Acute Bacterial Meningitis

Acute bacterial meningitis is rapidly progressive bacterial infection of the meninges and subarachnoid space. Findings typically include headache, fever, and nuchal rigidity. Diagnosis is by CSF analysis. Treatment is with antibiotics and corticosteroids given as soon as possible. For neonatal meningitis, see Infections in Neonates: Neonatal Bacterial Meningitis

Pathophysiology
Most commonly, bacteria reach the subarachnoid space and meninges via hematogenous spread. Bacteria may also reach the meninges from nearby infected structures (eg, sinuses, the middle ear) or through a congenital or acquired defect in the skull or spine (eg, a penetrating head wound, a neural tube defect, an opening made during neurosurgery). Because WBCs, immunoglobulins, and complement are normally sparse or absent from CSF, bacteria initially multiply without causing inflammation. Later, bacteria release endotoxins, teichoic acid, and other substances that trigger an inflammatory response with mediators such as WBCs and TNF. Typically in CSF, levels of protein increase, and because bacteria consume glucose and because less glucose is transported into the CSF, glucose levels decrease. Inflammation in the subarachnoid space is accompanied by cortical encephalitis and ventriculitis. Complications are common and may include

Hydrocephalus (in some patients) Arterial or venous infarcts due to inflammation and thrombosis of arteries and veins in superficial and sometimes deep areas of brain Abducens palsy due to inflammation of the 6th cranial nerve Deafness due to inflammation of the 8th cranial nerve or structures in the middle ear Subdural empyema Increased intracranial pressure (ICP) due to cerebral edema Brain herniation (the most common cause of death during the acute stages) Systemic complications (which are sometimes fatal), such as septic shock, disseminated intravascular coagulation (DIC), or hyponatremia due to syndrome of inappropriate antidiuretic hormone secretion (SIADH)
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Etiology
Likely causes depend on

Patient age Route of entry Immune status of the patient

Age: In children and young adults, the most common causes are

Neisseria meningitidis Streptococcus pneumoniae

N. meningitidis meningitis occasionally causes death within hours. Sepsis caused by N. meningitidissometimes results in bilateral adrenal hemorrhagic infarction (Waterhouse-Friderichsen syndrome). Haemophilus influenzae type B, previously the most common cause of meningitis in children < 6 yr and overall, is now a rare cause in the US and Western Europe, where the H. influenzae vaccine is widely used. However, in areas where it is not widely used, H. influenzae is a common cause, particularly in children aged 2 mo to 6 yr. In middle-aged adults and in the elderly, the most common cause of meningitis is

S. pneumoniae

Less commonly, N. meningitidis causes meningitis in middle-aged and older adults. As host defenses decline with age, patients may develop meningitis due to L. monocytogenes or gram-negative bacteria.

Table 2

Causes of Bacterial Meningitis by Patient Age

Age Group
Children and young adults

Bacteria
Neisseria meningitidis Streptococcus pneumoniae S. aureus* Haemophilus influenzae (rare in developed countries but still seen in countries where the H. influenzae type B vaccine is not widely used)

Middle-aged adults

S. pneumoniae S. aureus* N. meningitidis (less common in this age group)

The elderly

S. pneumoniae S. aureus* Listeria monocytogenes Gram-negative bacteria

*S. aureus occasionally causes severe meningitis in patients of all ages, It is the most common cause of meningitis that develops after a penetrating head wound.

Route: Routes of entry include the following:

By hematogenous spread (the most common route) From infected structures in or around the head (eg, sinuses, middle ear, mastoid process), sometimes associated with a CSF leak Through a penetrating wound After a neurosurgical procedure (eg, if a ventricular shunt becomes infected) Through congenital or acquired defects in the skull or spine

Having any of the above conditions increases the risk of acquiring meningitis.

Table 3

Causes of Bacterial Meningitis by Route

Route Infection in or around the head (eg, sinusitis, otitis, mastoiditis), sometimes with a CSF leak Bacteria Streptococcus pneumoniae Haemophilus influenzae Anaerobic and microaerophilic streptococci Bacteroides sp Staphylococcus aureus Penetrating head wound Damaged skin (eg, skin infections, abscesses, pressure ulcers, large S. aureus S. aureus

burns) An infected shunt A neurosurgical procedure S. epidermidis Gram-negative bacteria (eg, Klebsiella pneumoniae,Acinetobacter calcoaceticus, Escherichia coli)

Immune status: Overall, the most common causes in immunocompromised patients are

S. pneumoniae L. monocytogenes Pseudomonas aeruginosa Mycobacterium tuberculosis N. meningitidis Gram-negative bacteria

But the most likely bacteria depend on the type of immune deficiency:

Defects in cell-mediated immunity (eg, in AIDS, Hodgkin lymphoma, or drug-induced immunosuppression):L. monocytogenes or mycobacteria Defects in humoral immunity or splenectomy: S. pneumoniae or, less frequently, N. meningitidis (both can cause fulminant meningitis) Neutropenia: P. aeruginosa or gram-negative enteric bacteria

In very young infants (particularly premature infants) and the elderly, T-cell immunity may be weak; thus, these age groups are at risk of meningitis due to L monocytogenes.

Symptoms and Signs

In most cases, bacterial meningitis begins with 3 to 5 days of insidiously progressive nonspecific symptoms including malaise, fever, irritability, and vomiting. However, meningitis may be more rapid in onset and can be fulminant, making bacterial meningitis one of the few disorders in which a previously healthy young person may go to sleep with mild symptoms and never awaken. Typical meningeal symptoms and signs include fever, tachycardia, headache, photophobia, changes in mental status (eg, lethargy, obtundation), nuchal rigidity (although not all patients report it), and sometimes, when Staphylococcus aureus is the cause, back pain. Seizures occur early in up to 40% of children with acute bacterial meningitis and may occur in adults. Up to 12% of patients present in coma. Severe meningitis may cause papilledema, but papilledema may be absent early, even when ICP is increased. Accompanying systemic infection by the organism may cause rashes, petechiae, or purpura (which suggest meningococcemia); pulmonary consolidation (often in meningitis due to S. pneumoniae); or heart murmurs (which suggest endocarditiseg, often caused by S. aureus or S. pneumoniae). Atypical presentations in adults : Fever and nuchal rigidity may be absent or mild in immunocompromised or elderly patients and in alcoholics. Often, in the elderly, the only sign is confusion in those who were previously alert or altered responsiveness in those who have dementia. In such patients, starting appropriate antibiotics before head CT or MRI may be prudent. If bacterial meningitis develops after a neurosurgical procedure, symptoms often take days to develop.

Diagnosis

CSF analysis As soon as acute bacterial meningitis is suspected, blood cultures and lumbar puncture for CSF analysis (unless contraindicated) are done. If the patient is very ill, antibiotics are given immediately. The need for confirmation should not delay treatment.

Clinicians should suspect bacterial meningitis in patients with typical symptoms and signs, usually fever, changes in mental status, and nuchal rigidity. However, clinicians must be aware that symptoms and signs are different in neonates and infants and may be absent or initially mild in the elderly, alcoholics, and immunocompromised patients. Diagnosis can be challenging in patients who have had a neurosurgical procedure (because such procedures can also cause changes in mental status and neck stiffness) and in the elderly and alcoholics (because changes in mental status may be due to falls and subdural hematomas). Focal seizures or focal neurologic deficits may indicate a focal lesion such as a brain abscess. Because untreated bacterial meningitis is lethal, tests should be done if there is even a small chance of meningitis. Testing is particularly helpful in infants, the elderly, alcoholics, immunocompromised patients, and patients who had neurosurgical procedure because symptoms may be atypical.

Sidebar 1

Pearls & Pitfalls

Do a lumbar puncture even if findings are not specific for meningitis, particularly in infants, the elderly, alcoholics, immunocompromised patients, and patients who have had neurosurgery.

If findings suggest acute bacterial meningitis, routine tests include

CSF analysis CBC and differential Metabolic panel Blood cultures plus PCR (if available)

Lumbar puncture: Unless contraindicated, lumbar puncture is done immediately to obtain CSF for analysis, the mainstay of diagnosis. Contraindications to immediate lumbar puncture are signs suggesting markedly increased ICP or a mass; typically, these signs include focal deficits, papilledema, deterioration in consciousness, and seizures. In such cases, lumbar puncture may cause brain herniation and thus is deferred until neuroimaging (typically contrast-enhanced CT or MRI) is done to check for increased ICP or a mass. When lumbar puncture is deferred, treatment is best begun immediately (after blood sampling for culture and before neuroimaging). After ICP, if increased, has been lowered or if no mass is detected, lumbar puncture can be done. CSF should be sent for analysis: cell count, protein, glucose, Gram staining, culture, PCR (if available), and other tests as indicated clinically. Simultaneously, a blood sample should be drawn and sent to have the CSF:blood glucose ratio determined. CSF cell count should be determined as soon as possible because WBCs may adhere to the walls of the collecting tube, resulting in a falsely low cell count; in extremely purulent CSF, WBCs may lyse. Typical CSF findings in bacterial meningitis include increased pressure, fluid that is often turbid, a high WBC count (consisting predominantly of PMNs), elevated protein, and a low CSF:blood glucose ratio. A C SF glucose level of 18 mg/dL or a CSF:blood glucose ratio of < 0.23 strongly suggests bacterial meningitis. However, changes in CSF glucose may lag 30 to 120 min behind changes in blood glucose. In acute bacterial meningitis, an elevated protein level (usually 100 to 500 mg/dL) indicates blood-brain barrier injury. CSF cell count and protein and glucose levels in patients with acute bacterial meningitis are not always typical. Atypical CSF findings may include

Normal in early stages except for the presence of bacteria Predominance of lymphocytes in about 14% of patients, particularly in neonates with gram-negative meningitis, patients with meningitis due to L. monocytogenes, and some patients with partially treated bacterial meningitis Normal glucose in about 9% of patients Normal WBC counts in severely immunosuppressed patients

Table 4

CSF Findings in Meningitis

Condition
Normal CSF

Predominant Cell Type*

All lymphocytes (05 cells/L) Leukocytes (usually PMNs), often greatly increased

Protein* Glucose* Specific Tests

< 40 mg/dL > 50 % of blood glucose < 50% of blood glucose (may be extremely low) Usually normal None

Bacterial meningitis

Elevated

Gram staining (yield is 5 high if 10 colony-forming units of bacteria/ mL are present) Bacterial culture PCR if available PCR (to check for enteroviruses or herpes simplex, herpes zoster, or West Nile virus) IgM (to check for West Nile virus or other arboviruses)

Viral meningitis

Lymphocytes (may be mixed; PMNs and lymphocytes during the first 2448 h) PMNs and lymphocytes (usually pleocytosis)

Elevated

Tuberculous meningitis

Elevated

< 50% of blood glucose (may be extremely low)

Acid-fast staining PCR Mycobacterial culture (ideally using a CSF sample of 30 mL) Interferon- tests of serum and (if available) CSF

Fungal meningitis

Usually lymphocytes

Elevated

< 50% of blood glucose (may be extremely low)

Cryptococcal antigen test Serologic tests forCoccidioides immitis orHistoplasmasp antigen, especially if patients have recently spent time in an endemic area Fungal culture (ideally using a CSF sample of 30 mL) India ink (forCryptococcussp)

*Changes in cell count, glucose, and protein may be minimal in severely immunocompromised patients.

In tuberculous meningitis, CSF acid-fast staining can be insensitive, sensitivity of PCR is only about 50%, and culture requires up to 8 wk. Positive CSF interferon- tests indicate tuberculous meningitis, but serum interferon- tests may only indicate prior infection. Thus, confirming a diagnosis of tuberculous meningitis is difficult, and if it is strongly suspected, even if not confirmed, it is treated presumptively.

A small number of cells may be present normally in neonates or after a seizure.

PCR = polymerase chain reaction; PMNs = polymorphonuclear neutrophils.

Identification of the causative bacteria involves Gram staining, culture, and, when available, PCR. Gram staining provides information rapidly, but the information is limited. For bacteria to be reliably detected with Gram stain, about 105 bacteria/mm3 must be present. Results may be falsely negative if CSF is handled carelessly, if bacteria are not adequately resuspended after CSF has been allowed to settle, or if errors in decolorization or reading of the slide occur. Diagnosis of the specific bacteria and determination of antibiotic sensitivity requires bacterial culture. If clinicians suspect an anaerobic infection or other unusual bacteria, they should tell the laboratory before samples are plated for cultures. Prior antibiotic therapy can reduce the yield from Gram staining and culture. PCR, if available, may be a useful adjunctive test, especially in patients who have already received antibiotics. Until the cause of meningitis is confirmed, other tests using samples of cerebrospinal fluid or blood may be done to check for other causes of meningitis, such as viruses (particularly herpes simplex), fungi, and cancer cells. Samples from other sites suspected of being infected (eg, urinary or respiratory tract) are also cultured .

Prognosis
For children < 19 yr, the mortality rate may be as low as 3% but is often higher; survivors may be deaf and neuropsychologically impaired. The mortality rate is about 17% for adults < 60 yr but up to 37% in those > 60. Community-acquired meningitis due to S. aureus has a mortality rate of 43%. In general, mortality rate correlates with depth of obtundation or coma. Factors associated with a poor prognosis include

Age > 60 yr Coexisting debilitating disorders A low Glasgow coma score at admission Focal neurologic deficits A low CSF cell count Increased CSF pressure (particularly)

Seizures and a low CSF:serum glucose ratio may also indicate a poor prognosis.

Treatment

Antibiotics Corticosteroids to decrease cerebral inflammation and edema

Antibiotics are the mainstay of therapy. In addition to antibiotics, treatment includes measures to decrease brain and cranial nerve inflammation and increased ICP. Most patients are admitted to an ICU. Antibiotics: Antibiotics must be bactericidal for the causative bacteria and must be able to penetrate the blood-brain barrier. If patients appear ill and findings suggest meningitis, antibiotics (see Meningitis: Initial Antibiotics for Acute Bacterial Meningitis ) are started as soon as blood cultures are drawn. If lumbar puncture is delayed pending neuroimaging results, treatment begins before neuroimaging. If patients do not appear very ill or have atypical symptoms and the diagnosis is less certain, antibiotics can wait until CSF results are known.

Sidebar 2

Pearls & Pitfalls

If patients appear ill and acute meningitis is suspected, treat them with antibiotics and corticosteroids as soon as blood for cultures is drawn.

Appropriate empiric antibiotics depend on the patient's age and immune status and route of infection (see Meningitis: Initial Antibiotics for Acute Bacterial Meningitis ). In general, clinicians should use antibiotics that are effective against S. pneumoniae,N. meningitidis, and S. aureus. Sometimes (eg, in neonates and some immunosuppressed patients), herpes simplex encephalitis cannot be excluded; thus, acyclovir

is added. Antibiotic therapy may need to be modified based on results of culture and sensitivity testing. Commonly used antibiotics include 3rd-generation cephalosporins for S. pneumoniae andN. meningitidis, ampicillin

for L monocytogenes, andvancomycin for penicillin-resistant strains of S. pneumoniae and for S. aureus.

Table 5

Initial Antibiotics for Acute Bacterial Meningitis

Patient Group
Age
< 3 mo Streptococcus agalactiae Escherichia coli or other gramnegative bacteria Listeria monocytogenes Staphylococcus aureus* plus Ceftriaxone or cefotaxime Ampicillin

Suspected Bacteria

Provisional Antibiotics

3 mo18 yr

Neisseria meningitidis S. pneumoniae S. aureus* Haemophilus influenzae

Cefotaxime or ceftriaxone

plus Vancomycin

1850 yr

S. pneumoniae N. meningitidis S. aureus*

Ceftriaxone or cefotaxime

plus Vancomycin

> 50 yr

S. pneumoniae L. monocytogenes S. aureus Gram-negative bacteria

Ceftriaxone or cefotaxime

N. meningitidis(unusual in this age group)

plus Ampicillin

plus Vancomycin

Route
Sinusitis, otitis, CSF leaks S. pneumoniae H. influenzae Gram-negative bacteria includingPseudomonas aeruginosa Anaerobic or microaerophilic streptococci Bacteroides fragilis S. aureus* plus Metronidazole or meropenem plus Ceftazidime

Vancomycin

Penetrating head wounds, neurosurgical procedures, shunt infections

S. aureus S. epidermidis Gram-negative bacteria includingP. aeruginosa S. pneumonia

Vancomycin

plus Ceftazidime

Immune status
AIDS, other conditions that impair cell-mediated immunity S. pneumoniae L. monocytogenes Gram-negative bacteria includingP. aeruginosa S. aureus* plus Ceftazidime Ampicillin

plus Vancomycin

*S. aureus is an uncommon cause of meningitis except when the route is a penetrating head wound or a neurosurgical procedure. However, it can cause meningitis in all patient groups. Thus, vancomycin or other antistaphylococcal antibiotics should be given if clinicians think that this bacteria is a possible, even if unlikely, cause.

S. pneumoniae is the most common causative bacteria in patients with a CSF leak or acute otitis. Such patients may be treated with vancomycin and ceftriaxone orcefotaxime . However, when meningitis is accompanied by subdural empyema or develops after a neurosurgical procedure, other bacteria, including P. aeruginosa, are more likely to be present; in such cases, initial treatment should include vancomycin plusceftazidime

plus metronidazole .

H. influenzae should be considered in children < 5 yr with no record of H. influenzae type b conjugate vaccination.

Table 6

Specific Antibiotics for Acute Bacterial Meningitis

Bacteria
Gram-positive bacteria (unidentified)

Age Group

Antibiotics*

Comments

Children Vancomycin and adults plus Ceftriaxone (cefotaxime ) andampicillin

Gram-negative bacilli (unidentified)

Children Cefotaxime and adults (or ceftriaxone ,meropenem , or ceftazidime

) plus Gentamicin , tobramycin

, oramikacin

if systemic infection is suspected Haemophilus influenzae type b Children Ceftriaxone and adults (cefotaxime ) Neisseria meningitidis Children Ceftriaxone and adults (cefotaxime ) Streptococcus pneumoniae Children Vancomycin and adults and ceftriaxone (cefotaxime ) Staphylococcus aureus and S. epidermidis Children Vancomycin and adults with or withoutrifampin Vancomycin is used for methicillinresistant strains, ornafcillin or oxacillin Penicillin G

is used for susceptible strains after sensitivities are known. Penicillin G

may be used for susceptible strains after sensitivities are known.

may be used after sensitivities are known. Rifampin

is added if no improvement occurs withvancomycin or nafcillin

. Listeria sp Children Ampicillin and adults (penicillin G Penicillin G

is used for susceptible strains after sensitivities are known. Trimethoprim/sulfamethoxazole

) or Trimethoprim/sulfamethoxazole

is used in patients who are allergic to penicillin.

Enteric gram-negative bacteria (eg,Escherichia coli, Klebsiellasp, Proteus s p)

Children Ceftriaxone and adults (cefotaxime ) plus Gentamicin , tobramycin

, oramikacin

if systemic infection is suspected Pseudomonassp Children Meropenem and adults (ceftazidime

orcefepime ), usually alone but sometimes with an aminoglycoside or Aztreonam

*Alternative antibiotics are in parentheses.

If gram-positive bacteria are pleomorphic, ampicillin

is included to cover Listeria sp.

Amikacin

is used in areas where gentamicin resistance is common. Because aminoglycosides have poor CSF penetration, they are infrequently used for treatment of meningitis. When required, they may have to be given intrathecally or via an Ommaya reservoir, especially in patients with Pseudomonas meningitis. When aminoglycosides are used, renal function should be monitored.

Table 7

Common IV Antibiotic Dosages for Acute Bacterial Meningitis*

Antibiotic Dosage Children > 1 mo
Ceftriaxone 50 mg/kg q 12 h

Adults
2 g q 12 h

Cefotaxime

50 mg/kg q 6 h

2 g q 4 6 h

Ceftazidime

50 mg/kg q 8 h

2gq8h

Cefepime

2 g q 12 h

2 g q 812 h

Ampicillin

75 mg/kg q 6 h

23 g q 4 h

Penicillin G

4 million units q 4 h

4 million units q 4 h

Nafcillin and oxacillin

50 mg/kg q 6 h

2gq4h

Vancomycin

15 mg/kg q 6 h

1015 mg/kg q 8 h

Meropenem

40 mg/kg q 8 h

2gq8h

Gentamicin andtobramycin

2.5 mg/kg q 8 h

2 mg/kg q 8 h

Amikacin

10 mg/kg q 8 h

7.5 mg/kg q 12 h

Rifampin

6.7 mg/kg q 8 h

600 mg q 24 h

Chloramphenicol

25 mg/kg q 6 h

1gq6h

*For neonatal dosages, see Table 1: Infections in Neonates: Recommended Dosages of Selected Parenteral Antibiotics for Neonates .

Renal function should be monitored.

Corticosteroids: Dexamethasone

is used to decrease cerebral and cranial nerve inflammation and edema; it should be given when therapy is started. Adults are given 10 mg IV; children are given 0.15 mg/kg IV.Dexamethasone

is given immediately before or with the initial dose of antibiotics and q 6 h for 4 days. Other measures: The effectiveness of other measures is less well-proved. Patients presenting with papilledema or signs of impending brain herniation are treated for increased ICP: elevation of the head of the bed to 30, hyperventilation to a PCO2 of 27 to 30 mm Hg to cause intracranial vasoconstriction, and osmotic diuresis with IV mannitol

. Usually, adults are given mannitol

1 g/kg IV bolus over 30 min, repeated prn q 3 to 4 h or 0.25 g/kg q 2 to 3 h, and children are given 0.5 to 2.0 g/kg over 30 min, repeated prn. Supportive measures can include IV fluids, anticonvulsants, treatment of concomitant infections, and treatment of specific complications (eg, corticosteroids for Waterhouse-Friderichsen syndrome, surgical drainage for subdural empyema).

Prevention
Use of vaccines for H. influenzae type B and, to a lesser extent, for N. meningitidis and S. pneumoniae has reduced the incidence of bacterial meningitis.

Physical measures: Keeping patients in respiratory isolation (using droplet precautions) for the first 24 h of therapy can help prevent meningitis from spreading. Gloves, masks, and gowns are used. Vaccination: Vaccination can prevent certain types of bacterial meningitis. A conjugated pneumococcal vaccine effective against 7 serotypes, including > 80% of organisms that cause meningitis, is recommended for all children (see Immunization: Pneumococcal Disease and Table 12: Approach to the Care of Normal Infants and Children: Recommended Immunization Schedule for Ages 0 6 yr ). Routine vaccination against H. influenzae type b is highly effective and begins at age 2 mo. A quadrivalent meningococcal vaccine is given to

Children who are 2 to 10 yr if they have an immunodeficiency or functional asplenia All children at age 11 to 12 yr Older children, college students living in dormitories, and military recruits who have not had the vaccine previously Travelers to endemic areas Laboratory personnel who routinely handle meningococcal specimens

During an epidemic, the population at risk (eg, college students, a small town) must be identified, and its size must be determined before proceeding to mass vaccination. The effort is expensive and requires public education and support, but it saves lives and reduces morbidity. The meningococcal vaccine does not protect against serotype B meningococcal meningitis; this information should kept in mind when a vaccinated patient presents with symptoms of meningitis. Chemoprophylaxis: Anyone who has prolonged face-to-face contact with a patient who has meningitis (eg, household or day care contacts, medical personnel and other people who are exposed to the patient's oral secretions) should be given postexposure chemoprophylaxis. For meningococcal meningitis, chemoprophylaxis consists of one of the following:

Rifampin

600 mg (for children > 1 mo, 10 mg/kg; for children < 1 mo, 5 mg/kg) po q 12 h for 4 doses

Ceftriaxone 250 mg (for children < 15 yr, 125 mg) IM for 1 dose

For adults, a fluoroquinolone (ciprofloxacin

or levofloxacin

500 mg or ofloxacin 400 mg) po for 1 dose Chemoprophylaxis against H. influenzae type b is rifampin

20 mg/kg po once/day (maximum: 600 mg/day) for 4 days. There is no consensus on whether children < 2 yr require prophylaxis for exposure at day care. Chemoprophylaxis is not usually needed for contacts of patients with other types of bacterial meningitis.

Key Points

Common causes include N. meningitidis and S. pneumoniae in children and adults and Listeria sp in infants and the elderly; S. aureus occasionally causes meningitis in people of all ages. Typical features may be absent or subtle in infants, alcoholics, the elderly, immunocompromised patients, and patients who develop meningitis after a neurosurgical procedure. If patients have focal neurologic deficits, obtundation, seizures, or papilledema (suggesting increased ICP or a mass), lumbar puncture is deferred pending results of neuroimaging. Acute bacterial meningitis, unless atypical or mild, is treated as soon as possible, before the diagnosis is confirmed. Common empirically chosen antibiotic regimens often include 3rd-generation cephalosporins (for S. pneumoniae and N. meningitidis), ampicillin

(for L. monocytogenes), and vancomycin SOME TRADE NAMES

VANCOCIN Click for Drug Monograph

(for penicillin-resistant strains of S. pneumoniae and for S. aureus).

Routine vaccination for S. pneumoniae and N. meningitidis and chemoprophylaxis against N. meningitidishelps prevent meningitis.