Meningitis in Children - I.V. Bohadelnikov 2005

Secondary purulent meningitis in children. General data
Staphylococcal meningitis

Staphylococcal meningitis is a Purulent meningitis caused predominantly by Staphylococcus aureus (S. aureus). It typically develops against the Background of a localized or generalized staphylococcal infection and is characterized by a severe clinical course, a high tendency toward cerebral abscess formation, and unfavorable outcomes.

Etiology. The causative agents are ubiquitous microorganisms. Staphylococci are non-motile cocci measuring 0.5–1.5 µm in diameter, appearing in smears singly, in pairs, or in clusters. The optimal Temperature for their GROWTH AND REPRODUCTION is 30°C–37°C, with a slightly alkaline medium reaction. These microbes thrive on media containing Blood, CARBOHYDRATES, or milk. They are resistant to drying and heat while retaining their virulence, yet sensitive to sunlight (dying within 10–12 hours) and common disinfectants. Most staphylococci are aerobes. Infections, including meningitis, are most frequently caused by S. aureus, and less commonly by S. epidermidis or S. saprophyticus, particularly in immunocompromised infants.

Pathogenic factors of staphylococci include a microcapsule that protects the Bacteria from Complement-mediated phagocytosis by polymorphonuclear leukocytes, promotes microbial adhesion, and facilitates tissue dissemination; Cell wall components that stimulate inflammatory responses by activating macrophages and The Complement System; Enzymes such as catalase and coagulase; and toxic substances, including hemolysins (4 antigenic types), exfoliative toxins A and B, toxic Shock syndrome toxin, and enterotoxins A–F.

Epidemiology. Staphylococcus aureus is a normal component of the human microflora. The source of infection includes patients and staphylococcal carriers, with "healthy carriers" accounting for up to 30% of the healthy population worldwide. Transmission occurs via airborne droplets, direct contact, and the alimentary route.

Carriers among medical personnel and individuals suffering from various staphylococcal lesions of the Skin and Upper Respiratory Tract pose the highest risk of transmission. Currently, a significant proportion of Staphylococcal infections are endogenous, where the infectious mechanism involves the translocation of the pathogen from colonization sites to other body areas.

Staphylococcal meningitis most frequently affects infants and children in their first three months of life with underlying perinatal pathology. This vulnerability is due to immature specific and non-specific Immunity, while Hypoxia and birth trauma significantly increase blood-Brain barrier (BBB) permeability.

Pathogenesis. Depending on the route of pathogen entry into the brain, staphylococcal meningitis is classified into contact, hematogenous, and post-traumatic forms. Contact forms arise from the direct extension of an inflammatory process to the Meninges. This occurs when the primary focus of infection is situated in close proximity to the Central Nervous system, such as in ethmoiditis, HEAD or facial Phlegmon, cranial or spinal Osteomyelitis, purulent otitis media, brain abscesses, infected epidural cysts and subdural hematomas, and occasionally following surgical interventions.

Post-traumatic meningitis develops following cranial and facial bone injuries, which not only compromise the integrity of the Skull but also increase BBB permeability, thereby creating favorable conditions for staphylococci to invade the central nervous system.

Hematogenous forms of meningitis, which occur in children with purulent Conjunctivitis, staphylodermatitis, Omphalitis, Pneumonia, or enterocolitis, follow the most severe clinical course. The Development of hematogenous staphylococcal meningitis requires at least one primary focus of infection combined with depressed cellular and humoral immunity and increased BBB permeability. The systemic Circulation of the pathogen leads to damage across various Organs and systems, including the central nervous system. This damage occurs both directly—via the action of cell wall components, bacterial Proteolytic Enzymes, and toxins—and indirectly through the activation and elevation of BIOLOGICALLY ACTIVE SUBSTANCES in the blood, such as histamine, kallikrein, bradykinin, and proteases. High levels of these mediators induce hemodynamic and microcirculatory disturbances as well as Metabolic Disorders, which in turn increase the permeability of cellular and vascular membranes and the BBB, facilitating The entry of staphylococci into the central nervous system.

Clinical Manifestations. The clinical course of staphylococcal meningitis is characterized by an acute onset, rapid development of meningeal syndrome, seizures, and focal neurological deficits.

The disease begins acutely and abruptly, with body temperatures rising to 39°C–40°C, fever, severe headache, and vomiting. The patient's condition is critical: periods of general restlessness alternate with lethargy, accompanied by limb tremors and cutaneous hyperesthesia. Altered states of consciousness, ranging up to coma, are common, alongside pronounced meningeal signs and rapidly progressive focal neurological deficits such as paresis and paralysis. In infants, the anterior fontanelle becomes tense and bulging, accompanied by hyperesthesia, hand tremors, and seizures. In severe cases, encephalitic symptoms may appear as focal neurological deficits resulting from the involvement of cranial nerve nuclei (III, V, VII, and IX Cranial Nerves) or their respective roots. Frequently, the typical clinical picture of staphylococcal meningitis is masked by a severe septic state, during which meningeal signs in infants may be absent or incomplete. In such cases, clinicians must pay close attention to a progressively deteriorating condition, generalized hyperesthesia, tremors of the chin and hands, frequent regurgitation, refusal to nurse, and unresponsiveness to ongoing therapy.

The disease follows a prolonged, sluggish course, frequently leaving persistent neurological sequelae. Distinctive features of staphylococcal meningitis include: a) a strong tendency to form brain abscesses and obstruction of the CEREBROSPINAL FLUID pathways, whereby well-demarcated, often multiple and communicating purulent cavities can be detected in the meninges and brain parenchyma as early as 7–10 days after onset; b) the presence of numerous antibiotic-resistant staphylococcal strains or their high capacity to rapidly develop resistance during Treatment; and c) difficulties in eradicating the primary focus of infection. Accounting for these features is a mandatory prerequisite for successful treatment. In clinical practice, however, prominent central nervous system symptoms often overshadow the primary focus, the local clinical manifestations of which typically subside under METABOLISM/18.html">The Influence of massive therapy. Nevertheless, an undertreated and unsanitized primary focus remains the primary driver behind a protracted clinical course, disease relapses, and purulent meningitis.

Prognostically, staphylococcal meningitis is among the most unfavorable forms, associated with high mortality rates reaching 20%–60%.

Recovery following staphylococcal meningitis is frequently incomplete, with a significant proportion of children exhibiting residual deficits in the form of organic central nervous system damage.

Main Diagnostic Criteria for Staphylococcal Meningitis:

1. Epidemiological history: the disease develops against the background of localized or generalized staphylococcal infection spreading via contact or hematogenous routes; it predominantly affects infants and children in their first 3 months of life.

2. Acute onset characterized by high fever, along with systemic infectious and general cerebral symptoms.

3. Rapid development of meningeal syndrome, impaired consciousness ranging up to coma, and The Emergence of pronounced focal neurological signs including paresis and paralysis.

4. A distinct clinical propensity for multiple cerebral abscesses and the obstruction of cerebrospinal fluid pathways.

5. A protracted, sluggish clinical course marked by high mortality and frequent residual effects manifested as persistent neurological disorders.

Laboratory Diagnostics. Complete blood count: peripheral blood reveals marked leukocytosis, neutrophilia, a left shift in the leukocyte formula toward immature forms (band neutrophils and myelocytes), and a significantly elevated ERYTHROCYTE SEDIMENTATION RATE (ESR).

Cerebrospinal Fluid (CSF) Analysis: The CSF appears turbid and grayish, often with a yellowish or greenish tint. It is characterized by a high protein content (3–9 g/L) with moderate pleocytosis (1,200–1,500 Cells per µL), predominantly neutrophilic, alongside a depressed glucose level.

Bacteriological examination: Pathogen isolation is performed using blood, pus, sputum, pharyngeal and nasal mucus, CSF, and stool samples. Culturing is routinely carried out on yolk-salt Agar, milk-yolk-salt agar, and blood agar following standard microbiological protocols.

Bacterioscopic Examination: Following isolation, the pathogen is identified via Gram staining (staphylococci are Gram-positive microbes), the coagulase test (detecting the clotting factor characteristic of staphylococci), The ability to ferment mannitol, the synthesis of thermostable DNase, and latex agglutination or sensitized sheep erythrocyte agglutination assays. Further identification is achieved using specific Bacteriophages.

Serological Testing: Antibodies against teichoic acid (a species-specific antigen) are detected using the double agar gel diffusion method. Staphylococcal enterotoxin is identified via gel diffusion precipitation, passive hemagglutination inhibition, and fluorescent antibody assays.