Streptococcal meningitis in children. Streptococcal meningitis is a life-threatening condition. Forms of the course of meningitis


Streptococcal meningitis is characterized by rapid onset and severe course. As a rule, it is secondary and is associated with hematogenous drift into the meninges of the brain of streptococcus. Occurs, for example, with erysipelas, sepsis, infective endocarditis, usually in children and the elderly, as well as in those suffering from metabolic diseases, alcoholism and cachexia (N.K. Rosenberg). It is possible in persons who have received glucocorticoids for a long time, against the background of any purulent-inflammatory diseases of streptococcal etiology. Pathogens are found everywhere. Group A streptococci colonize human skin and mucous membranes, group B streptococci colonize the gastrointestinal tract, skin, nasopharynx, and vagina. Streptococcal infections are spread by a sick person or a carrier. The carriage of streptococci in organized groups can reach 30%. CNS damage in the case of streptococcal meningitis is always of secondary origin and is, in fact, a manifestation or complication of streptococcal sepsis. The most significant are hematogenous and contact, less - lymphogenous ways of infection of the membranes and brain substance. Symptoms. Clinical manifestations of streptococcal meningitis do not have specific features that distinguish it from other secondary purulent meningitis. The disease begins acutely, with fever, chills, headache, vomiting, sometimes repeated, severe meningeal symptoms. Perhaps the development of encephalic manifestations in the form of impaired consciousness, clonic-tonic convulsions, tremor of the extremities. Signs of severe septicemia are characteristic of streptococcal meningitis: high body temperature with large swings, hemorrhagic rash, enlargement of the heart, deafness of heart tones. Naturally, the functions of parenchymal organs suffer, hepatolienal syndrome, renal failure, and damage to the adrenal glands occur. In the acute course of the disease, signs of severe septicemia and encephalic manifestations may prevail over meningeal symptoms. Streptococcal meningitis in endocarditis is often accompanied by lesions of the brain vessels with hemorrhages in the subarachnoid space, early onset of focal symptoms. The development of edema-swelling of the brain is characteristic, but brain abscesses develop rarely. Diagnostics. In the hemogram - the presence of leukocytosis, accelerated ESR. During lumbar puncture, the cerebrospinal fluid is cloudy, flows out under high pressure. Neutrophilic pleocytosis is typical (800–1200 cells per 1 µl), the protein content is increased to 2–4 g/l. Typical is a decrease in the glucose content in the cerebrospinal fluid. The etiology of streptococcal meningitis is established by the isolation of the culture of the pathogen during bacteriological cultures of cerebrospinal fluid and blood. Conduct a study of paired sera. Apply setting (latex agglutination). Treatment. The prognosis for streptococcal meningitis is severe. In the absence of antibiotic therapy, 95% of streptococcal meningitis is fatal. In the era of antibiotics, the death rate from streptococcal meningitis, despite the development of high medical technology, continues to remain at the level of 5-8%. Often, the patient simply does not have time to provide the necessary medical care, so it is very important to provide the necessary medical care in the early stages of the disease. When the first signs of streptococcal meningitis are detected, the patient must be urgently hospitalized. Patients with this disease are treated in specialized intensive care units. Streptococcal meningitis can be complicated by hydrocephalus, hearing impairment, up to its loss, visual impairment, developmental delay, epilepsy.

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Streptococcal meningitis

What is streptococcal meningitis -

Streptococcal meningitis- (m. streptococcica) purulent meningitis that occurs when a streptococcal infection is generalized or when pathogens enter the meninges from nearby organs (middle ear, paranasal sinuses, etc.). It is characterized by a rapid onset with the development of edema-swelling of the brain, encephalic focal symptoms, and damage to other organs and systems.

What provokes / Causes of Streptococcal meningitis:

The causative agent of meningitis are streptococci, which are spherical or ovoid cells 0.5–2.0 μm in size, arranged in pairs or short chains in smears, under adverse conditions can acquire an elongated or lanceolate shape, resembling coccobacilli. They are immobile, do not form spores and capsules, anaerobes or facultative anaerobes, the optimum temperature is 37 °C. According to the presence of specific carbohydrates in the cell wall, 17 serogroups are distinguished, denoted by capital letters of the Latin alphabet.

Group A hemolytic streptococci are the main pathogens in humans. They are responsible for pharyngitis, scarlet fever, cellulitis, erysipelas, pyoderma, impetigo, streptococcal toxic shock syndrome, septic endocarditis, acute glomerulonephritis and other diseases.

Group B Streptococcus inhabit the nasopharynx, gastrointestinal tract and vagina. Serovars 1a and 111 are tropic to the tissues of the central nervous system and respiratory tract and most often cause meningitis and pneumonia in newborns, as well as lesions of the skin, soft tissues, pneumonia, endocarditis, meningitis and endometritis, lesions of the urinary tract and complications of surgical wounds during caesarean section.

The causative agent of meningitis is a hemolytic or viridescent streptococcus, which has pronounced toxic properties that determine the virulence of the microbe and its aggressiveness. The main ones are: fimbrial protein, capsule and C5a-peptidase.

The fimbrial protein is the main virulence factor, which is a type-specific antigen. It prevents phagocytosis, binds fibrinogen, fibrin and their degradation products, adsorbs them on its surface, masking receptors for complement components and opsonins, causes activation of lymphocytes and the formation of antibodies with low affinity.

The capsule is the second most important virulence factor. It protects streptococci from the antimicrobial potential of phagocytes and promotes adhesion to the epithelium.

The third virulence factor is C5a-peptidase, which inhibits the activity of phagocytes. An important role in pathogenesis is also played by streptokinase, hyaluronidase, erythrogenic (pyrogenic) toxins, cardiohepatic toxin, streptolysin O and S.

Despite the widespread streptococcal infection with extensive and varied pathology, purulent meningitis of a streptococcal nature is rare. The causative agents are hemolytic and viridescent streptococci (I. G. Weinstein, N. I. Grashchenkov, 1962). Emphasizing the rarity of the disease, Noone and Herzen (1950) indicate that in the world literature until 1948 they found only 63 cases of streptococcal meningitis. According to statistics, streptococcal meningitis is observed mainly in infants and young children, more often occurring during streptococcal septicemia with purulent otitis media, erysipelas of the face, inflammation of the paranasal cavities, endocarditis, thrombophlebitis of the cerebral sinuses and other purulent foci (Biedel, 1950; Baccheta, Digilio, 1960; Mannik, Baringer, Stokes, 1962). In a significant percentage of cases, the source of purulent meningitis remains unclear (Hoyne, Herzen, 1950).

Recently, there have been reports by a number of authors in which there is a marked increase in the proportion of streptococcal meningitis among other forms. This is written by Schneeweiss, Blaurock, Jungfer (1963), who from 1956 to 1961 counted 2372 reports of purulent meningitis caused by streptococcus in the literature. The clinical picture of streptococcal meningitis has no specific features. In the vast majority of cases, the disease is characterized by an acute onset, an increase in temperature to significant numbers, repeated vomiting, lethargy or anxiety of the child.

Epidemiology
The reservoir is a sick person or a carrier. The main routes of transmission are contact, airborne and alimentary (through contaminated food products, such as milk). Children of any age are ill, but more often newborns in whom meningitis develops as a manifestation of sepsis. In 50% of newborns, infection most often occurs vertically - when the fetus passes through the birth canal infected with streptococci.

Significant colonization of the birth canal of the mother with streptococci leads to the early development of meningitis (within the first 5 days), and in children infected with a small dose, meningitis develops much later (from 6 days to 3 months). In 50% of sick newborns who do not have a specific focus of infection, meningitis develops within 24 hours, while mortality reaches 37%. Of the total number of children with late manifestations of infection, the development of meningitis and bacteremia, 10–20% die, and 50% of surviving children have gross residual effects. In patients with septic endocarditis, meningitis may occur as a result of meningeal embolism.

Pathogenesis (what happens?) during Streptococcal meningitis:

Most often, the entrance gates of infection are damaged skin (diaper rash, areas of maceration, burns, wounds), as well as mucous membranes of the nasopharynx, upper respiratory tract (streptoderma, phlegmon, abscess, purulent-necrotic rhinitis, nasopharyngitis, otitis media, tracheobronchitis, etc.) . However, in most cases, the source of development of purulent meningitis cannot be identified. The outcome of infection with streptococcus in a newborn child directly depends on the state of its cellular and humoral protection factors and the magnitude of the infectious dose.
At the site of introduction, streptococcus causes not only catarrhal, but also purulent-necrotic inflammation, from where it quickly spreads throughout the body by lymphogenous or hematogenous. Streptococcus in the blood, its toxins, enzymes, lead to the activation and increase in the level of biologically active substances, impaired hemostasis, metabolic processes with the development of acidosis, increased permeability of cell and vascular membranes, as well as the BBB. This contributes to the penetration of streptococcus into the central nervous system, damage to the meninges and brain matter.

Streptococcal meningitis symptoms:

Clinical manifestations of streptococcal meningitis do not have specific features that distinguish it from other secondary purulent meningitis.

The disease begins acutely, with fever, anorexia, chills, headache, vomiting, sometimes repeated, severe meningeal symptoms. Perhaps the development of encephalic manifestations in the form of impaired consciousness, clonic-tonic convulsions, tremor of the extremities. Signs of severe septicemia are characteristic of streptococcal meningitis: high body temperature with large swings, hemorrhagic rash, enlargement of the heart, deafness of heart tones. Naturally, the functions of parenchymal organs suffer, hepatolienal syndrome, renal failure, and damage to the adrenal glands occur. In the acute course of the disease, signs of severe septicemia and encephalic manifestations may prevail over meningeal symptoms. Streptococcal meningitis in endocarditis is often accompanied by lesions of the brain vessels with hemorrhages in the subarachnoid space, early onset of focal symptoms. The development of edema-swelling of the brain is characteristic, but brain abscesses develop rarely.

Staphylococcal and streptococcal meningitis, as a rule, are secondary. Allocate contact and hematogenous forms. Contact purulent meningitis develops with osteomyelitis of the bones of the skull and spine, epiduritis, brain abscess, chronic purulent otitis media, sinusitis. Hematogenous meningitis occurs with sepsis, acute staphylococcal and streptococcal endocarditis. The inflammatory process in the membranes of the brain is characterized by a tendency to abscess formation.

The onset of the disease is acute. The main complaint is severe headaches of a diffuse or local nature. From the 2-3rd day of the disease, meningeal symptoms, general skin hyperesthesia, and sometimes convulsive syndrome are detected. Often the cranial nerves are affected, pathological reflexes may appear, in severe cases, disorders of consciousness and impaired stem functions are observed. Cerebrospinal fluid is opalescent or cloudy, its pressure is sharply increased; pleocytosis is predominantly neutrophilic or mixed in the range from several hundred to 3-3 thousand cells in 1 μl; the content of sugar and chlorides is reduced, protein is increased. A blood test reveals neutrophilic leukocytosis, an increase in ESR. The diagnosis is based on the history, clinical manifestations and the results of blood and cerebrospinal fluid tests (detection of the pathogen in them).
Early active treatment of the primary purulent focus is necessary against the background of antibiotic therapy with oxacillin, aminoglycosides, cephalosporins, biseptol, etc. (depending on the sensitivity of the isolated pathogen strain). Antibacterial therapy is combined with the use of antistaphylococcal gamma globulin, antistaphylococcal plasma, bacteriophage, immunomodulators. The prognosis is severe, determined both by the direct lesion of the central nervous system and the course of the general septic process.

Diagnosis of Streptococcal meningitis:

The main diagnostic criteria for streptococcal meningitis are:
1. Epidemiological anamnesis: the disease develops against the background of streptococcal sepsis, less often - another streptococcal disease, the pathogen spreads hematogenously or lymphogenously, children of any age are ill, but more often newborns.
2. The onset of meningitis is acute, with the development of signs of severe septicemia: a significant range of temperature reactions, the presence of a hemorrhagic rash, hepatolienal syndrome and severe meningeal symptoms.
3. Quite often, edema-swelling of the brain, encephalic focal symptoms develop rapidly.
4. Often occurs with the involvement of other vital organs and systems (liver, heart, lungs, adrenal glands) in the infectious process.
5. Isolation of hemolytic streptococcus from CSF, blood confirms the etiological diagnosis.

Laboratory diagnostics
General blood analysis. In the peripheral blood, leukocytosis, neutrophilia, a shift in the blood formula to the left, and an increased ESR are detected.
Liquor research. In the cerebrospinal fluid, a high neutrophilic pleocytosis (thousands of cells in 1 µl), an increase in protein content (1–10 g/l) and a decrease in glucose levels are detected. Bacterioscopy reveals Gram-negative cocci.
bacteriological research. Isolation of the pathogen is the most reliable method. It is produced by sowing blood, mucus from the nose and throat, sputum, cerebrospinal fluid on blood agar. On liquid media, streptococci give a benthic, upward growth. For differentiation, the identified microorganisms are inoculated on a thioglycol medium, semi-liquid agar.
bacterioscopic examination. Bacterioscopy in smears reveals typical gram-positive cocci forming short chains, but polymorphic forms can also be detected.
Serological study. Serotyping is carried out in the reaction of latex agglutination or coagglutination using monoclonal antibodies labeled with fluorescins.

Treatment for streptococcal meningitis:

Secondary purulent meningitis is no less severe than meningococcal meningitis. Treatment should begin already at the prehospital stage with the introduction of penicillin. It is prescribed for 200,000 - 300,000 units / kg of body weight per day intramuscularly.

With pneumococcal meningitis, the dose of penicillin is 300,000-500,000 IU / kg per day, in severe condition - 1,000,000 IU / kg per day. With streptococcal meningitis, penicillin is prescribed at 200,000 IU / kg per day.

With staphylococcal and streptococcal meningitis, semi-synthetic penicillins (methicillin, oxacillin, ampicillin) are also used intramuscularly at a dose of 200-300 mg / kg per day. You can prescribe chloramphenicol sodium succinate at a dose of 60-80 mg / kg per day, klaforan - 50-80 mg / kg per day.

With meningitis caused by Pfeiffer-Afanasiev bacillus, Escherichia coli, Friedlander bacillus or salmonella, the maximum effect is given by chloramphenicol sodium succinate, which is prescribed at a dose of 60-80 mg / kg per day intramuscularly with an interval of 6-8 hours. Neomycin sulfate is also effective - 50,000 IU / kg 2 times a day.

They also recommend morphocycline - 150 mg 2 times a day intravenously.
With staphylococcal meningitis, staphylococcal toxoid is administered at a dose of 0.1-0.3-0.5-0.7-1 ml intramuscularly, antistaphylococcal gamma globulin - 1 - 2 doses intramuscularly for 6 - 10 days, immunized antistaphylococcal plasma - 250 ml 1 time in 3 days.

Prevention of streptococcal meningitis:

IN prevention of streptococcal meningitis an important role is played by the popularization of information about the ways of spreading the infection, since the disease is more often transmitted by airborne droplets, the patient and others should know that infection is possible when talking, coughing, sneezing. Hygiene skills and living conditions play an important role in the prevention of meningitis.

Which doctors should you contact if you have Streptococcal meningitis:

Are you worried about something? Do you want to know more detailed information about Streptococcal meningitis, its causes, symptoms, methods of treatment and prevention, the course of the disease and diet after it? Or do you need an inspection? You can book an appointment with a doctor– clinic Eurolaboratory always at your service! The best doctors will examine you, study the external signs and help identify the disease by symptoms, advise you and provide the necessary assistance and make a diagnosis. you also can call a doctor at home. Clinic Eurolaboratory open for you around the clock.

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Streptococcal meningitis- (m. streptococcica) purulent meningitis that occurs when a streptococcal infection is generalized or when pathogens enter the meninges from nearby organs (middle ear, paranasal sinuses, etc.). It is characterized by a rapid onset with the development of edema-swelling of the brain, encephalic focal symptoms, and damage to other organs and systems.

What causes streptococcal meningitis:

The causative agent of meningitis are streptococci, which are spherical or ovoid cells 0.5–2.0 μm in size, arranged in pairs or short chains in smears, under adverse conditions can acquire an elongated or lanceolate shape, resembling coccobacilli. They are immobile, do not form spores and capsules, anaerobes or facultative anaerobes, the optimum temperature is 37 °C. According to the presence of specific carbohydrates in the cell wall, 17 serogroups are distinguished, denoted by capital letters of the Latin alphabet.

Group A hemolytic streptococci are the main pathogens in humans. They are responsible for pharyngitis, scarlet fever, cellulitis, erysipelas, pyoderma, impetigo, streptococcal toxic shock syndrome, septic endocarditis, acute glomerulonephritis and other diseases.

Group B Streptococcus inhabit the nasopharynx, gastrointestinal tract and vagina. Serovars 1a and 111 are tropic to the tissues of the central nervous system and respiratory tract and most often cause meningitis and pneumonia in newborns, as well as lesions of the skin, soft tissues, pneumonia, endocarditis, meningitis and endometritis, lesions of the urinary tract and complications of surgical wounds during caesarean section.

The causative agent of meningitis is a hemolytic or viridescent streptococcus, which has pronounced toxic properties that determine the virulence of the microbe and its aggressiveness. The main ones are: fimbrial protein, capsule and C5a-peptidase.

The fimbrial protein is the main virulence factor, which is a type-specific antigen. It prevents phagocytosis, binds fibrinogen, fibrin and their degradation products, adsorbs them on its surface, masking receptors for complement components and opsonins, causes activation of lymphocytes and the formation of antibodies with low affinity.

The capsule is the second most important virulence factor. It protects streptococci from the antimicrobial potential of phagocytes and promotes adhesion to the epithelium.

The third virulence factor is C5a-peptidase, which inhibits the activity of phagocytes. An important role in pathogenesis is also played by streptokinase, hyaluronidase, erythrogenic (pyrogenic) toxins, cardiohepatic toxin, streptolysin O and S.

Despite the widespread streptococcal infection with extensive and varied pathology, purulent meningitis of a streptococcal nature is rare. The causative agents are hemolytic and viridescent streptococci (I. G. Weinstein, N. I. Grashchenkov, 1962). Emphasizing the rarity of the disease, Noone and Herzen (1950) indicate that in the world literature until 1948 they found only 63 cases of streptococcal meningitis. According to statistics, streptococcal meningitis is observed mainly in infants and young children, more often occurring during streptococcal septicemia with purulent otitis media, erysipelas of the face, inflammation of the paranasal cavities, endocarditis, thrombophlebitis of the cerebral sinuses and other purulent foci (Biedel, 1950; Baccheta, Digilio, 1960; Mannik, Baringer, Stokes, 1962). In a significant percentage of cases, the source of purulent meningitis remains unclear (Hoyne, Herzen, 1950).

Recently, there have been reports by a number of authors in which there is a marked increase in the proportion of streptococcal meningitis among other forms. This is written by Schneeweiss, Blaurock, Jungfer (1963), who from 1956 to 1961 counted 2372 reports of purulent meningitis caused by streptococcus in the literature. The clinical picture of streptococcal meningitis has no specific features. In the vast majority of cases, the disease is characterized by an acute onset, an increase in temperature to significant numbers, repeated vomiting, lethargy or anxiety of the child.

Epidemiology
The reservoir is a sick person or a carrier. The main routes of transmission are contact, airborne and alimentary (through contaminated food products, such as milk). Children of any age are ill, but more often newborns in whom meningitis develops as a manifestation of sepsis. In 50% of newborns, infection most often occurs vertically - when the fetus passes through the birth canal infected with streptococci.

Significant colonization of the birth canal of the mother with streptococci leads to the early development of meningitis (within the first 5 days), and in children infected with a small dose, meningitis develops much later (from 6 days to 3 months). In 50% of sick newborns who do not have a specific focus of infection, meningitis develops within 24 hours, while mortality reaches 37%. Of the total number of children with late manifestations of infection, the development of meningitis and bacteremia, 10–20% die, and 50% of surviving children have gross residual effects. In patients with septic endocarditis, meningitis may occur as a result of meningeal embolism.

Pathogenesis (what happens?) during Streptococcal meningitis:

Most often, the entrance gates of infection are damaged skin (diaper rash, areas of maceration, burns, wounds), as well as mucous membranes of the nasopharynx, upper respiratory tract (streptoderma, phlegmon, abscess, purulent-necrotic rhinitis, nasopharyngitis, otitis media, tracheobronchitis, etc.) . However, in most cases, the source of development of purulent meningitis cannot be identified. The outcome of infection with streptococcus in a newborn child directly depends on the state of its cellular and humoral protection factors and the magnitude of the infectious dose.
At the site of introduction, streptococcus causes not only catarrhal, but also purulent-necrotic inflammation, from where it quickly spreads throughout the body by lymphogenous or hematogenous. Streptococcus in the blood, its toxins, enzymes, lead to the activation and increase in the level of biologically active substances, impaired hemostasis, metabolic processes with the development of acidosis, increased permeability of cell and vascular membranes, as well as the BBB. This contributes to the penetration of streptococcus into the central nervous system, damage to the meninges and brain matter.

Streptococcal meningitis symptoms:

Clinical manifestations of streptococcal meningitis do not have specific features that distinguish it from other secondary purulent meningitis.

The disease begins acutely, with fever, anorexia, chills, headache, vomiting, sometimes repeated, severe meningeal symptoms. Perhaps the development of encephalic manifestations in the form of impaired consciousness, clonic-tonic convulsions, tremor of the extremities. Signs of severe septicemia are characteristic of streptococcal meningitis: high body temperature with large swings, hemorrhagic rash, enlargement of the heart, deafness of heart tones. Naturally, the functions of parenchymal organs suffer, hepatolienal syndrome, renal failure, and damage to the adrenal glands occur. In the acute course of the disease, signs of severe septicemia and encephalic manifestations may prevail over meningeal symptoms. Streptococcal meningitis in endocarditis is often accompanied by lesions of the brain vessels with hemorrhages in the subarachnoid space, early onset of focal symptoms. The development of edema-swelling of the brain is characteristic, but brain abscesses develop rarely.

Staphylococcal and streptococcal meningitis, as a rule, are secondary. Allocate contact and hematogenous forms. Contact purulent meningitis develops with osteomyelitis of the bones of the skull and spine, epiduritis, brain abscess, chronic purulent otitis media, sinusitis. Hematogenous meningitis occurs with sepsis, acute staphylococcal and streptococcal endocarditis. The inflammatory process in the membranes of the brain is characterized by a tendency to abscess formation.

The onset of the disease is acute. The main complaint is severe headaches of a diffuse or local nature. From the 2-3rd day of the disease, meningeal symptoms, general skin hyperesthesia, and sometimes convulsive syndrome are detected. Often the cranial nerves are affected, pathological reflexes may appear, in severe cases, disorders of consciousness and impaired stem functions are observed. Cerebrospinal fluid is opalescent or cloudy, its pressure is sharply increased; pleocytosis is predominantly neutrophilic or mixed in the range from several hundred to 3-3 thousand cells in 1 μl; the content of sugar and chlorides is reduced, protein is increased. A blood test reveals neutrophilic leukocytosis, an increase in ESR. The diagnosis is based on the history, clinical manifestations and the results of blood and cerebrospinal fluid tests (detection of the pathogen in them).
Early active treatment of the primary purulent focus is necessary against the background of antibiotic therapy with oxacillin, aminoglycosides, cephalosporins, biseptol, etc. (depending on the sensitivity of the isolated pathogen strain). Antibacterial therapy is combined with the use of antistaphylococcal gamma globulin, antistaphylococcal plasma, bacteriophage, immunomodulators. The prognosis is severe, determined both by the direct lesion of the central nervous system and the course of the general septic process.

Diagnosis of Streptococcal meningitis:

The main diagnostic criteria for streptococcal meningitis are:
1. Epidemiological anamnesis: the disease develops against the background of streptococcal sepsis, less often - another streptococcal disease, the pathogen spreads hematogenously or lymphogenously, children of any age are ill, but more often newborns.
2. The onset of meningitis is acute, with the development of signs of severe septicemia: a significant range of temperature reactions, the presence of a hemorrhagic rash, hepatolienal syndrome and severe meningeal symptoms.
3. Quite often, edema-swelling of the brain, encephalic focal symptoms develop rapidly.
4. Often occurs with the involvement of other vital organs and systems (liver, heart, lungs, adrenal glands) in the infectious process.
5. Isolation of hemolytic streptococcus from CSF, blood confirms the etiological diagnosis.

Laboratory diagnostics
General blood analysis. In the peripheral blood, leukocytosis, neutrophilia, a shift in the blood formula to the left, and an increased ESR are detected.
Liquor research. In the cerebrospinal fluid, a high neutrophilic pleocytosis (thousands of cells in 1 µl), an increase in protein content (1–10 g/l) and a decrease in glucose levels are detected. Bacterioscopy reveals Gram-negative cocci.
bacteriological research. Isolation of the pathogen is the most reliable method. It is produced by sowing blood, mucus from the nose and throat, sputum, cerebrospinal fluid on blood agar. On liquid media, streptococci give a benthic, upward growth. For differentiation, the identified microorganisms are inoculated on a thioglycol medium, semi-liquid agar.
bacterioscopic examination. Bacterioscopy in smears reveals typical gram-positive cocci forming short chains, but polymorphic forms can also be detected.
Serological study. Serotyping is carried out in the reaction of latex agglutination or coagglutination using monoclonal antibodies labeled with fluorescins.

Treatment for streptococcal meningitis:

Secondary purulent meningitis is no less severe than meningococcal meningitis. Treatment should begin already at the prehospital stage with the introduction of penicillin. It is prescribed for 200,000 - 300,000 units / kg of body weight per day intramuscularly.

With pneumococcal meningitis, the dose of penicillin is 300,000-500,000 IU / kg per day, in severe condition - 1,000,000 IU / kg per day. With streptococcal meningitis, penicillin is prescribed at 200,000 IU / kg per day.

With staphylococcal and streptococcal meningitis, semi-synthetic penicillins (methicillin, oxacillin, ampicillin) are also used intramuscularly at a dose of 200-300 mg / kg per day. You can prescribe chloramphenicol sodium succinate at a dose of 60-80 mg / kg per day, klaforan - 50-80 mg / kg per day.

With meningitis caused by Pfeiffer-Afanasiev bacillus, Escherichia coli, Friedlander bacillus or salmonella, the maximum effect is given by chloramphenicol sodium succinate, which is prescribed at a dose of 60-80 mg / kg per day intramuscularly with an interval of 6-8 hours. Neomycin sulfate is also effective - 50,000 IU / kg 2 times a day.

They also recommend morphocycline - 150 mg 2 times a day intravenously.
With staphylococcal meningitis, staphylococcal toxoid is administered at a dose of 0.1-0.3-0.5-0.7-1 ml intramuscularly, antistaphylococcal gamma globulin - 1 - 2 doses intramuscularly for 6 - 10 days, immunized antistaphylococcal plasma - 250 ml 1 time in 3 days.

Prevention of streptococcal meningitis:

IN prevention of streptococcal meningitis an important role is played by the popularization of information about the ways of spreading the infection, since the disease is more often transmitted by airborne droplets, the patient and others should know that infection is possible when talking, coughing, sneezing. Hygiene skills and living conditions play an important role in the prevention of meningitis.

Brain diseases can leave behind irreversible consequences and often lead to death. Meningitis is one of them and is an inflammation of the meninges. It is caused by bacteria, viruses and fungi, and the disease spreads by airborne droplets and contact (depending on the nature of the disease). Both soft and arachnoid membranes (leptomeningitis) and hard ones (pachymeningitis) can become inflamed, but it is the first type that is considered the main one. The disease can be an independent process (primary type) or occur as a complication (secondary type). Meningococcal infection is the primary type, and staphylococcal meningitis is the secondary. The disease is divided into serous and purulent forms. The first type refers to most types of the disease, and the second is mainly the result of a bacterial infection.

Staphylococcal meningitis is a purulent type of leptomeningitis. It is caused by a bacterium called Staphylococcus aureus. The disease can manifest itself in the form of pinpoint foci or generalized (throughout the meninges). The staphylococcal species is characterized by the severity of manifestations and has not the most favorable prognosis.

This disease affects all age groups, but due to weak immunity, it occurs mainly in children. According to statistics, it appears in every 11 newborn due to an infection introduced into the body. Microbes that can cause pathology belong to the group of aerobes of the immobile type. They are sensitive to light and disinfectants, but quite resistant to drying and heat. Microbes enter the body by airborne droplets and contact.

Often, staphylococcal meningitis is transmitted from healthcare workers who are not even aware that they have the bacteria in their bodies. Increase the chances of a pathological process occurring during childbirth and fetal hypoxia.

Meningococcal infection

The meningococcal species is a common representative of the generalized form of this disease. This type of leptomeningitis occurs due to the ingestion of meningococcus. It has an extremely acute onset of the course and manifests itself in the form of meningeal symptoms, which is accompanied by signs of intoxication.

Meningococcus is immobile and dies extremely quickly in the external environment. It is aerobic and susceptible to cold, heat and sunlight. This bacterium is protected by a special capsule that allows it to survive external stimuli and is destroyed after it enters a favorable environment (the human body). Such meningitis has an acute course due to the endotoxin produced by the pathogen. It is similar to the toxins synthesized by enterobacteria, but is much stronger than them.

You can get meningococcal meningitis through the air. Often this happens during a conversation or when an infected person coughs and sneezes. Such meningitis is not transmitted by contact.

pneumococcal infection

Pneumococcal meningitis is a purulent leptomeningitis. The causative agent of the disease are pneumococci. Occurs mainly in children over 10 years of age.

This type of disease is quite common and comes immediately after meningococcal infection. For the first time it became known about pneumococcal meningitis in the XIX century. During these years, it became known that the bacterium causing the disease is aerobic. It is immobile, protected by an outer capsule, and represents the Streptococcus family.

Pneumococcal meningitis occurs due to airborne droplets entering the body. It can be transmitted by both sick and healthy people who are carriers of the infection. More likely to catch the disease in autumn and spring.

streptococcal infection

Streptococcal meningitis is a purulent type. Leptomeningitis of this variety occurs after the direct spread of streptococci or due to infection from other places (ear, nose). The disease is characterized by an acute onset with cerebral edema and damage to internal organs.

Transmitted by airborne droplets and contact. Children, especially newborns, suffer from pathology. They have streptococcal meningitis due to sepsis. In every 2 cases, infection occurs during childbirth due to the presence of streptococci in the birth canal. The rate of development of the disease depends on the number of bacteria. At high concentrations, streptococcal meningitis appears no later than 5 days after birth. If the colony of streptococci is very small, then the disease can occur within 3 months.

Sometimes the pathology does not have a specific lesion. In this case, it manifests itself within a day and a third of sick babies die from this type of disease. In other cases, death occurs in about 15% of cases, and at the same time, every second baby has the consequences of the pathology.

Otogenic type of disease

Otogenic meningitis is a purulent type of leptomenigitis. It occurs mainly due to bacteria that have entered the brain from the ear cavity. Basically, this happens due to chronic and acute otitis media. It is divided into the following types:

  • Primary. The infection came from the ear cavity directly to the meninges;
  • Secondary. The disease developed as a result of intracranial pathological processes (abscesses, sinus thrombosis).

With purulent otitis media, microflora is sown. It is because of it that otogenic meningitis develops. It is characterized by the appearance of cerebral edema, massive discharge of pus, the development of encephalitis and an increase in the amount of cerebrospinal fluid (cerebrospinal fluid).

fungal infection

Cryptococcal meningitis is caused by the ingestion of a yeast fungus (cryptococcus neoformans). Pathology occurs due to weakened immune defenses and is transmitted by airborne droplets. With this meningitis, the symptoms are not distinguished by anything special and are characteristic of any form of leptomenigitis. However, if left untreated, the patient may fall into a coma and die.

Cryptococcal meningitis does not occur in healthy people and is common in patients suffering from AIDS and other pathologies that depress the immune system. A fungal infection enters the body mainly from the excrement of birds.

Previously, it often manifested itself after transplantation and taking glucocorticosteroids and thymocyte immunoglobulin. To date, the disease in most cases occurs in people with the immunodeficiency virus.

Timely detection of cryptococcal meningitis is extremely difficult, since initially its manifestations resemble tuberculosis. The fungal infection is localized mainly in the human brain. However, sometimes the disease may return due to the accumulation of cryptococcus neoformans in the prostate gland.

Viral infection

Aseptic meningitis is a viral infection that can spread even to healthy people and can be fatal. In most cases, the peak of the development of the disease occurs after a week, then the patient begins to recover. This is possible if the disease is treated immediately. People who do not want to undergo therapy often become disabled or die. Symptoms of the disease are not much different from inflammation of the meninges caused by a bacterial infection.

Aseptic meningitis is virtually always the result of enteroviruses. Outbreaks of morbidity are more often observed in summer and autumn. Enteroviruses are transmitted by airborne droplets. In more rare cases, it occurs after contact with an infected person or thing. The virus is also found in human feces. This mode of transmission is typical for babies and people who change diapers for such children. Usually the disease manifests itself after an incubation period, which lasts about a week, but from the 3rd day the patient can infect others.

herpes virus

Herpetic meningitis refers to the viral forms of inflammation of the meninges. It is called herpes 1 and 2 types, but it is the second type that most often becomes its cause of development. Occurs in every 5 people who first had this type of virus. In the future, the body is much less likely to perceive the appearance of herpes so acutely. Herpes meningitis is diagnosed simply, as vesicular rashes are often visible in the genital area. In addition to a rash, patients are often tormented by frequent urination, back pain, as well as impaired sensitivity and signs of paresthesia in the anogenital zone (anus and genital area).

Herpetic meningitis is transmitted by airborne droplets. After entering the body, it settles mainly in the ganglia and periodically manifests itself due to weakened immunity.
In women, herpetic meningitis occurs more often than in men.

According to statistics, the first appearance of type 2 herpes ends badly enough for the female, and a third of the girls fall ill with this pathology. In males, the situation is slightly better and only every 10 men develop this pathology. Herpetic meningitis tends to come back and relapses are observed in every 5 people.

Syphilis

Syphilis is a severe sexually transmitted disease. It is divided into several stages of development, and each of them has its own complications. Syphilitic meningitis manifests itself in 2 stages and proceeds mostly secretly, but sometimes quite acutely. It is characterized by high fever and other meningeal symptoms.

Inflammation of the meninges of the brain after surgery

Only 0.6% of people who have had brain surgery suffer from postoperative meningitis. This pathology occurs due to infection during surgery. In most cases, such meningitis develops within 48 hours after infection and is extremely acute.

Symptoms

All types of meningitis, including staphylococcal, have similar symptoms and differ mainly in the severity of manifestations. Basically, in humans with inflammation of the meninges, the following symptoms are observed:

  • General weakness;
  • Heat;
  • Photophobia;
  • mental disorders;
  • Nausea up to vomiting;
  • Headache, aggravated by movement and due to exposure to external stimuli (light, sound, vibration, etc.);
  • Increased tone of the occipital muscles;
  • Restriction of head movements;
  • Pulsation and swelling of the fontanel in babies;
  • Skin blanching;
  • Deterioration of concentration;
  • Violation of the behavior of infants;
  • Loss of appetite;
  • Increased breathing and heart rate;
  • The appearance of shortness of breath;
  • pressure reduction;
  • Taking unusual postures;
  • The appearance of abnormal involuntary reflexes;
  • Increased sensitivity in the head area;
  • Convulsive seizures;
  • The appearance of a rash.

The appearance of several of these symptoms should be a signal to go to the hospital. The doctor will conduct an examination and prescribe examinations to identify the presence of the disease and its cause. For this, MRI, CT, tests and lumbar puncture are used to remove cerebrospinal fluid.

The course of treatment depends on the nature of the infection, as antivirals, antifungals, and antibiotics may be needed to eliminate the bacteria. It also includes drugs to improve blood flow, anti-inflammatory drugs and analgesics.

Staphylococcal, meningococcal and other types of inflammation of the meninges are dangerous to health. The course of meningitis in most cases is quite acute and the patient may remain disabled or die. You can prevent this, but for this you will have to strengthen the immune system and avoid meeting with infected people.

Despite the widespread streptococcal infection with extensive and varied pathology, purulent meningitis of a streptococcal nature is rare. The causative agents are hemolytic and viridescent streptococci (I. G. Weinstein, N. I. Grashchenkov, 1962). Emphasizing the rarity of the disease, Noupe and Herzen (1950) indicate that in the world literature until 1948 they found only 63 cases of streptococcal meningitis. According to statistics, streptococcal meningitis is observed mainly in infants and young children, more often occurring during streptococcal septicemia with purulent otitis media, erysipelas of the face, inflammation of the paranasal cavities, endocarditis, thrombophlebitis of the cerebral sinuses and other purulent foci (Biedel, 1950; Baccheta, Digilio, 1960; Mannik, Baringer, Stokes, 1962). In a significant percentage of cases, the source of purulent meningitis remains unclear (Hoyne, Herzen, 1950).
Recently there have been reports by a number of authors (Gerlini, Natoli, 1960), in which there is a marked increase in the proportion of streptococcal meningitis among other forms. This is written by Schneeweiss, Blaurock, Jungfer (1963), who from 1956 to 1961 counted 2372 reports of purulent meningitis caused by streptococcus in the literature. The clinical picture of streptococcal meningitis has no specific features. In the vast majority of cases, the disease is characterized by an acute onset, an increase in temperature to significant numbers, repeated vomiting, lethargy or anxiety of the child.
However, as with staphylococcal meningitis, the clinical picture of the disease is often dominated by the features of meningoencephalitis - depression of consciousness, frequent clonic-tonic convulsions, early focal symptoms along with signs of severe septicemia (high temperature with large fluctuations, subcutaneous hemorrhages, deafness of heart tones, increased liver and spleen). The cerebrospinal fluid is turbid, with a high protein content (4.5-9% 0) and pleocytosis of a predominantly neutrophilic nature.
Along with acute forms, in which there is a rapid disappearance of cerebral, meningeal and cerebrospinal fluid changes, more common are severe forms with prolonged toxicosis, persistent fever and prolonged anorexia, and persistent changes in the composition of the cerebrospinal fluid. A similar example of a flow can be the following observation.
Oleg M., 1 month 10 days old, was admitted to the clinic on the 2nd day of illness. The disease swayed sharply, the temperature rose to 39.2°, lethargy was replaced by periods of severe anxiety, repeated vomiting. The next day, the mother noticed the child's lack of movement in the left arm and leg, repeated convulsions in the left half of the body.
Upon admission, the patient's general condition was severe, consciousness was darkened, convulsive twitching of the hands, temperature 39.3° (Fig. 16). The skin is pale, around the mouth and wings of the nose with cyanotic staining. No pathological changes were found in the lungs. Heart sounds are sharply muffled, the pulse is weak filling. There are no meningeal symptoms. General muscle hypotension was noted. Lumbar puncture yielded a slightly turbid liquid, 2100 cells per 1 mm3 (mainly neutrophils), 6.34% protein. Streptococcus was isolated bacterioscopically.
The treatment was carried out with massive doses of penicillin, to which streptomycin was added on the 6th day of therapy. The further course of the disease was characterized by prolonged, irregular fever, periodic convulsions (until the 9th day of treatment), while cerebral phenomena and signs of toxicosis persisted until the 11th day, anorexia - 14 days. The cerebrospinal fluid was sanitized by the 23rd day of the child's stay in the hospital. By the time of discharge, no complications were noted.
In the few reports on the description of the clinic of streptococcal meningitis, the severity of this form of meningitis and often occurring complications are emphasized (Baccheta, Digilio, 1960; Natoli, Gerlini, 1961). Thus, of the 2 cases described by Natoli and Gerlini /1961), both had severe complications (encephalitic symptoms, hydrocephalus). De Matteis (1958) also draws attention to the frequency of severe complications in this disease. According to Appelbaum (1961), mortality in streptococcal meningitis averages 35%.
Rare forms of purulent meningitis. In recent years, due to the widespread use of antibiotics, especially penicillin, there have been marked changes in the usual microbial landscape. The practical significance of gram-negative bacilli (Pseudomonas aeruginosa, Proteus vulgaris, Friedlander's bacillus) has increased, which, along with E. coli, increasingly began to participate in various forms of infectious pathology of newborns and children in the first months of life (V. A. Tabolin et al., 1968). Infections caused by these microbes have created new aspects of the infectious pathology of early childhood.

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