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Classic stigmata of congenital syphilis SNHL, interstitial keratitis, Hutchinson teeth (notched incisors), mulberry molars, Clutton joints (bilateral painless knee effusions), nasal septal perforation & saddle deformity& frontal bossing. Acute bacterial meningitis is a fulminant, often fatal pyogenic infection beginning in the meninges. Meningococci exist in the nasopharynx of about 5% of people and spread by respiratory droplets and close contact.
Gram-negative organisms (most often Escherichia coli, Klebsiella sp, or Enterobacter sp) can cause meningitis in infants, in immunocompromised patients, or after CNS surgery, CNS trauma, bacteremia (eg, due to GU manipulation), or hospital-acquired infections. Staphylococci can cause meningitis after penetrating head wounds or neurosurgical procedures (often as part of a mixed infection) or after bacteremia (eg, due to endocarditis). Listeria typically cause meningitis in the very young, the very old, and patients of any age who are immunocompromised because of chronic renal failure, hepatic disorders, or corticosteroid or cytotoxic therapy after organ transplantation.
Bacteria typically reach the meninges by hematogenous spread from sites of colonization in the nasopharynx or other foci of infection (eg, pneumonia). Bacteria can also enter CSF by direct extension from nearby infections (eg, sinusitis, mastoiditis) or through exterior openings in normally closed CSF pathways (eg, due to meningomyelocele, spinal dermal sinus, penetrating injuries, or neurosurgical procedures).
Bacterial surface components, complement, and inflammatory cytokines (eg, tumor necrosis factor, IL-1) draw neutrophils into the CSF space. Occasionally, bilateral adrenal hemorrhagic infarction (Waterhouse-Friderichsen syndrome) results, particularly with meningococcal infection. A respiratory illness or sore throat often precedes the more characteristic symptoms of fever, headache, stiff neck, and vomiting. Elderly: The elderly may also have nonspecific symptoms (eg, confusion with or occasionally without fever).
Patients with partially treated meningitis: Patients seen early in the disease, before typical findings of meningitis appear, are sometimes diagnosed with otitis media or sinusitis and given oral antibiotics. Acute bacterial meningitis is suspected in children < 2 yr with lethargy, progressive irritability, a high-pitched cry, a bulging fontanelle, meningeal signs, or hypothermia. Because acute bacterial meningitis, especially meningococcal, can be lethal within hours, it must be treated as soon as the diagnosis is suspected. Imaging tests: CT, when done, may be normal or show small ventricles, effacement of the sulci, and contrast enhancement over the convexities. Other tests: Peripheral blood tests include blood cultures (positive in 50%), cell count with differential, electrolytes, glucose, renal function, coagulation tests, and PCR for bacterial pathogens (where available). Alternate diagnoses: Disorders that resemble bacterial meningitis can usually be differentiated by clinical presentation, neuroimaging, and routine CSF tests. Viral encephalitis, especially herpes encephalitis, also causes fever, headache, confusion, seizure and coma, which can be confused with bacterial meningitis. Subarachnoid hemorrhage causes severe headache and a stiff neck, but onset is explosive and fever is usually absent; CT shows hemorrhage, or the CSF contains RBCs or is xanthochromic. Brain abscess can cause fever, headache, and impaired consciousness, but the neck is typically supple unless abscess contents have ruptured into the CSF space, causing a fulminant secondary meningitis. Severe systemic infections (eg, sepsis, infective endocarditis) can impair cognition or consciousness by causing fever and compromising tissue perfusion; CSF is normal or contains a small number of WBCs, and the neck is supple. Cerebellar tonsillar herniation can cause impaired consciousness (secondary to obstructive hydrocephalus) and neck stiffness but usually not fever, and it can be differentiated by CT or MRI. Cerebral vasculitis (eg, due to SLE) and cerebral venous thrombosis can cause mild fever, headache, altered mental status, and mild to moderate meningeal inflammation, typically producing CSF test results similar to those of viral encephalitis. Fungal meningitis or amebic ( Naegleria ) meningoencephalitis occasionally causes acute, fulminant meningitis with clinical findings and routine CSF test results similar to those of bacterial meningitis. TB meningitis is usually subacute or chronic but is occasionally acute; CSF characteristics are usually intermediate between those of acute bacterial and aseptic meningitis. Waterhouse-Friderichsen syndrome: This disorder should be suspected in any febrile patient who remains in shock despite adequate volume replacement and who has rapidly evolving purpura and evidence of DIC. Immediate empirical treatment with corticosteroids, antibiotics, and supportive care have improved outcome and reduced mortality to < 10%. In immunocompromised patients, the benefits of Dexamethasone in reducing intracranial pressure must be weighed against the risk of worsening immunodeficiency.
Third-generation cephalosporins (eg, ceftriaxone, cefotaxime) are effective against pathogens common in patients of all ages., a 4th-generation cephalosporin, can be substituted for a 3rd-generation cephalosporin in children and can be useful for Pseudomonas infection. Because herpes encephalitis can resemble bacterial meningitis at presentation, acyclovir is usually included with the initial empirical therapy.
Reevaluation: As the results of blood, CSF, and other tests become available and the pathogen and drug susceptibility are identified, antibiotics are adjusted accordingly.
If no pathogen is identified in the CSF, addition of antibiotics for TB should be considered, especially if CSF glucose levels are very low.

Lumbar puncture should be repeated 24 to 48 h after starting antibiotics to confirm CSF sterility and conversion to lymphocytic predominance. Other measures: Supportive therapy includes treatment of fever, dehydration, electrolyte disorders, seizures, and shock. If Waterhouse-Friderichsen syndrome is suspected, high-dose hydrocortisone(eg, 100 to 200 mg IV q 4 to 6 h or as a continuous infusion after an initial bolus) is given; treatment should not be delayed pending measurement of hormone levels. If infants up to 1 yr of age have subdural effusion, daily subdural taps through the cranial sutures usually help. Patients with severe meningococcal meningitis may benefit from drotrecogin alfa activated protein C), which downregulates the inflammatory response. Physical measures: Spread of meningitis is prevented by keeping patients in respiratory isolation (droplet precautions) for the first 24 h of therapy. A conjugated pneumococcal vaccine effective against 7 serotypes, including > 80% of organisms that cause meningitis, is recommended for all children.
A quadrivalent meningococcal vaccine is given to children aged 2 to 10 yr with immunodeficiencies or functional asplenia, all children at age 11 to 12 yr (and older children, college students living in dormitories, and military recruits who have not had the vaccine previously), travelers to endemic areas, and laboratory personnel who routinely handle meningococcal specimens.
Chemoprophylaxis: Anyone who has face-to-face contact with the patient (eg, family, medical staff members) should receive postexposure chemoprophylaxis. Chemoprophylaxis is not usually needed for contacts of patients with pneumococcal meningitis. Skeletal findings osteochondritis& periostitis of long bones SNHL, interstitial keratitis, Hutchinson teeth (notched incisors), mulberry molars, Clutton joints (bilateral painless knee effusions), nasal septal perforation & saddle deformity& frontal bossing. Only a small fraction of carriers develop meningitis; what makes them susceptible is unknown. Especially at risk are alcoholics and people with chronic otitis, sinusitis, mastoiditis, CSF leaks, recurrent meningitis, pneumococcal pneumonia, sickle cell disease, or asplenia. Pseudomonas sp occasionally causes meningitis in immunocompromised or colonized patients. Why some bacteria are more prone to colonize CSF is not clear, but binding pili and encapsulation appear to play a role. In those < 2 mo, symptoms and signs are often nonspecific, particularly in early disease. Serum Na is monitored for evidence of SIADH, and coagulation results are monitored for evidence of DIC. MRI and CSF testing are helpful in distinguishing viral encephalitis from bacterial meningitis. With hemorrhagic necrosis of the adrenal glands, adrenocorticol insufficiency develops rapidly. However, if meningitis is treated late or occurs in neonates, the elderly, or immunocompromised patients, death is common. If the diagnosis is unclear and the patient does not appear ill, antibiotics may be withheld pending CSF test results. Dexamethasone may prevent hearing loss and other neurologic sequelae by inhibiting release of proinflammatory cytokines triggered by antibiotic-induced bacterial lysis. However, because cephalosporin-resistant pneumococci are becoming increasingly prevalent, vancomycin, with or without rifampin, is usually added.
When initial CSF tests are inconclusive, a repeat lumbar puncture in 8 to 24 h (or sooner if the patient deteriorates) may help. If brain herniation is suspected, hyperventilation (Paco2, 25 to 30 mm Hg acutely), mannitol, and additional dexamethasone(4 mg IV q 4 h) can be used; barbiturate-induced coma may be considered. In patients with sepsis due to meningitis, intracranial bleeding occurs more frequently, with or without drotrecogin alfa treatment. Haemophilus influenzae type b meningitis, now uncommon because of widespread vaccination, can occur in immunocompromised patients or after head trauma in unvaccinated people. Receptors for pili and other bacterial surface components in the choroid plexus facilitate penetration into CSF. Fever, hypothermia, poor feeding, lethargy, vomiting, and irritability are common presenting symptoms. Patients may appear less ill and have milder meningeal signs and slower disease progression.
Prompt lumbar puncture with or without prior CT is required, but these procedures should not delay immediate treatment with corticosteroids and antibiotics. Scans should be scrutinized for evidence of brain abscess, sinusitis, mastoiditis, skull fracture, and congenital malformations. Serum procalcitonin and C-reactive protein are elevated to a much greater degree with bacterial than with viral infections.

In such cases, CSF is checked for cryptococcal polysaccharide antigen, Histoplasma polysaccharide antigen, and Coccidioides immitis complement fixation antibodies; CSF is also examined using India ink and cultured for fungi.
A poor outcome is predicted by persistent leukopenia or development of Waterhouse-Friderichsen syndrome. Giving antibiotics before lumbar puncture slightly increases the probability of false-negative cultures, particularly with pneumococci, but does not affect other test results.
If clinical and CSF findings continue to suggest aseptic meningitis, antibiotics are withheld.
If effusion persists after 3 to 4 wk of taps, surgical exploration for possible excision of a subdural membrane is indicated. The result is vasculitis and thrombophlebitis (which cause focal ischemia or infarction) and brain edema. Seizures, a high-pitched cry, and bulging or tight fontanelles are possible but often occur late.
Arthritis may restrict neck motion, often in multiple directions, and should not be mistaken for meningismus. In amebic meningoencephalitis, ameboid movement can be detected in unspun wet mounts of CSF, and the amebas can be cultured. Survivors occasionally have deafness, other cranial nerve deficits, cerebral infarction, recurrent seizures, or intellectual disability. If the patient's condition is serious, especially if antibiotics have been given (possibly causing falsely sterile cultures), antibiotics should be continued.
If ventricles are enlarged, intracranial pressure may be monitored and CSF drained, but outcome is usually poor. During an epidemic, the population at risk must be identified (eg, college students, a small town) and its size determined before proceeding to mass vaccination. There is no consensus on whether children < 2 yr require prophylaxis for exposure at day care.
Treatment requires antibiotics, often beginning empirically with a 3rd- or 4th-generation cephalosporin, vancomycin, and ampicillin; corticosteroids are usually given. It also tends to occur in epidemics among closed populations (eg, in military barracks, college dormitories, and boarding schools).
Cranial nerve abnormalities (eg, 3rd [oculomotor] or 7th [facial] cranial nerve palsy; occasionally, deafness) and other focal deficits occur in 10 to 20%.
Examination of the head, ears, spine, and skin may reveal a source or route of infection.
Subdural effusions may develop after several days; typical signs are seizures, persistent fever, and enlarging head size. Aminoglycosides penetrate the CNS poorly but are still used empirically to cover gram-negative bacteria in neonates (see Infections in Neonates: Treatment). The effort is expensive and requires public education and support, but it saves lives and reduces morbidity.
The purulent exudate in the CSF blocks CSF reabsorption by the arachnoid villi, causing hydrocephalus. In patients > 2 yr, changes in consciousness progress through irritability, confusion, drowsiness, stupor, and coma. Spinal dimples, nevi, or tufts of hair suggest a spinal dermal sinus that communicates with the meninges and provides a portal for bacteria entry.
Cultures are positive in 90%; they may be falsely negative in patients who are partially treated.
When meningitis due to a gram-negative anaerobe is a consideration (eg, because of otitis, sinusitis or mastoiditis), meropenem should be added. For meningitis patients with a recent neurosurgical procedure or with an intraventricular shunt, vancomycin, meropenem, plus metronidazoleprovide coverage against staphylococci, gram-negative bacteria, and anaerobes. However, these tests are not always routinely done because they probably add little to other routine CSF tests.
This test and the latex agglutination tests may be helpful when patients have received prior antibiotics (partial treatment), when patients are immunocompromised, or when other CSF tests do not identify the causative organism. Broad range bacterial PCR for 16S ribosomal DNA testing can be useful if CSF cultures detect no organisms.

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