Transcript Lecture 1 Bacterial meningitis

Lecture 1
Bacterial meningitis
Dr. Abdelraouf A. Elmanama
Islamic University-Gaza
Medical Technology Department
Lecture outlines
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Introduction
Simplified anatomy of the CNS
Etiology (causes of bacterial meningitis)
Pathophysiology
Clinical manifestations
Objectives
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Define meningitis
Describe prevalence of meningitis
Explain pathophysiology
Identify clinical manifestations
Know the appropriate antibiotic
treatment per age group
Definition
Meningitis: inflammation of the
leptomeninges (the tissues
surrounding the brain and spinal cord)
• Bacterial meningitis
• Aseptic meningits: infectious or
noninfectious
Viral, Rickettsiae,
Mycoplasma
Fungal, spirochetes: syphilis, Lyme
Protozoa: malaria
Malignancy
Lupus erythematous
Lead or mercury poisoning
Anatomy
Meningies
CNS infections
• Meningitis
Infection of the subarachnoid space with meningeal
involvement
• Encephalitis
Inflammation of brain
• Meningoencephalitis
Inflammation of brain with meningeal involvement
• Brain Abscess
Pathogens may be bacterial, TB, viral, fungal, or
parasitic
CSF
• About 85% of CSF produced by the
choroid plexus which also controls the
constituency of CSF
• CSF volume varies by age with a
normal adult having a steady state
volume of ~150cc
Meningitis Bacterial Pathogens
• Mechanical Barriers Intact
S. pneumoniae (pneumococci)
N. meningitidis (meningococci, Groups A,B,C,Y, &
W135)
H. influenzae (type B or Hib)
Immunizations may also affect likely pathogen
Special situations B. anthracis
• Traumatic alteration or other risk factors
S. aureus
E. coli or P. aeruginosa
May depend on circumstances
Meningitis Bacterial Pathogens
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Neonatal
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Children < 1 month of age
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Pathogens acquired from birth canal
• E. coli
• Group B Streptococci (S. agalactiae)
Initial symptoms and signs
Symptoms or Sign
Relative frequency%
Headache
>90
Fever
>90
Meningismus
>85
Altered sensorium
>80
Kernig’s or Brudzinski’s
>50
signs
Focal findings
10-20
Papilledema
<1
DESCRIPTION of symptomes
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Severe headache .A person with meningitis may describe the headache as the worst one they’ve
ever had.
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High fever. The infection can cause a high fever (39°C or over) which does not get lower with a
tepid bath or fever-reducing medicine.
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Stiff neck. Swelling in the meninges (membranes around the spinal cord and brain) causes a stiff
neck that makes it extremely painful to move the neck or head.
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Nausea and vomiting. Vomiting is common with many illnesses. However, if vomiting happens
with the other symptoms listed, it may be caused by meningitis.
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Numbness or loss of feeling. Sepsis (also known as blood poisoning) can reduce the amount of
blood that gets to a person’s hands and feet, causing numbness, coldness, or loss of feeling.
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Light sensitivity. A person with meningitis may find it painful to look at bright lights, and will try to
avoid them.
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Confusion. Swelling around the brain can make a person confused and seem "out of it.“
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Rash. Purple spots that do not turn white when you press on them are a sign of sepsis (also
known as blood poisoning) .
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Seizures. Sometimes people with meningitis have seizures similar to the kind that people with
epilepsy have
Rashes
Pathophysiology
Nasopharyngeal colonization
Local invasion
Bacteremia
Meningeal invasion
Bacterial replication in the subarachnoid space
Release of bacterial components (cell wall, LOS)
Cerebral microvascular endothelium
Macrophages, neutrophils, other CNS Cells
Cytokines
Increased BBB
permeability
Cerebral
vasculitis
Subarachnoid space inflammation
Increased CSF outflow resistance
Cytotoxic edema
Vasogenic edema
Hydrocephalus
Interstitial edema
Cerebral
infarction
Increased intracranial pressure
Decreased cerebral blood flow and loss of cerebrovascular autoregulation
Pathophysiology
• Meningitis:
– Infection of meninges (dura, arachnoid, pia
mater).
– Caused by:
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Bacteria, viruses, fungi, parasites, or toxins.
Bacterial ***25% mortality in adults
Viral meningitis
Fungal meningitis
• Bacterial Meningitis:
– Infection of the pia mater and arachnoid, the
subarachnoid space, the ventricular system, and the
CSF.
– Infectious agents:
• Meningococcus (Neisseria meningitidis)
• pneumococcus (streptococcus pneumoniae)
– URI---blood borne---CNS entry
– Inflammatory response by meninges, CSF, ventricles.
– Neutrophils migrate producing exudate that plugs off
CSF flow around the brain and spinal cord.
Organism
Site of entry
Neisseria meningitidis
Nasopharynx
Streptococcus pneumoniae
Nasopharynx or direct extension
across
skull fracture
Listeria monocytogenes
GI tract, placenta
Haemophilus influenzae
Nasopharynx
Staphylococcus aureus
Bacteremia, skin, or foreign body
Staphylococcus epidermidis
Skin or foreign body
• Once in CSF, the absence of antibodies &
complement components allows bacterial infection to
flourish
• Cascade of events:
– Cell wall and membrane products of organism
disrupt capillary endothelium of CNS (BBB)
– Margination and transmigration of PMNs across
endothelia in CSF
• Release of cytokines and chemokines into the
CNS
– Inflammation of subarachnoid space
• Mortality: 3 to 13%
– Rate varies with organism
– Higher with gram negative organism
• Neurologic Sequelae: 10 % of surviving patients
Long-term Neurological Complications
Adverse Outcomes at One Year of Age of
12 Infants With Bacterial Meningitis
Category of Disability
Number
Development delay
10
Cerebral palsy
1
Microcephaly
3
Hemiparesis
3
Hearing loss
1
Blindness
2
Seizure disorder
3
Total number of disabilities exceeds the number of infants owing to the presence of
multiple disabilities in most subjects
Pathogenesis
– Majority of cases are hematogenous in
origin
– Organisms have virulence factors that
allow bypassing of normal defenses
• Proteases
• Polysaccharidases
Pathology and Pathogenesis
– Sequential steps allow the pathogen into the
CSF
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Nasopharyngeal colonization
Nasopharyngeal epithelial cell invasion
Bloodstream invasion
Bacteremia with intravascular survival
Crossing of the BBB and entry into the CSF
Survival and replication in the subarachnoid space
• Pathology
– Hallmark
• Exudate in the subarachnoid space
• Accumulation of exudate in the dependent areas of
the brain
• Large numbers of PMN’s
• Within 2-3 days inflammation in the walls of the
small and medium-sized blood vessels
• Blockage of normal CSF pathways and blockage
of the normal absorption may lead to obstructive
hydrocephalus