Cns infections
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Transcript of Cns infections
CNS INFECTIONSCNS INFECTIONS
PROF. DR. SHAHENAZ M. HUSSEINPROF. DR. SHAHENAZ M. HUSSEIN
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.
Acute Bacterial MeningitisAcute 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.
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.
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 • Kernig’s 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 sutures3- Cranial nerve neuropathies.4- Hypertension with bradycardia 5- Apnea or hyperventilation, stupor and coma.
Signs of meningeal irritation: • Nuchal rigidity and back pain • Kernig’s 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 sutures3- 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 (<50% of S. glucose)5- Physical appearance:Turbid with elevated pressure (100-300
mm H2O).
Normal CSF shows: Normal pressure (50-80 mm H2O), leucocytes (<5/mm3), proteins (20-45 mg/dl) and glucose (75% of the level of serum glucose).
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 (<50% of S. glucose)5- Physical appearance:Turbid with elevated pressure (100-300
mm H2O).
Normal CSF shows: Normal pressure (50-80 mm H2O), leucocytes (<5/mm3), proteins (20-45 mg/dl) and glucose (75% of the level of serum glucose).
COMPLICATIONS
• Deafness• Hydrocephalus• Brain abscess• Subdural effusion• Motor disabilities
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 β- 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.
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.
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.
ENCEPHALITISDefinition: 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).
ENCEPHALITISDefinition: 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).
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; (Meningoencephalitis).
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.
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; (Meningoencephalitis).
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.
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 Simplex;and varicella-zoster
infections, Acyclovir is used.