Brain infections

Acute bacterial meningitis

• is an acute purulent infection within the sub-arachnoid
space.
• The meninges, the subarachnoid space, and the brain
parenchyma are all frequently involved in the
inflammatory reaction (meningoencephalitis).
• Etiology
– Strptococcus pneumoniae 30-60%
– Haemophylus influenzae <10%
– Neisseria meningitidis 10-35%
– Listeria monocyytogenes
– Gram negative organisms
– Staphlococcus-VP shunt,trauma or surgery
• Risk factors for pneumococcal meningitis
– Pneumococcal pneumonia
– acute or chronic pneumococcal sinusitis or otitis
media,
– alcoholism,
– diabetes,
– splenectomy,
– hypogammaglobulinemia, complement deficiency
– head trauma with basilar skull fracture and CSF
rhinorrhea
 pathophysiology
• Microorganism and virus reach the nervous
through many routes main route is blood
stream and bacteria in URTI
• Microrganism in the csf in the subarachnoid
space becomes infected
• Infection spreads through meninges and
invades the ventricles
• Inflammatory response to infection tends to
increase the CSF production with moderate
increase in pressure .
 Continuation of pathophysiology

• If the process extends into the brain ,parencyma

or if concurrent encephalitis is present ,cerebral
oedema and increased intracranial pressure
• Pathological alteration includes hyperaemia of
meningeal vessels,edema of brain tissues ,and
generalized inflammatory reactions with the
exudation of WBC into subarachnoid .
• Hydrocephalus may be caused by exudates
blocking the small passage between ventricles.
 Clinical features
• Fever
• Headache
• Stiff neck
• Photosensitivity
• Altered mental status
• 2 of 4 found in 95% of patients
• Examination
– Kernig sign passive resistance to extension of
flexed knee at 90 degree
– Nuchal rigidity
– Brudzinski sign-flexion of knee and hip when neck
passively flexed
– Focal neurological sign-hemiparesis,aphasia etc
– Fundoscopy-papiloedema
– Rash-maculopapular,petechia etc
• Investigation
– Blood culture before antibiotics
– White cell count >10,000
– CT SCAN brain prior to lumbar puncture if
immunosuppressed,seizure,focal deficit,altered
mental status
– Lumbar puncture CSF
• turbid
• Gram stain and culture
• White cell >20
• Protein >0.45g/l or 45mg/dl
• Glucose <2.5mmol
Types of meningitis glucose protein cells

Acute bacterial low high PMNS often >300/mm

Acute viral low Normal or high Mononuclear

<300mm

tuberculous low high Mononuclear and

PMNs,<300/mm

Fungal low high <300/mm

malignant Low high Usually mononuclear

 treatment
• Normal adult-ceftriaxone 2gm BD for two
weeks in pneumococcal.if resistance
suspected then add vancomycin
• Crytsalline penicillin 24mu/day every 4-6
hours
 Complications
• Brain damage
• Build up of fluid between skull and
brain(subdural effusion)
• Hearing loss
• Hydrocephalus
• seizures
 VIRAL MENINGITIS

• headache, fever, and signs of meningeal

irritation coupled with an inflammatory CSF
profile
• Constitutional signs can include malaise,
myalgia, anorexia, nausea and vomiting etc
• Drowsiness and lethargy
• Alteration in mental status,marked stupor or
confusion suggest encephalitis
• Etiology-enterovirus,HSV2,HIV are common
 diagnosis
• CSF
– lymphocytic pleocytosis (25–500 cells/L),
– a normal or slightly elevated protein
concentration [0.2–0.8 g/L (20–80 mg/dL)],
– a normal glucose concentration,
– and a normal or mildly elevated opening pressure
(100–350 mmH2O)
 VIRAL ENCEPHALITIS

• Viral infection of the brain parenchyma with

evidence of neurologic dysfunction
• Etiology
– HSV
– HZV
– Arbovirus
– Enterovirus
– Others HIV/CMV/JC virus
– mumps
• Fever,Headache Mental status change
seizures and focal neurological findings
• Diagnostic
– Lumbar puncture:
• lymphocytic pleocytosis;
• PCR for Human herpes virus
• Treatment of viral meningitis/encephalitis
– Acyclovir 15-30mg/kg TID
 Subacute and chronic meningitis
• Tuberculosis meningitis-
– Index of suspicion- combination of
unrelenting headache, stiff neck, fatigue,
night sweats, and fever
– PLUS
– with a CSF lymphocytic pleocytosis and a mildly
decreased glucose concentration is highly
suspicious for tuberculous meningitis.
Characteristic of CSF
• elevated opening pressure,
• lymphocytic pleocytosis (10–500 cells/L),
• elevated protein concentration in the
range of 1–5 g/L, and
• decreased glucose concentration in the
range of 1.1–2.2 mmol/L (20–40 mg/dL).
• Diagnosis of TBM is via culture or PCR plus the
biochemistry of high protein and low glucose
and lymphocytic pleocytosis
• Treatment
– isoniazid,rifampcin,pyrazinamide,ethambutol
– Pyridoxine 50mg/day
– Dexamethasone 12-16mg tapered after three
weeks
• Cryptococcal meningitis
– Caused by cryptococcus neoformans almost
exclusively in HIV postive individuals
– CSF –
• mononuclear or lymphocytic pleocytosis, an increased
protein concentration, and a decreased glucose
concentration.
• Indian ink stains the fungi
• Cryptococcal antigen test is highly sensitive
• Treatment
– Induction phase of two weeks
• Amphotericin B 0.7-1mg/kg
– Plus
• Fluconazole 1200mg/day
– Consolidation for 8 weeks
• Fluconazole at 400-800mg/day
– Maintenance
• Fluconazole 200mg/day for minimum one year and
CD4 >100 on at least two occasion 6 months apart
 Brain abscess
• Focal, suppurative infection within the brain
parenchyma, typically surrounded by a
vascularized capsule.
• Develop from
– direct spread from a contiguous cranial site of
infection, such as paranasal sinusitis, otitis media,
mastoiditis, or dental infection;
– following head trauma or a neurosurgical procedure
– (3) as a result of hematogenous spread from a remote
site of infection
– Cryptogenic in 25%,source unknown
• Etiology
– streptococci,
– Bacteroides spp.,
– Pseudomonas spp.,
– Haemophilus spp
– Enterobacteriaceae.
– staphylococci,
– Bacteroides spp.
– , Fusobacterium spp.,
• Clinical features-presents as an expanding intracranial
mass lesion rather than as an infectious process
• Median hospital presentation is 11–12 days following
onset of symptoms.
• The classic clinical triad of headache, fever, and a focal
neurologic deficit in <50%
• Others-focal or generalised seizure
• Focal deficit-hemiparesis,aphasia,visual field
defects,ataxia
• Signs of ICP-vomiting,nausea,vomiting,drowsiness
• Diagnosis-MRI or CT SCAN head.MRI is superior
moreso at earl stage
• Treatment
– third- or fourth-generation cephalosporin (e.g.,
cefotaxime, ceftriaxone, or cefepime) and
metronidazole
– Duration 6-8 weeks
– Intravenous dexamethasone therapy (10 mg every 6
h) is usually reserved for patients with substantial
periabscess edema and associated mass effect and
increased ICP and tapered rapidly