Meningitis in Children - I.V. Bohadelnykov 2005

Secondary purulent meningitis in children. General data
Streptococcal meningitis

Streptococcal meningitis is a Purulent meningitis that develops against the Background of streptococcal Sepsis or other streptococcal infections. It is characterized by an acute onset with The Development of cerebral edema and Swelling, focal encephalitic symptoms, and involvement of other Organs and systems.

Etiology. The CAUSATIVE AGENT OF the disease is streptococci, which are spherical or ovoid Cells ranging in size from 0,5-2,0 µm, appearing in smears in pairs or short chains. Under adverse conditions, they can acquire an elongated or lanceolate shape resembling coccobacilli. They are non-motile, do not form spores or capsules, and are anaerobic or facultative anaerobic Bacteria with an optimum Temperature of 37° C. Based on specific CARBOHYDRATES in The Cell wall, 17 serogroups are distinguished, designated by capital letters of the Latin alphabet.

Group A hemolytic streptococci are the primary human pathogens. They are responsible for pharyngitis, scarlet fever, cellulitis, erysipelas, impetigo, streptococcal toxic Shock syndrome, infective endocarditis, acute Glomerulonephritis, and other diseases.

Group B streptococci colonize 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 frequently cause meningitis and Pneumonia in newborns, as well as Skin and soft tissue infections, pneumonia, endocarditis, meningitis, endometritis, Urinary Tract infections, and surgical wound complications following Cesarean Section.

The causative agent of meningitis is hemolytic or viridans group streptococcus, which possesses pronounced toxic properties that determine the microbe's virulence and aggressiveness. The main factors include fimbrial protein, capsule, and C5a peptidase. Fimbrial protein is the primary virulence factor and a type-specific antigen; it inhibits phagocytosis, binds fibrinogen, fibrin, and their degradation products, adsorbs them onto its surface (masking receptors for Complement components and opsonins), and induces lymphocyte activation and The production of low-affinity Antibodies. The capsule is the second most important virulence factor. It protects streptococci from the antimicrobial potential of phagocytes and promotes their adhesion to the epithelium. The third virulence factor is C5a peptidase, which suppresses phagocyte activity. Streptokinase, hyaluronidase, erythrogenic (pyrogenic) toxins, cardiohepatic toxin, and streptolysins O and S also play an important role in Pathogenesis.

Epidemiology. The reservoir of infection is an infected person or a bacterial carrier. The main transmission routes are contact, airborne droplet, and alimentary (via contaminated food products, such as milk). Children of any age can be affected, but infants are most commonly afflicted, in whom meningitis develops as a manifestation of sepsis. In 50% of infants, infection most frequently occurs vertically—during the passage of the fetus through birth channels infected with streptococci. Significant colonization of the mother's birth canal with streptococci leads to the Early Development of meningitis (within the first 5 days), whereas in infants infected with a smaller dose, meningitis develops much later (from 6 days to 3 months). In 50% of affected infants without a specific focus of infection, meningitis develops within 24 hours, with a mortality rate reaching 37%. Among children with late-onset manifestations of infection, complicated by meningitis and bacteremia, 10–20% die, and 50% of the survivors exhibit severe residual effects. In patients with infective endocarditis, meningitis may arise As a result of embolism of the meningeal vessels.

Pathogenesis. Most frequently, the entry portals of infection are damaged skin (diaper rash, maceration areas, Burns, wounds), as well as the mucous membranes of the nasopharynx and Upper Respiratory Tract (streptoderma, Phlegmon, abscess, purulent-necrotic rhinitis, nasopharyngitis, otitis, tracheobronchitis, etc.). However, in a significant percentage of cases, the source of purulent meningitis cannot be identified. The outcome of streptococcal infection in a newborn directly depends on the state of their cellular and humoral defense factors and the size of the infecting dose.

At the site of penetration, streptococcus causes not only catarrhal but also purulent-necrotic inflammation, from which it rapidly spreads throughout the body via lymphogenic or hematogenous pathways. Streptococcus present in the Blood, along with its toxins and Enzymes, leads to the activation and increased levels of BIOLOGICALLY ACTIVE SUBSTANCES, disruption of hemostasis, Metabolic Disorders accompanied by acidosis, and increased permeability of cellular and vascular membranes, as well as the blood-Brain barrier. This facilitates the penetration of streptococcus into the central nervous system, leading to damage to the Meninges and brain parenchyma.

Clinical manifestations. The Clinical Features of streptococcal meningitis do not possess specific characteristics that distinguish it from other secondary purulent meninges.

The disease begins acutely with elevated body temperature, anorexia, fever, headache, vomiting (sometimes recurrent), and pronounced meningeal signs. Encephalitic manifestations may develop in the form of impaired consciousness, clonic-tonic seizures, and limb tremor. Characteristic of streptococcal meningitis are signs of severe septicemia: high fever with wide fluctuations, hemorrhagic rash, cardiac enlargement, and muffled Heart sounds. Parenchymal organ Functions are consistently affected, resulting in hepatosplenomegaly, renal failure, and adrenal involvement. In the acute course of the disease, signs of severe septicemia and encephalitic manifestations may predominate over meningeal symptoms. Streptococcal meningitis in endocarditis is often accompanied by cerebrovascular involvement with hemorrhages into the subarachnoid space and the early onset of focal symptoms. Cerebral edema and swelling characteristically develop, whereas brain abscesses are rare.

Main diagnostic criteria for streptococcal meningitis:

1. Epidemiological history: the disease develops against the background of streptococcal sepsis or, less commonly, another streptococcal infection; the pathogen spreads hematogenously or lymphogenously; children of any age fall ill, but infants are most frequently affected.

2. The onset of meningitis is acute, accompanied by manifestations of severe septicemia: significant fluctuations in temperature response, the presence of a hemorrhagic rash, hepatosplenomegaly, and pronounced meningeal signs.

3. Cerebral edema and swelling, as well as focal encephalitic symptoms, frequently develop rapidly.

4. It often proceeds with the involvement of other vital organs and systems (Liver, heart, Lungs, adrenals) in the infectious process.

5. Isolation of hemolytic streptococcus from CEREBROSPINAL FLUID and blood confirms the etiological Diagnosis.

Laboratory Diagnostics. Complete blood count. Peripheral blood reveals leukocytosis, neutrophilia, a left shift in the leukocyte formula, and an elevated ESR.

Cerebrospinal fluid analysis. CSF examination reveals high neutrophilic pleocytosis (thousands of cells per 1 µm), elevated protein levels (1–10 g/L), and decreased glucose levels. Bacterioscopy reveals Gram-negative cocci.

Bacteriological examination. Isolation of the pathogen is the most reliable method. It is performed by culturing blood, nasal and pharyngeal mucus, sputum, and cerebrospinal fluid on blood Agar. In liquid media, streptococci produce sediment growth that extends upward. To differentiate the identified microorganisms, they are inoculated into thioglycollate medium or semisolid agar.

Bacterioscopic examination. Bacterioscopy of smears reveals typical Gram-positive cocci forming short chains, although polymorphic forms may also be detected.

Serological examination. Serotyping is performed using the latex agglutination or coagglutination test with fluorochrome-labeled Monoclonal Antibodies.