A detailed presentation of bacterial meningitis. Learn!

1. Principles of Management of
Bacterial Meningitis
Presentation by Dr Marcel Nchwang
Moderated by Dr Abdulrauf Tajudeen
Department of Internal Medicine
ATBUTH, Bauchi
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2. OUTLINE
• INTRODUCTION
• EPIDEMIOLOGY
• TYPES
• AETIOLOGY/PATHOGENESIS
• PATHOPHYSIOLOGY
• CLINICAL PRESENTATION
• MANAGEMENT
• DIFFERENTIAL DIAGNOSIS
• CONCLUSION
• REFERENCES
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3. INTRODUCTION
• Meningitis is an inflammatory process of the leptomeninges and CSF
within the Subarachnoid space.
• In bacterial meningitis, it is by the infectious agents, bacteria.
• Meningitis of bacterial origin are usually pyogenic and usually have an
acute course
• It is a medical emergency
• The inflammatory process classically affects the CSF and
leptomeninges (pia and arachnoid mater) but may affect the brain
parenchyma also-> meningoencephalitis
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5. EPIDEMIOLOGY
• Bacterial meningitis is the most common form of suppurative CNS infection, a
global health concern
• The disease occurs at any age but affects babies, preschool and young people
more
• Fatality rates reach 50% untreated, even with early diagnosis and treatment,
8-15% still die within 24 hours of symptom onset
• 10-20% develop various sequelae
• There several aetiologic agents and they differ by age and geography
• Strept pneumoniae is responsible for approx. 50% of cases, Neisseria 25%,
Group B streptococci about 15%, listeria about 10% and Haemophilus <10%
• The commonest cause across all age groups is the pneumococci and
meningococci
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6. EPIDEMIOLOGY
• The highest burden of disease is in the developing world, the meningitis belt
• The meningitis belt spans countries in sub-Saharan Africa including Nigeria which
had about 80,000 cases of suspected meningitis with 4000 deaths in 2009
• The disease may occur as sporadic cases, small clusters or epidemics
• It often shows seasonal variation particularly with Neisseria occurring about
every 5-12 years, Nigeria had it’s most recent peak outbreak in 2009 with about
4000 cases/week
• In Nigeria, Zamfara has the highest burden in the 21st century with 7,140 susp
cases and 553 deaths between December 2016 to 2017.
• Disease burden is more during the dry season, December to June where cases
may reach up to 1000 cases per 100,000 population
• The disease is rare in the USA, Europe, Australia and South America with cases of
0.12-3/100,000/year
• There is a generally a decline in cases due to improvement in vaccinations
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8. TYPES
• Acute
• Disease and symptoms evolving over 1-24 hours and up to 1 week
• Neisseria and pneumococcus are the most common agents responsible
• Chronic
• Disease and symptoms develop over greater than 1 week and last at least 4
weeks meningitic signs take weeks to develop
• Recurrent meningitis
• At least 2 episodes of signs and symptoms of meningeal inflammation with
asstd CSF findings separated by a period of full recovery
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9. AETIOLOGY
• Geographical distributions and age differ, these are the commonest
• Gram positive bacteria
• Streptoccocus pneumoniae
• Staphyloccocus aureus
• Listeria monocytogenes
• Other streptococci, enterococci
• Gram negative bacteria
• Neisseria meningitides
• Haemophilus influenzae
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10. STREPTOCOCCUS PNEUMONIAE
• Also called pneumococcus
• Are gram positive cocci occurring in pairs
• Are normal flora of the respiratory tract of most humans and its only
host able to cause an array of respiratory tract infections and
meningitis
• Has a capsule responsible for its antigenic and pathogenic properties
as well as IgA protease
• There are up to 91 types based on C-polysaccharide of which types 1-
8 are responsible for most infection and can be detected in CSF
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11. Neisseria meningitidis
• Is a gram negative coccus, kidney shaped and occurring in pairs
• Has at least 13 serogroups associated with meningitis of which A, B,
C, X, Y, W135 are implicated.
• These are responsible for epidemics; in Africa and these epidemics
are usually caused by the serogroup A (serotypes 2 and 15). other
groups cause epidemics in other parts of the world
• Has the capsule responsible for its antigenic properties as well as
toxins which cause fever, shock and others
• Also found in the nasopharynx (transient flora) of humans
transmitted via droplets and considered communicable
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12. AETIOPATHOGENESIS
• For disease to occur, there usually is an interaction between host,
agent and environment
• There are several factors that predispose to the occurrence or risk of
disease in humans
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13. HOST FACTORS….
• Age: younger and elderly are at higher risk due to absence or low
antibodies
• Source: agents in nasopharynx of cases and carriers. Carriers harbour
disease in inter-epidemic period
• Immune status: unvaccinated, suppressed immunity from HIV/AIDS,
DM, immune deficiencies-complements, hypogammagloubulinaemia
• Predisposing infection: URTIs, sinusitis, otitis, skull fracture,
pneumonia, Splenectomy
• Other predisposing conditions like SCA, spinal tube defects
• smoking
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14. ENVIRONMENTAL FACTORS
• Overcrowding: common in low income/socioeconomic societies,
refugees, barracks, hostels
• Seasons: more in the dry months of the year
• Transmission: by respiratory droplets, portal of entry is nasopharynx
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15. PATHOPHYSIOLOGY
• The model of the commonest organisms, strept pneumoniae and
Neisseria are used
• There may be direct inoculation of the agent directly to the SAS as in
skull fractures, recent neurosurgery
• Or the agent reaches the SAS from another focus of infection via
blood, haematogenous
• Commonly however, the infection starts as a invasion of the
nasopharynx by the agents
• Some pathogenic properties IgA protease, pili aid attachment to the
epithelial cells of the nasopharynx
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16. PATHOPHYSIOLOGY
• The agents colonize and multiply in the nasopharynx
• They then gain access to the intravascular space by being transported
across epithelial cells bound in vacuoles or invading the intravascular space
between gap junctions of the epithelial cells
• Once in the bloodstream they are able to avoid phagocytosis by
neutrophils and opsonisation by the complement system because of the
polysaccharide capsule. There is now bacteraemia
• They reach the SAS via blood to the choroid plexus whose endothelial cells
they invade
• They readily replicate in the SAS as the CSF contains no WBCs and small
amounts of complement proteins and immunoglobulins preventing
opsonisation
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17. PATHOPHYSIOLOGY
• The inflammatory process is propagated by invasion of the bacteria
and release of cell wall components (LOS, teichoic acid and
peptidoglycans), toxins
• These induce inflammation of the meninges and production of
inflammatory cytokines (IL-1B, TNF-a) and chemokines by microglia,
monocytes and endothelial cells (NO)
• This immune response caused by the bacteria is responsible for the
meningeal damage. Rational for steroids
• There is also production of other excitatory amino acids and reactive
O2 species that can cause direct brain neuronal death
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18. PATHOPHYSIOLOGY
• The inflammatory cytokines cause vasodilation and breakdown of the BBB.
• Flow of proteins, WBCs forms layers of pus which form adhesions and
obstruct CSF flow
• This results in hydrocephalus and interstitial oedema
• Furthermore, invasion of the endothelial cells and upregulation of selectins
cause infiltration of arterial wall by inflammatory cells.
• This leads to intimal thickening (vasculitis) and obstruction of blood flow
ischemia and infarction. Also by thrombosis (PAF)
• The interstitial, vasogenic and cytotoxic oedema  increased ICP, coma
and herniation
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21. CLINICAL PRESENTATION
• Presentation may be
• Acute: fulminant and occurs within hours
• Subacute: progressively worsens over days
• Chronic: over weeks
• There is the classical presentation of the meningitic syndrome
• Fever
• Nuchal rigidity
• headache
• Impaired consciousness from lethargy to coma
• Seizures
• photophobia
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22. CLINICAL PRESENTATION
• Vomiting
• Skin rash/petechiae
• Shock
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23. CLINICAL PRESENTATION
• Examination
• General
• Attitude, Fever, dehydration, skin rashes/petechiae
• CNS
• Impaired consciousness
• Pupils: 3rd nerve
• Irritable
• Meningeal signs: kernig and brudzinski
• Cranial nerve palsies: 3rd,6th, 8th
• Hemiplegia/hemiparesis
•
• CVS/RS: irregular respiration, bradycardia, tachycardia, HTN, hypotension
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26. Management
• Manage as an emergency
• Goal is commencement of antibiotics within 60 minutes of presentation
• Antibiotics are the mainstay of treatment
• Generally;
• History: biodata, symptoms, risk factors, complications, care
• Examination
• Investigations
• Treatment: specific and supportive
• Depends on presentation: acute fulminant cases require emergency care
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29. INVESTIGATIONS
• Lumbar puncture: pressure, macroscopy
• Microbiology
• CSF culture
• Gram staining
• Blood culture
• Chemistry
• Plasma glucose (RBS)
• CSF protein and CSF glucose
• CRP
• Hyponatremia
• Radiology/imaging:
• CT/MRI: oedema, meningeal enhancement;
• CXR
• PCR
• latex agglutination
• Haematology
• FBC/Diff, PCV GXM, clotting profile, RVS, VDRL
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30. LUMBAR PUNCTURE
• A procedure required in the emergency setting to obtain CSF for analysis for diagnosis of
ABM and others
• Indication in this case is ABM.
• CT before LP is indicated In suspicion of raised ICP, >60 years, immunosuppressed, known
CNS lesions, coma, FND, new onset seizure
• Contraindications to LP
• Absolute
• Infection at site of LP
• SOL with midline shift or posterior fossa
• Acute spinal trauma
• Relative
• Raised ICP
• Coagulopathy
• Spinal deformities
• Pt not cooperative
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31. LUMBAR PUNCTURE
• Do RBS before LP, CSF glucose is better interpreted viz-a-viz blood glucose
• Exclude contraindications
• Explain procedure to patient: benefits and risks
• Obtain consent
• Sterile procedure: obtain items
• Position patient: lateral recumbent vs sitting position
• Procedure: locate L3/L4 iliac crest to trace then use L2/L3 or L4/L5
• Clean, local anaesthesia
• Insert cephalad towards umbilicus, slowly until pop when dura is penetrated
• Attach manometer
• Collect CSF in appropriate sample contains
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36. TREATMENT
• Emergency: ABC
• Emperical
• Specific
• Adjunctive
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37. EMPERICAL THERAPY
• Commenced as soon as suspicion of BM is made; CSF and or blood
cultures are taken before commencement of therapy
• Influenced by age and geographical pattern and antibiotic resistance
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38. EMPERICAL THERAPY
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39. SPECIFIC THERAPY
• This follows culture and sensitivity blood and CSF culture tests
• The appropriate antibiotics are given over a specified period
depending on the organism isolated
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40. SPECIFIC THERAPY
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41. ADJUNCTIVE CARE
• Dexamethasone 0.6mk/kg or 10mg 6hrly for 4/7: given before or with
first dose of antibiotics
• Raised ICP: lift head of bed, mannitol
• Ventilatory support/intubation
• Shock? Fluid therapy
• Fever and pain
• Seizures: lorazepam 0.1mg/kg or phenobarbital loading and
maintenance
• Monitoring: vitals, ICP
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42. PREVENTION
• 2 major ways
• Vaccination
• For: house hold contacts, >65years, splenectomy, immunedeficienciess, travel to
endemic areas, dormitories
• Chemoprophylaxis
• Necessary to clear the nasopharynx of carriers
• Rifampin 600mg bd for 2/7 or ciprofloxacin 500mg as single dose or IM ceftriazone
250mg stat
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43. DIFFERENTIAL DIAGNOSIS
• Viral encephalitis
• Cerebral malaria
• Fungal meningitis
• SAH
• Chemical meningitis
• Meningitis due to inflammatory dx
• Amebic encephalitis
• Brain abscess
• Rocky mountain spotted fever-RMSF
• SAH
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44. COMPLICATIONS
• Early
• Seizures
• Shock
• Raised ICP
• DIC
• COMA
• Late
• Hydrocephalus
• hearing impairment
• gait abnormalities
• cranial nerve palsies
• intellectual disability
• seizures
• cerebral abscess
• Focal paralysis
• Blindness
• Waterhouse Friedrichson syndrome
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45. PROGONSIS
• Pneumococcus has the highest mortality-20%
• Mortality reaches 90% without treatment
• Poor prognostic factors
• Declining consciousness level on admission
• Signs of raised ICP
• Extreme of age
• Presence of comorbid conditions like shock
• Need for mechanical ventilation
• Hypoglycorrhachia
• CSF proteins >3g/L or 300mg/dl
• Delay in initiating antibiotic therapy
• Presence of skin rash
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46. CONCLUSION
• Bacterial meningitis is a common condition and medical emergency
• Largely a disease of developing world with high mortalities commonly
caused by strept pneumoniae and Neisseria meningiditis
• Prompt assessment and commencement of antibiotics could be life
saving and minutes could make the difference
• Has mimicks of which lumbar puncture and CSF analysis forms a
cornerstone in diagnosis and treatment
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47. REFERENCES
• Robbins and Cotran Pathologic basis of disease. 9th edition
• Acute meningitis. Kumar and Clark Clinical medicine. 10th edition
• Davidson’s Principles and Practice of Medicine. 24th edition
• Harrisons Principles of Internal Medicine. 24th edition
• Traveler’s Health. Centre for Disease Control.
https://wwwnc.cdc.gov/travel/yellowbook/2020/travel-related-
infectious-diseases/meningococcal-disease
• Hitting Early, Epidemic Meningitis Ravages Nigeria and Nigeria.
https://www.science.org/doi/full/10.1126/science.324.5923.20
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48. REFERENCES
• Global Etiology of bacterial meningitis: a systemic review and meta-
analysis. Internet.
https://www.journals.plos.org/plosone/article?id=10.1371/journal.po
ne.0198772
• Meningococcal Meningitis. Slideshare. Internet.
https://www.slidershare.net/harivanschopra/meningococcal-
meningitis-drharivansh-chopra-10917879
• Meningitis. E-medicine Medscape.
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49. Thank You!!!...
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