Meningitis - Acute and Chronic

Meningitis - Acute and Chronic : Infection inflammatory Aseptic Drug Toxin Autoimmune Paraneoplastic

1. MENINGITIS CHAIRPERSON- DR GAYATRI.B.H. STUDENT-DR NATARAJ G S

2. DEFINATIONS MENINGITIS : Inflammation of the meninges. Encephalitis : Inflammation of the brain parenchyma. Meningo encephalitis : Inflammation of meninges and brain parenchyma.

3. Meningitis is a clinical syndrome characterized by inflammation of the meninges. CAUSES: 1) INFECTIOUS 2) NON INFECTIOUS (MEDICATIONS AND CARCINOMATOSIS) MAY BE CLASSIFIED AS 1) ACUTE MENINGITIS :HOURS TO DAYS 2) CHRONIC MENINGITIS :AT LEAST 4 WEEKS.

4. CLASSIFICATION 1)Acute bacterial meningitis. 2)Acute aseptic meningitis. 3)Chronic meningitis. 4)Others (depend on specific pathogen) fungal , parasitic

5. PATHOPHYSIOLOGY Three major pathways. Hematogenous ( eg , from bacteremia, viremia , fungemia ). Retrograde neuronal pathway ( eg , Naegleria fowleri , rabies, HSV, VZV). Direct contiguous spread ( eg , sinusitis, otitis media, congenital malformations, trauma, direct inoculation during intracranial manipulation ).

6. PATHOPHYSIOLOGY

7. CLINICAL MANIFESTATIONS Fever , malaise Headache V omiting P hotophobia Hyperirritability N eck stiffness

8. C hanges in mental status Seizure ( 30 % of patients.) Triad of fever, nuchal rigidity, and change in mental status(2/3 of patients). Fever is the most common manifestation (95%), while stiff neck and headache are less common. However , the negative predictive value of these symptoms is high ( ie , the absence of fever, neck stiffness, or altered mental status eliminates the diagnosis of meningitis .).

9. Meningeal irritation signs Nuchal rigidity. 2) Kernig sign. 3) Brudzinsky sign .

10. PHYSICAL FINDING SENSITIVITY FEVER 85% NECK STIFFNESS 70% ALTERED SENSORIUM 67% ABSENCE OF ABOVE THREE 99% TO 100% SPECIFIC EXAM KERNIG SIGN 5% BRUDZINSKI SIGN 5% PHYSICAL EXAM FINDING

11. Signs of increase ICP 1)Papilledema. 2) Cushing’s triad. Bradycardia , Systolic Hypertension(widening of pulse pressure) and Irregular decreased breathing. 3) Changes in pupils. 4) Focal neurological deficit.

12. Atypical presentation Elderly , especially with underlying comorbidities ( eg , diabetes, renal and liver disease ), L ethargy and an absence of meningeal symptoms. Patients with neutropenia may present with subtle symptoms of meningeal irritation.

13. Others Immuno compromised hosts , I ncluding organ and tissue transplant recipients. P atients with HIV and AIDS patients with aseptic meningitis syndrome usually appear clinically nontoxic with no vascular instability

14. S exual contact and high-risk behavior HSV meningitis is associated with primary genital HSV infection and HIV infection Exposure to a patient with a similar illness is an important epidemiological clue when determining etiology ( eg , meningococcemia).

15. Intake of unpasteurized milk predisposes to brucellosis and L monocytogenes infection. Animal contacts rabies ( lymohocytic choriomeningitis ) virus Leptospira . History of neurosurgery - ventriculo peritoneal shunt cochlear implants.

16. Sinusitis or otitis suggests direct extension into the meninges, usually with S pneumoniae and H influenzae . Rhinorrhea / otorrhea suggests a CSF leak from a basilar skull fracture, with meningitis most commonly caused by S pneumoniae . Petechiae are seen in meningococcal disease with or without meningitis . The presence of a murmur suggests infective endocarditis with secondary bacterial seeding of the meninges .

17. Hepato splenomegaly and lymphadenopathy suggest a systemic disease, including viral ( eg , mononucleosis like syndrome in EBV, CMV, and HIV) and fungal ( eg , disseminated histoplasmosis ) disease . Vesicular lesions in a dermatomal distribution suggest varicella-zoster virus . Genital vesicles suggest HSV-2 meningitis

18. Acute infections of the nervous system are among the most important. clinical syndromes include 1) A cute bacterial meningitis , 2) V iral meningitis, 3) Encephalitis, 4) F ocal infections such as brain abscess and subdural empyema , and infectious thrombophlebitis

19. Acute bacterial meningitis S. pneumoniae gram-positive cocci , colonize at human nasopharynx . Most common bacterial cause of meningitis, accounting for 47% of cases with mortality rates 19-26% Mechanism: hematogenous or direct extension from sinusitis or otitis media

20. Risk factor B asilar skull fracture and CSF leak. Patients with hyposplenism or splenectomy hypogammaglobulinemia Multiple myeloma Glucocorticoids treatment D iabetes mellitus R enal insufficiency

21. Alcoholism Malnutrition Chronic liver disease Pneumonia Sinusitis Endocarditis

22. MANAGEMENT Key goals of early management are to emergently distinguish between these conditions. Identify the responsible pathogen , and initiate appropriate antimicrobial therapy.

23. The first task is to identify whether an infection predominantly involves the subarachnoid space ( meningitis ) or whether there is evidence of either generalized or focal involvement of brain tissue in the cerebral hemispheres, cerebellum, or brainstem . When brain tissue is directly injured by a bacterial or viral infection, the disease is referred to as encephalitis , whereas focal infections involving brain tissue are classified as either cerebritis or abscess , depending on the presence or absence of a capsule.

24. N. meningitidis Gram-negative diplococci in n asopharynx (10-15%) Leading cause of bacterial meningitis in children and young adults, accounting for 59% of cases. Meningococcal disease: purulent conjunctivitis, septic arthritis, sepsis +/- meningitis. Risk factors: household crowding ,college dormitories , military facilities chronic medical illness corticosteroid use .

25. H. influenzae - small, pleomorphic, gram-negative coccobacilli F requently found as normal flora in the upper respiratory tract of humans S pread by airborne droplets or direct contact with secretions. Meningitis is caused by the encapsulated type B strain It primarily affects infants younger than 2 years . Its isolation in adults suggests the presence of an underlying medical disorder, including sinusitis, otitis media, alcoholism, CSF leak following head trauma, hyposplenism and hypogammaglobulinemia .

26. L. monocytogenes small gram-positive bacillus O ne of the highest mortality rates (22%). Most human cases appear food-borne: coleslaw, milk, cheese Risk factor: infants and children , Elderly (>60 y) P regnant women Alcoholism Patients with CMI defect, immuno compromised.

27. Aseptic meningitis syndrome M ost common infectious syndrome affecting the CNS A cute onset of meningeal symptoms, fever, and cerebrospinal pleocytosis (usually prominently lymphocytic) with negative bacterial microbiologic data. Most episodes are caused by a viral pathogen but they can also be caused by bacteria, fungi, or parasites Importantly, partially treated bacterial meningitis accounts for a large number of meningitis cases with a negative microbiologic workup.

28. Aseptic meningitis syndrome HERPES (HSV, HZV, EBV, CMV ), ENTERO ( Echo,Coxakie,Polio,Enterovirus etc .) ARBO (JEV, Tick-bite encephalitis virus) Adenovirus LCMV HIV

29. VZV and CMV causes meningitis in immuno compromised hosts. Lymphocytic chorio meningitis virus(LCMV) transmit by aerosols and direct contact with rodents. may be associated with orchitis , arthritis, myocarditis, and alopecia. Mumps Meningitis usually follows the onset of parotitis , which clinically resolves in 7-10 days

30. HIV Aseptic meningitis may be the presenting symptom in a patient with acute HIV infection Always suspect HIV as a cause of aseptic meningitis in a patient with risk factors such as intravenous drug use and in individuals who practice high-risk sexual behaviors

31. Partially-treated bacterial meningitis L monocytogenes Brucella species Rickettsia rickettsii Ehrlichia species Mycoplasma pneumoniae Treponema pallidum Leptospira species Mycobacterium tuberculosis Nocardia species

32. Parasites N fowleri ( brain eating amoeba) Acanthamoeba species Angiostrongylus cantonensis or rat lung worm ( commenest cause of eosinophilic meningitis) Strongyloidiasis stercoralis (thread worm) Taenia solium ( cysticercosis )

33. FUNGI Cryptococcus neoformans C immitis H capsulatum Candida species Aspergillus species

34. Chronic meningitis S igns and symptoms of meningeal irritation associated with CSF pleocytosis that persists for longer than 4 weeks. B acterial V iral F ungal A septic (Lyme, syphillis ) TB Other causes of aseptic meningitis

35. Tuberculous meningitis A cid-fast bacilli  Patients generally have a prodrome of fever of varying degrees, malaise, and intermittent headaches Patients often develop central nerve palsies (III, IV, V, VI, and VII) suggesting basilar meningeal involvement 

36. MRC STAGINGOF TB MENINGITIS C linical staging of meningeal tuberculosis is based on neurologic status Stage 1 - no change in mental function with no deficits and no hydrocephalus.no definitive neurological symptom. Stage 2 - confusion and with or without evidence of neurologic deficit. signs of meningeal irritation. Stage 3 - stupor and lethargy. focal neurological deficits and involuntary movements.(50 %to 70%)

37. INFARCTION IN TBM

38. TUBERCULOMA

39. BORDER ZONE ENCEPHALITIS IN TBM

40. Spirochetal meningitis T pallidum modes of transmission: S exual contact D irect contact with an active lesion passage through the placenta blood transfusion (rare ). Syphilitic meningitis usually occurs during the primary or secondary stage . Its presentation is similar to other agents of aseptic meningitis

41. Other CNS syphilitic syndromes M eningovascular syphilis Parenchymatous neurosyphilis Gummatous neurosyphilis and T he symptoms are dominated by focal syphilitic arteritis ( ie , focal neurologic symptoms associated with signs of meningeal irritation)

42. Fungal meningitis C. neoformans A n encapsulated yeast-like fungus that found in high concentrations in aged pigeon droppings. 50-80% of cases occur in immunocompromised hosts. The infection is characterized by the gradual onset of symptoms, the most common of which is headache.  The onset may be acute, especially among patients with AIDS.

43. Parasitic meningitis Free-living amoebas ( ie , Acanthamoeba , Balamuthia,Naegleria ) infrequent but often life-threatening illness. N fowleri is the agent of primary amebic meningoencephalitis (PAM) . Infection occurs when swimming or playing in the contaminated water invade the CNS through the nasal mucosa and cribriform plate. 

44. Primary amebic meningo encephalitis ( PAM) An acute onset of high fever, photophobia, headache, and change in mental status, similar to bacterial meningitis with involvement of the olfactory nerves sensation. Death occurs in 3 days in patients who are not treated. Subacute or chronic form, is an insidious onset of low-grade fever, headache, and focal neurologic signs. Acanthamoeba and Balamuthia cause granulomatous amebic encephalitis, which spreads hematogenously from the primary site of infection (skin or lungs)

45. Helminthic eosinophilic meningitis Acantonensis cause eosinophilic meningitis ( pleocytosis with >10% eosinophils ). Acquire the infection by ingesting raw mollusks

46. On rare occasions, the larva can migrate into the CNS and cause eosinophilic meningitis. G spinigerum cause eosinophilic meningoencephalitis acquire the infection following ingestion of undercooked infected fish and poultry. This is common in Southeast Asia, China, and Japan

47. Differential diagnosis Encephalitis Brain Abscess. Noninfectious meningitis , M edication- induced meningeal inflammation Meningeal carcinomatosis Stroke CNS vasculitis Other causes of aseptic meningitis: malignancy NSAID’s chemo

48. Lumbar puncture Lumbar puncture for CSF examination is urgently warranted in individuals in whom meningitis is clinically suspected. CSF for Chemistry (glucose & protein) cell count & diff Gram stain ,AFB stain Culture for pathogens Other : India ink ,serology ,PCR ,Ag Identification ,cytology CSF Gram stain permits rapid identification of the bacterial cause in 60-90% of patients with bacterial meningitis. The presence of bacteria is 100% specific, but the sensitivity for detection is variable

49. Lumbar puncture Contraindications Increase risk of herniation(suspected space occupying lesion in CNS ). Skin & soft tissue infection at area of tap. Bleeding disorder. Respiratory distress (positioning ).

50. COMPLICATIONS Cerebral herniation. Post dural puncture headache . Traumatic tap ,Spinal trauma. Cerebral herniation following the lumbar tap procedure is rare in individuals with no focal neurologic deficits and no increased ICP. If it occurs, it usually happens within 24 hours following the lumbar puncture and should always be considered in the differential diagnosis if the patient's neurologic status deteriorates

51. Laboratory investigation CBC Peripheral smear HIV C ultures from other possible sites of infection. The utility of these cultures is most evident in cases when the performance of a lumbar puncture is delayed by the need for head imaging (risk for herniation in a patient with focal neurologic deficit or coma) and when antimicrobial therapy is rightfully initiated before the lumbar puncture and neuroimaging tests.

52. Imaging study CT or MRI of the brain INDICATIONS: Focal neurologic deficit Increased ICP Suspicious for space-occupying lesions Suspected basilar fracture Diagnosis is unclear

53. Helpful in the detection of CNS complications of bacterial meningitis, such as hydrocephalus, cerebral infarct, brain abscess, subdural empyema, and venous sinus thrombosis. Do not aid in the diagnosis of meningitis. Some patients may show meningeal enhancement, but its absence does not rule out the condition. CT scan of the brain may be performed prior to lumbar puncture in some patient groups with a higher risk of herniation newly onset seizures, moderate-to-severe impairment in consciousness

54. Treatment : Bacterial meningitis Bacterial meningitis is a neurological emergency that is associated with significant morbidity and mortality. The initiation of empiric antibacterial therapy is therefore essential for better outcome usually based on the known predisposing factors and/or initial CSF Gram-stain results. D elays in instituting antimicrobial treatment in individuals with bacterial meningitis could lead to significant morbidity and mortality Meningitis.

55. Treatment : Bacterial meningitis penicillins , certain cephalosporins ( ie , third- and fourth-generation cephalosporins ), the carbapenems , fluoroquinolones , and rifampin provide high CSF levels Once the pathogen has been identified and antimicrobial susceptibilities determined, the antibiotics may be modified for optimal targetted treatment Meningitis.

56. Antibiotics dosage Cefotaxime 12 g/day in divided doses 4h Ceftriaxone 4 g/day in divided doses 12h Gentamicin 7.5 mg/ kq /day 8h Meropenem 3 g/day divided doses 8h Metronidazole 400 mg/day divided doses 8h Nafcillin 9-12 g/day divided doses 4h Penicillin G 20-24 million U/day 4h Vancomycin 2 g/day 12h

57. Use of corticosteroid The use of corticosteroids such as dexamethasone as adjunctive treatment was significantly associated with a reduction in case-fatality rate and neurologic sequelae Strongly consider in patients with certain types of bacterial meninigitis , such as H influenzae , tuberculous , and pneumococcal meningitis S hould be administered prior to or during the administration of antimicrobial therapy May associate with decreased penetration into the CSF of some antimicrobials, such as vancomycin Dexamethasone (0.15 mg/kg per dose q6h for 2-4 d)

58. Viral meningitis Most viral meningitis are benign and self-limited. Often, they require only supportive care and do not require specific therapy. In certain instances, specific antiviral therapy may be indicated, if available Acyclovir (10 mg/kg IV q8h) for HSV-1 and HSV-2

59. Ganciclovir (induction dose of 5 mg/kg IV q12h, maintenance dose of 5 mg/kg q24h) and foscarnet (induction dose of 60 mg/kg IV q8h, maintenance dose of mg/kg IV q24h) for CMV meningitis in immunocompromised hosts. Instituting highly active antiretroviral therapy (HAART) may be necessary for patients with HIV meningitis that occurs during an acute sero conversion syndrome .

60. Tuberculous meningitis The demonstration of the acid-fast in the CSF is difficult and usually requires a large volume of CSF. The culture for Mycobacterium usually takes several weeks and may delay definitive diagnosis. Nucleic acid amplification for M tuberculosis have the advantage of a rapid, sensitive, and specific The need for mycobacterial growth in cultures remains because this offers the advantage of performing drug susceptibility assays.

61. Isoniazid (INH) and pyrazinamide (PZA) attain good CSF levels (approximate blood levels). Rifampin (RIF) penetrates the BBB less efficiently but still attains adequate CSF levels. U se the combination of the first-line drugs ( ie , INH, RIF, PZA, ethambutol , streptomycin. The dosage is similar to what is used for pulmonary tuberculosis(WEIGHT BAND).

62. A treatment duration of 12 months is the minimum, and some experts suggest a duration of at least 2 years . The use of corticosteroids is indicated for individuals with stage 2 or stage 3 disease ( ie , patients with evidence of neurologic deficits or changes in their mental function). The recommended dose is 0.15 mg/d, which may be tapered gradually during a span of 6 weeks.

63. Cryptococcal meningitis Diagnosis : identification of the pathogen in the CSF C neoformans culture from CSF. India ink preparation : sensitivity of only 50%, but highly diagnostic if positive CSF cryptococcal antigen : sensitivity of greater than 90% B lood cultures and serum cryptococcal antigen to determine if cryptococcal fungemia is present In many cases, cryptococcal meningitis is complicated by increased ICP

64. Cryptococcal meningitis in AIDS CD4<100/cu mm 2-7 cases/1000 with 89% CNS manifestation. 10,0000 cases world wide and 6,00000 death annualy . Relapse rate is 30 -50% Spreads haematogenously from pulmonary foci.

65. AIDS-related cryptococcal meningitis Induction therapy: amphotericin B ( 0.7 to 1 mg/kg/d IV) for at least 2 weeks Consolidation therapy: fluconazole (400 mg/d for 8 wk ). Itraconazole is an alternative Maintenance therapy: Long-term antifungal therapy with fluconazole (200 mg/d) In case of increased ICP. Make an effort to reduce such pressure by repeated lumbar puncture, a lumbar drain, or shunt In many cases, cryptococcal meningitis is complicated by increased ICP

66. cryptococcal meningitis in patients without AIDS Induction/consolidation: Administer amphotericin B (0.7-1 mg/kg/d) plus flucytosine (100 mg/kg/d) for 2 weeks . Then, administer fluconazole (400 mg/d) for a minimum of 10 weeks. A lumbar puncture is recommended after 2 weeks to document sterilization of the CSF. If the infection persists, longer therapy is recommended. Solid organ transplant recipients require prolonged therapy.

67. Fungal meningitis C. immitis H capsulatum Candida species Oral fluconazole (400 mg/d) or Itraconazole ( mg/d) Duration of treatment usually is life long. H capsulatum Amphotericin B at0.7to 1 mg/kg/d to complete a total dose of 35 mg/kg Fluconazole (800 mg/d) for an additional 9-12 months may be used to prevent relapse. Candida species amphotericin B (0.7mg/kg/d)+/- Flucytosine (25 mg/kg qid )

68. Syphilitic meningitis CSF SHOWS – Mild lymphocytic pleocytosis . E levated CSF protein levels & Decreased glucose levels may be observed in 10-70% of cases. Demonstrate the spirochete by using dark-field or phase- contrast microscopy on specimens collected from skin lesions ( eg , chancres and other syphilitic lesions).

69. CSF VDRL : sensitivity of 30-70% (a negative result does not rule out syphilitic meningitis) and a high specificity (a positive test result suggests the disease ). serologic tests to detect syphilis : VDRL test ,FTA-Abs , TPHA Isolating T pallidum from the CSF is extremely difficult and time consuming Always take care to not contaminate the CSF with blood during spinal fluid collection ( eg , traumatic tap).

70. Syphilitic meningitis P enicillin G (2-4 million U/d IV q4h) for 14 days , Often followed with benzathine penicillin G 2.4 million U IM. Alternative : administer procaine penicillin G (2.4 million U/d IM) plus probenecid (500 mg PO qid ) for 14 days, followed by IM benzathine penicillin G (2.4 million U). Repeat CSF examination : cell count , serologic titers Because penicillin G is treatment of choice, patients who are allergic to penicillin should undergo penicillin desensitization .

71. Lyme meningitis Neurologic complications of Lyme disease (other than Bell palsy) ideally require parenteral antibiotic administration. The drug of choice is ceftriaxone (2 g/d) for 14 to21 days . The alternative therapy is penicillin G (20 million U/d) for14to 21 days. Doxycycline (100 mg PO/IV bid) for14to21 days or chloramphenicol (1 g qid ) for14to 21 days has also been used.

72. Complications : Early increased intracranial pressure (ICP) V enous sinus thrombosis. Subdural empyema. Brain abscess. C ranial nerve palsies cerebral infarction result from impaired cerebral blood flow. Cranial nerve palsies and the effects of impaired cerebral blood flow, such as cerebral infarction, are caused by increased ICP.

73. Complications : Late Hearing impairment Obstructive hydrocephalus. Brain parenchymal damage

74. Further Inpatient Care Monitor the clinical course & response to medical treatment. Surveillance for the development of complications. Seizure precautions are indicated, especially for patients with impaired mental function Proper isolation precautions in cases of invasive meningococcal disease

75. Monitor patients for potential adverse effects of medications, S uch as hypersensitivity reactions, cytopenia , or drug toxicity Drug-level monitoring for some antibiotics such as vancomycin and aminoglycosides. Liver dysfunction

76. Isolation – Meningococcemia Capable of transmitting organism up to 24 hours after initiation of appropriate therapy Droplet precautions x 24 hours, then no isolation Incubation period days, usually <4 days

77. Meningococcemia - Prophylaxis Rifampin < 1 month 5 mg/kg PO Q 12 x 2 days >1 mo 10 mg/kg (max 600 mg) PO Q 12 x 2days. for adults 600mg 12 h for 2 days.or tab ciprofloxacin 500mg once. Ceftriaxone <1m 125 mg IM x 1 dose >1m 125 mg IM x 1 dose >15y 250 mg IMx 1 dose

78. Prognosis viral meningitis usually have a good prognosis for recovery. The prognosis is worse for patients at the extremes of age ( ie , <2 y, >60 y) and with significant comorbidities and underlying immunodeficiency. Patients presenting with an impaired level of consciousness are at increased risk for developing neurologic sequelae or dying . A seizure during an episode of meningitis also is a risk factor for mortality or neurologic sequelae . The presence of low-level pleocytosis (<20 cells) in patients with bacterial meningitis suggests a poorer outcome .

79. Meningococcemia - Prophylaxis Persons who have had “intimate contact” w/ oral secretions prior & during 1st 24 h of antibiotics “Intimate contact” – HIGH RISK (kissing , eating/ drinking utensils, mouth-to-mouth, suctioning, intubating ). Treat within 24 hours of exposure Chemoprophylaxis can be considered for people in close contact with patients in the endemic situation

80. CSF IN TB MENINGITIS ( 1) Elevated opening pressure, ( 2) Lymphocytic pleocytosis ( 10–500 cells/ Μ l) (3 ) Elevated protein concentration ( 4) Decreased glucose concentration in the range of 20–40 mg/ dL .

81. Cultures of CSF take 4–8 weeks to identify the organism and are positive in ~50% of adults. Culture remains the gold standard to make the diagnosis of tuberculous meningitis. PCR for the detection of M. tuberculosis DNA should be sent on CSF if available, but the sensitivity and specificity on CSF have not been defined. CDC recommends the use of nucleic acid amplification tests for the diagnosis of pulmonary tuberculosis.

82. The combination of unrelenting headache, stiffneck , fatigue, night sweats, and fever with a CSF lymphocytic pleocytosis and a mildly decreased glucose concentration is highly suspicious for tuberculous meningitis.

83. The last tube of fluid collected at LP is the best tube to send for a smear for acid-fast bacilli (AFB ). If there is a pellicle in the CSF or a cobweb-like clot on the surface of the fluid, AFB can best be demonstrated in a smear of the clot or pellicle. Positive smears are typically reported in only 10–40% of cases of tuberculous meningitis in adults.

84. CSF abnormalities in fungal meningitis A mononuclear or lymphocytic pleocytosis , an increased protein concentration, and a decreased glucose concentration. There may be eosinophils in the CSF in C. immitis meningitis . Large volumes of CSF are often required to demonstrate the organism on India ink smear or grow the organism in culture . If spinal fluid examined by LP on two separate occasions fails to yield an organism, CSF should be obtained by high-cervical or cisternal puncture.

85. The cryptococcal polysaccharide antigen test is a highly sensitive and specific test for cryptococcal meningitis. A reactive CSF cryptococcal antigen test establishes the diagnosis . The detection of the Histoplasma polysaccharide antigen in CSF establishes the diagnosis of a fungal meningitis B ut is not specific for meningitis due to H. capsulatum . It may be falsely positive in coccidioidal meningitis. The CSF complement fixation antibody test is reported to have a specificity of 100 % and a sensitivity of 75% for coccidioidal meningitis.

86. The diagnosis of syphilitic meningitis Reactive serum treponemal test (fluorescent treponemal antibody absorption test [FTA-ABS] or Micro hemagglutination assay– T. pallidum [MHA-TP]) is associated with a CSF lymphocytic or mononuclear Pleocytosis and an elevated protein concentration, or when the CSF Venereal Disease Research Laboratory (VDRL) test is positive .

87. A reactive CSF FTA-ABS is not definitive evidence of neurosyphilis . The CSF FTA-ABS can be falsely positive from blood contamination. A negative CSF VDRL does not rule out neurosyphilis . A negative CSF FTA-ABS or MHA-TP rules out neurosyphilis

88. TEST APPEARENCE PRESSURE WBC/micro lit PROTEIN mg/dl Glucose mg/dl Chloridemeq /l normal clear 90-180mm 0-8 lym 15-45 50-80 115-130 A. BACT MEN TURBID INCREASED 1000-10000 100-500 <40 DECRESED VIRAL CLEAR N ORMAL/ MODERATE 5-300RARELY>1000 N- MILD> NORMAL NORMAL TB MEN COB WEB 100-600 MIXED OR LYM 50-300 due to spinal block DECREASED DECREASED FUNGAL CLEAR 40-400 mixed 50-300 decreased decreased Ac syphilitic clear About 500lym > But <100 normal normal

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