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.