WHAT ARE CENTRAL NERVOUS SYSTEM INFECTIONS?

WHAT ARE CENTRAL NERVOUS SYSTEM INFECTIONS?

  1. 1
    WHAT IS THE MEANING OF CENTRAL NERVOUS SYSTEM INFECTIONS?
    • Central Nervous System (CNS) infections include a wide variety of clinical conditions and etiologies: meningitis, meningoencephalitis, encephalitis, brain and meningeal abscesses, and shunt infections. The focus of this chapter is meningitis.
  2. 2
    WHAT ARE THE CAUSES OF CENTRAL NERVOUS SYSTEM INFECTIONS?
    • Central nervous system infections are the result of hematogenous spread from a primary infection site, seeding from a parameningeal focus, reactivation from a latent site, trauma, or congenital disabilities in the CNS. Passive and active exposure to cigarette smoke and the presence of a cochlear implant that includes a positioner, both increase the risk of bacterial meningitis.
    • CNS infections may be caused by a variety of bacteria, fungi, viruses, and parasites. The most common causes of bacterial meningitis are Streptococcus pneumoniae, group B Streptococcus, Neisseria meningitides, Haemophilus influenza, and Listeria monocytogenes.
    • The critical first step in the acquisition of acute bacterial meningitis is nasopharyngeal colonisation of the host by the bacterial pathogen. The bacteria first attach themselves to nasopharyngeal epithelial cells and are then phagocytised into the host’s bloodstream.
    • A common characteristic of most CNS bacterial pathogens (e.g., H. influenza, Escherichia coli, and N. meningitidis) is the presence of an extensive polysaccharide capsule that is resistant to neutrophil phagocytosis and complement opsonisation.
    • The neurologic sequelae of meningitis occur due to the activation of host inflammatory pathways. Bacterial cell death causes the release of cell wall components such as lipopolysaccharide, lipid A (endotoxin), lipoteichoic acid, teichoic acid, and peptidoglycan, depending on whether the pathogen is gram-positive or gram-negative. These cell wall components cause capillary endothelial cells and CNS macrophages to release cytokines (interleukin-1, tumour necrosis factor, and other inflammatory mediators).
    • Proteolytic products and toxic oxygen radicals cause an alteration of the blood-brain barrier, whereas platelet-activating factor activates coagulation, and arachidonic acid metabolites stimulate vasodilation. These events lead to cerebral oedema, elevated intracranial pressure, cerebrospinal fluid (CSF) pleocytosis, decreased cerebral blood flow, cerebral ischemia, and death.
  3. 3
    WHAT ARE THE SIGNS AND SYMPTOMS OF CENTRAL NERVOUS SYSTEM INFECTIONS?
    • Meningitis causes CSF fluid changes, and these changes can be used as diagnostic markers of infection (Table 1–1).

    aInitial cerebrospinal fluid (CSF), while blood cell (WBC) count may reveal a predominance of polymorphonuclear neutrophils (PMNs).

    • Clinical presentation varies with age; generally, the younger the patient, the more atypical and the less pronounced is the clinical picture.
    • Patients may receive antibiotics before a diagnosis of meningitis is made, delaying presentation to the hospital. Prior antibiotic therapy may cause the Gram stain and CSF culture to be negative, but antibiotic therapy rarely affects CSF protein or glucose.
    • Classic signs and symptoms include fever, nuchal rigidity, altered mental status, chills, vomiting, photophobia, and severe headache. Kernig and Brudzinski signs may be present but are poorly sensitive and frequently absent in children.
    • Clinical signs and symptoms in young children may include bulging fontanelle, apneas, purpuric rash, and convulsions, in addition to those just mentioned.
    • Purpuric and petechial skin lesions typically indicate meningococcal involvement, although the lesions may be present with H. influenzae meningitis. Rashes rarely occur with pneumococcal meningitis.
    • Bacterial Meningitis Score is a validated clinical decision tool aimed to identify children older than 2 months with CSF pleocytosis who are at low risk of acute bacterial meningitis. This tool incorporates clinical features such as positive CSF Gram stain, presence of seizure, serum absolute neutrophil count of 10,000 cells/mm3 or more (≥10 × 109/L), CSF protein ≥80 mg/dL (≥800 mg/L), and CSF neutrophil count ≥1000 cells/mm3 (≥1 × 109/L). Treatment is recommended when one or more criteria are present. An elevated CSF protein of 50 mg/dL or more and a CSF glucose concentration less than 50% of the simultaneously obtained peripheral value suggest bacterial meningitis (see Table 1–1).
    • Gram stain and culture of the CSF are the most important laboratory tests performed for bacterial meningitis. When performed before antibiotic therapy is initiated, Gram stain is both rapid and sensitive and can confirm the diagnosis of bacterial meningitis in 75% to 90% of cases.
    • Polymerase chain reaction (PCR) techniques can be used to diagnose meningitis caused by N. meningitidis, S. pneumoniae, and H. influenza type b (Hib). Latex fixation, latex agglutination, and enzyme immunoassay tests provide for the rapid identification of several bacterial causes of meningitis, including S. pneumoniae, N. meningitides, and Hib. The rapid antigen tests should be used in situations in which the Gram stain is negative.
    • Diagnosis of tuberculosis meningitis employs acid-fast staining, culture, and PCR of the CSF.
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