Dr. Shatdal Chaudhary, M.D.
Universal College of Medical Sciences,
Brain abscess is a focal suppurative infection within
the brain parenchyma, typically surrounded by a
Cerebritis: is often employed to describe a
nonnencapsulated brain abscess.
Incidence~.3-1.3:100000 person per year
Brain abscess may develop by
1. Direct spread from a contiguous cranial site of infection
2. Head trauma, neurosurgical procedures
3. Hematogenous spread
25% cases : There isno primary source of infection
Pyogenic infection of chest or any other part of
Penetrating head injury
In immuno-compromised host
1. Early Cerebritis: 1-3days
2. Late Cerebritis: 4-9 days
Pus formationin necrotic center which is surrounded by
inflammatory cells and fibroblast
3. Early Capsule Formation: 10-13 days
A perivascular infiltration of inflammatory cells around a
central core of coagulation necrosis
A capsule that is better develop on corticalthen on ventricle
side of lesion
4. Late Capsule Formation: beyond 14 days
A well defined necrotic center surrounded by a dense
Typically presents as an expanding intracranial
mass rather than as a infectious process
Symptoms are gradual in onset
Patients present weeks to month
Usually presents 11-12 days following onset of
Classical triad: seen in <50% patients
Focal neurologic deficit 15-35%
MRI: better esp can detect early stages of cerebritis
CT Scan: a focal area of hypodensity surrounded by
ring enhancementwith surrounding edema
Combination of high dose parentral antibiotics
and neurosurgical drainage
Patients with neurodurgery/Head trauma
Modify antibiotics as per culture results
Duration: Min 6-8 weeks
Should continue atleast 3 months after resolution of
Role of steroids
Not given routinely
Usually reserved forof significant periabscess edema
with mass effect and raise ICP
Dexamethasone 10 mg 6 hrly
Aspiration and Drainage of the abscess under
Craniotomy and Complete excision of a
bacterial abscess: reserved for multiloculated
abscess or in those where aspiration is
Encephalitis is an acute inflammatory process affecting the brain
Viral infection is the most common and important cause, with over
100 viruses implicated worldwide
Incidence of 3.5-7.4 per 100,000 persons per year
~20,000 cases reported anually in USA
Causes of Viral Encephalitis
Herpes viruses – HSV-1, HSV-2, varicella zoster virus, cytomegalovirus, EpsteinBarr virus, human herpes virus 6
Measles, mumps, and rubella viruses
Arboviruses – examples: Japanese encephalitis; St. Louis encephalitis virus; West
Nile encephalitis virus; Eastern, Western and Venzuelan equine encephalitis virus;
tick borne encephalitis virus
Bunyaviruses – examples: La Crosse strain of California virus
Reoviruses – example: Colorado tick fever virus
Arenaviruses – example: lymphocytic choriomeningitis virus
What Is An Arbovirus?
Arboviruses = arthropod-borne viruses
Arboviruses are maintained in nature through
biological transmission between susceptible
vertebrate hosts by blood-feeding arthropods
Vertebrate infection occurs when the infected
arthropod takes a blood meal
Major Arboviruses That Cause
St. Louis encephalitis
Eastern equine encephalitis
Western equine encephalitis
La Crosse encephalitis
Flavivirus related to St. Louis
Most important cause of arboviral
encephalitis worldwide, with over
45,000 cases reported annually
Transmitted by culex mosquito,
which breeds in rice fields
Mosquitoes become infected by
feeding on domestic pigs and wild
birds infected with Japanese
encephalitis virus. Infected
mosquitoes transmit virus to
humans and animals during the
History of Japanese Encephalitis
1800s – recognized in Japan
1924 – Japan epidemic. 6125 cases, 3797 deaths
1935 – virus isolated in brain of Japanese patient who
died of encephalitis
1938 – virus isolated from Culex mosquitoes in Japan
Today – extremely prevalent in South East Asia.
30,000-50,000 cases reported each year.
Distribution of Japanese
Encephalitis in Asia, 1970-1998
West Nile Virus
Primary host – wild birds
vector – mosquitoes
Geographic distribution Africa, Middle East,
Western Asia, Europe,
St. Louis Encephalitis
human pathogen in the
Leading cause of
Eastern Equine Encephalitis
Caused by a virus transmitted to
humans and horses by the bite of
an infected mosquito.
200 confirmed cases in the US
Human cases occur relatively
infrequently, largely because the
primary transmission cycle takes
place in swamp areas where
populations tend to be limited.
Western Equine Encephalitis
639 confirmed cases in
the US since 1964
Important cause of
encephalitis in horses
and humans in North
America, mainly in the
Western parts of the US
La Crosse Encephalitis
On average 75 cases per year reported
to the CDC
Most cases occur in children under 16
Zoonotic pathogen that cycles between
the daytime biting treehole mosquito,
and vertebrate amplifier hosts
(chipmunk, tree squirrel) in deciduous
1963 – isolated in La Crosse, WI from
the brain of a child who died from
Summary – Confirmed and Probable
Human Cases in the US
Western Equine 1964-2000
Malaise, Anorexia, Nausea and Vomiting
Altered level of consciousness
Mild lethargy to Coma
Behavioral changes, hallucinations, agitations,
personality changes, frank psychosis
Focal neurologic deficits:
Virtually every possible focal neurological disturbance has
Weakness: Hemiparesis with hyperactive tendon reflexes
Cranial nerve deficits
Involantary movements- tremors, myoclonic jerks
Seizures >50% patients
Detailed history critical to determine the likely cause of encephalitis.
Prodromal illness, recent vaccination, development of few days → Acute
Disseminated Encephalomyelitis (ADEM) .
Biphasic onset: systemic illness then CNS disease → Enterovirus encephalitis.
Abrupt onset, rapid progression over few days → HSE.
Recent travel and the geographical context:
Africa → Cerebral malaria
Asia → Japanese encephalitis
High risk regions of Europe and USA → Lyme disease
Recent animal bites → Tick borne encephalitis or Rabies.
Forest worker, exposed to tick bites
Medical personnel, possible exposure to infectious diseases.
CSF examination: Should be performed in all the
patients until contraindicated
Diagnosis is usually based on CSF
Mild increase in protein
Inrease cells with predominantly lymphocytes
Absence of bacteria on culture.
Viruses occasionally isolated directly from CSF
Less than half are identified
CSF PCR techniques
Detect specific viral DNA in CSF
Usually available for HSVCMV, EBV, HHV6,
MRI/ CT Scan
Can exclude subdural bleeds, tumor, and sinus thrombosis
Focal or diffuse ence4phalitis process
In HSV encephalitis- 80% abnormalities in temporal lobe
In HSV: Periodic focal temporal lobe spikes on
a background of slow or low amplitude activity.
Is generally reserved for patients in whom CSF
PCR fail to lead a specific diagnosis
Reserved for patients who are worsening, have an
undiagnosed lesion after scan, or a poor response to
Treatment of raised ICP
Fever, dehydration, electrolyte imbalances, and
convulsions require treatment.
For cerebral edema severe enough to produce
herniation, controlled hyperventilation, mannitol, and
Patients with cerebral edema must not be
If these measures are used, monitoring ICP should
If there is evidence of ventricular enlargement,
intracranial pressure may be monitored in conjunction
with CSF drainage.
Acyclovir is a synthetic purine nucleoside
analogue with inhibitory activity against HSV-1
and HSV-2, varicella-zoster virus (VZV),
Epstein-Barr virus (EBV) and cytomegalovirus
In order of decreasing effectiveness
Acyclovir 10 mg/kg 8 hrly 14-21day
Thymidine Kinase (TK) of uninfected cells does not use acyclovir as a
TK encoded by HSV, VZV and EBV2 converts acyclovir into acyclovir
The monophosphate is further converted into diphosphate by cellular
guanylate kinase and into triphosphate by a number of cellular enzymes.
Acyclovir triphosphate interferes with Herpes simplex virus DNA polymerase
and inhibits viral DNA replication.
Acyclovir triphosphate incorporated into growing chains of DNA by viral
When incorporation occurs, the DNA chain is terminated.
Acyclovir is preferentially taken up and selectively converted to the active
triphosphate form by HSV-infected cells.
Thus, acyclovir is much less toxic in vitro for normal uninfected cells because:
1) less is taken up; 2) less is converted to the active form.
Ganicyclovir/Foscarnet: For CMV related CNS
Ganicyclovir 5mg/kg (over 1 hr) 12 hrly during
induction therapy the od in maintenance therapy
Foscarnet: 60mg/kg 8hrly during induction then
maintenance 60-120 mg/kg
Synthetic adrenocortical steroid
Potent anti-inflammatory effects
Dexamethasone injection is generally
administered initially via IV then IM
Side effects: convulsions; increased ICP after
treatment; vertigo; headache; psychic
The mortality rate varies with etiology, and epidemics due to the
same virus vary in severity in different years.
Bad: Eastern equine encephalitis virus infection, nearly 80% of survivors
have severe neurological sequelae.
Not so Bad: EBV, California encephalitis virus, and Venezuelan equine
encephalitis virus, severe sequelae are unusual.
Approximately 5 to 15% of children infected with LaCrosse virus have a
residual seizure disorder, and 1% have persistent hemiparesis.
Permanent cerebral sequelae are more likely to occur in infants,
but young children improve for a longer time than adults with
Intellectual impairment, learning disabilities, hearing loss, and other
lasting sequelae have been reported in some studies.
Prognosis w/ Treatment
Considerable variation in the incidence and severity of sequelae.
Hard to assess effects of treatment.
The incidence and severity of sequelae were directly related to the age of the
patient and the level of consciousness at the time of initiation of therapy.
Patients with severe neurological impairment (Glasgow coma score 6) at initiation
of therapy either died or survived with severe sequelae.
Young patients (<30 years) with good neurological function at initiation of
therapy did substantially better (100% survival, 62% with no or mild sequelae)
compared with their older counterparts (>30 years); (64% survival, 57% no or
Recent studies using quantitative CSF PCR tests for HSV indicate that clinical
outcome following treatment also correlates with the amount of HSV DNA
present in CSF at the time of presentation.
None for most Encephalitides
Appears to be 91% effective
There is no JE-specific therapy other than supportive care
Live-attenuated vaccine developed and tested in China
Vero cell-derived inactivated vaccines have been developed in
Appears to be safe and effective
Chinese immunization programs involving millions of children
2 millions doses are produced annually in China and Japan
Several other JE vaccines under development
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