Serdar Balcı

Infectious Diseases of CNS

Serdar BALCI, MD

Infectious Diseases of CNS

How do infectious agents reach the nervous system

Epidural and Subdural Infections

Bacterial or fungal infections

Usually as a consequence of direct local spread

Epidural Infections

Subdural Infections


Acute Pyogenic Meningitis (Bacterial Meningitis)

Acute meningitis

Exudate is within the leptomeninges over the surface of the brain

Meningeal vessels are engorged and prominent

Tracts of pus can be followed along blood vessels on the brain surface

When the meningitis is fulminant

-inflammatory cells infiltrate the walls of the leptomeningeal veins

-may spread into the substance of the brain (focal cerebritis)

-may extend to the ventricles, producing ventriculitis

Robbins Basic Pathology

Acute meningitis

Aseptic Meningitis (Viral Meningitis)

Chronic Meningitis



They may involve the brain parenchyma

Tuberculous Meningitis

Spirochetal Infections


Brain Abscesses

N Engl J Med 2014;371:447-56

N Engl J Med 2014;371:447-56

N Engl J Med 2014;371:447-56

N Engl J Med 2014;371:447-56

N Engl J Med 2014;371:447-56

Robbins Basic Pathology

Central liquefactive necrosis

İnflammatory cells

Edema and granulation tissue, vascularization

Fibrous capsule

Zone of reactive gliosis

Viral Encephalitis

Robbins Basic Pathology

**perivascular cuffing of lymphocytes **

**microglial nodules **

Robbins Basic Pathology

Herpes encephalitis showing extensive destruction of inferior frontal and anterior temporal lobes

Robbins Basic Pathology

HIV encephalitis: Accumulation of microglia forming a microglial nodule and multinucleate giant cell

Robbins Basic Pathology


HSV-1 encephalitis


Meningitis in adults

Disseminated severe encephalitis neonates born by vaginal delivery to women with active primary HSV genital infections

Varicella-zoster virus (VZV)

chickenpox during primary infection

Latent infection in neurons of dorsal root ganglia

Reactivation in the distribution of one or a few dermatomes



Rabies Virus

Virus enters the CNS by ascending along the peripheral nerves from the wound site

Incubation period depends on the distance between the wound and the brain

Human Immunodeficiency Virus

HIV encephalitis

Polyomavirus and Progressive Multifocal Leukoencephalopathy

Patchy, irregular, ill-defined areas of white matter destruction that enlarge as the disease progresses

Each lesion is an area of demyelination

Robbins Basic Pathology


-scattered lipid-laden macrophages

-reduced number of axons


-greatly enlarged oligodendrocyte nuclei whose chromatin is replaced by glassy-appearing amphophilic viral inclusions

Robbins Basic Pathology

Fungal Encephalitis

Cryptococcus neoformans

Robbins Basic Pathology

Robbins Basic Pathology

Cerebral Toxoplasmosis

Robbins Basic Pathology

Free tachyzoites are demonstrated by immunohistochemical staining

Bradyzoites are present as a pseudocyst

Robbins Basic Pathology


End-stage infection by the tapeworm Tenia solium

Develop into mature tapeworms, they encyst

Common within the brain and subarachnoid space

Mass lesion and can cause seizures

Intense inflammatory infiltrate in the surrounding brain, often including eosinophils

Associated with marked gliosis


Prion Diseases

Robbins Basic Pathology

Sporadic cases of prion disease (sCJD)

PrP c also may change its conformation spontaneously

**Extremely low rate **

Early-onset familial forms of prion disease (fCJD)

Certain mutations in the gene encoding PrP c ( PRNP ) accelerate the rate of spontaneous conformational change

α-Helical PrPc may spontaneously shift to the β-sheet PrPsc conformation, an event that occurs at a much higher rate in familial disease associated with germ line PrP mutations

Robbins Basic Pathology

PrPsc may also be from exogenous sources, such as contaminated food, medical instrumentation, or medicines. Once present, PrPsc converts additional molecules of PrPc into PrPsc through physical interaction

Robbins Basic Pathology

formation of pathogenic PrPsc aggregates

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Creutzfeldt-Jakob Disease

Pathognomonic finding is a spongiform transformation of the cerebral cortex and deep gray matter structures (caudate, putamen)

Uneven formation of small, apparently empty, microscopic vacuoles of varying sizes within the neuropil and sometimes in the perikaryon of neurons

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Advanced cases

Severe neuronal loss

Reactive gliosis

Expansion of the vacuolated areas into cystlike spaces (“status spongiosus”)

No inflammatory infiltrate is present

Immunohistochemical staining demonstrates the presence of proteinase K–resistant PrP sc in tissue

Western blotting of tissue extracts after partial protease digestion allows detection of diagnostic PrP sc .

Variant Creutzfeldt-Jakob Disease

Variant CJD (vCJD) is characterized by amyloid plaques (see inset) that sit in the regions of greatest spongiform change

Robbins Basic Pathology

Autopsy Pathology: A Manual and Atlas

Autopsy Pathology: A Manual and Atlas

Autopsy Pathology: A Manual and Atlas

Autopsy Pathology: A Manual and Atlas

Autopsy Pathology: A Manual and Atlas

Autopsy Pathology: A Manual and Atlas

Autopsy Pathology: A Manual and Atlas

Rubin’s Pathology 7th Ed Clinicopathologic Foundations Of Medicine