CNS Infections

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CNS Infections

• Amal Al Dabbagh,
• Consultant Pediatrician
• MBBCH, MSc, CABP

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Definitions

• Infection of the CNS may be diffuse or focal.
• Meningitis and encephalitis are examples of
  diffuse infection.
• Meningitis implies 1ry infection of the meninges.
• Encephalitis indicates brain parenchymal
  involvement.
• Many patients have meningeal parenchymal
  involvementmeningoencephalitis.
• Brain abscess is the best example of a focal
  infection.

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Epidemiology

• Risk factors
• Lack of immunity to specific pathogens associated
  with young age.
• Recent colonization with pathogenic bacteria.
• Close contact( household, daycare, dorms) with
  individuals having invasive disease caused by N.
  meningitides H. infl type b, crowding,
  poverty, black race male gender.
• Mode of transmission is person-person thru resp
  secretions or droplets.
• Infants children with occult bacteremia.

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Pathogenisis

• Inflammation of the meninges when cell wall
  membrane products of the organism disrupt the
  capillary endothelium of the CNS(BBB).
• Hematogenous or direct invasion.
• Disruption will lead to migration margination
  of PMNs across endothelia into CSF leading to a
  cascade of events (cytokine chemokines release
  within the CNS ) resulting in inflammation
  signs and symptoms of meningitis.

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Pathology

• Cerebral edema.
• Increased ICP.
• Thrombosis
• Infarction
• High CSF protein and low Glucose

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Associations risk factors

• Defects of complement system (C5-C8).recurrent
  meningococcal infection.
• Defects of the properdin system.lethal
  meningococcal disease.
• Splenic dysfunction ( SCD) or asplenia ( trauma,
  cong. ) .Pneumococcal, H.infl b, rarely
  meningococcal sepsis meningitis.
• T-lymphocyte defects ( malignancy, HIV)..L
  monocytogenes infections of the CNS.
• CSF leak across midline facial defect, middle
  ear, basal skull fracture.Pn.coccal meningitis.
• Lumbosacral dermal sinus mmcele.staph G-ve
  enteric bacterial meningitis.
• CSF shunt..coagulase ve staph meningitis.

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CNS Infections, Etiology

• Many microorganisms can cause infection,
  nonetheless, specific pathogens are identifiable
  and are influenced by the age ,immune status of
  the host epidemiology of the pathogen.
• Viral infections of the CNS are much more common
  than bacterial ones.
• Bacterial infections are in turn much more common
  than fungal, parasitic infections.
• Rickettsia ( Rocky mountain spotted fever) are
  relatively uncommon, but important under specific
  circumstances.
• Mycoplasma spp. Can also cause CNS infections,
  but their contribution is often difficult to
  determine.

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Etiology OF Bacterial Meningitis according to age

• Newborn Groups B D streptococci
  (enterococcus),gram ve enteric bacilli ( E-coli,
  Klebsiella), Listeria monocytogenous.
• Gp B D streptococci Listeria persist as
  important CNS pathogens through the 3rd mo of
  life.
• 2m-12yrs N. meningitides in the US, bacterial
  meningitis caused by S. Pneumoniae H.
  influenzae type b in incompletely vaccinated
  individuals or those in developing countries.

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Clinical Manifestations

• Regardless of etiology, most patients with CNS
  infection have similar clinical manifestations.
• Common symptoms include headache, nausea,
  vomiting, anorexia, restlessness, altered state
  of consciousness, and irritabilitynon specific.
• Common signs, in addition to fever, include
  photophobia, neck pain rigidity, obtundation,
  stupor, coma, seizures, focal neurologic
  deficits.
• The severity constellation of signs are
  determined by the specific pathogen, the host,
  the area of CNS affected.

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Meningeal Irritation signs

• Nuchal rigidity.
• Back pain.
• Kernig sign ( flexion of the hip 90 degrees with
  subsequent pain with extension of the leg) .
• Brudzinski sign ( involuntary flexion of the
  knees hips after passive flexion of the neck).
• Tripod posture The Patient sits with partial
  support from the arms which are held back
  straight with the hands on the sitting surface

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Other Findings

• Arthralgia, Myalgia.
• Transient arthritis.
• Peticheal or purpuric rash.
• Anemia.
• DIC picture

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Increased ICP

• Is due to cell death ( cytotoxic CE), cytokine
  induced increased cerebral permeability(
  vasogenic), and increased hydrostatic pressure (
  interstitial CE).
• Headache, emesis.
• Bulging fontanel, Diastasis of the sutures.
• Oculomotor or abducens nerve paralysis.
• Hypertension with bradycardia.
• Apnea or hyperventilation.
• Decorticate or decerebrate posturing.
• Stupor, coma or signs of herniation

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Papilledema

• Uncommon in uncomplicated meningitis.
• Suggest a more chronic process, as IC abscess,
  subdural empyema, or occlusion of a dural venous
  sinus.

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Diagnosis

• The diagnosis of CNS infections depends on
  examination of CSF, obtained by lumbar puncture.

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C/I to LP

• Increased ICP.
• Suspicion of mass lesion.
• Infection of LP site.
• Extreme patient instability.
• Hemorrhagic disease.

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Cerebrospinal Fluid Findings in Central Nervous
System Disorders
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Uncommon forms of meningitis
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Differential Diagnosis

• Other microorganisms which cause CNS infection
  with similar clinical manifestations.
• TB, Treponema pallidum, Borellia, fungi.
• Brain abscess parameningeal abscess.
• Acute viral meningoencephalitis.

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Acute Complications of Bacterial Meningitis

• Systemic effects
• Cardiovascular instability-? inotropes
• Depressed level of consciousness? intubation
• Prolonged seizure activity-? mechanical
  ventilation.
• SIADH-? fluid restriction
• Persistent fever.

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Persistent Fever

• Common with H. Influenza type b
• Subdural effusion.
• Pericardial or joint effusion.
• Drug Fever.
• Thrombophlebitis.
• Nosocomial Infections

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Acute complications of Bacterial Meningitis, cont

• Localized effects to the CNS
• Cerebral vascultis.
• Stenosis of cerebral arteries.
• Infarction.
• Intracerebral hemorrhage.
• Abscess formation especially with G-ve
  pathogens as Salmonella Citrobacter.
• Subdural effusion ventriculitis

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Long term sequelae of Bacterial Meningitis

• These findings occur in 25 to 50 of patients
  and include
• Spasticity
• Blindness.
• Hearing loss.
• Persistent seizures.
• Hydrocephalus.
• Developmental delay.
• Decreased IQ.
• Subtle cognitive deficits , learning disabilities
  school behavioral problems.

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Treatment

• Supportive
• Ventilation.
• Rx of shock/DIC
• Rx of Increased ICP/Seizure
• Rx of SIADH.
• Rx of complications

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Antibiotic Initial Therapy

• Ceftriaxone 100mg/kg/24hrs divided into 2 doses.
• Cefotaxime 200mg/kg/24hrs div. Into 4 doses.
• Penicillin G 300,000 iu/kg ,div. Into 4 doses for
  Str.pn Meningococcus.
• Penicillin Resistant Pneumococci.Ceftriaxone or
  Cefotaxime plus Vancomycin

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Antibiotics,Infantslt2months

• Ceftriaxone or
• Cefotaxime plus Ampicillin 300mg/kg/24hrsto
  cover Listeria.

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Treatment Course

• 7 days for Meningococcus
• 10 days for H.Influenza Str.Pn.
• Dexamethazone 0.15 mg/kg/dose Q 6hrs for 2 days
  for H.Influenza( 1-2 hrs before antibiotics
  initiated).
• Prior to discharge home give Rifampicin

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prevention

• H.Influenza ( Vaccines, Rifampicin)
• N.Meningitidis ( Vaccine, Rifampicin,
  Ciprofloxacin)
• Pneumococcal ( pneumovax, Prevnar).

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Mortality

• H.Influenza 8
• Meningococcus 15
• Pneumococcus 35

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Poor Prognosis

• Young Age
• Delayed Rx
• The organism
• Concn. of Organism or Ag in CSF.
• Late onset seizure.

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Poor Prognosis, cont

• Coma at presentation.
• Shock.
• Low or absent CSF WBC(with visible bacteria on
  gram stain)
• Immune compromised status.

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Acute Aseptic Meningitis

• An acute inflammation of the meninges is a common
  illness with many causes.
• Lymphocytic Pleocytosis.
• Normal Glucose in CSF.
• Slightly raised CSF protein.
• No bacterial growth.

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Acute Aseptic meningitis,Etiology

• Not always identified.
• Viruses usually responsible.
• Enteroviruses in 85 of cases (Coxackie virus
  B5. Eccho viruses 4,6,9,11).
• Arboviruses ( EEV, WEV, WNV).
• Herpes simples(12).

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Acute Aseptic Meningitis,Etiology

• HIV,Varicella,EBV.
• Lymphocytic Choriomeningitis.
• Natural or Vaccine related(MMR,Polio,Rabies)
• Influenza ParaInfluenza viruses.

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A A Meningitis,Etiology

• Mycoplasma
• Chlamydia
• Fungi
• Protozoa
• Parasites
• Post infectious
• Mycobacterium tuberculosis.

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Encephalitis

• Inflammation of the cerebral cortex with clinical
  symptoms ranging from slight confusion to coma.
• Symptoms usually are coupled with headaches
  photophobia.
• CSF shows fewer inflammatory cells(PMN) than
  meningitis.
• It is an unusual complication of common viral
  illness.

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Viral Encephalitis

• Virus gains access through
• Hematogenous (common arthropod borne viral
  disease).
• Neuronal ( Herpes Simplex,Rabies).

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Encephalitis,Etiology

• HSV,sporadic.
• Rabies, rare but important.
• M,M,R.
• Yellow Fever.
• Poliomyelitis, vaccine related.
• Picorna viruses(enteroviruses, coxackie, eccho
  viruses),also cause aseptic meningitis.

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Encephalitis,Etiology

• Arthropod-borne viruses
• St Louis Encephalitis,from bird reservoir.
• Eastern Equine Encephalitis.
• La Crosse Virus.
• Post Infectious Encephalomyelitis
• associated with URTI especially Influenza
  measles where vaccination is not a routine.

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Encephalitis,Epidemiology

• Winter Fall.
• HSV cause 10 of non neonatal virus infections.

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Encephalitis,clinical manifestation

• Confusion.
• Hallucinations.
• Memory loss.
• Combativeness.
• Seizure.
• Coma

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Differential Diagnosis

• BacterialTB
• ParasiticMalaria,Toxoplasma.
• Non infectiousVasculitis,Malignancy.
• EncephalopathyToxins,hypoglycemia,Reye Syndrome.

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Diagnosis

• Full history Exposure to animals
• Mosquito,Ticks
• Travel
• Full Examination.
• Investigations.

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Encephalitis,Investigations

• CSFcell,glucose,protein.
• CulturesCSF,throat,stool.
• SerologyInitial 2-3 wks later.
• EEG focal diffuse changes.
• CT,MRI.

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Encephalitis,Treatment

• Supportive care.
• Specific drugs
• acyclovir for HSV
• Zidovidin for HIV
• Doxycycline Erythromycin for Mycoplasma

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Encephalitis,Prognosis

• Most children recover without major sequelae.
• Poorer prognosis with
• HSV, Rabies,Mycoplasma
• Seizure,Coma

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Neisseria meningitidis in CSF G-ve diplococci
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Streptococcus pneumoniae in CSF(Gve diplococci)
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Haemophilus influenza in CSF(G-ve coccobacilli)
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Gp B streptococcus in CSF(Gve coccobacilli)
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Listeria monocytogenes in CSF( Gve rods and
coccobacilli)
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Meningococcal meninigitis
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Figure 1. A. CT of cerebral edema. Note "ground
glass" appearance, loss of normal gray-white
matter differentiation, and effacement of
left-sided sulci and gyri compared with the right
side. B. CT of epidural hematoma. Note midline
shift and compression of ipsilateral ventricle
and brain tissue
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