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Central Nervous System lnfections Subacute and Chronic Meningitis Subacute and chronic meningitis are defined by symptom duration between 5 and 30 days and more than 30 days, respectively. The most common infectious causes are Mgcobacterium tuberculosis and fungi. Tuberculous Meningitis Tuberculous meningitis classically presents as basilar menin- gitis with cranial neuropathies (particularly of cranial nerve VI), mental status changes, and the syndrome of inappropriate secretion of antidiuretic hormone. A history of tuberculosis exposure, an abnormal chest radiograph, a positive tuberculin skin test result, and a positive interferon-y release assay result are suggestive but can be absent. CSF examination shows a lymphocytic pleocytosis (leukocyte count of 100-500/pL [rOO- 500 x 106/Ll), elevated protein level, and hypoglycorrhachia. CSF acid-fast bacilli smear is insensitive, and culture results are positive in only 38% to 88% of patients. Culture sensitivity increases when LPs are performed serially for at least 3 days. Nucleic acid amplification testing should be performed when possible, especially when the acid-fast bacilli stain result is negative and suspicion is high, because it might increase diag- FIGURE 2. 0bstructive hydrocephalus and multiple cystic lesions in the lateral nostic yield. Antituberculous therapy should be administered ventricle resu lting from neu rocysticercosis.

Tuberculous Meningitis Tuberculous meningitis classically presents as basilar menin- gitis with cranial neuropathies (particularly of cranial nerve VI), mental status changes, and the syndrome of inappropriate secretion of antidiuretic hormone. A history of tuberculosis exposure, an abnormal chest radiograph, a positive tuberculin skin test result, and a positive interferon-y release assay result are suggestive but can be absent. CSF examination shows a lymphocytic pleocytosis (leukocyte count of 100-500/pL [rOO- 500 x 106/Ll), elevated protein level, and hypoglycorrhachia. CSF acid-fast bacilli smear is insensitive, and culture results are positive in only 38% to 88% of patients. Culture sensitivity increases when LPs are performed serially for at least 3 days. Nucleic acid amplification testing should be performed when possible, especially when the acid-fast bacilli stain result is negative and suspicion is high, because it might increase diag- FIGURE 2. 0bstructive hydrocephalus and multiple cystic lesions in the lateral nostic yield. Antituberculous therapy should be administered ventricle resu lting from neu rocysticercosis. for 1year, and adjunctive glucocorticoids should be given ini- tially because of their association with improved outcomes. (schistosomiasis), and Gnathostoma. Neurocysticercosis (Figure 2) is endemic in Mexico, Central and South America, Fungal Meningitis and Asia. It most commonly presents with seizures or hydro- Fungal pathogens, including Cryptococcus neoformans, cephalus, and CT scan of the head shows multiple cysts or calci- Coccidioides immitis, Histoplasma capsulatum, and endemic fied lesions. Treatment includes managing seizures and increased mycoses, are a significant cause of subacute or chronic menin- gitis syndromes. Fungal meningitis is discussed in the Fungal intracranial pressure and administering adjunctive glucocorti- coids and antiparasitic agents for viable cystic lesions. Calcified Infections chapter. lesions represent dead parasites and do not require therapy. Neurobrucellosis Neurobrucellosis occurs in 4% to 11% of patients with brucel- Noninfectious Causes losis, which is endemic to countries in the Mediterranean, Medications such as NSAIDS, antibiotics, and intravenous Middle East, and Central America. It may present with menin- immune globulin can occasionally cause aseptic meningitis. gitis, meningoencephalitis, cranial neuropathies, myelopathy, Meningeal involvement of leukemia, Iymphoma, and meta- radiculopathy, or stroke or as a brain abscess. A positive bru- static carcinoma can also present as aseptic meningitis, with cellosis culture or serologic test result in the CSF or blood the CSF cytolog5r showing atypical or immature cells and makes the diagnosis. Treatment is combination antibiotic severe hypoglycorrhachia (<rO mg/dl [0.0 mmol/LJ). Systemic

for 1year, and adjunctive glucocorticoids should be given ini- tially because of their association with improved outcomes. (schistosomiasis), and Gnathostoma. Neurocysticercosis (Figure 2) is endemic in Mexico, Central and South America, Fungal Meningitis and Asia. It most commonly presents with seizures or hydro- Fungal pathogens, including Cryptococcus neoformans, cephalus, and CT scan of the head shows multiple cysts or calci- Coccidioides immitis, Histoplasma capsulatum, and endemic fied lesions. Treatment includes managing seizures and increased mycoses, are a significant cause of subacute or chronic menin- gitis syndromes. Fungal meningitis is discussed in the Fungal intracranial pressure and administering adjunctive glucocorti- coids and antiparasitic agents for viable cystic lesions. Calcified Infections chapter. lesions represent dead parasites and do not require therapy. Neurobrucellosis Neurobrucellosis occurs in 4% to 11% of patients with brucel- Noninfectious Causes losis, which is endemic to countries in the Mediterranean, Medications such as NSAIDS, antibiotics, and intravenous Middle East, and Central America. It may present with menin- immune globulin can occasionally cause aseptic meningitis. gitis, meningoencephalitis, cranial neuropathies, myelopathy, Meningeal involvement of leukemia, Iymphoma, and meta- radiculopathy, or stroke or as a brain abscess. A positive bru- static carcinoma can also present as aseptic meningitis, with cellosis culture or serologic test result in the CSF or blood the CSF cytolog5r showing atypical or immature cells and makes the diagnosis. Treatment is combination antibiotic severe hypoglycorrhachia (<rO mg/dl [0.0 mmol/LJ). Systemic therapy for at least 6 months. lupus erythematosus, Behqet disease, Vogt-Koyanagi-Harada syndrome (uveomeningoencephalitis), and neurosarcoidosis Parasitic Meningitis can all present with aseptic meningitis. Finally, chemical men- Acute primary amebic meningoencephalitis caused by ingitis can be seen after intrathecal injections, intracranial Naegleria, Balamuthio, and Acanthamoebo species is a fatal hemorrhage, neurosurgical procedures, or spinal anesthesia. infection that clinically resembles bacterial meningitis or can t(Ev Potf,Ts present with a chronic granulomatous meningitis. Freshwater . Tuberculous meningitis classically presents as basilar exposure during the summer is a key historical clue. meningitis with cranial neuropathies, mental status Examination of a fresh CSF sample can reveal motile tropho- changes, and the syndrome of inappropriate secretion zoites, but the CDC should perform confirmatory testing by of antidiuretic hormone; it should be treated with PCR. Treatment should include miltefosine. antituberculous therapy for 1 year with initial adjunc- Helminth infections causing eosinophilic meningitis tive glucocorticoids. include Angiostrongylus cantonensis, Baglisascaris procy- (Continued) onis, Taenia solium (neurocysticercosis), Schistosomo species

therapy for at least 6 months. lupus erythematosus, Behqet disease, Vogt-Koyanagi-Harada syndrome (uveomeningoencephalitis), and neurosarcoidosis Parasitic Meningitis can all present with aseptic meningitis. Finally, chemical men- Acute primary amebic meningoencephalitis caused by ingitis can be seen after intrathecal injections, intracranial Naegleria, Balamuthio, and Acanthamoebo species is a fatal hemorrhage, neurosurgical procedures, or spinal anesthesia. infection that clinically resembles bacterial meningitis or can t(Ev Potf,Ts present with a chronic granulomatous meningitis. Freshwater . Tuberculous meningitis classically presents as basilar exposure during the summer is a key historical clue. meningitis with cranial neuropathies, mental status Examination of a fresh CSF sample can reveal motile tropho- changes, and the syndrome of inappropriate secretion zoites, but the CDC should perform confirmatory testing by of antidiuretic hormone; it should be treated with PCR. Treatment should include miltefosine. antituberculous therapy for 1 year with initial adjunc- Helminth infections causing eosinophilic meningitis tive glucocorticoids. include Angiostrongylus cantonensis, Baglisascaris procy- (Continued) onis, Taenia solium (neurocysticercosis), Schistosomo species 4

Central Nervous System lnfections commonly caused by anaerobes, aerobic and microaer-ophilic o Freshwater exposure in summertime is a key historical streptococci, S. aureus, and Enterobacteriaceae. Initial empiric clue in suspected acute primary amebic meningoen- therapy is guided by the likeiy predisposing condition (Table 4). cephalitis. Aspiration of the brain abscess for culture is preferred for o Medications such as NSAIDS, antibiotics, and intrave- definitive diagnosis; surgical or stereotactic drainage shouid be performed if the abscess is large (>2.S cm). Antibiotic therapy nous immune globulin can occasionally cause aseptic should be given for 4 to B weeks with follow-up cranial imag meningitis. ing to ensure resolution of the infection. Immunosuppressed patients (those with HIV or AIDS, Health Care-Associated Meningitis patients undergoing solid organ or bone marrow transplanta and Ventriculitis tion) are at risk for developing brain abscesses from several Health care-associated meningitis and ventriculitis, or noso opportunistic infections. See HIV/AIDS and Infections in comial meningitis, can occur after head trauma or a neuro Transplant Recipients for further discussion. surgical procedure (craniotomy, LP) or secondary to a device XEY POIT{TS infection (for example, CSF shunt or drain, intrathecal pump, deep brain stimulator). Normal or abnormal CSF cell count, o Brain abscesses in immunocompetent patients are glucose level, and protein level do not reliably confirm or rule treated empirically based on the likely predisposing fac out infection in these patients. Staphglococcus species and tor, with surgical or stereotactic drainage of abscesses enteric gram-negative bacteria are the most common causes, larger than 2.5 cm. but up to 50% of infections can have negative culture results. o If the predisposing condition is unknown, empiric The use of B-o-glucan and galactomannan CSF assays may intravenous treatment of a brain abscess should include aid in diagnosing health care-related fungal ventriculitis and vancomycin plus metronidazole and a third-generation meningitis. Empiric antimicrobial therapy is outlined in cephalosporin. Table 2 and should be accompanied by device removal, if present. CranialAbscess Cranial epidural and subdural abscesses can arise from under- . StaphAlococcus species and enteric gram-negative bac lying osteomyelitis complicating paranasal sinusitis (Pott puffy teria are the most common causes of health care,asso, tumor) or otitis media or after neurosurgical procedures or ciated meningitis and ventriculitis, but up to 50%, of head trauma. Rarely, they may arise as a complication of bac- infections can have negative culture results. terial meningitis. Cranial epidural abscesses usually grow r Empiric intravenous therapy for health care-associated slowly, presenting with subacute to chronic symptoms of headache, localized bone pain, and focal neuroiogic signs. In meningitis and ventriculitis is vancomycin plus either ceftazidime, cefepime, or meropenem. contrast, subdural empyema is a rapidly progressive infection with high mortali[z that represents a neurosurgical emer gency. The CSF formula in both parameningeal infections shows neutrophilic pleocytosis and a very high protein level, Focal Central Neruous frequently with negative Gram stain and culture r:esults. System lnfections Pathogen identification is best achieved by culture of the Brain Abscesses abscess obtained during surgical drainage. Brain abscesses can occur in any patient but are most com- monly seen in men. Predisposing conditions in immunocom- petent patients can be seen in Table 3. Brain abscesses are most . In cranial epidural and subdural abscess, pathogen identification is best achieved by culture of the abscess obtained during surgical drainage. TABLE 3" Predisposing Conditions for Brain Abscess Condition lncidence Contiguous foci of infection such as sinusitis -50"/" Spinal Epidural Abscess (frontal lobe)and otitis media (temporal lobe or Spinal epidural abscess most commonly results from hema- cerebellum) togenous dissemination. S. aureus accounts for approxi- Hematogenous, sometimes with multiple 2s% mately 50% of infections; streptococcus and gram negative a bscesses(odontogen ic resu lti n g from vi rida ns streptococci, endoca rditis, i njection d ru g use, bacilli such as Escherichia coli are also implicated. cardiac rig ht-to-left shunts) Predisposing factors for bacteremia include endocarditis, injection drug use, Iong term intravenous catheters (hemo- Cryptogenic (most likely odontogenic) 15"/" dialysis catheters, central lines), and urinary tract infection. Neurosurgery or penetrating head trauma 10% Spinal epidural abscess can also occur after neurosurgical

commonly caused by anaerobes, aerobic and microaer-ophilic o Freshwater exposure in summertime is a key historical streptococci, S. aureus, and Enterobacteriaceae. Initial empiric clue in suspected acute primary amebic meningoen- therapy is guided by the likeiy predisposing condition (Table 4). cephalitis. Aspiration of the brain abscess for culture is preferred for o Medications such as NSAIDS, antibiotics, and intrave- definitive diagnosis; surgical or stereotactic drainage shouid be performed if the abscess is large (>2.S cm). Antibiotic therapy nous immune globulin can occasionally cause aseptic should be given for 4 to B weeks with follow-up cranial imag meningitis. ing to ensure resolution of the infection. Immunosuppressed patients (those with HIV or AIDS, Health Care-Associated Meningitis patients undergoing solid organ or bone marrow transplanta and Ventriculitis tion) are at risk for developing brain abscesses from several Health care-associated meningitis and ventriculitis, or noso opportunistic infections. See HIV/AIDS and Infections in comial meningitis, can occur after head trauma or a neuro Transplant Recipients for further discussion. surgical procedure (craniotomy, LP) or secondary to a device XEY POIT{TS infection (for example, CSF shunt or drain, intrathecal pump, deep brain stimulator). Normal or abnormal CSF cell count, o Brain abscesses in immunocompetent patients are glucose level, and protein level do not reliably confirm or rule treated empirically based on the likely predisposing fac out infection in these patients. Staphglococcus species and tor, with surgical or stereotactic drainage of abscesses enteric gram-negative bacteria are the most common causes, larger than 2.5 cm. but up to 50% of infections can have negative culture results. o If the predisposing condition is unknown, empiric The use of B-o-glucan and galactomannan CSF assays may intravenous treatment of a brain abscess should include aid in diagnosing health care-related fungal ventriculitis and vancomycin plus metronidazole and a third-generation meningitis. Empiric antimicrobial therapy is outlined in cephalosporin. Table 2 and should be accompanied by device removal, if present. CranialAbscess Cranial epidural and subdural abscesses can arise from under- . StaphAlococcus species and enteric gram-negative bac lying osteomyelitis complicating paranasal sinusitis (Pott puffy teria are the most common causes of health care,asso, tumor) or otitis media or after neurosurgical procedures or ciated meningitis and ventriculitis, but up to 50%, of head trauma. Rarely, they may arise as a complication of bac- infections can have negative culture results. terial meningitis. Cranial epidural abscesses usually grow r Empiric intravenous therapy for health care-associated slowly, presenting with subacute to chronic symptoms of headache, localized bone pain, and focal neuroiogic signs. In meningitis and ventriculitis is vancomycin plus either ceftazidime, cefepime, or meropenem. contrast, subdural empyema is a rapidly progressive infection with high mortali[z that represents a neurosurgical emer gency. The CSF formula in both parameningeal infections shows neutrophilic pleocytosis and a very high protein level, Focal Central Neruous frequently with negative Gram stain and culture r:esults. System lnfections Pathogen identification is best achieved by culture of the Brain Abscesses abscess obtained during surgical drainage. Brain abscesses can occur in any patient but are most com- monly seen in men. Predisposing conditions in immunocom- petent patients can be seen in Table 3. Brain abscesses are most . In cranial epidural and subdural abscess, pathogen identification is best achieved by culture of the abscess obtained during surgical drainage. TABLE 3" Predisposing Conditions for Brain Abscess Condition lncidence Contiguous foci of infection such as sinusitis -50"/" Spinal Epidural Abscess (frontal lobe)and otitis media (temporal lobe or Spinal epidural abscess most commonly results from hema- cerebellum) togenous dissemination. S. aureus accounts for approxi- Hematogenous, sometimes with multiple 2s% mately 50% of infections; streptococcus and gram negative a bscesses(odontogen ic resu lti n g from vi rida ns streptococci, endoca rditis, i njection d ru g use, bacilli such as Escherichia coli are also implicated. cardiac rig ht-to-left shunts) Predisposing factors for bacteremia include endocarditis, injection drug use, Iong term intravenous catheters (hemo- Cryptogenic (most likely odontogenic) 15"/" dialysis catheters, central lines), and urinary tract infection. Neurosurgery or penetrating head trauma 10% Spinal epidural abscess can also occur after neurosurgical 5