CNS Bacterial infections Dr Abdirisaq JACDA .pptx

This updated 2025 cutting edge advances in CNS infections mainly
Bacterial meningitis
Brian abcess and
SEA

1. Presenter: Dr Abdirisaq Jacda IMR3 Moderator:- Dr Jama Ahmed Hirsi Neurologist 9/29/2025 Approach to Bacterial CNS Infections 2025 AU-HRU 1

2. 9/29/2025 2 Bacterial Infections of the Central Nervous System Meningitis Brain Abscess Spinal Epidural Abscess The Core topics FOR TODAY

3. 9/29/2025 3

4. 9/29/2025 4

5. 1. Acute Bacterial Meningitis 9/29/2025 5 Meningitis is an Inflammation of the leptomeninges ( pia and arachnoid mater ). Affects CSF in subarachnoid space and cerebral ventricles with increased WBCs Meningeal Anatomy: Pia mater Arachnoid mater Dura mater

6. Epidemiology 9/29/2025 6 Incidence:  ~1-3 cases per 100,000 adults annually in the US & Europe. Pathogen Distribution (Post-Vaccine Era, Harrison's 22nd Ed.): Streptococcus pneumoniae:   ~70%  of cases. The undisputed king. Neisseria meningitidis:   ~12%  of cases. Often in outbreaks (colleges, military). Listeria monocytogenes:   ~8%  of cases, concentrated in the >50 and immunocompromised. Group B Strep : ~7% of cases, often in those with diabetes. Haemophilus influenzae:   <2%  of cases, a true public health victory.

7. In Africa 9/29/2025 7 classic Picture (Pre-2010): Epidemic Cerebrospinal Meningitis (CSM) seasonal epidemics (December-June). Neisseria meningitidis  Serogroup A  was responsible for ~80-85% Attack Rates:  Could reach an astonishing  500-1000 cases per 100,000 The Modern Era (Post-2010): A Story of Success and Shifting Threats The Game-Changer:  The introduction of the  MenAfriVac ®  (meningococcal A conjugate vaccine) beginning in 2010. The Result:  A  >99% reduction  in Serogroup A meningitis cases in vaccinated regions. A monumental public health achievement.

8. 9/29/2025 8

9. Pathophysiology 9/29/2025 9 Colonization :  S. pneumoniae  or  N. meningitidis  colonize the nasopharynx. Invasion :  Bacteria breach the mucosal barrier and invade the bloodstream. Seeding the CNS :   Bacteria cross the blood-brain barrier into the CSF. Inflammatory crisis :  Rapid bacterial replication triggers a massive cytokine storm. This host "friendly fire" is what causes the real damage: cerebral edema, increased ICP, vasculitis, and neuronal injury.

10. 9/29/2025 10

11. Etiology 9/29/2025 11 Healthy Adults (<50 years):  Overwhelmingly  S. pneumoniae  and  N. meningitidis . Adults >50 years or Immunocompromised: (Alcoholism, Malignancy, Diabetes, Chronic Steroids) Think  S. pneumoniae , Gram-Negatives, and you MUST add coverage for  Listeria monocytogenes. Post-Neurosurgery or Head Trauma:  Think skin flora and nosocomial pathogens: Staphylococci ( MRSA! ),  Pseudomonas , and other Gram-negatives.

12. 9/29/2025 12

13. Listeria. M 9/29/2025 13 The Bug:  G+ rod acquired from contaminated food (soft cheeses, meats). The Vulnerable Host:  It evades T-cell mediated immunity. The elderly, alcoholics, pregnant women, patients on TNF-alpha inhibitors. The Unique Presentation:   Listeria  has a striking tropism for the  brainstem , causing a  rhombencephalitis.  This presents with a classic triad of ataxia, cranial nerve palsies, and altered mental status

14. Risk factors 9/29/2025 14 Immunocompromise (Critical to Identify): Asplenia (functional or surgical) Complement Deficiency (especially for  Neisseria ) HIV Infection / Hypogammaglobulinemia Chronic Steroid Use / Malignancy Common Comorbidities: Diabetes Mellitus Alcohol Use Disorder Cirrhosis Acute Predisposing Events & Exposures Recent Infections:  Otitis, sinusitis, or pneumonia (~43% of cases Head Trauma:  Especially BSF(rhinorrhea/otorrhea). Exposures:  Close contact with a known case, injection drug use, or travel to epidemic areas (e.g., Hajj pilgrimage for meningococcus).

15. 9/29/2025 15

16. Clinical features and the Classic Triad" is it a Myth? 9/29/2025 16 Textbook Triad:  Fever + Nuchal Rigidity + Altered Mental Status. The Reality:   Fewer than 50%  of patients present with all three The Reality Check:   95%  of patients will have at least  two  of the following four symptoms: Headache  (~87%),  Fever  (~77%),  Nuchal Rigidity  (~83%),  Altered Mental Status  (~69%)

17. 9/29/2025 17 Less common manifestations are Seizures (23 %), Aphasia or hemi or monoparesis (22 %), AMS ranging from lethargy to Coma (13 %), Cranial nerve palsy (9 %), Rash (8 %), and Papilledema (4 %). Concomitant infections may include sinusitis or otitis (34 %), pneumonia (9 %), and endocarditis (1%).

18. Physical Exam Signs - 9/29/2025 18 Meningococcal Rash:  A petechial or purpuric rash is highly specific for meningococcemia. Meningeal Signs (Kernig's & Brudzinski's): Clinical Pearl:  These signs have  high specificity but very low sensitivity ( 5-15%).   Their absence means nothing and should never be used to rule out meningitis. Jolt Accentuation:  More sensitive, but still not perfect.

19. 9/29/2025 19

20. 9/29/2025 20

21. Diagnostic algorithm 9/29/2025 21 Clinical picture Presence of atleast 2 of the four cardinal symtopms LP and or neuroomagine CT/MRI Doing pre-LP CT/MRI or directly to LP Other laboratory tests

22. Diagnostic algorithm 9/29/2025 22 Blood Cultures -> Steroids & Antibiotics -> CT -> LP .  The CT is only there to make sure the LP is safe; it does not help you diagnose meningitis it rules out complication s eg lile ???? The Rule (IDSA Guidelines):   Only get a CT scan before the LP if you suspect a mass or high ICP. Indications for Pre-LP CT (Remember "FAILS"): F ocal Neurologic Deficit (new),  A ltered Mental Status (severe),  I mmunocompromised,  L esion (new onset) Seizure,  S welling (Papilledema).

23. 9/29/2025 23 CT ​sulcal effacement and slight hyperattenuation on unenhanced CT but false positives are common  7 . MRI Increased FLAIR signal relative to normal cortex may be seen but this is not specific for meningitis  7 . On post-contrast MRI, the most common positive findings are thin and linear  leptomeningeal enhancement  (only seen in 50% of patients  7 ). More specifically, if seen, smooth or linear enhancement is more characteristic of acute pyogenic (bacterial) 

24. Radiopedia CT and MRI 9/29/2025 24

25. LP Technique: 9/29/2025 25 Patient Positioning:  Lateral decubitus Needle Choice:  Use a small gauge (22-25g)  atraumatic (pencil-point) needle   Tube Order:  Collect 4 tubes. Tube 1: Cell count & diff Tube 2: Glucose & protein Tube 3: Gram stain & culture Tube 4: Hold for special tests (e.g., VDRL, Cryptococcal antigen, PCR). Rationale:  Sending Tube 1 for cell count minimizes the impact of a traumatic tap on the culture tube.

26. CSF analaysis 9/29/2025 26

27. LP Technique: and findings 9/29/2025 27 Partially Treated Meningitis:  May show a  lymphocytic predominance  and a less dramatically low glucose. Early Viral Meningitis:  Can have a neutrophil predominance in the first 24-48 hours. TB Meningitis:  The great mimic.  Lymphocytic  pleocytosis with  very low glucose . Listeria  Meningitis :  Can also present with a lymphocytic predominance in up to 30% of cases.

28.  Modern CSF Diagnostics: Beyond the Gram Stain 9/29/2025 28 Gram Stain & Culture:  Still the gold standard but slow. Gram stain is only  ~60-80% sensitive. CSF Lactate:   . A lactate  >3.5 mmol/L  is highly specific for a bacterial process. PCR (e.g., BioFire Panel):   A revolutionary tool. Can detect DNA from 14 common pathogens in about an hour.  Sensitivity and specificity >95%. Doesn't provide antibiotic sensitivities. You still need the culture. Not available globaly

29. Management Step 1: The Dexamethasone Decision) 9/29/2025 29 To blunt the inflammatory response. ( de Gans et al., NEJM 2002):   This landmark trial showed that giving dexamethasone  improves mortality (RR 0.59)  and reduces neurologic sequelae in adults with  S. pneumoniae  meningitis. Give  Dexamethasone 10mg IV 15-20 minutes  BEFORE  or  WITH  the first dose of antibiotics. Why

30. Step 2: Empiric Antibiotics - "Hit Hard, Hit Fast") 9/29/2025 30 Healthy Adult (<50 yrs):   Ceftriaxone  (2g IV q12h) +  Vancomycin  (15-20 mg/kg IV q8-12h). Adult >50 or Risk Factors:  Ceftriaxone + Vancomycin +  Ampicillin  (2g IV q4h). Neurosurgery / Trauma:   Vancomycin  +  Anti-pseudomonal agent  (Cefepime, Meropenem).

31. When the Cultures Come Back 9/29/2025 31 de-escalate  to targeted therapy. S. pneumoniae :  If Penicillin-sensitive (MIC ≤0.06),  Penicillin G  is still the best drug. N. meningitidis :   Penicillin G  is the drug of choice. L. monocytogenes :   Ampicillin  ± Gentamicin for synergy. Duration of Therapy:  7 days for  N. meningitidis , 10-14 days for  S. pneumoniae , ≥21 days for  Listeria .

32. Complications of Meningitis: 9/29/2025 32 Increased ICP & Cerebral Edema:  Occurs in >50%. The most common cause of early death. Seizures:  Occur in  ~20-30% . Septic Shock & DIC:  Particularly with  meningococcemia . Hydrocephalus:  Occurs in ~15% of adults.

33. 9/29/2025 33

34. Complications of Meningitis: Long-Term 9/29/2025 34 Sensorineural Hearing Loss:  The most common in  ~10-20%  of survivors of pneumococcal meningitis. Cognitive Impairment:  Reported in up to  50%  of survivors. Focal Neurologic Deficits:  From vasculitic strokes. Epilepsy:  A long-term risk from the cortical scar highly variable 3-20%

35. Prognosis in Bacterial Meningitis 9/29/2025 35 Overall Mortality:  30% worse In LOW INCOME COUNTRIES Key Predictors of Poor Outcome (Bradley's 8th Ed.): Decreased level of consciousness on admission (GCS <10). Signs of high ICP. Cranial nerve palsies. Age >60. The Pathogen:   S. pneumoniae  has the highest mortality. Previous history of ABM Prolonged ICU stay

36. 9/29/2025 36

37. 2. BRAIN ABSCESS 9/29/2025 37 A brain abscess is a focal, encapsulated infection within the brain parenchyma, Localized area of cerebritis then pus surrounded by a vascularized capsule. The Evolution: Cerebritis to Abscess Days 1-3 (Early Cerebritis):  A poorly demarcated area of inflammation and edema. Days 4-9 (Late Cerebritis):  A necrotic center begins to form. Days 10-14+ (Capsule Formation):  Fibroblasts lay down a collagen capsule, "walling off" the infection. This capsule is what enhances with contrast.

38. Epidemiology & Risk Factors of Brain Abscess 9/29/2025 38 Incidence:  Much rarer than meningitis, ~0.5-1 per 100,000 person-years. Mortality:  Has improved from >40% to  <15%  with modern care. Sources of Infection: Contiguous Spread: ~50%  (Otitis, Sinusitis, Dental) Hematogenous Spread: ~25%  (Endocarditis, Lung Infections) Trauma / Neurosurgery: ~10% Cryptogenic (Unknown Source): ~15%

39. 9/29/2025 39

40. Etiology: A Polymicrobial 9/29/2025 40 The Bugs:  Often  polymicrobial , reflecting the source. Sinus/Dental source:   Viridans group streptococci and  anaerobes  ( Bacteroides ,  Prevotella ). Hematogenous source:   Staphylococcus aureus  (from endocarditis). Immunocompromised Host:   Nocardia ,  Toxoplasma , Fungi.

41. Clinical Presentation: The Insidious Space-Occupying Lesion 9/29/2025 41 Presents more like a slow-growing tumor than an acute infection. The Classic Triad (Headache, Fever, Focal Deficit):   present in  <20%  of patients. The Reality: Headache (70%):  Most common symptom. Dull, progressive, positional Fever (Only 50%):  Half of your patients will be afebrile! Focal Neurologic Deficits (50-60%):  Hemiparesis, aphasia, visual field cut. Seizures (25%):  Common.

42.  Diagnosis: 9/29/2025 42 Imaging Modality of Choice: Brain MRI with and without Gadolinium. The Signature Look:  A  ring-enhancing lesion  on T1 post-contrast imaging. The Lumbar Puncture : contraindicated why Why Not to do an LP?  An abscess is a mass. You risk  cerebral herniation. It's also low-yield. The CSF is often sterile. You get all the risk with almost no diagnostic benefit.

43. 9/29/2025 43 Differentiating a Ring-Enhancing Lesion) DDX M etastasis,  A bscess,  G lioblastoma,  I nfarct,  C ontusion,  D emyelination, Necrosis. The MRI : Diffusion Weighted Imaging (DWI) Brain Abscess:  The central pus is thick, restricting water movement. This appears  BRIGHT on DWI  and  DARK on ADC map. Necrotic Tumors:  The center is fluid-filled. It does  NOT  restrict diffusion. This is the single most useful imaging pearl to differentiate abscess from tumor and infract

44. Brain Abscess Management: 9/29/2025 44 CT-Guided Needle Aspiration:  The standard of care. It is both Diagnostic and Therapeutic: Diagnostic:  Provides pus for  aerobic AND anaerobic cultures. Therapeutic:  Debulks the abscess, reducing mass effect. When can you consider Medical Management Alone? (RARELY!) Abscess is very  small (<2.5 cm) Inaccessible location , or there are ???????? Multiple abscesses .

45.  Brain Abscess: Antibiotics & Steroids 9/29/2025 45 The Classic Empiric "Triple therapy" Vancomycin  (for  S. aureus ) Third-Generation Cephalosporin  (for Strep, GNRs) Metronidazole   (essential for anaerobes) The Duration:   LONG.  Typically  4-8 weeks of IV therapy. The Role of Steroids:  A Double-Edged Sword Use them ONLY  for patients with significant mass effect and clinical deterioration. Avoid them otherwise,  as they can mask treatment failure and impair antibiotic penetration.

46. Prognosis in Brain Abscess 9/29/2025 46 Mortality:  <15% in modern series. Significant neurologic deficits persist in  30-50%  of survivors. Epilepsy:   30-60%  of survivors due to the cortical scar, some studies reach up to 80%. Prophylactic AEDs are often considered class 2a Predictors of Poor Outcome:  Rupture of the abscess into the ventricles, delayed diagnosis, rapidly progressing deficits.

47. 9/29/2025 47 One of the most rapidly progressive and devastating CNS infections. A true neurosurgical emergency Location:  Infection in the potential space between the dura mater and the vertebral column. This space contains fat and a venous plexus. Mechanism of Spinal Cord Injury: Direct Compression:  The expanding abscess physically compresses the spinal cord and nerve roots. Vascular Compromise:  Inflammation can lead to septic thrombophlebitis of the epidural veins and thrombosis of spinal arteries, causing cord ischemia and infarction. 3. Spinal Epidural Abscess

48. 3. Spinal Epidural Abscess 9/29/2025 48 Incidence:  Increasing dramatically. Now estimated at  2-10 cases per 10,000 hospital admissions. Why the increase?  The rising prevalence of key risk factors: Diabetes, IV Drug Use, Spinal procedures. Mortality:   5-15% , often due to sepsis. Morbidity:  Up to  one-third  are left with permanent neurologic deficits. The #1 Culprit:   Staphylococcus aureus  is responsible for  60-70%  of cases. Assume MRSA.

49. Risk factors 9/29/2025 49 Diabetes Mellitus (Most Common) Intravenous Drug Use Recent Spinal Procedure  (e.g., epidural steroid injection) Indwelling Catheters  (vascular or urinary) Vertebral Osteomyelitis  (often co-exists) Distant Infection Source  (e.g., skin abscess, endocarditis)

50. Clinical Presentation: The Classic Triad 9/29/2025 50 Spinal Pain (Back or Neck Pain):  The earliest and most common symptom (>90%). Often severe, localized, and relentless. Fever:  Present in ~60-70%, but can be masked by antipyretics. Progressive Neurologic Deficits. The Pitfall:  This full triad is a LATE finding.  Waiting for neurologic deficits to appear before considering the diagnosis leads to permanent disability.

51. The Four Stages of SEA Progression 9/29/2025 51 Stage 1:  Back pain, focal tenderness, fever. Stage 2:  Radicular pain (nerve root irritation), paresthesias . Stage 3:  Motor weakness, sensory loss, bowel/bladder dysfunction (cauda equina syndrome). Stage 4:  Paralysis.

52. Diagnostic Tools 9/29/2025 52 Laboratory: ESR and CRP are almost always elevated.  An ESR > 20 mm/h has a sensitivity >95%. A normal ESR makes SEA highly unlikely. Blood Cultures:  Positive in 60% of cases. Essential to obtain before antibiotics. Imaging Gold Standard: MRI of the ENTIRE spine with and without gadolinium.  It is critical to image the entire spine as abscesses can be "skip lesions

53. Management: Time is Spine 9/29/2025 53 This is a surgical disease. Urgent Neurosurgical Consultation:  The moment the diagnosis is suspected, even before imaging is complete. Surgical Decompression:  Laminectomy and abscess washout is the definitive treatment to relieve cord compression. Empiric Antibiotics:  Should be started immediately after blood cultures are drawn.

54. Medical vs. Surgical Management: A Select Few 9/29/2025 54 Medical management ALONE may be considered ONLY if ALL criteria are met: No neurologic deficits. The patient is a prohibitive surgical risk. The organism is known and susceptible to antibiotics. The abscess is very small and there is no significant cord compression on MRI. Close neurologic monitoring in the hospital is possible. This is the exception, not the rule.

55. Empiric antibiotics 9/29/2025 55 Antibiotic Therapy Empiric Regimen:  Must cover  S. aureus  and Gram-negatives. Vancomycin  (for MRSA) + Ceftriaxone or Cefepime Duration:   6-8 weeks of intravenous antibiotics  are typically required, especially if there is associated vertebral osteomyelitis.

56. 9/29/2025 56 ANY questions