Meningitis, Encphalitis, Neurocystecercosis

Meningitis, Encephelitis &
Neurocysticercosis
Dr (Brig) YD Singh
MBBS, MD (Medicine), FIACM, DIT
Professor & Head, Unit of Medicine

FOM, AIMST University, Malaysia
Meninges: the Brain coverings
Meninges are 3 layers of protective tissue called

Dura mater, Arachnoid mater, and Pia mater
that surround the neuraxis.
The meninges of brain and spinal cord are continuous,
being linked through the foramen magnum.
March 3, 2022 Prof (Brig) YD Singh 2

Dura Mater (1)
• Most superior of meningeal layers
• Name means = "hard mother" in Latin
• It is tough and inflexible
• Forms several structures that separate the cranial cavity into compartments and
protect the brain from displacement.
• Falx cerebri separates cerebral hemispheres
• Falx cerebelli separates lobes of cerebellum
• Tentorium cerebelli = Cerebrum from Cerebellum
• It also forms several vein-like sinuses that carry blood back to the heart
• Superior sagittal sinus runs across top of brain in anterior-posterior direction

Dura Mater (2)
• Other sinuses include
• Straight sinus, Inferior sinus & transverse sinus
• Epidural space is a potential space between dura & skull.
• Subdural space another potential space between dura & arachnoid.
• Head injury may cause blood to collect in these potential spaces & cause brain
compression
• Epidural haematoma
• Subdural haematoma

Arachnoid Mater
• Term arachnoid = spider web like appearance of blood vessels within the
space
• It is middle layer of the meninges
• In some areas, it projects into sinuses formed by dura mater = Arachnoid villi
• Transfer CSF from ventricles back into blood
• Subarachanoid space lies between
• Arachnoid and pia mater & is filled with CSF
• All blood vessels entering the brain & cranial nerves pass through this
space

Pia Mater
• Pia mater is innermost layer of the meninges
• Unlike other layers
• Pia tissue adheres closely to the brain,
• Running down into sulci & fissures of cortex
• It fuses with the ependyma (membranous lining of brain ventricles) to form
structures called Choroid plexus which produce CSF

Cerebrospinal Fluid (CSF) (1)
• Purpose
• CSF is a clear liquid produced in ventricles
• Like saliva it is a blood filtrate
• It is also found inside the subarachnoid space (SAS) which surrounds Brain and
spinal chord
• Spinal chord central canal also contains CSF
• Average 150 mL of CSF circulates
• Forms @ 0.3–0.4 mL/min, 18-25 mL/hour and 430–530 mL/day
• It acts as a cushion for the neuraxis
• Supplies nutrients to Brain & spinal cord & removes waste from the
neuraxis

• Choroid Plexus
• All brain ventricles contain choroid plexuses which produce CSF by allowing certain
components of blood to enter the ventricles
• Choroid plexuses = Pia mater + Ependyma
• The Ventricles (there are 4 of them)
• 2 lateral + one third + one fourth ventricle
• All four ventricles are connected to each other
• They are filled with CSF & protect brain by cushioning it & supporting its weight.
• 2 lateral ventricles extend across a large area of brain. Anterior horns located in
frontal lobes

• Lateral Ventricles (continued)
• They extend posteriorly into parietal lobes
• Inferior horns are found in temporal lobes
• 3rd ventricle lies between 2 thalamic bodies
• Hypothalamus forms floor of 3rd ventricle
• 4th ventricle lies between Pons & Cerebellum
• Two interventricular foramina ( F of Munro)
• Link lateral ventricles to Third ventricle
• Aqueduct of Sylvius connects 3rd & 4th Vent
• 4th ventricle connected to brain SAS via two lateral foramina of Lushka and spinal
SAS by one medial foramen of Magendie

• CSF circulation & Subarachnoid Space
• CSF is manufactured in all ventricles
• It circulates through neuraxis in specific pattern
• Moving from Lat ventricle to 3rd to 4th ventricle
• Then passes into subarachnoid space where it circulates outside of brain & spinal cord
• Finally makes its way to superior sagittal sinus via the arachnoid villi
• In superior sagittal sinus CSF is reabsorbed into the blood stream.
• Total CSF is regenerated several times a day
• Endolymph & Perilymph (of inner ear) derived from CSF (process of ? Osmosis)

Cerebral ventricles: Various views

MRI showing pulsation of CSF

Definitions
• Meningitis = inflammation of meninges
• Encephalitis = inflammation of brain
parenchyma
• Meningo-encephalitis = inflammation of brain
paranchyma + meninges
• Aseptic meningitis = inflammation of meninges
with sterile CSF
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Prof (Brig) YD Singh 14
Acute infections of Nervous system
• Acute Bacterial meningitis
• Sub-acute / Chronic Bacterial meningitis
• Mycobacterium tuberculosis (Leading cause)
• Coxiella burnetii, Brucella, Leptospira, Actinomyces
• Viral meningitis,
• Encephalitis,
• Focal infections
• Brain abscess, Subdural empyema
• Thrombophlebitis

Acute Bacterial Meningitis
• Acute purulent infection within the subarachnoid space associated

with a CNS inflammatory reaction that may result in decreased
consciousness, seizures, raised intracranial pressure (ICP), and stroke

Epidemiology: Acute Bacterial Meningitis
• Streptococcus pneumoniae (~50%)
• N. meningitidis (~25%),
Above 2 most common causes of community acquired Acute bacterial meningitis
• Group B streptococci (~15%),
• Listeria monocytogenes (~10%)
• Most common predisposing factors
• Age >50 years, Diabetes, Chronic illness, Malignancy & immunosuppressive therapy / state
• H. influenzae now accounts for <10% of cases

Causes : Meningitis

Etiology- S. pneumoniae
• S. pneumoniae is the most common cause of

meningitis in adults >20 years of age
• Risk factors --coexisting acute or chronic

pneumococcal sinusitis or otitis media, alcoholism,
diabetes, splenectomy, hypo-gammaglobulinemia,
complement deficiency, and head trauma with basilar
skull fracture and CSF rhinorrhea

N. meningitidis
• 25% of all cases

• petechial or purpuric skin lesions
• fulminant
• nasopharyngeal colonization --asymptomatic carrier state or invasive
meningococcal disease
• complement deficiency -highly susceptible

Clinical signs of meningeal irritation

Listeria monocytogenes
• Neonates (<1 month of age), pregnant women, individuals >60 years,

and immunocompromised individuals
• Foodborne

H. influenzae type b meningitis in extremes
of age Neoantes & elders
• Declined dramatically since the introduction of the Hib conjugate

vaccine
• Others—Staphylococcus aureus and coagulase-negative staphylococci

Pathophysiology
• Initially colonize nasopharynx bloodstream

intraventricular choroid plexus, directly infect choroid
plexus epithelial cells, and gain access to the CSF
• Causes inflammatory reaction
• Multiply rapidly within CSF because of the absence of
effective host immune defenses
• Cytokines-TNF and IL-1
• Vasogenic edema and leakage of serum proteins into the
subarachnoid space

Symptoms : Meningitis
• Classic clinical triad of meningitis
• Fever, Headache, and Neck rigidity
• Headache = seen almost always present
• Photophobia = seen in 2/3rd patients
• Vomiting = seen in 2/3rd patients
• Neck stiffness = seen in 2/3rd patients
• Fever = seen in 2/3rd patients
• Altered mental status = seen in 2/3rd patients
• Myalgia = seen in 50 - 90 % patients
• Body rash = aetiology dependent (N. meningitidis)

Clinical Features & aetiology correlation in
Meningitis

Increased intracranial pressure (ICP)
• Papilledema
• Cushing’s triad
• Bradycardia
• Hypertension
• Irregular respiration
• Changes in pupils
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Meningococcemia – Petechiae/Purpura
March 3, 2022
Treatment of Raised ICP
• Elevation of the patient's head to 30–45°

• Elective intubation and
• Hyperventilation (PaCO2 25–30 mmHg)
• Mannitol IV

Meningitis - Acute complications
• Hydrocephalus
• Subdural effusion or
empyema ~30%
• Stroke
• Abscess
• Dural sinus thrombophlebitis
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Diagnosis – Lumbar puncture
March 3, 2022
• When patient presents
symptoms of Meningitis,
a sample of CSF is
acquired from a spinal
tap, which is then
analyzed for bacterial
presence.
March 3, 2022
Lumber Puncture
• Contraindications:
• Respiratory distress (positioning difficult)
•  ICP reported to increase risk of herniation
• Cellulitis at area of tap
• Bleeding disorder

Diagnosis : Acute Bacterial Meningitis
• Consistent Clinical picture with meningitis
• Performing lumbar puncture (LP)
• to evaluate meningeal inflammation & bacteria
• Gold standard for diagnosis is CSF pathogen identification on Gram stain & /or culture of CSF
• Brain imaging prior to LP is recommended
• Patients with any of the following do CT brain
• Altered level of consciousness,
• Focal neurological deficit , New-onset seizures
• Papilledema or other signs of raised ICP

Differential Diagnosis
• Viral meningoencephalitis
• Rickettsial disease
• Focal suppurative CNS infections
• Subarachnoid hemorrhage
• Chemical meningitis

Treatment :
Empirical Antimicrobial Therapy
• Begin antibiotic therapy within 60 min of a patient's arrival
in the emergency room
• S. pneumoniae & N. meningitidis
• Combination of a third-generation cephalosporin
( ceftriaxone or cefotaxime) + vancomycin
• Cefepime is a broad-spectrum fourth-generation
cephalosporin for Enterobacter species and Pseudomonas

Treatment :
Empirical Antimicrobial Therapy
• Ampicillin should be added to the empirical regimen for coverage of L.

monocytogenes in individuals <3 months of age, those >55, or those
with suspected impaired cell-mediated immunity
• Meropenem is a carbapenem antibiotic that is highly active in vitro
against L. monocytogenes

Specific Antimicrobial Therapy table
March 3, 2022
Prognosis –increased risk
• (1) Decreased level of consciousness on admission,

• (2) Onset of seizures within 24 h of admission,
• (3) Signs of increased ICP,
• (4) Young age (infancy) and age >50,
• (5) Presence of co-morbid conditions including shock and /or need
for mechanical ventilation,
• (6) Delay in the initiation of treatment.
• (7) Decreased CSF glucose concentration (<40 mg/dL)] and
markedly increased CSF protein concentration [>3 g/L)

Acute Viral Meningitis
• Headache, fever, and signs of meningeal irritation coupled with an

inflammatory CSF profile
• Headache-frontal or retro-orbital and often associated with
photophobia and pain on moving the eyes
• Constitutional signs
• Mild lethargy or drowsiness

Etiology

Laboratory Diagnosis - CSF Examination
• Lymphocytic pleocytosis (25–500 cells/ L)

• Normal or slightly elevated protein concentration (20–
80 mg/dL)
• Normal glucose concentration,
• Normal or mildly elevated opening pressure (100–350
mmH2O )
• CMV / Mumps virus—cell count in thousands

CSF Comparison

Lab diagnosis
• Polymerase Chain Reaction

(PCR )Amplification of Viral Nucleic Acid --enteroviral and HSV
infections
cytomegalovirus (CMV),
Epstein-Barr virus (EBV),
VZV, and human herpesvirus 6 (HHV-6).
* HSV PCR --recurrent episodes of "aseptic" meningitis

Lab diagnosis
• Viral Culture
• Serologic Studies –
seroconversion between acute-phase and convalescent sera (typically
obtained after 2–4 weeks ) OR
virus-specific IgM antibodies

Differential Diagnosis
• 1) Partially treated bacterial meningitis;

• (2) Early stages of meningitis caused by fungi, mycobacteria, or
Treponema pallidum
• (3) Meningitis caused by agents such as Mycoplasma, Listeria spp.,
Brucella spp., Coxiella spp., Leptospira spp., and Rickettsia spp.
• (4) Parameningeal infections;
• (5) Neoplastic meningitis

Enteroviruses
• >75% of cases
• CSF reverse transcriptase PCR (RT-PCR) is the diagnostic procedure of
choice
• summer months, especially in children (<15 years),
• stigmata of enterovirus infection

HSV-2 meningitis
• ~25% of women and 11% of men at the time of an initial (primary)

episode of genital herpes
• 20% - recurrent attacks of meningitis
• HSV-CSF PCR diagnostic

VZV meningitis
• Concurrent chickenpox or shingles

• VZV CSF IgM antibodies,
• Or by positive CSF cultures.

Others
• EBV infections
• HIV meningitis
• Mumps
• CMV infection

Acute Viral Meningitis: Treatment
• Symptomatic--analgesics, antipyretics, and antiemetics

• Oral or intravenous acyclovir --HSV-1 or -2 and in cases of severe EBV or
VZV infection
• Pleconaril –enteroviral
• Vaccination

Viral Encephalitis
• Brain parenchyma is mainly involved

• Evidence of associated meningitis (meningoencephalitis)
• Involvement of the spinal cord or nerve roots (encephalomyelitis,
encephalomyeloradiculitis).

Clinical Manifestations
• Altered level of consciousness (confusion, behavioral abnormalities), or

a depressed level of consciousness, ranging from mild lethargy to coma,
• Evidence of either focal or diffuse neurologic signs and symptoms.
• Hallucinations, agitation, personality change, behavioral disorders,
and, at times, a frankly psychotic state.
• Focal or generalized seizures

• aphasia, ataxia, upper or lower motor neuron patterns of weakness,
involuntary movements (e.g., myoclonic jerks, tremor), and cranial
nerve deficits
• hypothalamic-pituitary axis-- temperature dysregulation, diabetes
insipidus ,SIADH

Laboratory Diagnosis
CSF Examination
• Indistinguishable from that of viral meningitis
• CSF pleocytosis (>5 cells/ μL) occurs in >95% of patients with
documented viral encephalitis
• About 20% of patients with encephalitis will have a significant number
of red blood cells (>500/ μL) in the CSF in a nontraumatic tap

CSF PCR
• Primary diagnostic test for CNS infections caused by CMV, EBV, VZV,
HHV-6, and enteroviruses
• Initially negative HSV CSF PCR --positive when repeated 1–3 days later
• Generally not affected by 1 week of antiviral therapy

Serologic Studies and Antigen Detection
• HSV antibodies and antigen typically occurs after the first week of
illness
• Demonstration of West Nile Virus (WNV) IgM antibodies is diagnostic
of WNV encephalitis as IgM antibodies do not cross the blood-brain
barrier, and their presence in CSF is therefore indicative of intrathecal
synthesis

MRI, CT, EEG- HSV encephelitis
• Focal and diffuse encephelitis

• Focal findings include:
(1) areas of increased signal
intensity in the fronto-temporal
region of the brain on T2-
weighted, FLAIR, or diffusion-
weighted MRI images

MRI, CT, EEG in HSV Encephelitis
(2) Focal areas of low absorption, mass effect,
and contrast enhancement on CT; or
(3) Periodic focal temporal lobe spikes on a

background of slow or low-amplitude ("flattened")
activity on EEG

Differential diagnosis - Amoebic
• Amoeba Naegleria fowleri (primary amebic

meningoencephalitis),
• Acanthamoeba and Balamuthia -- subacute or
chronic granulomatous amoebic
meningoencephalitis.
• Naegleria -- immunocompetent children with a
history of swimming in potentially infected water.
• CSF resembles that of bacterial meningitis

D/D-Rabies encephelitis
• Encephelitic (furious) rabies =hydrophobia, aerophobia

• Paralytic (Dumb) rabies = acute ascending paralysis
• Myoclonus, seizures,and hallucinations
• Rabies virus antigen in brain tissue

Viral Encephalitis: Treatment
• Basic management and supportive therapy -careful

monitoring of ICP, fluid restriction, and suppression of
fever.
• Treatment of Seizures
• Acyclovir -started empirically in patients with suspected
viral encephalitis
• Dose-10 mg/kg of acyclovir intravenously every 8 h (30
mg/kg per day total dose) for a minimum of 14 days

Acyclovir- Complications
• Elevations in blood urea nitrogen and creatinine

levels (5%),
• Thrombocytopenia (6%),
• Gastrointestinal toxicity (nausea, vomiting, diarrhea)
(7%),
• Neurotoxicity (lethargy or obtundation,
disorientation, confusion, agitation, hallucinations,
tremors, seizures)

Treatment- contd
• Ganciclovir
5 mg/kg every 12 h given intravenously at a constant
rate over 1 h.
maintenance therapy of 5 mg/kg every day for an
indefinite period
• Foscarnet
60 mg/kg every 8 h for 14–21 days
• Cidofovir --CMV retinitis

Subacute Meningitis
• Unrelenting headache, stiff neck, low-grade fever, and lethargy for days
to several weeks before they present for evaluation.
• Duration > 4 weeks (defines chronicity)
• Cranial nerve abnormalities and night sweats may be present.

Etiology
• M. tuberculosis,
• C. neoformans,
• H. capsulatum,
• C. immitis, and
• T. pallidum

Tuberculous meningitis
• Haematogenous Spread
• millet seed size (miliary) tubercles form in brain
parenchyma during hematogenous spread of tubercle
bacilli in the course of primary infection – caseation in
proximity to the blood vessels in lungs
• Intense inflammatory reaction leads to thick exudate
production affecting
• Basilar cisterns, cranial nerves and major blood vessels
at the base of the brain.

Fungal infections
• abnormality in cell-mediated immunity

• Cryptococcus. neoformans. --soil and bird excreta
• H. capsulatum
• C. immitis

Syphilitic meningitis
• Painless chancre at the site of inoculation

• T. pallidum invades the CNS early in the course of syphilis.
• Cranial nerves VII and VIII are most frequently involved.

CSF in Tuberculous meningitis
• 1) Elevated opening pressure,

• 2) Lymphocytic pleocytosis(10–500 cells/ L),
• (3) Eevated protein concentration in the range of 1–5 g/L (10–500
mg/dL), and
• (4) Decreased glucose concentration in the range of 20–40 mg/dL
• (5) Cobweb-formation in CSF sample

Tuberculous meningitis : Diagnosis
• The combination of unrelenting headache, stiff neck, fatigue, night

sweats, and fever with a CSF lymphocytic pleocytosis and a mildly
decreased glucose concentration is highly suspicious for tuberculous
meningitis.

CSF in Fungal meningitis
• Mononuclear or Lymphocytic pleocytosis,

• Increased protein concentration, and
• Decreased glucose concentration.
• Eosinophils seen in - C. immitis meningitis

Cryptococcal meningitis
• cryptococcal polysaccharide antigen test

• India ink smear
Syphilitic meningitis –
• FTA-ABS
• MHA-TP

TB Meningitis: Treatment
• Empirical therapy of tuberculous meningitis-- on high index of
suspicion
• Initial therapy is a combination of
1.Isoniazid (300 mg/d),
2.Rifampin (10 mg/kg per day),
3.Pyrazinamide (30 mg/kg per day in divided doses),
4. Ethambutol (15–25 mg/kg per day in divided doses)
5. Pyridoxine (50 mg/d).
• Pyrazinamide and Ethambutol for 8 weeks
• Isoniazid and Rifampin for 6–12 months.
• Dexamethasone therapy is recommended for patients who develop
hydrocephalus.

Cryptococcus neoformans
• Amphotericin B (0.7 mg/kg IV per day) or AmBisome (5 mg/kg per day),
PLUS Flucytosine (100 mg/kg per day in four divided doses) for 2 weeks
or until CSF culture is sterile.
• 8–10-week course of Fluconazole (400–800 mg/d PO

Syphilitic meningitis
• Aqueous penicillin G
3–4 million units i.v.every 4 h for 10–14 days
• 2.4 million units of procaine penicillin G i.m.daily
500 mg of oral probenecid four times daily for 10–14 day

Chronic Encephalitis--Progressive Multifocal
Leukoencephalopathy (PML)
• Multifocal areas of demyelination of varying size throughout the brain

but sparing the spinal cord and optic nerves
• AIDS(80%)
• PML lesions are classically nonenhancing (90%) on MRI
• Treatment by Cytarabine

Subacute Sclerosing Pan-Encephalitis (SSPE)
• Rare chronic, progressive demyelinating disease of the CNS associated

with a chronic infection of brain tissue with measles virus
• progressive intellectual deterioration, seizures, myoclonus, ataxia, and
visual disturbances

Chronic and Recurrent Meningitis
• characteristic neurologic syndrome exists for > 4 weeks

• Persistent inflammatory response in the cerebrospinal fluid (CSF) (white
blood cell count >5/ L)

Etiology
(1) meningeal infections,

(2) malignancy,
(3) noninfectious inflammatory disorders,
(4) chemical meningitis,
(5) parameningeal infections.

• Persistent headache with or without stiff neck, hydrocephalus,
cranial neuropathies, radiculopathies, and cognitive or personality
changes are the cardinal features.

Infectious Causes of Chronic Meningitis
• Partially treated suppurative meningitis

• Parameningeal infection
• Mycobacterium tuberculosis
• Lyme disease -Borrelia burgdorferi
• Syphilis
• Fungal /Helminthic-Cysticercosis/ Viral

Noninfectious Causes of Chronic Meningitis
• Malignancy
• Chemical compounds
• CNS sarcoidosis
• Mollaret's meningitis (Recurrent meningitis )
• Systemic lupus erythematosus

Neurocysticercosis
• Taenia Solium (eggs) : under cooked pork
• Vegitarians equally at risk
• Vegitables contamination
• ICSOL/ Spinal mass
• Seizures/ evidence of raised intra-
cranial pressure.
• Primary infection – Asymptomatic –
Latency – Reactivation – (esp in –
immuno-compromised host)
• Fever, headache, focal signs

Clinical manifestations (1)
• Clinical manifestations are variable. Cysticerci can be found

anywhere in body
• Most commonly detected in brain, CSF, eye, skeletal muscle, subcutaneous
tissue
• Clinical presentation depends on number & location of cysticerci + extent of
associated inflammatory responses or scarring
• Neurologic manifestations are the most common

Clinical manifestations(2)
• Seizures are associated with inflammation surrounding cysticerci in

the brain parenchyma.
• These may be generalized, focal, or Jacksonian
• Hydrocephalus results from CSF flow obstruction by cysticerci &
accompanying inflammation

Clinical manifestations (3)
• Signs of increased intracranial pressure

• Headache, nausea, vomiting, changes in vision, dizziness, ataxia, onfusion are
seen
• Patients with hydrocephalus may develop papilledema or display
altered mental status
• When cysticerci develop at the base of the brain or in the
subarachnoid space, they may cause chronic meningitis or
arachnoiditis, or strokes.

Investigations
• CSF Elisa : 50% sensitivity
65% specificity.
• Serum Enzyme linked immuno-
transfer blot : 98% sensitivity
100% specificity.
• CT Brain : Parenchymal ring enhancing lesions, calcification.
• MRI Brain : Can distinguish active
from inactive cysts.

Ct Brain: Neurocysticercosis

Treatment :
•
Albendazole : 15 mg/kg/day,
2 split doses x 14 days.
Steroids @ 1mg/kg body wt per day : To reduce surrounding
oedema due to inflammation

Meningitis, Encphalitis, Neurocystecercosis

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Meningitis, Encephelitis &

Professor & Head, Unit of Medicine

Meninges are 3 layers of protective tissue called

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• Acute purulent infection within the subarachnoid space associated

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• S. pneumoniae is the most common cause of

• Risk factors --coexisting acute or chronic

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• 25% of all cases

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• Neonates (<1 month of age), pregnant women, individuals >60 years,

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• Declined dramatically since the introduction of the Hib conjugate

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• Initially colonize nasopharynx bloodstream

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• Elevation of the patient's head to 30–45°

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• Ampicillin should be added to the empirical regimen for coverage of L.

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• (1) Decreased level of consciousness on admission,

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• Headache, fever, and signs of meningeal irritation coupled with an

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• Lymphocytic pleocytosis (25–500 cells/ L)

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• Polymerase Chain Reaction

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• 1) Partially treated bacterial meningitis;

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• ~25% of women and 11% of men at the time of an initial (primary)

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• Concurrent chickenpox or shingles

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• Symptomatic--analgesics, antipyretics, and antiemetics

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• Brain parenchyma is mainly involved