Streptococcal meningitis is a life-threatening condition. G00.2 Streptococcal meningitis When having prophetic dreams

These diseases are usually of secondary origin and arise as a complication of inflammatory processes in the middle ear, paranasal cavities, erysipelas and other purulent foci. The most common pathogens are hemolytic and viridans streptococci, aureus and white staphylococci. Cases of meningitis caused by viridans streptococcus began to be described relatively recently. Goin and Gerzon found 63 cases of this meningitis in the world literature before 1948 (34 patients recovered and 29 died). According to statistical data, of all purulent meningitis, viridans streptococcus was detected in 0.3-2.4% of cases. The authors indicate that the source of meningitis caused by this pathogen in 13% of cases (out of 63) was heart disease (endocarditis lenta), in 31% - diseases of the ear, nose and throat, in 21% - diseases of other organs and in 35% of cases meningitis turned out to be “isolated”.

Staphylococcal meningitis is less common. Symptomatologically, streptococcal and staphylococcal meningitis occur basically like other purulent meningitis and are characterized by a pronounced clinical picture and severe course of the disease. The latter is due to the presence of a primary purulent focus in any organ and the fact that these purulent meningitis often represent only a partial manifestation of a general disease localized in the meninges.

The disease develops acutely, from the first days there is a high temperature, vomiting, Kernig's, Brudzinski's symptoms and stiff neck are clearly visible. When the medulla is involved in the process, depending on the location of the lesion, sometimes convulsions and rarely focal prolapses occur. The latter are usually associated with concomitant cerebral abscesses or thrombosis of cerebral vessels. With general sepsis or septicopyemia, skin rashes, enlarged liver and spleen, joint damage, pneumonia, purulent pleurisy, pericarditis, nephritis, etc. appear.

During a spinal tap, fluid leaks out under high pressure; sometimes in cases where it is of a pronounced purulent nature, the liquid may flow out slowly and with reduced pressure. The protein content is sharply increased, the cytosis is high, predominantly neutrophilic. The pathogen is determined bacterioscopically and bacteriologically in the liquid. However, often the liquid turns out to be sterile. We present cases of purulent meningitis from our own observations. Staphylococcus aureus was found in the blood of one patient, viridans streptococcus was found in the cerebrospinal fluid of another, and the pathogen was not found in the third, although furunculosis should be considered the source of his meningitis.

Clinic

1. Patient T., 39 years old. Received November 13th. Since November 3, he has been feeling unwell, with pain in the lumbar region and abdomen. On November 11, a severe headache and a temperature of 38.9° appeared. The patient consulted a doctor and was diagnosed with typhoid fever and was sent to the hospital. Upon admission, the condition was serious, the patient was lethargic and drowsy. There is no nausea or vomiting. Meningeal symptoms are pronounced. There is no skin rash. The tongue is coated, there is slight hyperemia in the pharynx. The liver is palpable in the hypochondrium, the spleen is not palpable. The respiratory and circulatory organs are unremarkable. Urination is free. A spinal puncture was performed: the fluid was cloudy, flowed out in frequent drops, protein 1.32%, 1050 cells per 1 mm 3, of which 90% were neutrophils, 10% lymphocytes. Blood test: l. 12,000, p. 9%, p. 74%. lymph. 13%, mon. 4%; ROE 37 mm per hour. The fundus is normal. No microflora was found in the liquid. Blood culture - Staphylococcus aureus. Diagnosis: purulent meningitis. Treatment with penicillin (endolumbar and intramuscular) and sulfathiazole was started. From November 21, the temperature dropped to normal levels and remained at this level until November 20, then rose again to 38.6° and remained at these levels for 4 days. Subsequently, until the patient was discharged, the temperature was normal. The meningeal syndrome had completely smoothed out by November 26, but during the period of repeated rise in temperature, it reappeared to a weak degree and lasted for 5 days. The cerebrospinal fluid on December 3 contained 0.26% protein, 46 cells per 1 mm 3, of which 90°/o lymphocytes, 10°/o neutrophils. In total, the patient received 13,600,000 units of penicillin and 30 g of sulfathiazole. Discharged in satisfactory condition.

2. Patient G., 56 years old. She was admitted to the hospital on November 19. The condition is serious, consciousness is darkened. According to her daughter, on November 18 the patient complained of a headache, runny nose, and congestion in the ears. Temperature 37.6°. I didn’t sleep well at night due to abdominal pain and vomiting. On the afternoon of November 19, she was taken to the hospital. For the last two years, the patient had high blood pressure (180/100 mm). A duodenal ulcer was discovered.

The patient is of normal build, the subcutaneous fat layer is pronounced. The borders of the heart are expanded to the left, heart sounds are muffled. Pulse 120 beats per minute. Blood pressure 180/90 mmHg. The tongue is dry, coated, the stomach is swollen. Lungs are within normal limits. Exophthalmos is greater on the right. The pupils are uniform, the reaction to light is preserved, there is a slight internal strabismus on the left. Tongue in the oral cavity in the midline. There are no paresis. Resists inspection. Tendon reflexes are alive and pathological are not caused. Nuchal rigidity, bilateral Kernig's sign. A more detailed examination cannot be carried out due to the serious condition of the patient. A spinal puncture was performed: the fluid is cloudy, the pressure is 500 mm of water column, the protein is 2.31%, the cytosis is 1600 cells per 1 mm 3, of which 95% are neutrophils, 3% lymphocytes and 2% plasma cells. Blood test: l. 12,500, p. 9%, p. 83%, lymph. 4%, mon. 4%; ROE 10 mm per hour. According to the otolaryngologist, there are no inflammatory changes in the ears. The fundus is normal. Diagnosis: purulent meningitis. Treatment with sulfonamides and penicillin intramuscularly and endolumbarally (100,000 units) was prescribed.

Upon repeated puncture (November 21), the cerebrospinal fluid contained 6000 cells per 1 mm, of which 50% were lymphocytes, 48% neutrophils, 2% eosinophils, 0.9% protein.

On November 23, her condition improved and the patient regained consciousness. Culture of the cerebrospinal fluid yielded growth of viridans streptococcus. Subsequently, the meningeal symptoms gradually smoothed out, the temperature dropped to normal, giving at times low-grade fevers. During the course of the disease, there was ulcerative stomatitis and an abscess on the inner surface of the left thigh below the inguinal fold. The abscess was opened. By November 29, the cerebrospinal fluid was sanitized, and on November 15, the patient was discharged from the hospital.

3. Patient M., 58 years old. He was admitted to the hospital on December 28 in a moderate condition with complaints of headache, weakness, chills and cough with sputum. I felt unwell since December 13, and on December 15, chills, muscle pain and a severe headache appeared. High temperature since December 27. He consulted a doctor and was hospitalized on December 28th. Upon admission, the patient had a profuse rash on the body, shortness of breath, shortening of the percussion sound on the right in the lower lobe of the lung, and the presence of dry and moist rales in this area. There were no significant changes in the cardiovascular system. The liver was palpable at the edge of the rib, the spleen was not palpable. There were no meningeal phenomena. On the right temple there are traces of a former boil, on the lower back there is an open boil in the stage of reverse development. Since December 29, consciousness has become darkened, the headache has intensified, and pronounced meningeal symptoms have appeared (stiff neck, Kernig's and Brudzinski's symptoms). During a spinal puncture, a turbid fluid was obtained that came out under high pressure, containing 2.64% protein, cytosis of 1280 cells per 1 mm (neutrophils 55°/o, lymphocytes 40%, microphages 1%, plasma cells 4%), sugar 83 mg% and chlorides 561 mg%. Blood test: l. 9000 S. 1%, e. 1%, p. 8%, p. 73%, lymph. 16%, mon. 2%; ROE 40 mm per hour. Repeated blood and fluid cultures are sterile. According to the ophthalmologist, neuroretinitis of the left eye. ENT organs are normal. Diagnosis: purulent meningitis.

Treatment was carried out with penicillin (endolumbar and intramuscular), sulfonamides, infusions of glucose and methenamine. The meningeal syndrome smoothed out by January 4, but pathological changes in the fluid persisted until November 20. The temperature has been normal since December 31st. Discharged on November 26.

Course of the disease usually acute, in some cases it is subacute, chronic, and sometimes remitting. Differential diagnosis of streptococcal and staphylococcal meningitis is carried out mainly on the basis of the following factors:

1. detection of the corresponding pathogen in the cerebrospinal fluid;
2. identification of a purulent focus in any organ.

Since cerebrospinal fluid is often sterile, you should more carefully look for primary lesions (purulent inflammation of the middle ear, boils, osteomyelitis, panaritium, etc.). It is necessary to conduct a detailed examination of the heart, lungs, kidneys and other organs. Usually the primary source of purulent meningitis can be found, but in some cases this is impossible. During an epidemic of meningococcal meningitis, the diagnosis is established without much difficulty; in sporadic cases of this disease, differential diagnosis is very difficult, since the symptoms of meningococcal meningitis and other purulent meningitis are similar, especially in the first days of the disease. The course of the disease and the therapeutic effect of the drugs used can also help in the differential diagnosis. It should be taken into account that for meningococcal meningitis, currently known treatment methods have a very beneficial effect on the course of the disease, while for purulent meningitis of other etiologies the therapeutic effect is relative. If with meningococcal meningitis abortive and mild forms of the course are often observed, then with staphylococcal and streptococcal meningitis this happens much less frequently. Finally, with meningococcal meningitis, in the vast majority of cases there is a favorable outcome (with the exception of young children), and with purulent meningitis of other etiologies, mortality is still significant.

Pathogenesis

Streptococcal and staphylococcal meningitis (meningitis streptococci et staphylococci) is usually a secondary purulent meningitis. Streptococcal meningitis is less common than pneumococcal meningitis. Streptococcal and staphylococcal meningitis can be a complication of purulent otitis, mastoiditis, inflammatory processes of the paranasal cavities and other purulent and septic processes. In otogenic meningitis, streptococcus is more common than other microorganisms. In purulent meningitis, which complicates furunculosis, the causative agent is usually Staphylococcus aureus.

Symptomatology

The clinical picture of streptococcal and staphylococcal meningitis is the same as with other purulent meningitis. An etiological diagnosis is possible only with bacteriological examination of the cerebrospinal fluid.

Treatment

The prognosis of streptococcal meningitis before the use of sulfonamides and antibiotics was unfavorable: mortality reached 97%. With the introduction of sulfonamide therapy, it decreased to 21%. Since the use of antibiotics, the prognosis has improved significantly.

Hemolytic streptococcus is sensitive to sulfonamides, and viridans - to penicillin. Asvold believes that for purulent meningitis caused by hemolytic streptococcus, treatment with large doses of penicillin (1,000,000 units after 2 hours) in combination with sulfonamides is very effective. Hoan and Herzon, citing 9 cases of recovery (out of 12), note that in connection with treatment with sulfonamides and penicillin, the prognosis of meningitis caused by viridans streptococcus has improved. While only 9 cases of recovery were published in the world literature before 1947, in subsequent years 34 out of 63 patients recovered.

As for purulent meningitis caused by Staphylococcus aureus, a good effect is observed when treated with penicillin. There are also indications of greater effectiveness of streptomycin. However, it should be taken into account that staphylococci relatively quickly acquire resistance to antibiotics.

Meningitis is a clinical syndrome that characterizes the development of inflammatory processes in the membranes of the brain or spinal cord. Classic symptoms of meningitis are fever, headache and neck stiffness. Other symptoms may include vomiting, photophobia, drowsiness, confusion, irritability, delirium, and coma. Patients with viral meningitis often exhibit preliminary symptoms (eg, muscle pain, fatigue, anorexia, etc.). Infants may experience bulging of the fontanel, causeless irritability, and hypotension.

Diagnosing meningitis can be difficult. A comprehensive blood test is required, as well as other diagnostic methods, which we will talk about later.

Inflammatory processes developing in the central nervous system can be divided into two forms: inflammatory processes in which the membranes of the brain are involved (meningitis) and inflammatory processes limited to the parenchyma (encephalitis).

Risk factors

Experts have identified factors that increase the risk of meningitis. We list the main risk factors:

Patient's age (under five years and over sixty years);

Splenectomy and sickle cell disease;

Thalassemia;

Drug use;

Bacterial endocarditis;

Posthemorrhagic hydrocephalus;

Listeriosis disease;

Traumatic brain injuries.

Forms of meningitis

There are three forms of meningitis:

Purulent meningitis (bacterial);

Granulomatous meningitis;

Aseptic meningitis.

The most common cause of inflammatory processes affecting the meninges are bacterial or viral infections. Microorganisms penetrate the meninges through the blood.

Bacterial (purulent) meningitis. Bacterial meningitis is an inflammation of the membranes of the brain that develops as a result of a bacterial infection. The bacterial form can be divided into the following types (depending on the causative agent of the disease):

Pneumococcal meningitis;

Haemophilus influenzae meningitis;

Staphylococcal meningitis;

Tuberculous meningitis;

Bacterial meningitis in pediatric patients.

Pachymeningitis. This is purulent meningitis resulting from a bacterial infection (usually staphylococcal or streptococcal). The bacteria most often spread to the meninges through sinus infection or osteomyelitis.

Haemophilus influenzae meningitis. The disease develops when polymorphic gram-negative coccobacteria get on the membranes of the brain. Haemophilus influenzae meningitis is often observed after influenza.

Pneumococcal meningitis. Pneumococcal meningitis is the most common form of bacterial meningitis. Its development is associated with focal infectious processes (for example: pneumonia, sinusitis, endocarditis). The risk of pneumococcal meningitis increases in people with alcoholism and chronic liver disease.

Streptococcal meningitis. Streptococcal meningitis develops when infected with streptococci. It is this form of meningitis that most often occurs in newborns.

Meningococcal meningitis. The cause of development is infection with gram-negative diplococci.

Listeria meningitis. Occurs in cases of listeriosis. The risk group for this disease includes pregnant women, infants and children under 5 years of age, elderly people (over 60 years of age), as well as people with chronic liver disease, kidney disease or diabetes.

Staphylococcal meningitis. This form of meningitis develops after neurosurgical operations and with traumatic brain injuries.

Symptoms of meningitis

The classic symptoms of meningitis (the so-called classic triad) are fever, headaches and neck stiffness. This symptom complex is observed in 44% of all patients with meningitis. Other symptoms may also occur:

Photophobia (so-called photophobia);

Drowsiness;

Confusion;

Increased irritability;

Meningitis can provoke the development of the following complications:

Septic shock;

Seizures (seizures occur in 40% of pediatric patients and 30% of adult patients);

Brain swelling;

Septic arthritis;

Exudative pericarditis;

Hearing loss (up to absolute deafness);

Hydrocephalus;

Ataxia;

Loss of vision (up to complete blindness).

Diagnostics

If the patient has the classic triad of symptoms, then most likely he has meningitis and the specialist only needs to carry out additional diagnostic procedures to make an accurate diagnosis. However, it must be remembered that the above symptom complex occurs only in 44% of all patients, so the diagnostician must pay attention to signs of irritation of the patient’s cerebral membranes (stiff neck muscles, Kernig’s sign, etc.).

To accurately detect meningitis, in addition to examining the patient and neurological examination, it is necessary to conduct a cerebrospinal puncture, computed tomography (CG) and electroencephalography.

Other diagnostic procedures are also carried out, depending on the cause of meningitis and the form of its course.

It is necessary to carry out differential diagnosis with the following diseases:

Brain abscess;

Delirium tremens;

Malignant neoplasms of the brain and spinal cord;

Febrile seizures;

Subarachnoid hemorrhage.

Treatment of meningitis

Treatment of meningitis requires an integrated approach and directly depends on the form of the disease and the severity of the patient’s condition. In the acute form of meningitis, after identifying the causative agent of the disease, a course of antibiotic therapy is carried out (the causative agent of the disease must be tested for drug resistance). It is very important to start treatment as early as possible so that the brain is not damaged and irreversible changes occur.

For chronic meningitis, treatment is also carried out; after identifying the pathogen, antibacterial therapy (antibiotic therapy) is carried out.

Special attention of physicians should be focused on the prevention and, if necessary, treatment of complications (we are talking primarily about hypotension or shock, hypoxia, hyponatremia, arrhythmia and ischemia). Intracranial pressure (ICP) and any manifestations of hydrocephalus should also be continuously monitored.

Newborns are treated with a course of ampicillin and gentamicin. Older children are prescribed cefotaxime and ceftriaxone.

Children over seven years of age and adult patients (up to 50 years of age) are prescribed cefotaxime, ceftriaxone and vancomycin.

For patients over 50 years of age, ceftriaxone and ampicillin are prescribed (if the patient's condition is severe, doxycycline is added).

In addition to antibiotic therapy, a course of steroid drugs (corticosteroids) may be prescribed.

When treating viral meningitis, maintenance therapy is mainly prescribed. A course of acyclovir may be prescribed, but there is no consensus on this matter (many experts are confident that viral meningitis does not require specific therapy).

Forecast

The development of various neurological complications, as well as death, is possible. Timely therapy increases the chances of a favorable prognosis.

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Clinical picture of encephalitis: fever, headache, dizziness, drowsiness, paralysis of the extraocular muscles, nystagmus, sometimes excessive salivation, greasiness of the face. Recently, the disease is more often abortive. Increased drowsiness or insomnia in combination with mild oculomotor disorders are observed, so patients can endure the disease on their legs. It is possible that it is not the entire oculomotor nerve that is involved in the process, but its branches that innervate individual muscles. The muscle that lifts the upper eyelid is especially often affected (ptosis develops) and the internal rectus muscle (convergence paresis is observed). The most characteristic symptoms of epidemic encephalitis are moderate fever, drowsiness and oculomotor disorders “Economeau's triad”. Depending on the severity and severity of the disease, the cerebrospinal fluid is either normal or has slight lymphocytic pleocytosis and hyperalbuminosis. For meningitis, the development of meningeal syndrome is typical against the background of fever and other general infectious symptoms. There may be prodromal phenomena - general malaise, runny nose, abdominal or ear pain, etc. Meningeal syndrome consists of general cerebral symptoms that reveal tonic tension in the muscles of the limbs and trunk. Vomiting occurs without preliminary nausea, suddenly after a change of position, without connection with food intake, during an intensification of the headache. Percussion of the skull is painful. Excruciating pain and skin hyperesthesia are typical. A constant and specific symptom of any meningitis is a change in the cerebrospinal fluid. The pressure is increased to 250–400 mm water. Art. Cell-protein dissociation syndrome is observed - an increase in the content of cellular elements (neutrophilic pleocytosis - in purulent meningitis, lymphocytic - in serous meningitis) with a normal (or relatively small) increase in protein content. Analysis of cerebrospinal fluid, along with serological and virological studies, is crucial in making a differential diagnosis and establishing the form of meningitis.

Streptococcal meningitis is a purulent meningitis that develops during the generalization of streptococcal infection or when pathogens from nearby organs (paranasal sinuses, middle ear) invade the meninges. It is characterized by a rapid onset with the formation of encephalic focal symptoms, edema-swelling of the brain, and damage to other organs and systems. Causative agents of meningitis- streptococci, which are spherical cells 0.5–2.0 microns in size, located in smears in pairs or short chains, under certain conditions can acquire a lanceolate or elongated shape. They are immobile, do not form capsules or spores, are anaerobes or facultative anaerobes, temperature optimum is 37 °C. Mostly entrance gate of infection There are damaged skin (burns, wounds, diaper rash, areas of maceration), mucous membranes of the upper respiratory tract and nasopharynx. But most often the source of the formation of purulent meningitis cannot be determined. The result of streptococcal infection of a newborn child is directly related to the state of its cellular and humoral defense factors and the magnitude of the infectious dose. Streptococcus causes not only catarrhal, but also purulent-necrotic inflammation at the site of penetration, from where it quickly spreads throughout the body hematogenously or lymphogenously. Streptococcus residing in the blood, its enzymes and toxins, cause activation and increase in the level of biologically active substances, disruption of hemostasis, metabolic processes with the formation of acidosis, increased permeability of vascular and cellular membranes, as well as the BBB. This promotes the introduction of streptococcus into the central nervous system, damaging the brain and meninges.

treatment

Treatment begins already at the prehospital stage with the use of penicillin. It is administered intramuscularly at 200,000 - 300,000 units/kg body weight per day. Semi-synthetic penicillins (oxacillin, ampicillin, methicillin) are also used at a dose of 200-300 mg/kg per day. Levomycetin sodium succinate and klaforan are also prescribed.

prevention

In the prevention of streptococcal meningitis, the popularization of information about the ways of spreading the infection is of primary importance, since the disease is mainly transmitted by airborne droplets. The patient and others must know that infection is possible during conversation, coughing, and sneezing. Living conditions and hygiene skills are important in the prevention of meningitis.

symptoms

Clinical symptoms of streptococcal meningitis do not have specific features that distinguish it from other secondary purulent meningitis. The disease develops acutely, with an increase in body temperature, chills, headache, anorexia, vomiting, sometimes repeated, and meningeal symptoms. The formation of encephalic manifestations in the form of a disorder of consciousness, tremor of the limbs, and clonic-tonic convulsions is likely. Signs of severe septicemia are characteristic of streptococcal meningitis:

• hemorrhagic rash,
• increase in heart size,
• high and significant body temperature,
• dullness of heart sounds.

As a rule, the functions of parenchymal organs are impaired, renal failure, hepatolienal syndrome appear, and damage to the adrenal glands occurs. In the acute course of the disease, symptoms of severe septicemia and encephalic signs may dominate over meningeal symptoms. With endocarditis, streptococcal meningitis is often accompanied by damage to the blood vessels of the brain, accompanied by hemorrhages in the subarachnoid area, and the early appearance of focal symptoms. The formation of edema-swelling of the brain is typical, but brain abscesses are rare.

Despite the widespread occurrence of streptococcal infection with extensive and varied pathology, purulent meningitis of streptococcal nature is rare. The causative agents are hemolytic and viridans streptococci (I. G. Vainshtein, N. I. Grashchenkov, 1962). Emphasizing the rarity of the disease, Knope and Herzen (1950) indicate that in the world literature before 1948 they found only 63 cases of streptococcal meningitis. According to statistical data, streptococcal meningitis is observed mainly in infants and small children, more often occurring during the period of streptococcal septicemia with purulent otitis, erysipelas, 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, reports have appeared from a number of authors (Gerlini, Natoli, 1960), which note a noticeable increase in the proportion of streptococcal meningitis among other forms. Schneeweiss, Blaurock, Jungfer (1963) write about this, who from 1956 to 1961 counted 2372 reports in the literature of purulent meningitis caused by streptococcus. 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 levels, repeated vomiting, lethargy or restlessness of the child.
However, as with staphylococcal meningitis, the disease picture is often dominated by features of meningoencephalitis - depression of consciousness, frequent clonic-tonic convulsions, early focal symptoms along with signs of severe septicemia (high temperature with wide fluctuations, subcutaneous hemorrhages, dullness of heart sounds, 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 liquorological changes, severe forms with prolonged toxicosis, persistent fever and prolonged anorexia, persistent changes in the composition of the cerebrospinal fluid are more common. A similar example of flow would be the following observation.
Oleg M., 1 month 10 days, was admitted to the clinic on the 2nd day of illness. The disease progressed acutely, the temperature rose to 39.2°, lethargy was replaced by periods of severe anxiety and repeated vomiting. The next day, the mother noticed a lack of movement in the child's left arm and leg, and repeated convulsions in the left half of the body.
Upon admission, the 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 a cyanotic coloration. No pathological changes were detected in the lungs. Heart sounds are sharply muffled, the pulse is weak. There are no meningeal symptoms. General muscle hypotonia was noted. Lumbar puncture yielded slightly cloudy fluid, 2100 cells per 1 mm3 (mainly neutrophils), 6.34% protein. Streptococcus was bacterioscopically isolated.
Treatment was carried out with penicillin in massive doses, to which streptomycin was added on the 6th day of therapy. The further course of the disease was characterized by prolonged, irregular type of fever, periodic convulsions (until the 9th day of treatment), while general 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 hospital stay. At the time of discharge, no complications were noted.
The few reports describing the clinical picture of streptococcal meningitis emphasize the severity of this form of meningitis and the frequent complications (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 with this disease. According to Appelbaum (1961), the mortality rate for 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 normal microbial landscape. The practical importance of gram-negative bacilli (Pseudomonas aeruginosa, Proteus vulgaris, Friedlander's bacillus) has increased, which, along with Escherichia 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 infectious pathology in early childhood.

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