AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

INTRODUCTION

Section 2 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

Background

Meningitis due to Staphylococcus aureus accounts for 1-9% of cases of bacterial meningitis and is associated with mortality rates of 14-77%. It usually is associated with neurosurgical interventions (such as cerebrospinal fluid [CSF] shunts), trauma, or underlying conditions such as malignancy, decubitus ulcers, cellulitis, infected intravascular grafts, chronic alcoholism, diabetes mellitus, osteomyelitis, or perirectal abscess. It is uncommon in immunocompetent individuals in the absence of focal infection (eg, pneumonia, osteomyelitis, endocarditis, parameningeal infection, psoas or epidural abscess, sinusitis, tropical pyomyositis), neurosurgical interventions, or congenital dermal sinus. When staphylococcal endocarditis is the source, blood cultures and peripheral and echocardiographic manifestations will point to that etiology.

Pathophysiology

Neonates are colonized by S aureus soon after birth; major niches include umbilical stump, perineal area, skin, and gastrointestinal tract. Later in life, major niches include anterior nares, and about 25% of children and adults become carriers. Health professionals; individuals with diabetes receiving insulin injections, hemodialysis, or peritoneal dialysis; patients with dermatologic conditions or HIV infection; intravenous (IV) drug users; and trauma patients have higher carriage rates. Carriers experience more postsurgical infections than noncarriers.

The next step after colonization is penetration through the epithelial or mucosal surface. The mechanisms underlying penetration are not completely understood, but trauma, surgery, immunosuppression, and other infections are predisposing conditions. After penetration and complement activation, S aureus is coated by C3b, immunoglobulin G (IgG), or both (opsonization). Staphylococci are then ingested and killed by polymorphonuclear cells and monocytes. Failure of these defense mechanisms can lead to recurrent or chronic infection. Inherited or acquired defects of chemotaxis, opsonization, or polymorphonuclear leukocyte function (eg, due to severe bacterial infections, rheumatoid arthritis, decompensated diabetes mellitus) predispose patients to continuation of the infection process.

Foreign body infection leads to an acquired phagocytic defect. After hours or days of contact with the foreign body, S aureus produces a polysaccharide/adhesin substance that causes it to adhere to the foreign body and protects it from the environment. The resident phagocytic population close to the foreign body is not able to kill the invading strain. Anchoring of S aureus to foreign substances also modifies its susceptibility to antimicrobial agents. These factors explain the inability of antibiotics alone to eradicate foreign body infection.

S aureus meningitis has 2 different pathogenic mechanisms, as follows:

In the first form, bacteria are introduced during surgery or by trauma or local spreading (especially coagulase-negative staphylococci) from contiguous infection. Bacteria introduced during surgery cause foreign body infection and subsequent postoperative meningitis. Attachment of S aureus to foreign surfaces involves interaction with proteins of the extracellular matrix: fibrinogen, fibronectin, laminin, thrombospondin, vitronectin, elastin, bone sialoprotein, and collagen. S aureus ligands for these host proteins have been characterized, cloned, and sequenced. Patients with this type of infection have a lower mortality rate than those with hematogenous meningitis, which may be explained by early recognition and less systemic involvement.

In the second group, hematogenous or spontaneous meningitis, S aureus is disseminated systemically. Infection is more often community acquired, and the incidence of positive blood culture results is higher, as is mortality rate. S aureus attachment to endothelial cells during septicemia is complex and involves interaction with fibronectin, fibrinogen, and laminin. After adhesion, phagocytosis by endothelial cells and induction of tissue factor procoagulant activity occur. Any localized S aureus infection can lead to bacteremia. In the pre-antibiotic era, mortality rate was 82%. Recent studies reported mortality rates between 30% and 40% in non–drug-using patients with S aureus septicemia.

Patients with S aureus bacteremia can be divided into 2 groups. The first comprises elderly patients with a recognizable primary site of infection and underlying disorders, who usually are already hospitalized when infection starts. Endocarditis and secondary disease foci affect only 10% of such patients, and the relapse rate is lower than in the second group. The second group comprises young patients without identifiable primary infection; they usually have community-acquired bacteremia due to drug use and a high incidence of endocarditis and metastatic foci. The mechanisms responsible for spreading to the meninges are not fully understood. Sustained bacteremia is important but not the sole mechanism responsible for CNS invasion.

The site of CNS invasion during septicemia is still not clear. It may involve the dural venous system or choroid plexus, where receptors for pathogens have been found. Transcytosis through microvascular endothelial cells is another possible mechanism of meningeal invasion during meningitis. Once bacteria are in the subarachnoid space, host mechanisms are inadequate to control the infection. Meningeal inflammation increases CSF complement concentrations. However, complement concentration is still insufficient and, despite the increased number of leukocytes, opsonic and bactericidal activity are suboptimal, leading to multiplication of bacteria in the CSF.

Once bacteria enter and replicate within the CSF, inflammation of the subarachnoid space ensues because of bacterial (eg, cell wall components) and host factors (eg, prostaglandins, tumor necrosis factor alpha). Alteration of blood-brain barrier permeability leads to cerebral edema and increased intracranial pressure. Meningitis also modifies blood flow throughout the subarachnoid space, resulting in vasculitis and ischemia. Oxygen radicals may contribute to the increased water content, increased intracranial pressure, and changes in blood flow seen in meningitis.

Frequency

United States

In the United States, S aureus meningitis accounts for 1-3% of cases of meningitis and is associated with a high mortality rate (about 50% in adults); however, the prognosis for CSF shunt infections is more favorable.

International

Worldwide, S aureus meningitis constitutes 0.3-8.8% of all cases of bacterial meningitis. Hospitals with active neurosurgical services generate more cases of staphylococcal meningitis (eg, infection of CSF shunts). S aureus is the second most common cause of CSF shunt infections, outnumbered only by Staphylococcus epidermidis.

In one study, 38 of 154 (25%) cases of bacterial meningitis during a 7-year period were nonpneumococcal gram-positive coccal infections. The majority of cases were due to S aureus and S epidermidis. In another study, S aureus was present in 21 of 720 (3%) cases of meningitis. Thirteen of the 21 cases were patients in the postoperative period after a neurosurgical procedure, and 3 of the remaining 8 patients had endocarditis or a parameningeal focus of infection.

Mortality/Morbidity

Staphylococcal meningitis is associated with a high mortality rate (about 50% in adults), particularly hematogenous S aureus meningitis (mortality rate, 18-56%). The prognosis for CSF shunt infections is more favorable, probably because of earlier recognition.

Race

Data not available

Sex

Data not available

Age

Newborn nurseries seem to experience waves of staphylococcal epidemics that occur in cycles (ie, epidemics occurred in the 1900s, late 1920s, early 1950s, early 1970s, late 1980s, and early 1990s). S aureus was the most common staphylococcal pathogen in the nursery from the 1950s to the 1970s.

CLINICAL

Section 3 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

History

With a high index of suspicion, making the diagnosis of bacterial meningitis, in general, is not difficult. All febrile patients with lethargy, headache, or confusion of sudden onset, even if fever is only low grade or the patient is a confused alcoholic, should undergo an urgent lumbar puncture, since a definitive diagnosis of meningitis can be made only by examination of CSF. In patients who have not undergone a neurosurgical procedure, presentation of S aureus meningitis may be similar to that of other types of bacterial meningitis. Patients with septicemia have additional systemic signs and symptoms, including septic shock.

• Shunt infections can be insidious, although a fulminant postoperative course can be seen with S aureus infection. Coagulase-negative staphylococci (CoNS) are normal inhabitants of the human skin and mucous membranes. Patients most at risk for CoNS infection frequently have a disruption in their host defense mechanisms due to surgery, foreign body placement, or immunosuppression. Because CoNS are common contaminants of cultures, the diagnostic definition of adult CoNS meningitis is different from the meningitis caused by other common pathogens and, hence, is defined with a more strict criteria.
  • Common presentations include low-grade fever in 14-92% of cases, malaise, poor feeding, and irritability. Signs of meningeal irritation are not usually present, since no functional communication exists between the infected ventricles and CSF spaces in most of the cases.
  • Redness of the skin overlying the shunt, if it occurs, is a highly specific sign. Infections with symptoms referable to the distal portion of the shunt are more specific: shunts that end in a vessel lead to bacteremia, while shunts that end in the pleural or peritoneal space cause peritonitis or pleuritis.
  • In immunosuppressed patients, the classical meningeal signs may be absent.
• In IV drug users, S aureus from bacterial vegetations on cardiac valves is most commonly the starting point for systemic involvement and meningitis.
• In one clinical series, CoNS were reported to be 52.8% of pathogens of ventriculoperitoneal shunt infections in pediatric patients younger than 8 years. Data on adult CoNS meningitis were not given as these had not been specifically examined in the literature.

Physical

• Classic signs include the following:
• • Neck stiffness
  • Altered consciousness (drowsiness, confusion, stupor, coma)
  • Generalized or focal seizures
  • Brudzinski sign (flexion at the hip and knee in response to forced flexion of the neck)
  • Kernig sign (inability to completely extend the legs)
• In S aureus septicemia, look for signs of systemic embolization/seeding, which include Roth spots, Janeway lesions, petechiae, subconjunctival hemorrhages, and cardiac murmurs.

Causes

• Hospitals with active neurosurgical services generate more cases of staphylococcal meningitis (eg, infection of CSF shunts) than other clinical facilities.
• In one study, 38 of 154 (25%) cases of bacterial meningitis during a 7-year period were nonpneumococcal gram-positive coccal infections; the majority of cases were due to S aureus and S epidermidis.

DIFFERENTIALS

Section 4 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

Other Problems to be Considered

Behçet disease
Chemical meningitis (eg, after spinal anesthesia, myelography)
Epstein-Barr virus infections
Fungal meningoencephalitis
Legionnaire disease
Leptospiral meningoencephalitis
Listeria monocytogenes meningoencephalitis
Necrotizing cerebral angiitis
Neoplastic angioendotheliosis
Mycoplasmal pneumonia
Rickettsial encephalitides

WORKUP

Section 5 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

Lab Studies

• CBC with differential demonstrates polymorphonuclear leukocytosis with left shift.
• CSF analysis is the diagnostic test of choice for suspected meningitis.
• • CSF lactate dehydrogenase (LDH) appears to be diagnostic and has a prognostic value in bacterial meningitis. Increase in total LDH is observed consistently in bacterial meningitis, mostly due to increases in fractions 4 and 5, which are derived from granulocytes. LDH fractions 1 and 2, derived presumably from brain tissue, are elevated only slightly in bacterial meningitis but rise sharply in patients who develop neurologic sequelae.
  • Leukocyte count in the CSF ranges from 250-100,000/µL. Counts above 50,000 raise the possibility of a brain abscess having ruptured into a ventricle. Neutrophils predominate early in infection, but mononuclear cells (lymphocytes, plasma cells, histiocytes) steadily increase as the infection continues.
  • Protein content is higher than 45 mg/dL in greater than 90% of cases. In most cases, the protein ranges from 100 to 500 mg/dL.
  • Glucose content is usually diminished to below 40 mg/dL or to less than 40% of blood glucose level.
  • Gram stain of CSF sediment permits identification of the causative agent in most cases.
• Other laboratory methods for identification of causative organisms include counterimmunoelectrophoresis (CIE), radioimmunoassay (RIA), latex particle agglutination (LPA), enzyme-linked immunosorbent assay (ELISA), and—most sensitive of all—gene amplification by polymerase chain reaction (PCR).
• Blood cultures should always be obtained. They are positive in 40-60% of patients with Haemophilus influenzae, meningococcal, or pneumococcal meningitis, but data are scarce for staphylococcal meningitis. Blood cultures may provide the only definite clue as to the causative agent if CSF cultures are negative and if more sophisticated diagnostic identification procedures are not readily available.
• Because of earlier antibiotic intervention in patients presenting with signs suggestive of bacterial meningitis, a noted rise occurs in culture-negative CSF and blood cultures in some laboratories. This makes the use of a non–culture-based system to detect and identify the causal agents increasingly important. It is here that the 16S rRNA PCR becomes a valuable molecular tool to aid in the detection on nonculturable etiologic agents of meningitis. With the advent of polyacrylamide gel electrophoresis (PAGE) to separate mixed 16S rRNA amplicons prior to sequencing without the need of cloning, the PCR technique is increasingly being used to augment staphylococci identification.
• 16S rRNA genes exist in all bacteria and accumulate mutations at a slow constant rate over time; therefore, they may be used as "molecular clocks." Highly variable portions of the 16S rRNA sequence provide unique signatures to any bacterium and useful information about relationships between them. These properties provide important aids in microbiologic diagnostics, especially in equivocal cases.
• Complement levels and immunoglobulin levels should be part of the evaluation of every patient with bacterial meningitis.
• Antibody levels should be monitored and pneumococcal and meningococcal vaccines should be given to those with recurrent bacterial meningitis because this is common in those with previous head trauma, skull fracture, or dural CSF leak, as well as those with deficiencies of any of the complement components or hypogammaglobulinemia.

Imaging Studies

• Chest x-rays are important because they may show an abscess or pneumonitis, an important consideration for infants and immunocompromised patients.
• Sinus and skull x-rays may show the presence of cranial osteomyelitis, paranasal sinusitis, or mastoiditis.
• CT scans of the head are usually normal but may reveal nonspecific cerebral edema or show previous neurosurgical interventions. CT scans reveal eroding skull lesions and routes for bacterial invasion (eg, mastoiditis, sinusitis, tumors, sinus wall defects, brain abscess, subdural empyema). In patients with immunosuppression or with focal findings, papilledema, or other signs of increased intracranial pressure, a CT scan of the head must be done before the spinal tap to detect mass lesions that could result in herniation. Those with space-occupying lesions do not undergo lumbar puncture because the withdrawal of CSF removes counterpressure from below, thus increasing the effect of compression from above and exacerbating the brain shift already present. CT scan should be preceded by blood cultures and the initiation of antibiotic therapy.
• MRI with contrast enhancement may demonstrate cortical reactions, including infarctions, hydrocephalus, and meningeal exudates. The role of MRI with contrast T1 and T2 sequences is not well established.
• Transthoracic and transesophageal echocardiograms are helpful for the evaluation of endocarditis. Negative tests do not rule out endocarditis, since neither technique is sensitive enough to detect small vegetations, which may require more than 10 days to develop.

Other Tests

• Lumbar puncture: CSF pressure is elevated consistently (>180 mm H₂O), but pressures greater than 400 mm H₂O suggest the potential for herniation.

Histologic Findings

Pia-arachnoiditis with edema and microinfarcts is observed. Polymorphonuclear leukocytes fill the subarachnoid space in severely affected areas and are found predominantly around the leptomeningeal blood vessels in less severe cases. In fulminant meningitis, the inflammatory cells infiltrate the walls of the leptomeningeal veins and produce a venulitis that can lead to venous occlusion and subsequent hemorrhagic infarction of the underlying brain.

TREATMENT

Section 6 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

Medical Care

Bacterial meningitis is a medical emergency. Once purulent meningitis is confirmed by CSF analysis, initial measures include administration of antibiotics with effective CNS penetration and maintenance of adequate blood pressure. Initial antibiotic selection should be based on Gram stain or rapid bacterial antigen tests. If the spinal tap is delayed or the organism cannot be identified rapidly, empiric selection of an antibiotic with effective CNS penetration should be based on age and underlying disease status, since delay in treatment is associated with adverse clinical outcome.

• Standard empirical therapy varies according to age, as follows:
• • In infants younger than 4 weeks, it consists in ampicillin plus cefotaxime or an aminoglycoside.
  • Infants aged 4-12 weeks should be treated with ampicillin plus a third-generation cephalosporin.
  • In children aged 12 weeks to 18 years, a third-generation cephalosporin or ampicillin plus chloramphenicol is an appropriate combination.
  • Adults aged 18-50 years and individuals with basilar skull fracture should be treated with a third-generation cephalosporin, while individuals older than 50 should be treated with ampicillin plus a third-generation cephalosporin.
• Immunocompromised patients should receive the combination of vancomycin, ampicillin, and ceftazidime.
• Patients who have experienced head trauma, have a CSF shunt, or have undergone a neurosurgical procedure should be treated with vancomycin and ceftazidime.
• Vancomycin should be added to empirical regimens when highly penicillin- or cephalosporin-resistant strains of Streptococcus pneumoniae are suspected.
• Ampicillin should be added to empirical treatment at any age if Listeria monocytogenes is a consideration.
• If allergy to penicillins and cephalosporins preclude their use, chloramphenicol is a reasonable alternative.
• Dose calculations are based on a patient's age and renal and hepatic functions.
• Once S aureus meningitis is confirmed and sensitivity determined, therapy may be altered or simplified by using vancomycin, oxacillin, or nafcillin alone. For methicillin-sensitive S aureus, nafcillin or oxacillin is standard therapy. If the infective organism is methicillin-resistant S aureus (MRSA) or S epidermidis, vancomycin is the drug of choice.
• Most experts recommend addition of rifampin if the patient shows no clinical improvement 72 hours after initial treatment of S aureus meningitis.
• Most cases of bacterial meningitis are treated for a period of 10-14 days, except when a parameningeal focus of infection persists (as in most cases of staphylococcal meningitis). In such cases, treatment should be continued for a longer period. Effects of therapy should be tagged to clinical improvement.
• Use of steroids in S aureus meningitis is controversial. While adjunctive dexamethasone is beneficial for H influenzae type B and pneumococcal meningitis, and some authors favor its use in all types of bacterial meningitis, at present the routine use of dexamethasone is not recommended.
• Shunt removal is often necessary to optimize therapy. If infection is suspected, CSF should be removed from the shunt and sent for studies. Treatment should be started if initial results point to meningeal inflammation and should be modified according to culture results. If infections are difficult to eradicate or if the shunt cannot be removed, direct instillation of the antimicrobial agent is warranted. Daily intraventricular vancomycin doses range from 4-10 mg. Gentamicin doses are 1-2 mg/day for children and 4-8 mg/day for adults. Combination with an IV agent is always required. Intraventricular teicoplanin also has been employed successfully. Since the entire shunt has a propensity to be contaminated once one section is infected, partial shunt revision is not recommended.

Surgical Care

In cases of S aureus meningitis due to septicemia, once the source of infection is identified, surgical debridement or excision may be indicated.

Consultations

Obstructive or normal pressure hydrocephalus may complicate the clinical picture, leading to further obtundation. When either of these is present, neurosurgical consultation for shunting should be considered.

Activity

Bed rest and general supportive measures are needed until the acute illness phase has passed; thereafter, physical activity may be increased gradually as tolerated.

MEDICATION

Section 7 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

The goals of pharmacotherapy are to eradicate the infection, reduce morbidity, and prevent complications.

Drug Category: Antibiotics

The agents named are effective in treatment of susceptible bacterial infections such as meningitis due to penicillinase-producing strains of S aureus.

FOLLOW-UP

Section 8 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

Further Outpatient Care

• Monitoring recovery in all aspects is important, including cognitive sequelae, normal pressure hydrocephalus, and seizures.

Complications

• Seizures are more frequent after H influenzae meningitis than after S aureus meningitis.
• In fulminant meningitis, incidence of strokes is increased because of venulitis, which leads to microinfarcts.

Prognosis

• Untreated bacterial meningitis is usually fatal. A disproportionate number of deaths occur in infants and elderly persons; mortality rate is highest in neonates.
• The presence of bacteremia, coma, seizures, or various underlying diseases (eg, alcoholism, diabetes mellitus, multiple myeloma, head trauma) significantly worsens the prognosis; therefore, an aggressive approach should be used in these settings.
• The likelihood of complete recovery, disability, and employability depends on the underlying condition and the severity of the meningitis.

Patient Education

• For excellent patient education resources, visit eMedicine's Brain and Nervous System Center and Procedures Center. Also, see eMedicine's patient education articles Meningitis in Adults, Meningitis in Children, and Spinal Tap.

MISCELLANEOUS

Section 9 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

Medical/Legal Pitfalls

• Low-grade fever, malaise, poor feeding, and irritability in patients with CSF shunts should raise suspicion of meningitis, even when high fever, stiff neck, severe headache, and nausea/vomiting are absent. Failure to consider meningitis may constitute negligence.
• If the patient does not respond to antistaphylococcal antibiotics, appropriate antibiotic coverage must be sought, for instance, by the addition of rifampin.

ACKNOWLEDGMENTS

Section 10 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

The authors and editors of eMedicine gratefully acknowledge the contributions of previous author Timothy Brannan, MD to the development and writing of this article.

REFERENCES

Section 11 of 11

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• References

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• Schwartz JF, Balentine JD. Recurrent meningitis due to an intracranial epidermoid. Neurology. Feb 1978;28(2):124-9. [Medline].
• Shinefeld HR. Staphylococcal infections. In: Remington & Klein's Infectious Diseases of the Fetus and Newborn Infant. 4th ed. 1995:1105-1141.
• Spotkov J, Garber SZ, Ruskin J. Staphylococcal meningitis: a complication of psoas abscess. Neurology. Jan 1985;35(1):110-1. [Medline].
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• Weinstein MP, LaForce FM, Mangi RJ, Quintiliani R. Non-pneumococcal Gram-positive coccal meningitis related to neurosurgery. J Neurosurg. Aug 1977;47(2):236-40. [Medline].
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Article Last Updated: Mar 27, 2007