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CNS infections

14/08/14. CNS infections. Dr. A. Ksheera Cariappa Asst Professor. CONTENTS. INTRODUCTION & KEY WORDS TUBERCULOUS MENINGITIS VIRAL MENINGITIS BACTERIAL MENINGITIS BRAIN ABSCESS. INTRODUCTION & KEY WORDS. THE MENINGES. 3 Layers : Dura mater, Arachnoid mater and Pia mater

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CNS infections

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  1. 14/08/14 CNS infections Dr. A. KsheeraCariappa Asst Professor

  2. CONTENTS • INTRODUCTION & KEY WORDS • TUBERCULOUS MENINGITIS • VIRAL MENINGITIS • BACTERIAL MENINGITIS • BRAIN ABSCESS

  3. INTRODUCTION & KEY WORDS

  4. THE MENINGES • 3 Layers : Dura mater, Arachnoid mater and Pia mater • DURA MATER: tough fibrous covering of the brain composed of dense collagen which is closely attached to the skull on its inner layer. • In the region of spinal canal, it encloses a potential space, the epidural space, between the bone and the dura.

  5. PIA-ARACHNOID (LEPTOMENINGES): The leptomeninges (lepto=thin, slender) form the delicate vascular membranous covering of the central nervous system. • The pia mater is closely applied to the brain and its convolutions, while the arachnoid mater lies between the pia mater and the dura mater without dipping into sulci. • Thus, a space is left between the two layers of leptomeninges, known as subarachnoid space, which contains the CSF.

  6. The major arteries and veins run in the subarachnoid space and small nutrient arteries pass into the cortex. • Extension of the subarachnoid space between the wall of blood vessels entering the brain and their pial sheaths form a circumvascular space called Virchow-Robin space. • Another important potential space is enclosed between the dura and the arachnoid membrane known as subdural space.

  7. ‘WORDS’ • Pachymeningitis -- ?? • Arachnoiditis -- ?? • Leptomeningitis / Meningitis -- ?? • Encephalitis -- ?? • Meningoencephalitis -- ?? • Abscess -- ??

  8. D. Pathophysiology of infection Injury to blood-brain barrier Separation of tight junctions Increased albumin in CSF, increased intracranial pressure Edema (vasogenic and inflammatory mediators) Spinal nerve root and nerve (neck stiffness) Vasculitis; infarction Direct cytopathic/toxic effect A. Central nervous system (CNS) protection • Cerebrospinal fluid (CSF) lacks host defense (cells) • Meninges • Blood-brain barrier B. Routes of infection • Hematogenous • Direct implantation • Local spread • Along PNS C. Factors in infection • Number of organisms • Host immune system • Type of organism

  9. TUBERCULOUS MENINGITIS

  10. Mycobacterium tuberculosis (TB) 1. Epidural - Extension from vertebral infection (Pott’s disease) - Compression of cord - Rarely causes meningitis 2. Subdural - Miliary or tuberculoma-en-plaque Tuberculoma = abscess Granulomas with caseous necrosis, usually small and multiple , may act as a mass, enhancing on CT scan - TB meningitis— Exudate and fibrin along base of brain. • Clinical features: Tuberculous meningitis manifests clinically as headache, confusion, malaise and vomiting.

  11. MORPHOLOGIC FEATURES • Grossly, in Tb meningitis, the subarachnoid space contains thick exudate, particularly abundant in the sulci and the base of the brain. Tubercles, 1-2 mm in diameter, may be visible, especially adjacent to the blood vessels. Primary focus – Rich’s focus • Microscopically, Tb meningitis shows exudate of acute and chronic inflammatory cells, and granulomas with or without caseation necrosis and giant cells. • Acid fast bacilli may be demonstrated. Late cases show dense fibrous adhesions in the subarachnoid space and consequent hydrocephalus

  12. The brain is markedly swollen (with flattened gyri and narrowed sulci).There is a thick, fibrinousexudate limited to the region of the basal cisterns. It envelopes the circle of Willis and several cranial nerves, in particular the 1st (optic) and the 3rd.

  13. Tuberculous encephalitis of the brain.

  14. CSF studies, 1. Naked eye appearance shows a clear or slightly turbid CSF which may form fibrin web on standing. 2. Raised CSF pressure (above 300 mm water). 3. Mononuclear leucocytosis consisting mostly of lymphocytes, plasma cells and some macrophages (100-1000 cells/μl). 4. Raised protein content. 5. Normal / lowered glucose concentration. 6. Tubercle bacilli may be found on microscopy of centrifuged deposits by Ziehl-Neelsen staining 7. Culture still remains gold standard for diagnosis; molecular biological techniques (PCR) can also detect the bacilli

  15. VIRAL MENINGITIS

  16. Acute lymphocytic meningitis is aka viral or aseptic meningitis, especially common in children and young adults. • Among the etiologic agents are numerous viruses such as enteroviruses, mumps, ECHO viruses, coxsackie virus, Epstein-Barr virus, herpes simplex virus-2, arthropode-borne viruses and HIV. • Routes of spread – Hematogenous (polio, arbovirus) – Peripheral nerve (rabies) – Olfactory mucosa, trigeminal nerve (herpes) • However, evidence of viral infection may not be demonstrable in about a third of cases.

  17. Clinical features: are much the same as in bacterial meningitis with features of acute onset meningeal symptoms and fever. • However, viral meningitis has a benign and self-limiting clinical course of short duration and is invariably followed by complete recovery without the life threatening complications of bacterial meningitis.

  18. MORPHOLOGICFEATURES • Grossly, some cases show swelling of the brain while others show no distinctive change. • Microscopically, there is mild lymphocytic infiltrate inthe leptomeninges mainly perivascularly along with few plasma cells and macrophages. • Common histopathological features – Nerve cell alterations – Degeneration — chromatolysis, eosinophilia, nuclear changes, neuronophagia – Eosinophilic nuclear inclusions (Cowdry) – Type A—intranuclear, spherical, halo (e.g. CMV, herpes, PML) – Type B—small, multiple, no nucleolar displacement (e.g., polio) – Intracytoplasmic inclusions • Reactive endothelial changes • Tissue necrosis or demyelination with certain viruses

  19. The CSF findings in viral meningitis are as under: 1. Naked eye appearance shows clear or slightly turbid CSF. 2. CSF pressure increased (above 250 mm water). 3. Lymphocytosis in CSF (10-100 cells/μl). 4. CSF protein usually normal or mildly raised. 5. CSF sugar concentration usually normal. 6. CSF bacteriologically sterile = Aseptic meningitis “Aseptic meningitis” • Refers to any culture negative meningitis • Many viruses—coxsackie and echo virus in most cases • Low mortality • characteristically show meningeal and choroid plexus lymphocyte infiltration

  20. BACTERIAL MENINGITIS

  21. ETIOPATHOGENESIS. The causative organisms vary with age of pt: 1. Escherichia coliinfection is common in neonates with neural tube defects, Group B streptococci is next common 2. Haemophilusinfluenzaeis commonly responsible for infection in infants and children. Rates have decreased in neonates. 3. Neisseriameningitidiscauses meningitis in adolescent and young adults and is the causative agent for epidemic meningitis. 4. Streptococcus pneumoniaeis causative for infection at extremes of age and following trauma. ListeriaMonocytogenesis next common. • Routes of infection in acute pyogenic meningitis are: 1. Most commonly from the blood stream. 2. From an adjacent focus of infection. 3. By iatrogenic infection such as introduction of microorganisms at operation or during lumbar puncture.

  22. Clinical features: • Acute bacterial meningitis is a medical emergency. The immediate clinical manifestations are fever, severe headache, vomiting, drowsiness, stupor, coma, and occasionally, convulsions. • The most important clinical sign is stiffness of the neck on forward bending (nuchal rigidity), Kernig’s and Brudzinski’s signs

  23. MORPHOLOGICAL FEATURES • Grossly, pus accumulates in the subarachnoid space so that normally clear CSF becomes turbid or frankly purulent. The turbid fluid is particularly seen in the sulci and at the base of the brain where the space is wide. Tracts of pus can be followed along blood vessels on the brain surface. • In fulminant cases, some degree of ventriculitis is also present having a fibrinous coating on their walls and containing turbid CSF. In addition, purulent material may interfere with CSF flow and result in obstructive hydrocephalus. • Microscopically, there is presence of numerous polymorphonuclearneutrophils in the subarachnoid space as well as in the meninges, particularly around the blood vessels. • Gram-staining reveals varying number of causative bacteria.

  24. Pyogenic meningitis. A thick layer of suppurativeexudate covers the brainstem and cerebellum and thickens the leptomeninges

  25. Acute suppurative meningitis

  26. The diagnostic alterations in the CSF in acute pyogenic meningitis are as under: 1. Naked eye appearance shows cloudy or frankly purulent CSF. 2. Elevated CSF pressure (above 180 mm water). 3. Polymorphonuclearneutrophilicleucocytosis in CSF (between 10-10,000/μl). 4. Raised CSF protein level (higher than 50 mg/dl). 5. Decreased CSF sugar concentration (lower than 40 mg/ dl). 6. Bacteriologic examination by Gram’s stain or by CSF culture reveals causative organism.

  27. CSF FINDINGS SUMMARISED

  28. BRAIN ABSCESS

  29. Abscess  localized suppuration within brain substance • Brain abscesses may arise by one of the following routes: 1. By direct implantation of organisms e.g. following compound fractures of the skull. 2. By local extension of infection e.g. chronic suppurativeotitis media, mastoiditis and sinusitis. 3. By haematogenous spread e.g. from the heart such as acute bacterial endocarditis, and from lungs such as in bronchiectasis. egs. Streptococcus (#1), gram-negative bacilli (#2), Staphylococcus (#3); may see anaerobes and aerobes, usually multiple organisms

  30. MORPHOLOGIC FEATURES • Grossly, it appears as a localised area of inflammatory necrosis and oedema surrounded by fibrous capsule. • Early: central—pus; middle—granulation tissue; outer—astrocytosis/edema • Later: central—liquefactive necrosis; middle— collagenous wall; outer—astrocytosis / reactive gliosis • Microscopically, the changes consist of liquefactive necrosis in the centre of the abscess containing pus. It is surrounded by acute and chronic inflammatory cells, neovascularisation, oedema, septic thrombosis of vessels, fibrous encapsulation and zone of gliosis. • The CSF and overlying meninges also show evidence of acute and chronic inflammation.

  31. Frontal abscesses (arrows).

  32. Clinically, there is usually evidence of reactivation of infection at the primary site preceding the onset of cerebral symptoms. • The features of abscess are fever, headache, vomiting, seizures and focal neurological deficits depending upon the location of the abscess. Brain abscess is most common in cerebral hemispheres and less frequent in the cerebellum and basal ganglia. • CSF FINDINGS: • Increased pressure • TC (Polymorphonuclear cells) are raised • Protein concentration increased • Glucose content is Normal.

  33. Consequences – Organization – pressure effect – Formation of daughter abscesses – Abscess rupture  Ependymitis / Ventriculitis / venous sinus thrombosis – Leptomeningitis and permanent neurologic deficits – Increased ICP & progressive herniation fatal

  34. THANK YOU!!!

  35. References • Robbins & Cotran Pathologic basis of Diseases, 8thed • Harsh Mohan Textbook of Pathology, 6thed • Neuropathology Review, 2nded

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