Meningitis. Dr; Abdulrahman Al shaikh

definition Inflammatory disease of leptomeninges, the tissue surrounding the brain and spinal cord. The meninges consist of three parts : the pia, arachnoid ; and dura maters. It involves the arachnoid mater and the cerebrospinal fluid in the subarachnoid space as well as in the cerebral ventricles.

Types Acute either pyogenic or viral. Chronic due to tuberculosis or fungal.

Pyogenic meningitis.

: ETIOLOGICAL AGENT " Normal" Adults (6-21 yrs) Neisseria meningitidis Streptococcus pneumoniae Children (3 months - 6 years) Haemophilus influenzae Neisseria meningitidis Streptococcus pneumoniae Staphylococcus aureus Mycobacterium tuberculosis Infants (½ - 3 months) Streptococcus, Group B Listeria monocytogenes Escherichia coli

Neonates Escherichia coli Streptococcus, Group B Staphylococcus aureus Listeria monocytogenes Streptococcus, Group A Diabetics, alcoholics, elderly, debilitated, diseased (untreated) Listeria monocytogenes Streptococcus pneumoniae Treponema pallidum

Clinical feature. Fever and headache in majority. Headache severe and generalized. Most have fever but small percentage have hypothermia. CNS symptoms: photophobia, and cloudy sensorium. Changes in mentation and level of consciousness, seizures, and focal neurological signs tend to appear later in the course of the disease.

Nuchal rigidity. The patients might not complain of neck stiffness but easy to find it by passive or active flexion of the neck will usually result in inability to touch the chin to the chest. Brudzinski sign refers to spontaneous flexion of the hips during attempted passive flexion of the neck. The kernig signs refers to the inability to allow full extension of the knee when the hip is flexed 90 degree.

Other finding. Skin manifestation in form of petechiae and palpable purpura.( N. meningitides ). If sequelae of infection in other part of the body, there may the feature of that infection. ( sinusitis and otitis).

Laboratory features. Increased WBC. Low platelets if there is intravascular coagulation. Electrolytes abnormalities mainly low sodium. ( SIADH ). Blood culture at least one half have positive before antibiotics.

CSF. Can be diagnostic should be done in all only if there is contraindication. Can distinguish viral from bacterial. Gram stain should be done if suspected bacterial.

Complication. Cerebrovascular involvement. Cerebral odema. Hydrocephalus. Septic shock. Disseminated intravascular coagulation. Acute respiratory distress syndrome.

Treatment. Empiric ceftriaxone has a potent activity for causative organism except Listeria. Ampicilin should be added if Listeria infection possible. Dexamethazone reduced the complication.

H- influenza. Ceftriaxone 2 gm twice a day. Cefotaxime 2gm 6 hourly. Rifampicin 6oo mg daily for 4 days to clear the colonization. Should be treated 5 – 7 days.

Neisseria meningitis. Penicillin, but there resistant cases. Third generation cephalosporin. Treatment for 5 days at least. Rifampicin if penicillin used in treatment. Rifampicin or ciprobay for contact.

months of age. PREVENTION: Neisseria meningitidis - each dose of the multivalent vaccine provides A, C, Y and W-135 capsular polysaccharides. Effective in children over 3 months of age. Streptococcus pneumoniae - each dose of the multivalent vaccine provides 23 types of capsular polysaccharide covering the majority of strains causing meningitis. Recommended for children over 2 years of age. Haemophilus influenzae – each dose of the monovalent vaccine provides the capsular polysaccride from serotype b. organisms. Recommended for children over 18 months of age.

Viral meningitis

Mumps virus Polio virus Coxsackie B virus Echovirus Arboviruses Human Herpesvirus 1 (Herpes simplex 1 virus) Lymphocytic choriomeningitis viruses-Arenavirus Encephalomyocarditis viruses Louping ill virus Pseudolymphocytic meningitis virus Hepatitis viruses Adenovirus Rhinovirus Coxsackie A virus ETIOLOGICAL AGENTS :

NAMES OF DISEASE: Fungal meningitis Cryptococcosis Torulosis Tubercular meningitis Amoebic meningitis Syphilitic meningitis CHRONIC MENINGITIS

Cryptococcus neoformans (Serotypes A,B,C,D) Treponema pallidum ) All slow Mycobacterium tuberculosis ) growers in Naegleria fowleri ) the CNS Human immunodeficiency virus ) Coccidioides immitis ) ETIOLOGICAL AGENTS:

Fungal meningitis-predisposing factors. 1. Glucosteroid therapy 2. Malignancy (particularly of the lymphoreticular system) 3. Collagen - vascular disease. 4. Sarcoidosis - a disorder involving many organs where there is formation of epithelioid cell tubercles. 5. Diabetes mellitus 6. Pregnancy 7. Alcoholism 8. Genetic impairment of host defense mechanisms - 50%. T- cell diseases (Di George Syndrome, Nezelof's syndrome) 9. AIDS

Clinical feature: fungal. 1. Headache - frontal, temporal or retro-orbital. Most common feature and it becomes progressively more frequent and severe. 2. Mental aberrations (from simple irritability to psychosis) 3. Motor abnormalities (altered reflexes to paralyses) 4. Cranial nerve dysfunctions (aphasia, visual disturbances, hearing loss) 5. Cerebellar signs (dyssynergia, dysmetria, dysrhythmia, intentional tremor, slurring of speech) 6. Evidence of increased intracranial pressure 7. Fever in about 1/3 of patients

CSF: in fungal 1. Increased CSF pressure 2. Protein is elevated 3. Leukocytosis (40-400/mm 3 - mostly mononuclear cells) 4. Glucose is decreased (45% of blood glucose) 5. C. neoformans present in India ink preparations 6. Serological tests for cryptococcal antigen

TREATMENT: 1. Amphotericin B injected I.V. and into the subarachnoid space. NOTE: This is poorly absorbed into CSF. Treat for 6 weeks. Toxic. 2. Flucytosine (5-fluorocytosine)-penetrates into all body fluids, including CSF. Less toxic but higher doses required. 3. Miconazole-an imidazole derivative 4. Amphotericin B methyl ester

Tuberculous meningitis. Clinical feature. Diagnosis. Treatment.

Clinical feature: TB. Atypical presentations : Rapid progressive as pyogenic or slow dementia. Stage 1: lucid with no focal neurological signs. Stage 11 are confused or focal signs such as hemiparesis or cranial nerve palsies. Stage 111 advanced illness with delirium, stupor, coma and dense hemiplegia.

Diagnosis. High degree of suspicion. CSF – high protein, low sugar and a mononuclear pleocytosis. Early in the illness the cellular reaction is atypical with low cell or polymorphonuclear leukocyte. AFB smear in 37%. Polymerase chain reaction = 70%. CT Scan of the brain with contrast or MRI.

Treatment. INH, Rifampicin and pyrazinamid for 2 months then discontinue PYZ. In endemic areas where resistance to INH is high the streptomycin or ethambutol added. The duration for 12 months but if PYZ not tolerated the duration extended to 18 months and in case multiple drugs resistance for months. Steroid improve morbidity and mortality, prednisone 60 mg to be tapered over 4 weeks. Surgery in case of hydrocephalus or increase intracranial pressure.( deterioration in conscious level and stupor).