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Bacterial meningitis

Bacterial meningitis. meningitis. An inflammation of the leptomeninges . bacterial meningitis is a common complication of septicemia in children and must be treated as an emergency. Caused by : bacteria, viruses , or rarely fungi .

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Bacterial meningitis

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  1. Bacterial meningitis

  2. meningitis • An inflammation of the leptomeninges . • bacterial meningitis is a common complication of septicemia in children and must be treated as an emergency. • Caused by : bacteria, viruses , or rarely fungi . viral infection of the CNS are much more common than bacterial infection

  3. meningitis • Bacterial meningitis is one of the most potentially serious infection ,in infants and older children . • Associated with a high rate of acute complications and risk of long-term morbidity. • The etiology of meningitis in the neonate and the treatment are generally distinct from in older children

  4. meningitis • A limited number of bacteria are associated with meningitis in normal hosts . • the principle of supportive management and the initial choice of antibiotics can be generalized.

  5. Etiology of meningitis • 2 month – 12yr: S .pneumonia, N . Meningitidis ,H .influenza type b. H .influenza type b is the most common cause of meningitis in children < 4-yr

  6. Etiology and epidemiology of meningitis • 2 month : maternal flora and environment . Group B and D. streptococci gram – negative enteric bacilli . and listeria monocytogenes. may be due H.Influenza type b and nonecapsulate and other pathogens

  7. Etiology and epidemiology of meningitis • Lack of immunity ( IgM or igG anti capsularantibody ) to specific pathogens with young age. • recent colonization with pathogenic bacteria . • Close contact with invasive disease ( respiratory tract secration) • Crowding , poverty , black race , male . • Defect in complement (C5- C8 ) associated with recurrent meningococcal infection .

  8. Etiology and epidemiology of meningitis • ventricular-peritoneal shunts: Coagulase negative staphylococci and corynebacteria . • CSF leaks due to fracture cribriform palate or paranasal sinus ( pneumococcal ). • head trauma or neurosurgical procedures ( staphylococci )

  9. Etiology and epidemiology of meningitis • Splenic disfunction (sickle cell anemia or asplenia ) increased risk of pneumococcal , H.influenza type b ,rarely meningococcal sepsis and meningitis . • Immuno-suppressed patients with T-cell defects (AIDS, and malygnancy) : Cryptococcal and L.monocytogens. • Open neural tube defect : Meningomyelocele and lombosacral dermal sinus associated with staphylococci -Aureus and gram – negative .

  10. pathogenesis • Bacterial meningitis is usually hematogenous. (endocarditis , pneumonia , or thrombophlebitis , burns , indwelling catheters ) • Bacteremia precedes the condition or occur at the same time. • microorganisms leads to nasopharyngeal colonization , replication , invasion , and bacteremia .

  11. pathogenesis • Bacteria entry to the CSF through the choroid plexus.and meningeal seeding , binding to specific receptors and production of local cytokines initiates inflammation. • Neutrophilic infiltration , increase vascular premeablity , alterations of blood- brain barrier , and cerebral edema .

  12. pathogenesis • Meningitis rarely may be follow bacterial invasive from a contiguous focus of infection ; Paranasal synusitis , otitis media ,mastoiditis , orbital cellulitis, cranial osteomyelitis , penetrating cranial trauma ,meningomyeloceles , More often brain abscesses or epidural or subdural empyema follows contiguous infection .

  13. Clinical manifestation • Onset has two patterns; • The more dramatic and less common is sudden onset(< 1 day ) rapidly progressive of shock ,purpura , DIC ,and reduce level of consciousness frequntly resulting in death in 24 hr ( S.pneumoniae , or N. meningitidis ) • More often is preceded by several days of upper respiratory tract symptoms or GI symptoms . Subacute 2-3day .(H. influenzae)

  14. Clinical manifestation • In the young infants: fever usually is present and irritablity ,poor feeding , restlessness,may be noted. signs of meningeal inflammation may be minimal. • Older child : confusion , back pain , usually Kernig and Brudzinski signs in some children particularly age < 12-18 mo are not present

  15. Clinical manifestation • Increased ICP headache , diolopia , emesis , bulging fontanel 3 or 6 nerve paralysis, hypertension with bradicardia ,apnea or hyperventilation ,stupor coma ( brain herniation ) • inflammation of the meninges is associated with (headache ,nausea , vomiting , irritability , nuchal regidity , photophobia ) • Arthritis ,arthralgia ,myalgia , anemia , petechia ,purpura

  16. Clinical manifestation • Papilledema is uncommon . intracranial abcess , subdural empyema or occlusion of a dural venous sinus • Focal neurologic signs are due to vascular occlusion (10-20% ) • Seizuresoccur in 20-30% Seizures that occure on presentation or within the first 4 days of onset are no prognostic significance

  17. Clinical manifestation • Seizures cerebritis, infarction , electrolyte • Alteration of mental status increased ICP,cerebritis ,hypotension

  18. Clinical manifestation • Kernig sign: Flexion of the hip 90 degrees with subsequent pain with extension of the leg . • Brudzinski sign : Involuntary flexion of the knees and hips after passive flexion of the neck while supine.

  19. diagnosis • Blood culture ( reveal responsible bacteria 50-90% ) • LP analysis CSF for WBC count with diff ,protein, glucose ,Gram stain helpful in 90% , culture) CSF leukocyte count elevated >1000 and neutrophil (75-95%) • In tramatic LP Gram stain ,culture , glucose level may not be influenced.

  20. diagnosis  LP should be performed in every child when bacterial meningitis is suspected. Except : • when signs of increased ICP are present . • Infection at the LP site. • Suspicion of a mass lesion. • Extreme patient instability. • Thrombocytopenia is a relative contraindication.

  21. diagnosis • Patient in the flexed lateral decubitus position . • Intervertebral space L3-L4 or L4-L5.  Turbid CSF when CSF leukocyte count >200-400. • Pleocytosis may be absent and is a poor prognostic sign. • Pleocytosis with a lymphocytosis may be present during early stage of acute meningitis

  22. Differential diagnosis • Acute viral meningoencephalytis(PMN may be prodominant) • Partial treatment of a acute bacterial meningitis . (glucose , protein , neutrophile are not aletread) • TB ,fungal , spirochete ,,brain abcess , encephalitis bacterial endocarditis with embolism ,subdural empyema , subarachnoid hemmorhage , • Careful examination CSF ,and additional laboratory tests are important .

  23. CSF findings pressure leukocyte proteinmg/dl glucosemg/dl Normal 50-180mm <4 ,60-70%lymph 20-45 >50 or75% blood Bacterial1 00-60,000 100-500<40 Partial treatN1-10,000 100N Viral N 1000, lymph 20-100 generally N AbscessN 0-100 PMN 20-200N

  24. treatment • Decreasing CSF damage caused by the inflammation response with dexamethasone 0.6mg/kg/24hr for 2 days • Sterilization of CSF . • Supportive therapy : Maintenance of adequate CNS systemic perfusion. Treatment shock , DIC, SAIDH , seizures , ICP increased ,apnea ,arrhythmia ,coma .

  25. complication • Seizure ,increased ICP ,nerves palsies ,stroke ,cerebral or cerebellar herniation ,thrombosis venous sinuses, • Subdural effusion : in 10-30% that asymtomatic in 85-90%. In Symptomatic patient with increased ICP depressed consciousness aspiration must be done. Fever alone is not indication of aspiration.

  26. treatment • Empirical choice must cover S.pneumoniae . • Many of which are Relatively resistance to penicillin (mic0.1-1) is more common than high – level resistance . • Cefotaxime (200-300 mg/kg/24) or ceftrixone (100mg/kg/24) plus vancomycin (60 mg/kg/24). • Cefotaxime and ceftrixonealso cover N.meningitidis or H .influenza type b. • if L-monocytogenes is suspected ( infant<2 mo ) Ampicillin 200/kg/24hr plus ceftriaxone .

  27. Duration of treatment • S. Pneumoniae ( 10 -14 days) • N.Meningitidis ( 7days) • H.influenza (10 days) • Gram negative meningitis should be treated for 3 WK or 2 WK after CSF sterilization . • Patients with evidence of acute bacterial meningitis but no identifiable pathogen cetrixone for7-10 days.

  28. repeat CSF examination • Repeat LP indicated ; • in neonate • Gram negative meningitis • In β – lactam resistance S, pneumoniae . • CSF should be sterile within 24- 48 hr

  29. Prevention in meningococcal meningitidis • Chemoprophylaxis: for all close contacts of patients with meningococcal meningitis. with the rifampin10mg/kg every 12 hr for 2 days (600mg) • Close contacts : household,daycare ,direct exposure with oral secration ,

  30. Prevention ( H, influenza) • Rifampin should be given to all closefamily. 20 mg/kg /24hr once each day for 4 days.

  31. prognosis • Mortality rate H,influenza 8% , meningococcal 15%, for pneumococcal 25%. • 35% survivors have some sequelae; Deafness:is the most common neurologic sequelae. 30% withpneumococcal meningitis and 10%meningococ ,5-20% H.influ. seizures ,learning disability ,blindness ,paresis , ataxia , hydrocephallus ,mental retardation

  32. Poor prognosis • Young age .(< 6mo) • long duration of illness before antibiotic therapy. • late –onset seizure (>4days). • shock ,coma, focal neurologic sign • low or absent CSF WBC in the presence of visible bacteria on gram stain of CSF . • immuno compromised status.

  33. Thanks… But it’s not the end !!

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