2. Ilos
 Enumerate the commonest causative organism of the
brain abscess.
 Discuss the pathogenesis of brain abscess
 Discuss the epidemiology of the commonest CNS
bacterial abscess.
 Describe the gross & histopathological features of
the different stages of brain abscess.
 Describe the radiological features.
 Describe the possible clinical presentation
 Discuss diagnosis & differential diagnosis
 Discuss in details treatment of brain abscess

4. ACUTE FOCAL SUPPURATIVE CNS
INFECTIONS
 Brain abscess
 Subdural Empyema
 Extradural Abscess
 Spinal epidural abscess
 Spondylodiscitis epidural abscess

6.  1) Cell of origin & pathogenesis
 2) Epidemiology
 3) Macroscopic features
 4) Microscopic features
 5) Immunohistochemistry
 6) Genetic & Ultra structures features
 7) Radiological features
 8) Pattern of growth & Spread
 9) Staging & behavior
 10) Prognosis

7. Pathogenesis
 50% - Local Source
 Otitis media, sinusitis, dental infection
 Direct extension through infected bone
 Spread through emissary/diploic veins, local lymphatics
 25% Hematogenous spread
 adults - lung abscess, bronchiectasis and empyema
 children - cyanotic congenital heart disease (4-7%)
 pulmonary AVM - Osler-Weber-Rendu syndrome (5%)
 rarely bacterial endocarditis
 10% trauma / surgery
 15-20% cryptogenic

8. Microbiology
AGENT FREQUENCY (%)
Streptococci (S. intermedius, including S. anginosus) 60–70 %
Bacteroides and Prevotella spp. 20–40
Enterobacteriaceae 23–33
Staphylococcus aureus 10–15
Fungi * 10–15
Streptococcus pneumoniae <1
Haemophilus influenzae <1
Protozoa, helminths † (vary geographically) <1
*Fungi (Aspergillus Agents of mucor Candida Cryptococci Coccidiodoides
Cladosporium trichoides Pseudallescheria boydii)
†Protozoa, helminths (Entamoeba histolytica, Schistosomes Paragonimus
Cysticerci)

9. Pathogen
PREDISPOSING
CONDITION USUAL MICROBIAL ISOLATES
 otitis/mastoiditis. Mixed flora of Streptococci (anaerobic or aerobic), Bacteroides and Prevotella spp.,
Enterobacteriaceae
Sinusitis (frontoethmoid …….+ Staph. aureus, Haemophilus spp.
or sphenoid)
post-traumatic or S. aureus, streptococci, Enterobacteriaceae, Clostridium spp
postneurosurgical
Bacterial endocarditis S. aureus, streptococci
Congenital heart disease Streptococci, Haemophilus spp.
Lung abscess, empyema, Fusobacterium, Actinomyces, Bacteroides , Prevotella spp., streptococci, Nocardia
bronchiectasis
Neutropenia Aerobic gram-negative bacilli, Aspergillus , Mucorales, Candidaspp
AIDS Toxoplasmosis, Nocardia, Mycobacterium Tuberculosis
Diabetic: Klebsiella pneumoniae
Posttransplant Nocardia, Aspergillus, Candida
Transplantation Aspergillus spp., Candida spp., Mucorales, Enterobacteriaceae, Nocardia spp.,
Toxoplasma gondii
Neonates Citrobacter, Proteus, Pseudomonas, Serratia, Staphylococcus aureus

10. Pathogen
 Streptococci most commonly (70%)
 Bacteroides and Prevotella in 20% to 40%
 Enteric gram-negative bacilli (e.g., Proteus
species, Escherichia coli, Klebsiella and Pseudomonas)
in 23% to 33%
 Staphylococcus aureus for 10% to 15%
 Rarely <1% of cases
 Haemophilus influenzae
 Streptococcus pneumoniae
 Listeria monocytogenes ( Immunocompromised 85%)
 facultative gram-negative organisms ( Citrobacter
diversus, Proteusm, Serratia marcescens, Enterobacter)

11.  1) Cell of origin & pathogenesis
 2) Epidemiology
 3) Macroscopic features
 4) Microscopic features
 5) Immunohistochemistry
 6) Genetic & Ultra structures features
 7) Radiological features
 8) Pattern of growth & Spread
 9) Staging & behavior
 10) Prognosis

12. Epidemiology
 Incidence:
 Sex: M:F = 2:1
 Race:
 Age: any age but most common during 3rd-4th
decades
 Risk factors:
 IVDA (2.5%)
 Congenital heart disease (6.1%)
 HIV infection (1.2%)
 Immunosuppression (3.7%)
 Diabetes mellitus (3.1%)

13.  1) Cell of origin & pathogenesis
 2) Epidemiology
 3) Macroscopic features
 4) Microscopic features
 5) Immunohistochemistry
 6) Genetic & Ultra structures features
 7) Radiological features
 8) Pattern of growth & Spread
 9) Staging & behavior
 10) Prognosis

14. Macroscopic features
 Site: frontal > Parietal > other lobes
 Size: Variable, 5 mm – several cms
 Number: 10-50 % are multiple
 Character: According to stages
 Early cerebritis - poorly demarcated from surrounding
brain
 Late cerebritis - reticular marix (collagen precursor) and
developing necrotic center
 Early capsule formation - neovascularity, necrotic
center, developing capsule
 Late capsule formation - collagen capsule, necrotic
center, gliosis surrounding capsule

15. Macroscopic features
 Site: frontal > Parietal > other lobes
 Size: Variable, 5 mm – several cms
 Number: 10-50 % are multiple
PREDISPOSING LOCATION OF ABSCESS
CONDITION
 Character: According to stages
Otitis/mastoiditis - poorly demarcated Cerebellum
 Early cerebritis Temporal lobe, from surrounding
brain
Frontal/ethmoid Frontal lobe Early (Late Stage)
Later Cerebritic / Abscess Stage
 Late cerebritis - reticular marix (collagen precursor) and
Mature abscess
sinusitis
developing necrotic center
Sphenoidal sinusitis Frontal lobe, Sellanecrotic center,
 Early capsule formation - neovascularity, turcica
developing capsule
Dental infection Frontal > temporal lobe.
 Late capsule formation - collagen capsule, necrotic center,
Remote source
gliosis surrounding capsule cerebral artery
Middle
distribution (often multiple)

16.  1) Cell of origin & pathogenesis
 2) Epidemiology
 3) Macroscopic features
 4) Microscopic features
 5) Immunohistochemistry
 6) Genetic & Ultra structures features
 7) Radiological features
 8) Pattern of growth & Spread
 9) Staging & behavior
 10) Prognosis

17. Microscopic features

18.  1) Cell of origin & pathogenesis
 2) Epidemiology
 3) Macroscopic features
 4) Microscopic features
 5) Immunohistochemistry
 6) Genetic & Ultra structures features
 7) Radiological features
 8) Pattern of growth & Spread
 9) Staging & behavior
 10) Prognosis

19.  1) Cell of origin & pathogenesis
 2) Epidemiology
 3) Macroscopic features
 4) Microscopic features
 5) Immunohistochemistry
 6) Genetic & Ultra structures features
 7) Radiological features
 8) Pattern of growth & Spread
 9) Staging & behavior
 10) Prognosis

20.  1) Cell of origin & pathogenesis
 2) Epidemiology
 3) Macroscopic features
 4) Microscopic features
 5) Immunohistochemistry
 6) Genetic & Ultra structures features
 7) Radiological features
 8) Pattern of growth & Spread
 9) Staging & behavior
 10) Prognosis

21. Radiological features: CT

22. Radiological features: MRI
Early cerebritis

23. Radiological features: MRI
Early capsule

24. Radiological features: MRI
Late capsule

25. Pattern of growth & Spread
 1) Cell of origin & pathogenesis
 2) Epidemiology
 3) Macroscopic features
 4) Microscopic features
 5) Immunohistochemistry
 6) Genetic & Ultra structures features
 7) Radiological features
 8) Pattern of growth & Spread
 9) Staging & behavior
 10) Prognosis

26.  Capsule being thinner on the deep aspect
unfortunately promoting possible rupture into the
ventricular system. Because differences in
vascularity between cortical gray and white matter
allowed greater fibroblast proliferation on the
cortical side of the abscess

27.  1) Cell of origin & pathogenesis
 2) Epidemiology
 3) Macroscopic features
 4) Microscopic features
 5) Immunohistochemistry
 6) Genetic & Ultra structures features
 7) Radiological features
 8) Pattern of growth & Spread
 9) Staging & behavior
 10) Prognosis

28.  1) Cell of origin & pathogenesis
 2) Epidemiology
 3) Macroscopic features
 4) Microscopic features
 5) Immunohistochemistry
 6) Genetic & Ultra structures features
 7) Radiological features
 8) Pattern of growth & Spread
 9) Staging & behavior
 10) Prognosis

29. Prognosis
 Mortality: 0-24%
 Morbidity: 45%
 Seizure in 30-60%
 Neuro deficits 30-50%
 Late focal or generalized seizures - 27%

30. Poor Prognostic Factors
• Delayed or missed diagnosis
• Inappropriate antibiotics
• Multiple, deep, or multi-loculated abscesses
• Poor localization, especially in the posterior fossa
• Ventricular rupture (80%–100% mortality)
• Fungal , resistant pathogens
• Degree of neurological compromise at presentation
• Rapidly progressive neuro. impairment
• Immunosuppressed host
• Extremes of age Modified from CTID,2001

32.  Usually non-specific symptoms
 Increase intracranial pressure:
 Neurological deficits:
 Seizure:
 Ventriculitis:

34. Laboratory
 Aspirate:
 Stains: Gram/AFB/fungal stains
 Cultures: aerobic, anaerobic, fungal & TB
 cytopathology (+/-PCR for TB)
 WBC: Normal in 40%, only moderate
leukocytosis in ~ 50%, & only 10% have WBC
>20,000
 CRP: almost always elevated
 ESR : Usually (75%) moderately elevated
 Blood Cultures : Often negative, BUT Should
still be done

35. Radiological: CT

36. Radiological: MRI

37. Radiological: MRI

38. Radiological: MRI (DWI)

39. Radiological: M RI (DWI)

40. Radiological: M RI (DWI)

41. Radiological: M RI (DWI)

42. Radiological: M RI (DWI) differentiation
between abscess and mets

43. MRS

44. MRS

48. History

49. History : Diagnostic methods

50. History: Instillation of AB

51. History: Surgical Enuculation

52. Treatment
 Treatment of abscess:
 Eradication of primary infected foci

53. Medical Treatment
 When? Medical therapy alone is more successful if
 Treatment is begun before complete encapsulation
 Lesion is ≤ 0.8-2.5cm (3.0 cm is the typical cutoff)
 Duration of symptoms is < 2 weeks
 The patients should show improvement in the first 2 weeks
of treatment
 What?
 Antibiotics:
 Steroids: Advantages / Disadvantages
 Dehydrating measures:
 Anticonvulsant therapy:

54. MONITOR RESPONSE CLOSELY WITH
SERIAL IMAGING every week

55. Before Rx
Contrast enhancement at the site of the abscess may persist
for several months [3]. Thus, this finding alone is not an
After completion of Rx
indication for continued antibiotic treatment or for surgical
exploration. Cavuşoglu et al Neurosurg Focus 2008; 24:E9

56. Antibiotics
 What?
 Likely pathogen: considering primary source, underlying
condition, & geography
 Biopsy proved:
 -Antibiotic characteristics: MICs for usual pathogens,
CNS penetration, activity in abscess cavity
 For how long?
 Usually parental AB 6-8 wks followed by oral AB for 2-6
months)
 After surgical excision, a shorter course may suffice

57. What ? “Mandell 6th ed.”
Predisposing Condition Antimicrobial Regimen
Vancomycin + 3rd -generation
Unknown
cephalosporin+ metronidazole
Penetrating trauma or Vancomycin + 3rd generation
postneurosurgical cephalosporin
Otitis media, Metronidazole + 3rd generation
mastoiditis, or Sinusitis cephalosporin
Vancomycin + gentamicin or
Bacterial endocarditis
(nafcillin + ampicillin + gentamicin)
Congenital heart disease 3rd-generation cephalosporin
Lung abscess, empyema, Penicillin + metronidazole+
bronchiectasis sulfonamide

58. Another way of Thinking

59.  Flagyl:
 15 mg/kg IV as a loading dose,
 Followed by 7.5 mg/kg /8h
 Vancomycin: 15 mg/kg/12 h
 Claforan:
 Adult dose (50 kg or more) 2 g/ 4-6 h.
 Pediatric dose (less than 50 kg): 50 to 180 mg/kg/d
divided into 4-6 doses
 Rociphen:
 Adult dose 2 / 12 hours.
 Pediatric dose 50mg/kg /12 h
 Maxipime:
 Adult dose: 2g /8h.
 Pediatric dose: 50mg/kg every 8 hours

60. Surgical Treatment: Indications
1. Significant mass effect on CT (lesions > 2.5 cm).
2. Difficulty in diagnosis.
3. Proximity to ventricle.
4. Significantly increased intracranial pressure.
5. Poor neurological condition.
6. Traumatic abscess associated with foreign
material
7. Fungal abscess.
8. Multiloculated abscess.
9. CT scans can not be obtained every 1- 2 weeks
10. Failure of medical treatment for at least 2 weeks

61. Surgical Treatment: Methods
 Needle aspiration:
 Free hand:
 Stereotactic:
 Deep seated.
 Multiple or multiloculated
 Local instillation of AB:
 Surgical excision:

62. References
 Anne G. Osborn et al 2004: Infection and Demyelinating
Disease. In: Diagnostic imaging Brain. First Edition.
Amirsys Inc, Salt Lake City, Utah. part I/section 8/ pp 4-
82
 Srevenc. Bausermanandk. Gillnaul (2001). Bacterial,
fungal, and parasitic diseases of the central nervous
system. In: Principles and practice of neuropathology, 2nd
ed (James S. Nelson, Hernando Mena, Joseph E. Parisi and
Sydney S. Schochet) Oxford University Press, Inc. pp.45-
77
 Tunkelv A.R. et al. (2000). Brain Abscess. In: Principles
and Practice of Infectious Diseases, 5th ed. (Mandell,
Bennett and Dolin, eds.) pp. 1016–1028.