Purulent Meningitis in Children Jiang Li Department of Neurology Children's Hospital Chongqing University of Medical Sciences
Purulent Meningitis in Children Jiang Li Department of Neurology Children’s Hospital Chongqing University of Medical Sciences
Purulent Meningitis Acute infection of central nervous system(CNS) 90% of cases occur in the age of 1mo-5yr The inflammation of meninges caused by various bacteria. Common features in clinical practices include: fever, increased intracranial pressure, meningeal irritation One of the most potentially serious infections, associated with high mortality(about 10%)and morbidity
Acute infection of central nervous system(CNS). 90% of cases occur in the age of 1mo-5yr. The inflammation of meninges caused by various bacteria.Common features in clinical practices include: fever, increased intracranial pressure, meningeal irritation. One of the most potentially serious infections, associated with high mortality (about 10%) and morbidity. Purulent Meningitis
1. Etiology 1.1 Pathogens: Main pathogens: Neissria meningitidis, streptoccus pneumoniae, Haemophilus influenzae. (2/3 of purulent meningitis are caused by these pathogens) Pathogens in special populations(neonate <3mo infants, malnutrition, immunodeficiency) gramnegative enteric bacilli, group B streptococci, staphlococcus aureus
1.Etiology 1.1 Pathogens: Main pathogens: Neissria meningitidis, streptoccus pneumoniae, Haemophilus influenzae. (2/3 of purulent meningitis are caused by these pathogens) Pathogens in special populations (neonate & <3mo infants , malnutrition, immunodeficiency): gramnegative enteric bacilli, group B streptococci, staphlococcus aureus
1.2 Major risk factors for meningitis Immature immunologic function and attenuated immunologic response to pathogens Low level of immunoglobulin defects of complement and properdin system Immature or impaired blood-brain-barrier(BBB) Immature BBB function maturation at about 1yr Impaired BBB: Congenial or acquired defects across mucocutaneous barrier
1.2 Major risk factors for meningitis Immature immunologic function and attenuated immunologic response to pathogens • Low level of immunoglobulin, defects of complement and properdin system Immature or impaired blood-brain-barrier (BBB) • Immature BBB function: maturation at about 1yr • Impaired BBB: Congenial or acquired defects across mucocutaneous barrier
1.3 Access of bacteria invasion Typical access---hematogenous dissemination o Bacteria colonizing the mucous membranes of the nasopharynx→> invasion into local tissue→ bacteremia -> hematogenous seeding to the subarachnoid space Mode of transmission: Person to person contact through respiratory tract secretions or droplets
1.3 Access of bacteria invasion Typical access---hematogenous dissemination • Bacteria colonizing the mucous membranes of the nasopharynx →invasion into local tissue → bacteremia → hematogenous seeding to the subarachnoid space • Mode of transmission: Person to person contact through respiratory tract secretions or droplets
Access of bacteria invasion o Bacteria spread to the meninges directly through anatomic defects in the skull or head trauma Invasion from parameningeal organs such as paranasal sinuses or middle ear
Bacteria spread to the meninges directly: through anatomic defects in the skull or head trauma Invasion from parameningeal organs: such as paranasal sinuses or middle ear Access of bacteria invasion
2. Pathology o Structure of meninges Cranial bone venous sinus Extradural Arachnoid villus Dura mater Subdural space Arachnoid mater Subarachnoid Cerebral space blood vessel Subpial space Pla mater Brain Perivascular space Fig. 1. The meninges
2. Pathology Structure of meninges
Pathology o Characterized by leptomeningeal and perivascular infiltration with polymorphonuclear leukocytes and an inflammatory exudate Exudate which may be distributed from convexity of brain to basal region of cranium Exudate is more thickness due to streptococcus pneumoniae than other pathogens
Characterized by leptomeningeal and perivascular infiltration with polymorphonuclear leukocytes and an inflammatory exudate. Exudate which may be distributed from convexity of brain to basal region of cranium. Exudate is more thickness due to streptococcus pneumoniae than other pathogens. Pathology
3. Clinical manifestations The younger the child is, the higher incidence of meningitis will be. 12-2/3 of cases occur less than lyr of age ◆ Mode of presentation Acute or fulminant onset: symptoms and signs of sepsis; meningitis evolve rapidly over a few hours and death within 24 hours, usually infected with Neissria meningitides (N. meningitides)
3. Clinical manifestations The younger the child is, the higher incidence of meningitis will be. ½-2/3 of cases occur less than 1yr of age. Mode of presentation: • Acute or fulminant onset: symptoms and signs of sepsis; meningitis evolve rapidly over a few hours and death within 24 hours; usually infected with Neissria meningitides (N. meningitides)
Mode of presentation ● Subacute onset: Precede by several days of upper respiratory tract or gastrointestinal symptoms; difficult to pinpoint the exact onset of meningitis; usually with meningitis due to Haemophilus influenzae (H influenzae)and streptoccus pneumococcus (S pneumococcus)
• Subacute onset: Precede by several days of upper respiratory tract or gastrointestinal symptoms; difficult to pinpoint the exact onset of meningitis; usually with meningitis due to Haemophilus influenzae (H influenzae) and streptoccus pneumococcus (S pneumococcus). Mode of presentation