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Meningitis Group- 5 Tutor:Dr.Rajiv Shrestha

meningitis

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Page 1: meningitis

Meningitis

Group- 5 Tutor:Dr.Rajiv Shrestha

Page 2: meningitis

Group Members• Sagun Baral• Ashkal Basi• Ashutosh Ghimire• Kamal Ghimire• Anup Subedi• Samir Raut• Prasesh Dhakal• Prastuti Shrestha• Saugat Lamichhane• Kriti Pandey• Shravya Rayilla

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What is meningitis??• Meningitis refers to an inflammatory process of

leptomeninges and CSF within the sub-arachnoid space.

• Meningitis is generally caused by an infection, but chemical meningitis may also occur in response to a bacterial irritant injected into the sub-arachnoid space.

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CLASSIFICATION

• Infectious meningitis is broadly classified into three groups :- Acute Pyogenic (Bacterial) Meningitis- Aseptic (usually acute viral) Meningitis- Chronic (usually tuberculous / fungal) Meningitis

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CAUSATIVE AGENTS OF

MENINGITIS

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- BACTERIAL AGENTS: Neonatal: E. coli

Group B StreptococciInfants: Hemophilus influenzaeAdolescents and young adults:

Niesseria meningitidis(most common)Streptococcus pneumoniae

Elderly: Listeria monocytogensStreptococcus pneumoniae

- VIRAL AGENTS: Enterovirus(most common), Mumps virus, Coxsackie virus, HSVII, EBV

- FUNGAL AGENTS: Candida albicans, Cryptococcus neoformans, Blastomyces dermatidis, Coccidiodesimitis

- PARASITES: Protozoa, Nematodes, Cestodes

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Routes of Infection :There are 4 methods by which microbes enter the nervous system

1. Hematogenous route : through arterial and venous spread; is the most common route of entry

2. Direct implantation : it may be traumatic or rarely iatrogenic i.e. through a lumbar puncture needle

3. Local extension : through air sinuses, infected tooth or a surgical site.

4. Through peripheral nervous system : as occurs with certain viruses.

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Pathogenesis of bacterial meningitis: Nasopharynx

Nasopharyngeal colonisation (in epithelial cells)

Local invasion into intravascular spacebacteria transported across epithelial cells in membrane bound vacuoles OR by

creating separations in apical tight junctions

Bacteremia (avoid phagocytosis due to presence of polysaccharide capsule)

Reach choroid plexus / Adhere to cerebral capillary endothelium

Bacteria gain access to CSF

Rapid multiplication in CSF

Lysis of bacteria …contd

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Release of bacterial component Cytotoxic edema (lipopolysaccharide, endotoxin, peptidoglycan, teichoic acid)

Cerebral microvascular endothelium Macrophages activated and release cytokines

IL-1,TNFIncrease BBB permeability; Vasculitis Subarachnoid space inflammation

Vasogenic edema and ↑CSF outflow Exudates leakage of serum proteins resistance; ↑ICP into the sub arachnoid space

CSF flow obstruction & Hydrocephalus ↓CSF reabsorption ↓cerebral blood flow Interstital edema Coma

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Morphology of Bacterial MeningitisGROSS:

• Exudates in the leptomeninges and the surface of brain.

• Engorged meningeal vessels.• In H. influenzae exudates are

localized to the base.• In Pneumococcal meningitis

the exudate is seen over cerebral convexities near the sagittal sinus.

• When the meningitis is fulminant, the inflammation may extend to the ventricles producing ventriculitis.

MICROSCOPY:• Neutrophils fill the entire

subarachnoid space. • In severe cases they

infilterate the vessel wall and even the brain.

• Untreated cases can follow leptomeningeal fibrosis and

hydrocephalus.

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Acute pyogenic meningitis showing purulent exudates

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Clinical Features• Fever, chills and rigor

• Headache, nausea, vomiting

• Seizures, cranial nerve palsies

• Signs of meningeal irritation– Neck rigidity– Photophobia

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Signs

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Complications:

• Bacterial : - Waterhouse-Friderichsen syndrome - obstructive hydrocephalus - chronic adhesive arachnoiditis - focal cerebritis - phlebitis leading to venous occlusion and hemorrage of underlying brain.

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Cerobrospinal Fluid (CSF) in Normal individuals and in different types of meningitis

Characteristics Normal CSF Acute pyogenic meningitis

Tuberculous meningitis

Viral meningitis

Pressure Normal (<20cm H20)

Highly increased

Moderately increased

Slightly increased

Direct examinationA. Cell count/cumm and predominant cell

1-3Lymphocytes

1,000-20,000Neutrophils(90-95%)

50-500Lymphocytes(90%)

10-500Lymphocytes

B. Biochemical analysis1. Protein (mg

%)2. Sugars (mg

%)

30-45

40-80

Highly increased(100-600)Diminished (10-20)

Moderately increased(80-120)Diminished(10-20)

Slightly increased(60-80)Normal

Bacteriological examinationA. MicroscopyGram stain

ZN-staining

Nil

Nil

GPC,GNC,GNB,GPB etcNil

-

Acid fast bacilli

-

B. Culture Nil Specific medium

In LJ medium Cell cultures

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References

Harrison’s Principles Of Internal Medicine

Pathologic Basis Of DiseaseRobbins and Cotran

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K YOU

THANK YOU