Brain abscess is a focal infection within the brain parenchyma, typically surrounded by a capsule. It has an incidence of 0.3-1.3 per 100,000 people per year. Common causes include direct spread from a contiguous infection like sinusitis, hematogenous spread from infections elsewhere in the body, and head trauma. Clinical presentation is usually gradual onset of nonspecific symptoms like headache, fever, and focal neurological deficits. Diagnosis involves neuroimaging like MRI or CT scan showing a brain lesion, and microbiological evaluation of aspirated pus. Treatment consists of high dose intravenous antibiotics plus surgical drainage of the abscess. Prognosis depends on causative organism and ability to control infection, with a mortality rate of

1. Brain Abscess
Dr. Shatdal Chaudhary, M.D.
Associate Professor
Universal College of Medical Sciences,
Bhairahawa, Nepal
Email: shatdalchaudhary@yahoo.com

2. Definition

Brain abscess is a focal suppurative infection within
the brain parenchyma, typically surrounded by a
vascularized capsule.

Cerebritis: is often employed to describe a
nonnencapsulated brain abscess.

3. Epidemiology


Relatively uncommon
Incidence~.3-1.3:100000 person per year

4. Etiology

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

5. Predisposing conditions







Otitis media
Mastoiditis
Paranasal sinusitis
Pyogenic infection of chest or any other part of
body
Penetrating head injury
Neurosurgical procedure
Dental infection

6. In Immunocompetent persons:
 Streptococcus spp. (aerobic, Anaerobic and
viridans) 40%
 Enterobacteriaceae (Proteus, E.coli, Klebsella) 25%
 Anaerobes (Bacteroides, Fusobacterium) 30%
 Staphylococci 10%
 Taenia solium(NCC)
 Mycobacterial infection (tuberculoma)

7. In immuno-compromised host
 Nocardia
 T gondii
 Aspergillus
 Candida
 C. neoformans

8. Stages

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
collageous capsule

9. Clinical Presentation




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
symptoms.

10. Symptoms

Classical triad: seen in <50% patients
Headache 75%
 Fever 50%
 Focal neurologic deficit 15-35%


11. 
Focal neurologic deficit
Aphasia
 Hemiparesis
 Visual field defect
 Ataxia
 Nystagmus
 Seizures
 Raised ICP-Papilledema
 Meningismus Uncommon unless abscess rupture in
ventricle


12. Investigations




TLC, DLC
ESR, CRP
Blood cultures
Neuroimaging studies:
MRI: better esp can detect early stages of cerebritis
 CT Scan: a focal area of hypodensity surrounded by
ring enhancementwith surrounding edema
(hypodensity)


13. MRI

14. CT Scan

15. Microbiological Evaluation
CT-guided stereotactic needle aspiration
Gram’s Stain
 Culture : Aerobic, Anaerobic, Mycobacterial and
fungal cultures

Blood Culture
LP: do not perform

16. D/D







Bacterial Meningitis
Meningoencephalitis
Acute disseminated encephalomyelitis
Empyema
Saggital Sinus Thrombosis
Primary or Secondary brain tumor
CVA

17. Treatment



Combination of high dose parentral antibiotics
and neurosurgical drainage
Third/fourth grneration
cephalosporin+Metronidazole
Patients with neurodurgery/Head trauma
Vancomycin+Ceftazidine
 Meropenem+Vancomycin



Modify antibiotics as per culture results
Duration: Min 6-8 weeks

18. 
Prophylactic anticonvulsant


Should continue atleast 3 months after resolution of
abscess
Role of steroids
Not given routinely
 Usually reserved forof significant periabscess edema
with mass effect and raise ICP
 Dexamethasone 10 mg 6 hrly


19. 

Aspiration and Drainage of the abscess under
stereotactic guidance
Craniotomy and Complete excision of a
bacterial abscess: reserved for multiloculated
abscess or in those where aspiration is
unsucessful.

20. Prognosis


Mortality rate <15%
Neurological sequelae ≥20% of survivors

24. Acute Viral Meningitis






Enterovirus(coxaschie viruses, echovirus,human
enterovirus68-71
HSV 2
HIV
Arbovirus
VZV
EBV

25. Introduction

Encephalitis is an acute inflammatory process affecting the brain
parenchyma



Meningoencephalitis
Encephalomyelitis
Encephalomyeloradiculitis

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


26. Causes of Viral Encephalitis










Herpes viruses – HSV-1, HSV-2, varicella zoster virus, cytomegalovirus, EpsteinBarr virus, human herpes virus 6
Adenoviruses
Influenza A
Enteroviruses, poliovirus
Measles, mumps, and rubella viruses
Rabies
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

27. 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

28. Major Arboviruses That Cause
Encephalitis

Flaviviridae
Japanese encephalitis
 St. Louis encephalitis
 West Nile


Togaviridae
Eastern equine encephalitis
 Western equine encephalitis


Bunyaviridae

La Crosse encephalitis

30. Japanese Encephalitis

31. Japanese Encephalitis



Flavivirus related to St. Louis
encephalitis
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
feeding process.

32. 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.

33. Distribution of Japanese
Encephalitis in Asia, 1970-1998

34. West Nile Virus

35. West Nile Virus




Flavivirus
Primary host – wild birds
Principal arthropod
vector – mosquitoes
Geographic distribution Africa, Middle East,
Western Asia, Europe,
Australia, North
America, Central
America
http://www.walgreens.com/images/library/healthtips/july02/westnilea.jpg

36. St. Louis Encephalitis

37. St. Louis Encephalitis



Flavivirus
Most common
mosquito-transmitted
human pathogen in the
US
Leading cause of
epidemic flaviviral
encephalitis

38. Eastern Equine Encephalitis




Togavirus
Caused by a virus transmitted to
humans and horses by the bite of
an infected mosquito.
200 confirmed cases in the US
1964-present
Human cases occur relatively
infrequently, largely because the
primary transmission cycle takes
place in swamp areas where
populations tend to be limited.

39. Western Equine Encephalitis




Togavirus
Mosquito-borne
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
and Canada

40. La Crosse Encephalitis





Bunyavirus
On average 75 cases per year reported
to the CDC
Most cases occur in children under 16
years old
Zoonotic pathogen that cycles between
the daytime biting treehole mosquito,
and vertebrate amplifier hosts
(chipmunk, tree squirrel) in deciduous
forest habitats
1963 – isolated in La Crosse, WI from
the brain of a child who died from
encephalitis

41. Summary – Confirmed and Probable
Human Cases in the US
Virus
Years
Total cases
Eastern Equine
1964-2000
182
Western Equine 1964-2000
649
La Crosse
1964-2000
2,776
St. Louis
1964-2000
4,482
West Nile
1999-present
> 9,800

42. Clinical Manifestations

43. Symptoms

Fever

Headache,
Malaise, Anorexia, Nausea and Vomiting
Abdominal pain
Altered level of consciousness





Mild lethargy to Coma
Behavioral changes, hallucinations, agitations,
personality changes, frank psychosis

44. 
Focal neurologic deficits:

Virtually every possible focal neurological disturbance has
been reported.

Aphasia
Ataxia
Weakness: Hemiparesis with hyperactive tendon reflexes
Cranial nerve deficits
Involantary movements- tremors, myoclonic jerks






Seizures >50% patients
SIADH

45. Patient History





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.
Occupation


Forest worker, exposed to tick bites
Medical personnel, possible exposure to infectious diseases.

46. Lab Investigation

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
 Normal glucose
 Absence of bacteria on culture.
 Viruses occasionally isolated directly from CSF


Less than half are identified

47. Laboratory Diagnosis

CSF PCR techniques
Detect specific viral DNA in CSF
 Usually available for HSVCMV, EBV, HHV6,
ENTEROVIRUS, VZV


CSF CULTURE

48. MRI/ CT Scan


Can exclude subdural bleeds, tumor, and sinus thrombosis
Help by


Focal or diffuse ence4phalitis process
In HSV encephalitis- 80% abnormalities in temporal lobe

49. MRI

50. MRI

51. EEG

In HSV: Periodic focal temporal lobe spikes on
a background of slow or low amplitude activity.

52. Brain Biopsy

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
acyclovir.

53. D/D












Tuberculosis, Fungal, Rickettsia, Mycoplasma, Bacterial
Anoxic/Ischemic conditions
Metabolic disorders
Nutritional deficiency
Toxic (Accidental & Intentional)
Systemic infections
Critical illness
Malignant hypertension
Hashimoto’s encephalopathy
Traumatic brain injury
Epileptic (non-convulsive status)
CJD (Mad Cow)

54. Treatment

Suppportive
Vital monitoring
 ABC
 IVF
 Treatment of raised ICP
 Bed Care
 Nutrition
 DVT prophylaxis


55. Supportive Therapy



Fever, dehydration, electrolyte imbalances, and
convulsions require treatment.
For cerebral edema severe enough to produce
herniation, controlled hyperventilation, mannitol, and
dexamethasone.
 Patients with cerebral edema must not be
overhydrated.
 If these measures are used, monitoring ICP should
be considered.
If there is evidence of ventricular enlargement,
intracranial pressure may be monitored in conjunction
with CSF drainage.

56. Acyclovir

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
(CMV)
In order of decreasing effectiveness
 Acyclovir 10 mg/kg 8 hrly 14-21day


57. Acyclovir Action








Thymidine Kinase (TK) of uninfected cells does not use acyclovir as a
substrate.
TK encoded by HSV, VZV and EBV2 converts acyclovir into acyclovir
monophosphate.
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
DNA polymerase.
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.

58. 
Ganicyclovir/Foscarnet: For CMV related CNS
infection
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


59. Dexamethasone




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
disturbances

60. Prognosis

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
similar infections.

Intellectual impairment, learning disabilities, hearing loss, and other
lasting sequelae have been reported in some studies.

61. Prognosis w/ Treatment

Considerable variation in the incidence and severity of sequelae.


NIAID-CASG trials:




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
mild sequelae).
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.

62. Vaccination


None for most Encephalitides
JE



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
China


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