Infections of the Central Nervous System

Michelle VanDemark

Joanne V. Hickey

Infections of the central nervous system (CNS) can be life-threatening and require early recognition and treatment to improve outcomes. A comprehensive medical history and physical examination provide critical information in establishing the cause of the CNS infection and appropriate nursing interventions. This chapter will focus on meningitis, encephalitis, and abscesses. Other selected nervous system infections are briefly presented in tabular format.

MENINGITIS

Meningitis is an inflammation of the meninges that surround the brain and spinal cord. Primary causes of meningitis are bacterial or viral infections but meningitis can also be due to a fungus or parasite. Infections can occur when an organism gains access to the meninges via the blood-borne route or through the spread of nearby infections such as sinusitis, mastoiditis, otitis media, osteomyelitis of the skull or vertebrae, or pneumonia.¹ Other sources of cerebrospinal fluid (CSF) contamination include neurosurgical procedures, lumbar puncture (LP), and penetrating head wounds. Infections of the meninges also result from preexisting connections between the CNS and dural defects, congenital sinuses, or occult encephaloceles.²

Bacterial Meningitis

Bacterial meningitis is a pyogenic (purulent or suppurative) infection that involves the pia-arachnoid layers of the meninges and the subarachnoid space (SAS), including CSF. Common risk factors for the development of bacterial meningitis include immunocompromised conditions such as organ transplantation, cancer, diabetes mellitus, asplenia, chronic steroid therapy, HIV infection, intravenous
drug use, alcoholism, or malnutrition. Other risk factors include penetrating head trauma, otorrhea, rhinorrhea, or neurosurgical procedures. Also, living in close quarters such as college dormitories or military barracks can enhance the spread of meningitis; and travel to endemic areas such as sub-Saharan Africa is also a risk factor for meningitis.³

The annual incidence of bacterial meningitis is 4 to 6 cases per 1,00,000 adults (persons older than 16 years of age).⁴ In the United States, the annual incidence of people acquiring bacterial meningitis has decreased to 1.38 cases per 1,00,000 population with the median age shifting up to 41.9 years.⁵, ⁶, ⁷ The two populations that remain the greatest risk for acquiring meningitis are the very young (<2 months) and the elderly.⁷ Two factors have changed the epidemiology of bacterial meningitis significantly over the past 15 years. The first one is the advent of the Haemophilus influenzae type b (Hib) vaccine, conjugate pneumococcal vaccine, and recently the conjugated meningococcal vaccine. The incidence of meningococcal disease has decreased dramatically since the meningococcal vaccine; however, it does not contain serogroup B which is a causative agent of meningococcal disease.⁸ Secondly, there is an increasing emergence of antimicrobial resistant organisms, making treatment challenging.

Common Causative Organisms

The common causative organisms for bacterial meningitis tend to differ by age group. In older children and adults, Streptococcus pneumoniae and Neisseria meningitides are the most common causative organisms of meningitis.⁸ S. pneumoniae is the primary agent responsible for community-acquired bacterial meningitis. In older adults (50 years of age and older), S. pneumoniae is likely to cause meningitis in association with pneumonia or otitis media. Other common causative organisms include group B streptococcus (GBS) and Listeria monocytogenes. L. monocytogenes is responsible for meningitis in people who are immunosuppressed.⁸ In addition, gram-negative bacilli Enterobacteriaceae (Escherichia coli, Klebsiella pneumoniae, Pseudomonas, Enterobacter, and Serratia) are the organisms likely to cause meningitis in association with chronic lung disease, sinusitis, neurosurgical procedures, or chronic urinary tract infection in older patients (Table 29-1). Except during summer when incidence decreases, the rate of cases of meningitis is relatively constant throughout the year.

TABLE 29-1 COMMON CAUSATIVE ORGANISMS OF BACTERIAL MENINGITIS IN ADULTS^a

DISEASE	ORGANISM	COMMENTS
Pneumococcal meningitis	Streptococcus pneumoniae (gram-positive diplococci)	Most common type of meningitis with worldwide distribution Most common in young children and older adults Occurs mostly in winter and early spring Predisposing conditions include pneumonia, sinusitis, alcoholism, and head trauma
Haemophilus influenzae meningitis	H. influenzae (gram-negative cocci)	Used to occur most often in infants and children, but occurring more in adults Incidence has decreased in half due to H. influenzae vaccine Often follows upper respiratory or ear infections
Meningococcal meningitis	Neisseria meningitidis (gram-negative diplococci)	Highest incidence in children and young adults Presentation includes petechial rash, purpuric lesions, or ecchymosis that develop in 50% of patients About 10% develop a fulminating infection with overwhelming septicemia (meningococcemia); creates a medical emergency (high fever, circulatory collapse from adrenocortical insufficiency secondary to hemorrhage and necrosis of the adrenals called Waterhouse-Friderichsen syndrome); disseminated intravascular coagulation may also occur Death can result hours after onset
Listeria monocytogenes meningitis		Fourth most common cause of meningitis in nonsurgical bacterial meningitis
Less common sources	Staphylococcus aureus Streptococcus group A Streptococcus group B	Increased incidence of nosocomial infections noted Often introduced during neurosurgical procedures (craniotomy) or related to brain abscess, epidural abscess, or head trauma
Less common sources	Klebsiella Proteus Pseudomonas	Related to lumbar puncture, spinal anesthesia, or shunting procedure
Tuberculosis meningitis	Myobacterium tuberculosis	Secondary infection resulting from bacterial seeding of the meninges from tuberculosis elsewhere in the body Most common in children Incidence reflects the rate of tuberculosis in a country (relatively low in the United States)
^aThe organisms presented here are responsible for 80-90% of the cases of bacterial meningitis worldwide; these organisms are normally found in the nasopharynx of a significant portion of the population.

Pathophysiology

Both H. influenzae and S. pneumoniae organisms are associated with the respiratory tract and gram-negative rod organisms. Enterobacteriaceae, associated with the enteric tract, often inhabit the nasopharynx and are the major organisms causing bacterial
meningitis in children and adults. These bacteria attach to mucous epithelium by secreting a substance known as immunoglobin A (IgA) protease and then enter the bloodstream. In the blood, bacteria are inactivated by complement-mediated bactericidal activity and phagocytosis by neutrophils. However, protection from these mechanisms is afforded by a capsular polysaccharide coating. Bacteria that are able to survive in the circulation enter the CSF through the choroid plexus of the lateral ventricles and other areas of the altered blood-brain barrier. The CSF is an area of impaired host defense because of a lack of sufficient numbers of complement components and immunoglobulins for the opsonization (the rendering of bacteria and other cells subject to phagocytosis) of bacteria.⁹

The pathophysiologic events related to meningitis are well described by Roos.⁸ Bacteria multiply rapidly in the SAS. Both this multiplication and lysis of bacteria by bactericidal antibiotics cause the release of bacterial cell wall components. These components stimulate the formation of the inflammatory cytokines, interleukin-1 (IL-1), and tumor necrosis factor (TNF) by monocytes, macrophages, brain astrocytes, and microglial cells. Blood-brain barrier permeability is altered; polymorphonuclear leukocytes are recruited. All these events contribute to the formation of purulent exudate in the SAS. Concurrently, IL-1 and TNF induce the formation of molecules that adhere to leukocytes on vascular endothelial cells. This allows neutrophils to traverse the blood-brain barrier. The large numbers of leukocytes in the SAS add to the purulent exudate and obstruction of flow of CSF. Adhesion of leukocytes to the cerebral capillary endothelial cells increases their permeability and allows plasma proteins to leak through open intercellular junctions. This results in vasogenic brain edema and subsequent increased intracranial pressure (ICP).

In the acute phase of meningitis, the cerebral cortex undergoes little change except for perivascular inflammation with some infiltration into the cortex. In subacute cases, there may be diffuse degenerative changes, with necrosis and glial proliferation within the superficial areas of the brain, spinal cord, or cranial nerves. The optic and acoustic nerves are often affected, although the oculomotor, trochlear, abducens, and facial nerves can also be involved.

The resolution of meningitis depends on the extent of the infection and how quickly effective treatment is initiated. If the process is arrested early, resolution may be complete, without major sequelae. However, the arachnoid layer may undergo fibrotic changes and scar tissue formation. Adhesions and effusions can develop in the SAS, thereby interfering with the normal circulation of CSF. Fibrotic changes in the structures responsible for the production and absorption of CSF may result, contributing to the development of hydrocephalus. Some organisms may produce an abscess. Much of the outcome from bacterial meningitis depends on early and aggressive treatment to prevent the development of complications.

Signs and Symptoms

Bacterial meningitis requires prompt recognition and treatment to improve outcomes. Bacterial meningitis may have an insidious course progressing over 3 to 5 days or a rapidly fulminating course developing over hours to 2 days. Although many different organisms are capable of producing meningitis, all produce common signs and symptoms. The classic triad of meningitis includes fever, stiff neck, and altered mental status, though this triad is not particularly common. A study of 696 cases of bacterial meningitis in adults reported that only 44% of patients presented with the classic triad but 95% presented with at least two of four symptoms: headache, fever, neck stiffness, and altered mental status.¹⁰ Other common symptoms of bacterial meningitis include photophobia (light sensitivity), phonophobia (sound sensitivity), hyperalgesia, muscular hypotonia, back, abdominal and extremity pain, irritability, confusion, nausea vomiting, malaise, syndrome of inappropriate secretion of antidiuretic hormone (SIADH), and in severe cases, seizures. Bacteremia may cause systemic complications such as septic shock, disseminated intravascular coagulation (DIC), acute respiratory distress syndrome (ARDS), and septic or reactive arthritis.

Headache and Fever. The headache, which is usually the initial symptom, is described as severe. This symptom is attributed to irritation of the pain-sensitive dura and traction on related vascular structures. Fever is the rule with bacterial meningitis, and can vary from 101°F to 103°F (38°C to 39.5°C) or higher. The temperature remains high throughout the course of the illness and can rise to 105°F (40.5°C) and higher in the terminal stages because of decompensation of increased ICP on the brainstem.

Stiff Neck/Nuchal Rigidity, and Other Signs of Meningeal Irritation. A stiff neck is an early sign of meningeal irritation. Attempts to flex the neck forward, either actively or passively, usually proves difficult. This resistance is caused by spasms of the extensor muscles of the neck. Forceful flexion produces severe pain which is referred to as nuchal rigidity. Two signs of meningeal irritation are Kernig’s and Brudzinski’s signs. Kernig’s sign is elicited by flexing the upper leg at the hip to a 90-degree angle and then attempting to extend the knee. In the presence of meningeal irritation, pain and spasm of the hamstrings and lower back occur when an attempt is made to extend the knee (Fig. 29-1). The pain is caused by inflammation
of the meninges and spinal roots. The spasms are a protective mechanism to deter painful flexion. Brudzinski’s sign is positive when passive flexion of the neck and head to the chest causes spontaneous involuntary flexion of both the hips and knees (Fig. 29-2).¹¹ This reflex is caused by irritating exudate around the roots in the lumbar region.

Figure 29-1 ▪ Kernig’s sign. With the patient lying on his back, flex one of the patient’s legs at the hip and knee. If pain or resistance is elicited as the knee is straightened, this is a positive Kernig’s sign, a sign of meningeal irritation.

Figure 29-2 ▪ Brudzinski’s sign. With the patient lying on his back, place your hand behind the patient’s neck and flex the neck toward the sternum. In a patient with meningeal irritation there is neck pain, neck stiffness, and flexion of the hips and knees.

Altered Consciousness. In the very early stages, lethargy and confusion are common. The patient becomes disoriented to time, place, and person; is easily bewildered; has poor memory; and appears to have difficulty following commands. Other patients may become restless, agitated, irritable, and disoriented. Adults may progress rapidly from lethargy to stupor and coma. In the older adult, fever, confusion, stupor, or coma is typical.

Other Signs. Photophobia (light sensitivity) is a common sign of meningeal irritation seen in bacterial meningitis, but the pathophysiology for this symptom is not clear. Other signs and symptoms noted include skin hypersensitivity, hyperalgesia, and muscular hypotonia, although motor function is well preserved. Sensory loss does not occur. Seizures occur in 40% to 50% of patients with bacterial meningitis usually within the first week.¹² Some patients develop hyponatremia or SIADH from excessive release of antidiuretic hormone. There are signs and symptoms of water retention, along with oliguria and hypervolemia. Nausea and vomiting are common. Bacteremia may cause systemic complications such as septic shock, DIC, ARDS, and septic or reactive arthritis.

Increased ICP accompanies bacterial meningitis because of accumulation of purulent exudate, cerebral edema, and hydrocephalus. Symptoms of brainstem pressure are reflected as Cushing’s response of vital sign changes such as widening of pulse pressure, decreased pulse, and ataxic respirations. Vomiting is a frequent finding and is related to increased ICP. If the infection is not aggressively treated or response to treatment is poor, cerebral herniation can occur.

Neonates and immunocompromised persons have a blunted or nonspecific clinical presentation and LPs should be performed quickly upon presentation. Atypical presentation in the neonate includes fever, lethargy, irritability, respiratory distress, apnea, heart rate changes, jaundice, poor feeding, vomiting, and diarrhea. Due to their immature immune system, neonates will not experience bulging fontanel, seizures and coma until late in the course of bacterial meningitis.⁸, ¹³

Meningococcal Meningitis. Some additional differential signs and symptoms are noteworthy with N. meningitidis infection. Very rapid development of delirium and stupor, a petechial or purpura rash, or large ecchymotic areas especially of the lower parts of the body, are seen in approximately 50% of people with meningococcal meningitis. The petechiae may be seen on the conjunctiva and other parts of the skin and mucous membranes. Fulminating meningococcemia, with or without meningitis, has a high mortality rate because of the associated vasomotor collapse and infective shock related to adrenocortical hemorrhage.¹⁴ The adrenal hemorrhage resulting in adrenal insufficiency followed by hypotension, cyanosis, respiratory distress, and circulatory collapse is known as Waterhouse-Friderichsen syndrome. If this occurs, immediate administration of adrenal corticosteroids is necessary along with other supportive therapies to treat this life-threatening event.¹⁵

Diagnosis

A diagnosis of bacterial meningitis is often difficult to recognize. A detailed history, physical examination, and laboratory data¹⁶ are important in the evaluation of a possible CNS infection. A history of recent infections, such as those involving the ears, sinuses, or respiratory tract, is a risk factor. Investigate whether the patient has recently traveled to an area that is endemic for meningitis. Blood and CSF cultures should be immediately obtained when bacterial meningitis is suspected. The blood should be sent for complete blood count with differential, basic metabolic panel, blood cultures, Gram stain, and lactate. CSF analysis is the “gold standard” in definitively diagnosing bacterial meningitis. During the physical examination, assess the patient first for signs of elevated ICP or risk factors for cerebral herniation which could be a contraindication for LP. Patients who are at high risk for cerebral herniation include patients with new onset seizures, immunocompromised conditions (HIV infection, immunosuppressive therapy or organ transplantation), papilledema, focal neurologic deficits or impaired consciousness.⁵, ¹⁷, ¹⁸, ¹⁹ If an elevated ICP is suspected, a computed tomography (CT) scan may be ordered first to assess for significantly elevated ICP. The CT scan of the head may identify such factors as hydrocephalus, cerebral mass, cerebral edema and/or midline shift risk factors for brain herniation. Also, the CT scan is useful for detection of abscesses and lesions that erode the skull and provide a route for bacterial invasion (e.g., tumors or sinus wall defects). Diagnostic testing should not delay empiric antimicrobial therapy. In the most sensitive organism, CSF sterilization occurs after 4 to 6 hours following the initiation of antimicrobial therapy.

Collection of CSF requires an LP or a sample of CSF from a ventriculostomy. The classic CSF abnormalities noted in bacterial meningitis include the following.

Increased opening pressure on LP
Polymorphonuclear leukocytic pleocytosis
Decreased glucose concentration
Increased protein concentration
Glucose ratio less than 40 mg/dL
White blood cell (WBC) count of CSF usually more than 100 cells/mm³³ and often more than 1,000 cells/mm³³
Protein count higher than 45 mg/dL (most often 100 to 500 mg/dL)

TABLE 29-2 COMPARISON OF THE CLASSIC CEREBROSPINAL FLUID (CSF) FINDINGS IN ACUTE BACTERIAL MENINGITIS AND ACUTE ASEPTIC (VIRAL) MENINGITIS

CSF CHARACTERISTICS (NORMAL)	ACUTE BACTERIAL MENINGITIS^a	ACUTE ASEPTIC (VIRAL) MENINGITIS
Appearance (crystal clear)	Turbid, cloudy	Clear; sometimes turbid
Cells: White Blood Cells count (cells/mm³) (0-5 cells/mm³)	Increased white blood cells (100-5,000 cells/mm³) (1,000-2,000/mm³ or more; mostly polymorphonuclear neutrophils [PMNs] predominate)	Increased white blood cells (10-500 cells/mm³) (300 cells/mm³; mostly mononuclear lymphocytes predominate)
Protein level (15-50 mg/dL)	Increased (100-500 mg/dL)	Normal or slightly increased
Glucose level (40-80 mg/dL) (approximately two third of blood glucose level)	Decreased (<40 mg/dL or about 40% of blood glucose level)	Normal
Smear and culture (negative)	Bacteria present on Gram stain and culture	No bacteria present on Gram stain or culture; the virus may be demonstrated by special techniques
Opening pressure on lumbar puncture (100-180 mm H₂O)	Elevated (>180 mm of water pressure)	Variable
^aAll patients do not follow this classic profile; about 30% of patients with bacterial meningitis show some of the findings seen in aseptic meningitis.
From: Somand, D., & Meurer, W. (2009). Central nervous system infections. Emergency Medicine Clinics of North America, 27(1), 89-100. doi:10.1016/j.emc.2008.07.004; Roos, K. L., & Greenlee, J. E. (2011). Meningitis and encephalitis. Continuum Lifelong Learning Neurology, 17(5), 1010-1023; and Ziai, W. C., & Lewin, J. J. (2008). Update in the diagnosis and management of central nervous system infections. Neurologic Clinics, 26(2), 427-468.

Table 29-2 provides a comparison between the basic CSF criteria for diagnosis of bacterial meningitis and the findings associated with aseptic (viral) meningitis. Tests to identify specific causative organisms include Gram stain, smear, and culture. Blood cultures may also be of diagnostic value as they are positive in 40% to 60% of patients with H. influenzae, meningococcal, and pneumococcal meningitis.¹² CSF Gram stain is rapid and accurate in identifying the causative organism in 60% to 90% of cases of community-acquired bacterial meningitis and has greater than 97% specificity. For patients who have received antibiotics prior to the LP, the yield of the Gram stain decreases by 20%, making it more difficult to establish a diagnosis.¹⁹, ²⁰ Newer laboratory techniques are making it possible to detect bacterial antigen in an hour or two. These options include counter-immunoelectrophoresis (CIE), a sensitive technique that permits the detection of bacterial antigens in the CSF in 30 to 60 minutes; radioimmunoassay (RIA); latex particle agglutination (LPA); enzyme-linked immunosorbent assay (ELISA); and polymerase chain reaction (PCR).¹² PCR amplification of DNA is useful to detect common meningeal pathogens. PCR rapidly detects enteroviruses and aids in distinguishing enteroviral meningitis.²⁰, ²¹ At the same time, the serum glucose should be drawn to determine the CSF serum glucose ratio in which the CSF glucose is two thirds (0.67) of the serum glucose.⁸ CSF is normally clear and colorless. In bacterial meningitis CSF may have a xanthochromic appearance (brown/yellow color), which is due to the increased protein levels and/or the degradation of red blood cells.²¹ Finally, the distinction between bacterial and viral meningitis can be aided by CSF lactate dehydrogenase (LDH), C-reactive protein and serum procalcitonin levels, all of which are commonly elevated in bacterial meningitis.²¹ CSF lactate concentrations are useful in the diagnosis of bacterial meningitis in the postoperative neurosurgical patient and are considered positive when CSF lactate is greater than 4 mmol/L.¹⁹, ²⁰

Treatment

Bacterial meningitis is a medical emergency that requires a multidisciplinary approach.

Studies have shown that rapid assessment, diagnosis and treatment of bacterial meningitis with empiric antibiotics and corticosteroids early in the course of the disease will improve outcomes. The Infectious Disease Society of America (IDSA) guidelines state that antimicrobial therapy should be initiated as soon as bacterial meningitis is suspected. The antimicrobial therapy should be bactericidal for the suspected causative organism, and based on patient age, symptoms, geographic location, time of year and predisposing conditions.²⁰ Often high-dose broad-spectrum antibiotics that cross the blood-brain barrier and provide coverage for the most common bacterial pathogens will be started as soon as possible. These include penicillin (ampicillin or piperacillin) or third-generation cephalosporin (cefotaxime and ceftriaxone). Vancomycin may also be administered to provide optimal coverage of penicillinresistant and cephalosporin-resistant strains. Empiric acyclovir may be added to the antibiotic regime if there is a suspicion of herpes encephalitis diagnosis.⁵ Once the causative agent has been identified, the antibiotics can be modified for optimal therapy and the antibiotic course of 10 to 14 days will be completed. Table 29-3 outlines empiric antimicrobial therapy, and Table 29-4 lists recommendations for antimicrobial therapy based on a known organism. Practice Guidelines for the Management of Bacterial Meningitis is one of many resources to guide patient management.²⁰

Controversy regarding the administration of corticosteroids and anticonvulsant therapy exists. There is limited evidence to support use of corticosteroids in treating bacterial meningitis. However, dexamethasone, a corticosteroid, has been shown to decrease inflammation and edema associated with bacterial meningitis. Corticosteroids reduces neurological sequelae such as hearing loss and improve patient outcomes.¹¹, ²³ The IDSA Practice Guideline recommends use of dexamethasone as adjunctive therapy to be given before the first dose of antibiotics or at least given with the first dose. The recommended dose of dexamethasone is 0.15 mg/kg
administered intravenously every 6 hours for the first 4 days of therapy.⁹, ¹⁹, ²⁰ However, studies have shown that dexamethasone significantly decreases the efficacy of vancomycin penetrates into the CNS and achieves therapeutic concentrations, this is especially important in highly resistant S. pneumoniae.¹⁹ Concurrent use of a histamine-2 receptor antagonist or a proton pump inhibitor (PPI) is recommended to prevent gastrointestinal (GI) hemorrhage. Prophylactic use of anticonvulsant therapy is recommended by some to prevent seizures because about 40% of patients will have a seizure. Other physicians choose to begin phenytoin or levetiracetam (Keppra) only if the patient has had a seizure.

TABLE 29-3 EMPIRIC ANTIMICROBIAL THERAPY FOR BACTERIAL MENINGITIS

PATIENT GROUP	MOST LIKELY ORGANISM	ANTIMICROBIAL THERAPY
Adult: 2-50 yrs	Neisseria meningitides, Streptococcus pneumoniae, Haemophilus influenzae	Vancomycin plus a third-generation (ceftriaxone or cefotaxime) or fourth-generation (cefepime) cephalosporin
Adult: >50 yrs	S. pneumoniae, N. meningitides, Listeria monocytogenes, aerobic gram-negative bacilli, H. influenzae (add?)	Vancomycin plus ampicillin plus a third-generation (ceftriaxone or cefotaxime) or fourth-generation (cefepime) cephalosporin
Immunocompromised patients	Opportunistic organisms (L. monocytogenes, gram-negative bacilli, S. pneumoniae, N. meningitides, H. influenzae)	Vancomycin plus ampicillin plus a third-generation (ceftriaxone or cefotaxime) or fourth-generation (cefepime) cephalosporin
Postneurosurgery	Aerobic gram-negative bacilli (including Pseudomonas aeruginosa), Staphylococcus aureus, coagulase-negative staphylococci (especial S. epidermidis)	Vancomycin plus cefepime, or ceftazidime, or meropenem
Basal skull fracture (head trauma)	S. pneumoniae, H. influenzae, group A beta-hemolytic streptococci	Vancomycin plus a third-generation cephalosporin (ceftriaxone or cefotaxime)
Central nervous system shunts	Coagulase-negative staphylococci (especially S. epidermidis), S. aureus, aerobic gram-negative bacilli (including P. aeruginosa), Propionibacterium acne	Vancomycin plus cefepime, vancomycin plus ceftazidime, or vancomycin plus meropenem
From: Roos, K. L., & Greenlee, J. E. (2011). Meningitis and encephalitis. Continuum Lifelong Learning Neurology, 17(5), 1010-1023; Roos, K. L. (2002). Central nervous system infections. In J. Biller (Ed.). Practical neurology (2nd ed., pp. 562-573). Philadelphia: Lippincott Williams & Wilkins; Ropper, A. H., & Brown, R. H. (2005). Adams and Victor’s principles of neurology (8th ed., pp. 592-661). New York: McGraw-Hill; Ziai, W. C., & Lewin, J. J. (2008). Update in the diagnosis and management of central nervous system infections. Neurologic Clinics, 26(2), 427-468; and Tunkel, A. R., Hartman, B. J., Kaplan, S. L., Kaufman, B. A., Roos, K. L., Scheld, W. M., & Whitley, R. J. (2004). Practice guidelines for the management of bacterial meningitis. Clinical Infectious Diseases, 39(9), 1267-1284.

TABLE 29-4 RECOMMENDED ANTIMICROBIAL THERAPIES BY ORGANISM FOR BACTERIAL MENINGITIS IN ADULTS

ORGANISM	ANTIMICROBIAL DRUG
Streptococcus pneumoniae	Vancomycin plus a third-generation cephalosporin (ceftriaxone or cefotaxime)
Neisseria meningitidis	Penicillin G or third-generation cephalosporin (ceftriaxone or cefotaxime)
Haemophilus influenzae	Third-generation cephalosporin (ceftriaxone or cefotaxime)
Pseudomonas aeruginosa	Cefepime or ceftazidime
Listeria monocytogenes	Ampicillin or penicillin G
Staphylococcus aureus (methicillin sensitive)	Nafcillin or oxacillin
S. aureus (methicillin resistant)	Vancomycin
Enterobacteriaceae	Third-generation cephalosporin (ceftriaxone or cefotaxime)
From: Lin, A. L., & Safdieh, J. E. (2010). The evaluation and management of bacterial meningitis: Current practice and emerging developments. The Neurologist, 16(3), 143-151; Tunkel, A. R., Hartman, B. J., Kaplan, S. L., Kaufman, B. A., Roos, K. L., Scheld, W. M., & Whitley, R. J. (2004). Practice guidelines for the management of bacterial meningitis. Clinical Infectious Diseases, 39(9), 1267-1284; and Miranda, J., & Tunkel, A. R. (2009). Strategies and new developments in the management of bacterial meningitis. Infectious Disease Clinic of North America, 23(4), 925-943. doi:10.1016/j.idc.2009.06.014.

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Jul 14, 2016 | Posted by drzezo in NURSING | Comments Off

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