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CNS INFECTIONS

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CNS INFECTIONS PROF. DR. SHAHENAZ M. HUSSEIN OBJECTIVES By the end of this lecture you will be able to understand the followings: Etiology, clinical manifestations ... – PowerPoint PPT presentation

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Title: CNS INFECTIONS


1
CNS INFECTIONS
  • PROF. DR. SHAHENAZ M. HUSSEIN

2
OBJECTIVES
  • By the end of this lecture you will be able to
    understand the followings
  • Etiology, clinical manifestations,
    investigations, and treatment of acute bacterial
    meningitis.
  • Etiology, clinical manifestations, laboratory
    findings, diagnosis and management of
    encephalitis.
  • Slide and video demonstration of some
    neurological manifestations.

3
Acute Bacterial Meningitis
  • Etiology
  • First 2 months of life Group B Streptococcus,
    gram negative bacilli, S. pneumoniae, Neisseria
    meningitides, Haemophilus influenzae type b. and
    L. monocytogenes.
  • Children 2 mo-12yr of age 1- S. pneumoniae
  • 2-
    N. meningitides
  • Alterations of host defense
  • Pseudomonas aeruginosa, Staphylococcus aureus,
    Salmonella spp., and L. monocytogenes.
  • Mode of infection Bacterial meningitis most
    commonly results from hematogenous dissemination
    of microorganisms from a distant site of
    infection.

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  • Clinical Manifestations The onset of acute
    bacterial meningitis has two predominant
    patterns
  • 1- The more dramatic less common presentation is
    sudden onset with rapidly progressive
    manifestations of shock, purpura, DIC,
    unconsciousness, and frequently resulting in
    death within 24 hours.
  • 2- More often, meningitis is preceded by several
    days of fever with upper respiratory or GIT
    symptoms followed by nonspecific signs of CNS
    infection such as lethargy or irritability.
  • Non specific findings Fever,
    anorexia, poor feeding, myalgia, arthralgia,
    tachycardia, hypotension, and petechiae,or an
    erythematous macular rash.

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  • Signs of meningeal irritation
  • Nuchal rigidity and back pain
  • Kernigs sign flexion of the hip 90 degrees with
    subsequent pain and limitation with extension of
    the leg.
  • Brudzinski sign involuntary flexion of the knees
    and hips after passive flexion of the neck while
    the patient in supine position.
  • Symptoms and Signs of increased ICP
  • 1- Headache, and vomiting
  • 2- Bulging fontanel or widening of the sutures
  • 3- Cranial nerve neuropathies.
  • 4- Hypertension with bradycardia
  • 5- Apnea or hyperventilation, stupor and coma.

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  • Seizures (focal or generalized) due to,
    cerebritis, infarction or electrolyte
    disturbances. Seizures that occur on presentation
    or within the first 4 days of onset are usually
    of no prognostic significance.
  • Diagnosis
  • Lumbar puncture for CSF analysis should be
    performed
  • 1- Microorganisms on gram stain and culture.
  • 2- Neutrophil pleocytosis (300-2000/mm3).
  • 3- Elevated protein (100-500mg/dL)
  • 4- Reduced glucose concentration (lt50 of S.
    glucose)
  • 5- Physical appearanceTurbid with elevated
    pressure (100-300 mm H2O).
  • Normal CSF shows Normal pressure (50-80 mm H2O),
    leucocytes (lt5/mm3), proteins (20-45 mg/dl) and
    glucose (75 of the level of serum glucose).

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COMPLICATIONS
  • Deafness
  • Hydrocephalus
  • Brain abscess
  • Subdural effusion
  • Motor disabilities

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  • Treatment 1- Initial Antibiotic
    Therapy
  • -Ampicillin 200mg/kg with either cefotaxime or
    ceftriaxone100mg/kg, if gram-ve bacilli present
    give Ampicillin with Gentamycin for neonatal
    meningitis.
  • -Vancomycin 60mg/kg/24hr given every 6 hr in
    combination With either cefotaxime (200mg/kg/24hr
    given every 6 hours) or ceftriaxone
    (100mg/kg/24hr once or twice daily) in older
    infants and children.
  • -Patients allergic to ß- Lactam antibiotics can
    be treated with chloramphenicol, 100mg/kg/d,
    given every 6 hr. Duration of therapy At
    least for 7-14 days I.V.
  • -Corticosteroids I.V dexamethasone 0.15
    mg/kg/dose given every 6hr for 2 days for
    children older than 6wk with acute bacterial
    meningitis caused by H. influenzae type b to
    decrease the permanent auditory nerve damage.

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  • 2-Supportive and symptomatic therapy
    A-Good evaluation and monitoring are
    essential.
  • B-Correction of dehydration and electrolyte
    disturbances and proper nutrition.
  • C-Control of seizures
  • D- Management of neurological complications
  • Prevention
  • - Vaccination and antibiotic prophylaxis for
    susceptible at risk contacts.
  • Close contact should be treated with Rifampin
    10mg/kg/dose every 12hr, for 2 days (in N.
    meningitides) and 20mg/kg/day for 4 days in H.
    influenzae type b.

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  • ENCEPHALITIS
  • Definition Infection involving cerebral
    parenchyma, in some patients the meninges
    involved with the parenchyma causing
    meningoencephalitis.
  • Etiology
  • 1- Arthropod born virus Arbovirus Flavivirus
  • -St. Louis encephalitis. Birds (culex
    mosquitoes).West-Nile virus.
  • - Western equine encephalitis.Birds (Colisata
    mosquitoes).
  • - Eastern equine encephalitis. Birds ( Culisata
    mosquitoes).
  • - Venezuelan equine encephalitis. Hoarses ( 10
    species mosquitoes).
  • - California encephalitis (Bunya virus).
    Chipmunks (Aedes mosquitoes).
  • - Clorado tick fever (Wood tick).

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  • Etiology continue
  • 2-Herpes simplex virus.
  • 3- Varicella or vaccine.
  • 4- Measles or vaccine
  • 5-Influenza .
  • 6- Poliomyelitis.
  • 7- Congenital infections Cytomegalovirus,
    Rubella.
  • 8-HIV
  • 9-Rabies
  • 10-Rubella
  • 11-E.B.V.
  • 12-Mycoplasma pneumonia

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  • Clinical manifestations
  • - Duration of illness 2-5 days ----------up 3
    weeks.
  • Abrupt onset of fever, chills, headache, nausia,
    vomiting.
  • Generalized weakness, seizures, coma, ataxia,
    cranial nerve palsies.
  • Meningeal signs in some cases (Meningoencephaliti
    s).
  • Laboratory findings
  • Lymphocytosis in blood picture.
  • CSF 100-500 WBCs/ul pleocytosis (lymphocytes).
  • Serology Specific antibodies( IgM) in the 1st
    week.
  • PCR for viral antigens.
  • - Neuroimaging CT or MRI for brain.
  • - EEG for temporal lobe lesion of herpes
    simplex.
  • - Brain biopsy for undiagnosed cases.

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  • Complications
  • Acute disseminated encephalomyelitis ADEM
    usually follow measles or varicella diseases or
    vacination.
  • Mortality is variable according to the type of
    encephalitis 2-5 in St. Louis and 20 in
    Venezuelan equine. And 50 in Eastern equine.
  • Neurological sequelea ranging from 1 to more
    than 50 in Eastern equine encephalitis.
  • Therapy
  • Supportive except in Herpes Simplexand
    varicella-zoster infections, Acyclovir is used.
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