Meningitis Dr. Aso Faeq Salih Pediatric department

Meningitis Encephalitis Meningitis is an inflammation (swelling) of the protective membranes (meninges) covering the brain and spinal cord. A bacterial or viral infection of the fluid surrounding the brain and spinal cord usually causes the swelling. Inflammation of the brain parenchyma, presents as diffuse and/or focal neuropsychological dysfunction Most commonly a viral infection with parenchymal damage varying from mild to profound

Aetiology

Bacterial Cause Common cause: Neisseria meningitidis (In children 1 month to 12 month) Streptococcus pneumoniae and Haemophilus influenzae type b. less common pathogens such as Pseudomonas aeruginosa, Staphylococcus aureus, coagulase- negative staphylococci, Salmonella spp., and Listeria monocytogenes. (Due to Alterations of host defence, anatomic defects or immune deficits).

Neisseria meningitidis Gram negative, non motile, non sporing diplococcus Produces endotoxin responsible for circulatory collapse & DIC. Incubation period: 3-4 days (2- 10days average)

Viral Cause Viral meningitis comprises most aseptic meningitis syndromes. The viral agents for aseptic meningitis include the following: Enterovirus (polio virus, Echovirus, Coxsackievirus ) Herpesvirus (Hsv-1,2, Varicella.Z,EBV ) Paramyxovirus (Mumps, Measles) Togavirus (Rubella) Rhabdovirus (Rabies) Retrovirus (HIV)

Fungal Cause It’s rare in healthy people, but is a higher risk in those who have AIDS, other forms of immunodeficiency or immunosuppression. The most common agents are Cryptococcus neoformans, Candida, H capsulatum.

Acute Bacterial Meningitis

Acute Bacterial Meningitis One of the most potentially serious infections occurring in infants and older children. The incidence of bacterial meningitis is sufficiently high in febrile infants.

Epidemiology Major risk factor for meningitis- lack of immunity to specific pathogens associated with young age. Additional risks: recent colonization with pathogenic bacteria close contact (household, daycare centres) with individuals having invasive disease caused by N. meningitidis and H. influenzae type b, crowding, poverty Mode of transmission Probably person-to-person contact through respiratory tract secretions or droplets.

Defects of the complement system (C5- C8) have been associated with recurrent meningococcal infection. Splenic dysfunction (sickle cell anemia) or asplenia (due to trauma, or congenital defect) is associated with an increased risk of pneumococcal, H. influenzae type b (to some extent), and, rarely, meningococcal sepsis and meningitis.

Pathogenesis Bacterial meningitis most commonly results from haematogenous dissemination of microorganisms from a distant site of infection; bacteremia usually precedes meningitis or occurs concomitantly. Usual source of bacteremia: bacterial colonisation of naso-pharynx with potentially pathogenic microorganism.

Clinical Manifestations Common presentation is sudden onset rapidly progressive manifestations of shock Purpura disseminated intravascular coagulation (DIC)reduced levels of consciousness often resulting in progression to coma or death within 24 hr. More often, meningitis is preceded by several days of fever accompanied by upper respiratory tract or gastrointestinal symptoms, followed by nonspecific signs of CNS infection such as increasing lethargy and irritability.

Nonspecific findings include: Fever Anorexia Poor feeding Headache  The signs and symptoms of meningitis are related to the nonspecific findings associated with a systemic infection and to manifestations of meningeal irritation. Nonspecific findings include: Fever Anorexia Poor feeding Headache Symptoms of upper respiratory tract infection Myalgias Arthralgias Tachycardia Hypotension Various cutaneous signs, such as petechiae, purpura, or an erythematous macular rash

Meningeal irritation is manifested as: Nuchal rigidity- impaired neck flexion resulting from muscle spasm (not actual rigidity) of the extensor muscles of the neck; usually attributed to meningeal irritation. Back pain Kernig sign (flexion of the hip 90 degrees with subsequent pain with extension of the leg), and Brudzinski sign (involuntary flexion of the knees and hips after passive flexion of the neck while supine)

Testing for meningeal irritation (neck rigidity) Testing for meningeal irritation (Kernig’s test)

Meningococcal septicemia with purpuric skin rash with head retraction suggestive of Brudzinski’s contralateral reflex sign meningitis The childs hip and knee are passively flexed on one side Contralateral leg bends in reflex response

Diagnosis 1. CSF Study Lumbar Puncture is done for CSF collection.  Confirmed by analysis of the CSF, which typically reveals microorganisms on Gram stain and culture. Lumbar Puncture is done for CSF collection. Contraindications for an immediate LP include evidence of increased ICP, HTN. in patients in whom positioning for the LP would further compromise cardiopulmonary function. infection of the skin overlying the site of the LP.

>1,000/mm3 and, typically, there is a  The CSF leukocyte count in bacterial meningitis usually is elevated to >1,000/mm3 and, typically, there is a neutrophilic predominance (75- 95%).  Turbid CSF is present when the CSF leukocyte countexceeds 200-400/mm 3 . viral or bacterial meningitis have <5 leukocytes/mm3 in the CSF

2. Blood cultures  Blood cultures reveal the responsible bacteria in up to 80-90% of cases of meningitis. Elevations of the C- reactive protein,erythrocyte sedimentation rate, and procalcitonin have been used to differentiate bacterial (usually elevated) from viral causes of meningitis.

3. CT Scan Cranial computed tomography (CT) is of limited use in acute bacterial meningitis . CT in cerebral oedema may show slit- like lateral ventricle and areas of low attenuation.

Treatment A child with rapidly progressing disease of less than 24 hr duration, in the absence of increased ICP, should receive antibiotics as soon as possible after an LP is performed. If there are signs of increased ICP or focal neurologic findings, antibiotics should be given without performing an LP and before obtaining a CT scan

Initial Empirical Therapy  Vancomycin (60 mg/kg/24 hr, given every 6 hr) Because of the efficacy of third-generation cephalosporins in the therapy of meningitis caused by sensitive S. pneumoniae, N. meningitidis, and H. influenzae type b: Cefotaxime (300 mg/kg/24 hr, given every 6 hr) or Ceftriaxone (100 mg/ kg/24 hr administered once per day or 50 mg/kg/dose, given every 12 hr) Patients allergic to β-lactam antibiotics and >1 mo of age can be treated with Chloramphenicol, 100 mg/kg/24 hr, given every 6 hr. Another option for patients with allergy to β-lactam antibiotics is a combination of Vancomycin and Rifampin.

Coticosteroids  Use of intravenous dexamethasone 0.15 mg/kg/ dose given every 6 hr for 2 days, in the treatment of children older than 6 wk with acute bacterial meningitis caused by H. influenzae type b.  Among children with meningitis caused by H. influenzae type b, corticosteroid recipients have a shorter duration of fever (inflammation is reduced), lower CSF protein and lactate levels, and a reduction in sensorineural hearing loss (result of cochlear infection).

Complications During the treatment of meningitis, acute CNS complications can include seizures, increased ICP, cranial nerve palsies, stroke. Subdural effusions are especially common in infants Prolonged fever (>10 days) is noted in approximately 10% of patients. Prolonged fever is usually caused by intercurrent viral infection, nosocomial or secondary bacterial infection, thrombophlebitis, or drug reaction.

Prevention Neisseria meningitidis Vaccination and antibiotic prophylaxis of susceptible at- risk contacts represent the 2 available means of reducing the likelihood of bacterial meningitis. Neisseria meningitidis Two quadrivalent (A, C, Y, W-135), conjugated vaccines (MCV-4; Menactra and Menveo) are licensed by the FDA. Menactra is licensed for use in infants older than 9 mo of age, and Menveo for use in children older than 2 yr of age

Haemophilus influenzae Type B All children should be immunized with H. influenzae type b conjugate vaccine beginning at 2 mo of age. Streptococcus pneumoniae Routine administration of conjugate vaccine against S. pneumoniae is recommended for children younger than 5 yr of age. The initial dose is given at about 2 mo of age.

Prognosis Appropriate antibiotic therapy and supportive care have reduced the mortality of bacterial meningitis after the neonatal period to <10%. The highest mortality rates are observed with pneumococcal meningitis. Sensorineural hearing loss is the most common sequela of bacterial meningitis and, usually, is already present at the time of initial presentation.