsions.

In the first hours of meningitis, the CSF is either not changed at all, or the inflammatory changes are mild. From the end of the 1st day, the CSF becomes typical for purulent meningitis. Microscopy of smears of cerebrospinal fluid sediment in most cases reveals gram-negative diplococci, mainly intracellularly. Timely initiation of adequate therapy ensures recovery in most cases. ; in the absence of this, mortality reaches 50%.

Pneumococcal meningitis

Pneumococcal meningitis can be either primary or secondary (in this case it is preceded by otitis media or mastoiditis, pneumonia, sinusitis, traumatic brain injury, cerebrospinal fluid fistulas, etc.). It often occurs in persons with a burdened premorbid background: alcoholism, diabetes mellitus, splenectomy, hypogammaglobulinemia, etc.

The onset can be either rapid (25%) or gradual, over 2-7 days. Meningeal symptoms are detected later than with meningococcal meningitis, and in very severe cases they are completely absent. Most patients experience convulsions and impaired consciousness already in the first days of the illness. The clinical course is characterized by exceptional severity due to the involvement of brain matter in the pathological process. The encephalitis that develops as a result is manifested by focal symptoms in the form of paresis and paralysis of the limbs, ptosis, oculomotor disorders, etc. In cases where meningitis is one of the manifestations of pneumococcal sepsis, a petechial rash is observed on the skin, similar to that of meningococcemia.

The CSF is very turbid, greenish, the number of cells ranges from 100 to 10,000 or more in 1 μl, and cases with low cytosis are especially severe. The protein level increases to 3-6 g/l and higher, the sugar content decreases. When smear microscopy, gram-positive diplococci located extracellularly can be detected.

The prognosis for pneumococcal meningitis is worse than for meningococcal meningitis: even with early therapy, due to the rapid consolidation of pus, the process progresses and mortality reaches 15-25%.

Meningitis caused by Haemophilus influenzae type B

Meningitis caused by Haemophilus influenzae type B most often affects children under 1.5 years of age, but it can also occur in older children, in adults after 65 years of age, and sometimes in young and middle-aged people. According to some data, in recent years, up to 95% of all cases of GBM are caused by pneumococcus and Haemophilus influenzae type B (Hib).

The symptoms of Hib meningitis depend on the age of the patient and the duration of the disease. The onset can be sudden, with a sharp increase in body temperature to 39-400 C, repeated vomiting, and severe headache. After a few hours, convulsions, impaired consciousness, coma occur, and death may occur. A gradual development of the disease is also possible, with symptoms associated with the primary focus of Hib infection first appearing (epiglottitis, cellulitis, purulent otitis, arthritis, etc.), and then meningeal, cerebral and focal symptoms are added. The CSF is cloudy and green in color. There is a characteristic discrepancy between turbidity of the cerebrospinal fluid (it is caused by a high concentration of the pathogen in the CSF) and relatively low cytosis. Meningitis can occur sluggishly, in waves, with alternating periods of improvement and deterioration. Untimely and/or inadequate antibiotic therapy leads to death, the frequency of which reaches 33%.

Purulent meningitis of other etiologies (staphylo- and streptococcal, klebsiella, salmonella, caused by Pseudomonas aeruginosa, etc.) are usually secondary (oto- and rhinogenic, septic, after neurosurgical operations) and are relatively rare.

Diagnosis

The acute onset of the disease, a combination of fever, intoxication, meningeal syndrome, and characteristic changes in the CSF (high neutrophilic pleocytosis, increased protein content and decreased glucose levels) give grounds to diagnose purulent meningitis.

The etiology of GMB can be tentatively established by bacterioscopy of a CSF smear and clarified using bacteriological examination of CSF and blood. However, in patients who have already received antibiotics, the likelihood of detecting the pathogen using these methods is low. Therefore, various immunological methods are used to detect pathogen antigens and antibodies to them (VIEF, latex agglutination). The etiology of meningitis is most accurately determined using PCR. Differential diagnosis for both purulent and serous meningitis is carried out between meningitis of various etiologies, as well as with other diseases accompanied by meningeal syndrome and neurological disorders: cerebral and subarachnoid hemorrhage, brain injuries, brain abscess and other volumetric processes, cerebrovasculitis, infectious diseases with meningeal syndrome, etc.

Treatment

In case of GBM, unlike viral ones, it is carried out antibacterial therapy which is urgent. At the first stage, before establishing the etiology GBM, one of the following antibiotics is recommended: ampicillin/oxacillin (200-300 mg/kg per day); ceftriaxone (100 mg/kg/day) or cefotaxime (150-200 mgkg); in young children, a combination of ampicillin with ceftriaxone. In the future, antibacterial therapy is adjusted depending on the etiology of meningitis and the sensitivity of the pathogen. Antimicrobial drugs must be prescribed in maximum doses that provide bactericidal concentrations in the CSF. In patients with secondary GBM, sanitation of the primary lesion is necessary.

Tuberculous meningitis

Tuberculous meningitis most often affects children and the elderly . The disease in most cases is secondary in nature, spreading from primary foci in the internal organs (lungs, lymph nodes, kidneys). It is also possible to damage the membranes from subependymal caseous foci that existed for a long time without manifestations. Provoking factors are immunodeficiency states, alcoholism, exhaustion, drug addiction.

In the membranes of the base of the brain, dense infiltrates form with compression of the cranial nerves and vessels of the circle of Willis. The disease develops gradually, weakness, adynamia, sweating, increased fatigue, and emotional lability appear. A headache occurs, increasing in intensity, low-grade fever, and vomiting. Damage to the oculomotor nerves appears early.

In the CSF - lymphocytic pleocytosis, protein-cell dissociation, hypoglycorrhachia. The diagnosis is based on the determination of antigen and antibodies to Mycobacterium tuberculosis in the CSF using enzyme-linked immunosorbent assay (ELISA) and the use of PCR.

The treatment uses isoniazid (5 mg/kg/day) in combination with rifampicin (10 mg/kg/day) and pyrazinamide (15-30 mg/kg/day). Duration of treatment is 9-12 months.

Meningitis with syphilis

Meningitis in syphilis is observed in all stages of clinical manifestations of the disease and in asymptomatic cases. It may have a manifest or blurred clinical picture. From 10 to 70% of people with early syphilis have lymphocytic pleocytosis in the CSF, which is often combined with an increase in protein. In diagnosis, taking into account the polymorphic clinical picture, the main role is given to laboratory tests: a complex of serological reactions with cardiolipin and treponemal antigens in serum and CSF; Treponema pallidum microhemagglutination reactions. Treatment is carried out with penicillin (2-4 million units intravenously every 4 hours) or 2.4 million units/day intramuscularly with probenecid (500 mg orally 4 times/day). The course of treatment is 10-14 days.

Meningitis due to Lyme borreliosis

Meningitis in Lyme borreliosis is a common complication of the disease. It can be observed in combination with erythema migrans - a characteristic marker of the disease. The disease is usually preceded by ticks biting when visiting the forest. The course of meningitis is polymorphic, meningeal signs can be moderately expressed. In the CSF there is lymphocytic pleocytosis. Serological tests play a decisive role in the diagnosis: immunofluorescence reaction or ELISA with antigen B.burgdorferi . Treatment is carried out with intravenous penicillin 24 million units/day for 14-21 days or ceftriaxone 1 g 2 times a day.

Specific prevention

Specific prevention of bacterial meningitis. Currently, there are vaccines to prevent meningococcal meningitis, Haemophilus influenzae and pneumococcal infections. Vaccination is carried out in high-risk groups, as well as for epidemiological reasons.

The list of references can be found on the website http://www.site