menengitis

1. MENINGITIS
Acute infection of the meninges presents with a
characteristic tirade of
1. pyrexia,
2. headache
3. and meningism

3. BACTERIAL MENINGITIS
Acute infection of the meninges presents with a characteristic
triade of
1- pyrexia, 2- headache 3-and meningism
Meningeal signs :
1- stiffness of the neck
2- Kernig's sign (with the hip joint flexed, extension at the knee
causes spasm in the hamstring muscles)
3- Brudzinski's sign (passive flexion of the neck causes flexion of
the thighs and knees).
Etiology

4. MOST CAUSATIVE ORGANISM ACCORDING TO AGE:
Neonate E. Coli and Group B Strept , Listeria monocytogens
Infants H. Influenza, N. meningitidis . Pneumococcus
Teens/ young adults N. Meningitidis /H. Influenza, Pneumococcus
Elderly Pneumococcus, N. Meningitidis /H. Influenza,
Viral infection is the most common cause of meningitis, and
usually results in a benign and self-limiting illness requiring no
specific therapy

5. Clinical features
stiff neck, headache, fever, photophobia, vomiting, irritability, impairment
of consciousness, confusion, seizures and, morelikely in pneumococcal
meningitis, focal neurological signs and symptoms. Meningism is present
in the majority of patients, in deeply comatose patients this meningism
might be absent as it may be in the very early stage of the disease or in
very elderly patients.
The clinical signs and symptoms evolve rapidly, within few or several
hours, in some instances bacterial meningitis may also have a more sub
acute presentation (more typically in pneumococcal meningitis). The
detection of petechiae or a purpura fulminans on presentation is highly
suggestive of N. meningococcal infection

7. CSF
ANALYSIS

9. Cell count with differential, Glucose and protein concentration
Stain and culture
1. Gram’s stain and bacterial culture
2. India ink and fungal culture
3. Viral culture
4. Acid fast smear and M. tuberculosis culture
Polymerase chain reaction
1. Broad range bacterial PCR (16S ribosomal DNA)
2. Specific meningeal pathogen PCR
3. Reverse transcriptase PCR for enteroviruses
4. PCR for herpes simplex virus type 1 and 2
5. PCR for West Nile V
6. PCR for Epstein Barr virus 7. PCR for varicella zoster V
8. PCR for M. tuberculosis 9. PCR for HIV RNA

10.  Antigens
1-- Cryptococcal polysaccharide antigen
2-- Histoplasma polysaccharide antigen
 Antibodies
1. Herpes simplex virus (serum and CSF IgG to
calculate antibody ratio)
2. Varicella zoster virus IgM, and IgG antibody index
3. Arthropod-borne viruses (West Nile virus IgM)
4. Borrelia burgdorferi antibody index
5. C. immitis complement fixation antibody
6. HHV-6 IgM

11. Meningococcal infection
purulent meningitis 50%
sepsis syndrome in 25-35%
both sepsis and meningitis 15%
fulminating meningococcal septicemia, 10%
Diagnosis
-Elevated CSF cell count (>1000 WBC/μl, with more than 60% PMN)
-Elevated total protein content (>120mg/dl)
-Low CSF glucose concentration (CSF blood glucose ratio of less than <0,3)
-Identification of the bacterial pathogen in the CSF culture – CSF, blood,
skin biopsy microscopy of a gram stained smear antigen detection (latex particle agglutination
test)
Polymerase chain reaction (PCR) techniques can be used on both blood and CSF to identify
bacterial DNA

12. Cerebral complications
Brain edema with the risk of herniation
Arterial vascular complications: arteritis, vasospasm, focal cortical hyperperfusion,
altered cerebrovascular autoregulation
Septic sinus/venous thrombosis (in particular of the superior sagittal sinus) and Cortical
thrombophlebitis
Hydrocephalus
Cerebritis
Subdural effusion (in infants and children)
Rarely as a consequence of meningitis: brain abscess, subdural empyema
Vestibulocochlear involvement purulent labyrinthitis
Extracranial complications myocarditis
Septic shock
Disseminated intravascular coagulation
Adult respiratory distress syndrome (ARDS)
Arthritis (septic or reactive)
Electrolyte disturbances (hyponatremia, syndrome of inappropriate ADH secretion
(SIADH) or, rarely, central diabetes insipidus)
Spinal complications (e.g. myelitis, infarction)
complications

13. Therapeutic management
Empiric antimicrobial chemotherapy
initiate an antibiotic therapy without microbiological confirmation (neither by
gram stain nor by culture)
Recommended antibiotic
microorganism
Age
Cefotaxime plus ampicillin, or
ampicillin plus aminoglycoside
E. coli, Klebsiella, Enterobacter,
Proteus) L. monocytogenes
<1months
Ceftriaxone, plus vancomycin
S. pneumoniae, N. meningitidis
, H. Influenzae,E. coli
Preschool
and young
adult Ceftriaxone, plus vancomycin
N. meningitidis, S. pneumoniae
Listeria, Enterobacteriaceae
Ceftriaxone plus vancomycin plus
ampicillin
S. pneumoniae, N. meningitidis,
Listeria
>50 years

14. Recommended antibodies
Typical pathogens
Clinical condition
Ceftriaxone* plus
vancomycin †
plus ampicllin
S. pneumoniae, N.
meningitidis,
L. monocytogenes
Healthy, immunocompetent
(community-acquired)
Ceftazidime (or meropenem)
plus vancomycin ‡ or
fosfomycin
Staphylococci,
Enterobacteriaceae,
P. aeruginosa
Nosocomial (e.g. post-
neurosurgical
Or posttraumatic brain
injury)
=
=
shunt infection

15. N. meningitidis =======Penicillin G=== Ceftriaxone (or cefotaxime), Ampicillin,
rifampin
S. pneumoniae, penicillin susceptible=== Penicillin G (or Ampicillin)
====Ceftriaxone (or cefotaxime) Meropenem, cefepime
H. Influenzae Group streptococci==== Ceftriaxone (or cefotaxime) Penicillin G (±
gentamicin)=====Ampicillin plus chloramphenicol Ceftriaxone, Ampicillin (plus
gentamicin), vancomycin
Meningococci 7 days
Haemophilus influenzae type B 10-14 days
Pneumococci 14 days
Listeria monocytogenes >3 weeks
Gram negatives >3 weeks

16. Adjunctive therapy
Corticosteroids
management of increased intracranial pressure
anticonvulsants
Chemoprophylaxis
recommended for all people of the same household
Rifampicin (2x600mg/day for 2 days) is the drug most often recommended for
chemoprophylaxis, alternatives are ciprofloxacin (500mg orally once), or Ceftriaxone
(250-500mg i. m. once)
chemoprophylaxis is also recommended for the index patient at the time of discharge f
Vaccination
Haemophilus influenzae type B
serogroup C meningococcal meningitis
pneumococcal vaccine

17. I. recommended for patients with terminal complement component deficiency,
II. asplenia,
III. travellers to areas with epidemic meningococcal disease (so- called
meningococcal meningitis belt).
IV.splenectomised patients (or with functional asplenia),
V. chronic debilitating diseases
VI.such as diabetes mellitus
VII. with posttraumatic CSF leakage.

18. TUBERCULOUS MENINGITIS
Tuberculous meningitis,
Tuberculoma, or Tuberculous involvement of the spine with myelopathy (Pott's disease)
M. tuberculosis and
M. bovis
Clinical Features
low-grade fever, headache, and intermittent nausea and vomiting, followed by more
severe headache, neck stiffness, altered mentation, and cranial (usually III, but also II, VII,
and VIII) nerve palsies meningeal signs, seizures, and focal neurological deficits, including
hemiparesis, increasing drowsiness, and signs of increased ICP choroidal tubercles

19. TUBERCULOSIS
MODE OF TRANSMISSION:
 haematogenous dissemination of Mycobacterium
tuberculosis from primary pulmonary infection
 brain and spinal cord sub-pial and sub-ependymal
foci of infection (Rich foci)
I. rupture and release bacteria into the subarachnoid
space causing meningitis
II. enlarge to form tuberculomas without meningitis

20. Diagnosis.
tubercle bacilli on CSF acid-fast bacilli (AFB) smear or culture
CSF culture results are positive for M. tuberculosis in 45-70% of patients but may take 6-8
weeks to become positive.
CSF examination demonstrates normal or elevated opening pressure, elevated protein
{80^400 mg/dL), low glucose (<40 mg/dL), and pleocytosis (averaging 200-400 ]WBC/dL
with lymphocytic predominance
Tuberculomas, the parenchymal form of TB, occur as single
or multiple brain or spinal cord lesions and present with signs and symptoms of space-
occupying lesions.
polymerase chain reaction (PCR) technique has been applied and is now routinely
available for the diagnosis of TB meningitis, with
reported sensitivities of 70-75%.

21.  The diagnostic yield of Nucleic Acid
Amplifection [NAA] increases when large
volumes of CSF are processed. NAA tests are
more useful than conventional bacteriology after
the start of anti-tuberculosis treatment. NAA
assays can detect the rifampicin resistance
genotypes
 CSF adenosine deaminase activity is not
recommended as a routine diagnostic test for
CNS tuberculosis .
 The tuberculin skin test and IGRAs (using
peripheral blood) may provide indication of
previous tuberculosis
 Interferon-gamma release(QuantiFERON-TB
gold and T-SPOT.TB), are more accurate than
skin testing at diagnosing latent tuberculosis

22. TB MENINGITIS RADIOLOGICAL TESTS
 The brain of every patient with TBM should be imaged with
contrast enhanced CT either before the start of treatment(as part
of the diagnostic work-up), or within the first 48 h of treatment
 All patients with suspected cerebral tuberculoma or spinal cord
tuberculosis should be investigated by MRI which may show:
1. Communicating hydrocephalus
2. 40% vasculitis
3. Basal enhancement
4. Tuberculoma
5. Spinal = T1 isointense enhances with Gd

23.  50% of patients with TBM have chest X-rays suggesting
active or previous pulmonary tuberculosis
 Chest CT may reveal abnormalities missed by CXR
 The commonest cerebral CT features of TBM are
hydrocephalus and basal contrast enhancing exudates
 Infarctions as a result of ongoing vasculitis or
tuberculoma are found in approximately 20% of patients
at presentation Infarctions most commonly involve the
basal ganglia and the territories of the medial striate and
thalamoperforating arteries
 magnetic resonance spectroscopy (MRS) large lipid CH2
peak and choline/creatine ratio >1
 Patients should be treated for a minimum of 12 months

24. Isoniazid (INH) .5-10 (max 300 mg) PO, add pyridoxine to prevent
neuropathy (Child 25 mg/kg/day PO, Adult 50 /mg/kg/day PO)
side effect Hepatitis (1-2%), neuropathy (5%), seizures
Rifampin (RIF) Child 15 PO, Adult 10 PO"
side effect Hepatitis (1-2%),
Pyrazinamide 25 (max 2.5 g/day) PO
Arthralgia (5%!, hepatitis (1-5%), hyperuricemia, gout, rash
Streptomycin Child 30 IM Adult 15 (max 1 g/day) IM Hearing loss, vestibular imbalance
(1-5%)
Ethambutol 15-25 (max 2.5 g/day) PO Optic neuritis (3%), neuropathy (1-2%), rash

25. During treatment CSF is reexamined to monitor treatment efficacy and drug levels. Neuro
imaging studies are performed 2-3 months after the start of treatment and again at 3- to 6-month
intervals to verify improvement in lesions. Two years of treatment may be necessary for
tuberculomas.
Chemotherapy alone is effective treatment for most spinal TB without cord involvement.
Complications.
Progressive hydrocephalus
damage to the optic nerves and chiasm in the suprasellar cistern causes blindness
the syndrome of inappropriate secretion of antidiuretic hormone
vasculitis; stroke;
arachnoiditis;
spinal cord atrophy;
and syringomyelia.
2 1% mortality rate for immunocompetent patients and 33% for HIV-infected patients

26. Direct involvements
VIRAL INFECTIONS
meningitis
encephalitis (acute or chronic forms such as subacute sclerosing panencephalitis [SSPE]),
myelitis,
ganglionitis,
polyradiculitis
post infectious CNS inflammatory or autoimmune syndromes, such as acute
disseminated encephalomyelitis (ADEM)
Indirect involvements
Herpes viruses
1. HSV-type 1 and type 2
2. Varicella zoster virus (VZV),
3. Cytomegalovirus (CMV),
4. Epstcin-Barr virus (EBV),
5. Human herpes viruses {HHV-6, HHV-7, and HHV-S),
6. the simian {"monkey") Herpes B-virus.

27. Herpes Simplex Encephalitis (HSE),
HSV-1 is the most common viral cause of acute sporadic encephalitis
1. fever,
2. headache,
3. altered level of consciousness
4. behavioral changes,
5. an amnestic syndrome
6. focal or multifocal neurological deficit
7. focal or generalized seizure activity
8. hallucinations, particularly olfactory hallucinations
The diagnosis of HSE should be considered in any febrile patient with an altered level of
consciousness

28. Examination of cerebrospinal fluid (CSF)
Lymphocytic pleocytosis of 10-1000 white blood count (WBC)
Virus may be cultured from the CSF in less than 5% of cases
HSV DNA can be detected in the CSF with polymerase chain reaction (PCR)
techniques. CSF PCR testing has an estimated sensitivity of greater than 95% and
a specificity approaching 100%
CT and magnetic resonance imaging (MR1)
focal abnormalities in fronto-temporal regions
Electroencephalogram (EEG)
diffuse slowing, focal abnormalities in the temporal regions, or periodic lateralizing
epileptiform discharges (PLEDS).
Brain biopsy
the diagnosis remains in question or those who respond poorly to treatment
Therapy
Acyclovir[10] mg/kg every 8 hours for[ 14-21]
Dosing should be adjusted appropriately in patients with renal insufficiency. Treatment
with acyclovir reduces mortality of HSF from 70% to 20%
Foscarnet

30. Viral encephalitis
Tick borne encephalitis
Fever, malaise, stiff neck, sore throat, and nausea and vomiting, progressing to
stupor, coma, and convulsions.
Signs of an upper motor neuron lesion (exaggerated deep tendon reflexes, absent
superficial reflexes, pathologic reflexes, and spastic paralysis
Cerebrospinal fluid protein and opening pressure often increased, with lymphocytic
pleocytosis.
Mosquito-borne
Eastern equine Venezuelan equine St. Louis Japanese B
Murray Valley West Nile
Tick-borne complex
Far Eastern Central European
Russian spring-summer

31. AUTOIMMUNE ENCEPHALOPATHY
 Sub acute encephalopathy
 Cognitive and behavioral deficit
 Toxic ,Metabolic and infectious causes should
be excluded
 Elevated CSF protein with normal cells
 Presence of certain serum and CSF auto
antibodies
 Rapidly progressive causes of dementia should
be excluded