Meningitis in Children - I.V. Bohadelnykov 2005

Primary purulent meningitis in children. General data
Pneumococcal meningitis

Pneumococcal meningitis is an acute neuroinfection caused by Streptococcus pneumoniae, characterized by an acute onset, prominent general infectious and meningeal syndromes, frequent involvement of the Brain parenchyma, and high mortality rates.

Etiology. The CAUSATIVE AGENT OF meningitis is Streptococcus pneumoniae (pneumococcus), which is serologically heterogeneous and includes 84 serotypes. The bacterium was first isolated by Pasteur in 1881. It is a non-motile, non-spore-forming, and non-encapsulated microorganism (though encapsulated in clinical samples), functioning as an aerobe or facultative anaerobe. It appears as oval or lancet-shaped cocci with a diameter of approximately 1 µm. In smears from clinical material, they typically occur in pairs surrounded by a thick capsule. The bacterium grows well on media supplemented with Blood or serum, or 0.1% glucose solution, at a Temperature of 37°C.

Epidemiology. Pneumococcus is one of the primary pathogens responsible for bacterial infections globally. Infants, young children, and the elderly are the most susceptible. The source of infection includes patients and carriers (ranging from 25 to 50% of preschool children and 20 to 25% of adults). The primary transmission route is airborne droplets, although contact transmission is also possible. A sharp increase in incidence occurs during the cold season. An important factor contributing to The Development of the infection is a decrease in the body's resistance resulting from previous illnesses, surgeries, or hypothermia. Pneumococcal meningitis typically presents as

a sporadic disease, though epidemic outbreaks may also occur. Notably, pneumococcal meningitis often develops against the Background of viral respiratory infections, which increase the susceptibility of the Meninges to bacterial invasion within just a few hours of the initial viral injury. The source of infection can be either sick individuals or healthy carriers of the bacterium. The disease frequently develops secondary to acute or chronic Upper Respiratory Tract infections, as well as following traumatic brain injury.

Pathogenesis. The nasopharyngeal mucosa serves as the primary entry gate for pneumococcus. Due to the presence of pathogenicity factors, an inflammatory process develops at the site of entry. The primary virulence factor is the capsule, which protects the bacterium from the microbicidal action of phagocytes and opsonins. Substance C, represented by a Choline-containing teichoic acid in The Cell wall that interacts specifically with C-reactive protein, also plays a crucial role. This process is accompanied by the activation of The Complement System, excessive release of acute-phase inflammatory mediators, and stimulation of neutrophil leukocytes. All of these factors create favorable conditions for The formation of a primary inflammatory focus, leading to Pneumonia, otitis media, sinusitis, and other complications. From this primary focus, the pathogen spreads hematogenously throughout the body, causing endocarditis, Arthritis, and inflammation of the meninges resulting in Purulent meningitis, along with damage to other Organs and systems. Hematogenous dissemination of the pathogen is largely driven by a deficiency in specific Antibodies, as well as C1q and C4 complement components, which reflect an overall reduction in bactericidal activity.

Clinical Manifestations. Pneumococcal meningitis is one of the most severe forms of Purulent meningitis in children, ranking second in frequency only to Meningococcal meningitis. It predominantly affects children aged 1 to 5 years, and less commonly infants (6–12 months of age).

In the majority of primary infection cases, pneumococcal meningitis begins acutely, with body temperature rising to 39–40^oC, fever, and a rapid escalation of intoxication symptoms. Pronounced generalized hyperesthesia and meningeal signs are present. An early and frequent manifestation of pneumococcal meningitis is Central Nervous system (CNS) involvement, which presents as clonic seizures, cranial nerve palsies, mono- and hemiparesis, and varying degrees of altered consciousness. In infants under one year of age, hypertensive syndrome develops early and is often pronounced, manifesting as bulging and pulsating of the fontanelle, Separation of the cranial sutures, and enlargement of the HEAD. The Skin is pale or cyanotic, tachypnea is prominent, and hemodynamic disorders or hepatosplenomegaly may be observed. A specific feature of pneumococcal meningitis is its progression from the very first days of the illness as meningoencephalitis. Focal symptoms indicating the involvement of the brain parenchyma—such as limb paralysis or paresis, ataxia, and various hyperkinesias—appear early (on days 1–2 of the illness). Among the Cranial Nerves, the III, VI, VII, VIII, IX, and X pairs are most frequently affected. In A number of cases, the disease proceeds with the Clinical symptoms of ependymitis. Cerebral edema and Swelling develop more frequently in pneumococcal meningitis than in Other types of purulent meningitis and can be the cause of death within the first 3 days of illness. Occasionally, brain swelling and edema may develop at a later stage. In fulminant forms, particularly characteristic of young children, the meningeal syndrome may not have time to fully develop.

Pneumococcal meningitis developing against the background of a pre-existing primary inflammatory focus (suppurative otitis media, mastoiditis, sinusitis, pneumonia) has a subacute, pauci-symptomatic onset, yet it is characterized by a particularly severe clinical course and a higher mortality rate compared to primary pneumococcal meningitis. In septic presentations, a hemorrhagic skin rash may appear, resembling meningococcal rash in its nature and localization. However, early in the disease, the rash may be roseolopapular, transforming into hemorrhagic in subsequent days. Unlike the rash of meningococcal disease, the rash in pneumococcal meningitis is more persistent and resolves much more slowly. Unfavorable outcomes in such cases are typically attributed to delayed Diagnosis and late initiation of etiotropic Treatment. This explains the characteristic frequency of relapses in pneumococcal meningitis, as well as the fact that 22–24% of surviving children suffer from long-term neurological sequelae, including profound Hearing loss, blindness, amnesia, paralysis, and other manifestations of CNS damage.

The prognosis and outcomes of pneumococcal meningitis largely depend on timely diagnosis and the prompt initiation of appropriate therapy. Failure to meet these criteria leads to a protracted clinical course that frequently ends in fatality. Three main categories of fatal outcomes are distinguished (M.B. Titov, B.D. Lutsyk, 1990). The primary cause of death is meningoencephalitis with prominent signs of cerebral edema and swelling. The second cause is acute cardiopulmonary failure developing secondary to CNS involvement. The third cause is a septic process complicated by thrombohemorrhagic syndrome against the background of CNS damage.

Main diagnostic criteria for pneumococcal meningitis:

1. Epidemiological history: history of contact with a patient or a pneumococcal carrier, airborne or contact transmission routes, and high incidence among infants and young children.

2. Onset of meningitis following a primary pneumococcal infection such as pneumonia, otitis media, or sinusitis.

3. Acute and sudden onset of meningitis, accompanied by a rapidly progressive and pronounced general toxic syndrome, manifested by high fever with chills, bursting headaches, recurrent vomiting, and severe generalized hyperesthesia.

4. A fully developed meningeal syndrome encompassing the entire symptom complex, frequently complicated by cerebral edema and swelling.

5. Frequent involvement of the brain parenchyma in the pathological process, leading to meningoencephalitis.

6. A rapid increase in the severity of CNS involvement, characterized by impaired consciousness, generalized seizures, and cranial nerve palsies.

7. High severity of the disease, often following a protracted and relapsing course that may result in death.

8. Pronounced inflammatory Changes in the blood and CEREBROSPINAL FLUID (CSF), with bacteriological isolation of pneumococcus from blood or CSF confirming the etiological diagnosis.

Laboratory Diagnostics. Complete Blood Count. Peripheral blood typically shows leukocytosis with a marked left shift toward immature forms (band neutrophils and myelocytes), aneoosinophilia, and a significantly elevated ESR of up to 30–60 mm/h. In some cases, leukopenia is observed, which serves as an unfavorable prognostic sign.

CSF Analysis. The cerebrospinal fluid is turbid, frequently with a greenish tint, viscous, and characterized by marked neutrophilic pleocytosis (500–1500 Cells per 1 µL), a significant increase in protein levels (1–10 g/L), and decreased glucose content.

Bacteriological examination. Diagnostic specimens for identifying the pathogen include sputum, blood, pus, and CSF, which are inoculated onto blood or serum Agar.

Bacterioscopic Examination. The pneumococcal etiology of the disease is indicated by the presence of neutrophils and Gram-positive lancet-shaped diplococci (at least 10 per visual field) in smears of clinical specimens. Microscopic examination of the CSF reveals pneumococci as extracellular and intracellular Gram-positive lancet-shaped diplococci.

To differentiate pneumococcus from other streptococci, the following tests are used:

a) optochin test (inhibits the growth of streptococci);

b) deoxycholate test (the ability of pneumococcus to ferment inulin and its susceptibility to Bile distinguishes it from viridans streptococci);

c) the pathogen isolated from CSF must be serotyped using commercial Reagents for latex agglutination or co-agglutination assays, which detect capsular Antigens.

d) biological assay: intraperitoneal inoculation of white mice with the patient's specimen, followed by bacteriological and serological examination of the peritoneal exudate.