chronic bacterial & viral meningoencephalitis (2)

MeningoencephalitisGreek: meninges- membranes; enkephalos brain;

and -itis inflammation) is

a medical condition that simultaneously resembles both

meningitis, which is an infection or inflammation of the meninges, and

encephalitis, which is an infection or inflammation of the brain.

(.

Tuberculous Meningoencephalitis

T

contains a at

the

There may be scattered over the

The most common pattern of involvement

Mixtures of lymphocytes, plasma cells, and macrophages.

, often with and

with inflammatory infiltrates

can often be seen with acid-fast stains. The infectious process may spread to the

surface, traveling through the

In cases of may develop,

may result.

Tuberculoma:manifestation of the disease is

the development of a single (or )

( ), which may be

A may be as as several centimeters in diameter, causing significant

surrounded by ;

may occur in .

; and

, arterial occlusion and infarction.

When the process involves , may also be

affected.

and

.

• Also at risk for infection by .

• These lesions typically contain

with little or associated granulomatousreaction.

(Treponema Pallidum)

The major patterns of CNS involvement are 1.

ffected individuals often show most commonly the combination of tabes

dorsalis and paretic disease ( ).

The rate of progression and severity of the disease seem to be

, possibly for the same reason.

Morphology of Meningovascular neurosyphilis

A chronic meningitis involving: the base of the brain the cerebral convexities and the

spinal leptomeninges.

In addition, there may be an associated ( ) accompanied by a

distinctive

(plasma cell–rich mass lesions) may also occur in

byassociated with

(including delusions of grandeur) that terminate in .: Parenchymal damage in the cerebral cortex (particularly

the frontal lobe).by: loss of neurons, proliferations of microglia, gliosis, and

iron deposits. are demonstrable with the Prussian blue stain

perivascularly and in the neuropil, and are presumably the sequelae of small bleeds stemming from damage to the microcirculation.

can, at times, be demonstrated in .There is often an associated with damage to the

ependymal lining and proliferation of subependymal glia, called

Tabes dorsalis: damage by Treponema Pallidum to the

sensory nerves in the dorsal roots.impaired joint position sense and

resultant ataxia; loss of pain sensation, leading to skin and joint damage (Charcot joints); other sensory disturbances, particularly the characteristic “lightning pains”; and absence of deep tendon reflexes.

• : loss of both in the dorsal roots, with corresponding in the dorsal columns of the spinal cord.

• Organisms are not demonstrable in the cord lesions.

( )

caused by , transmitted by various species of ; involvement of the nervous system is called

.

include , and other ,

as well as . The rare cases that have come to autopsy have shown a

as well as (

A parenchymal infection of the brain associated with .

Types:Arthropod-Borne Viral Encephalitis Herpes Simplex Virus Type 1

(

Arthropod-Borne Viral Encephalitis

are an important cause of , especially in of the

world. Signs & Symptoms: generalized neurologic deficits, such as

seizures, confusion, delirium, and stupor or coma, and often focal signs, such as reflex asymmetry and

Involvement of the spinal cord in West Nile encephalitis can lead to a polio-like syndrome with paralysis.

The CSF is usually colorless but with a slightly elevated pressure and, initially, a neutrophilic pleocytosis that rapidly converts to lymphocytes; the protein concentration is elevated, but glucose content is normal.

Lymphocytic meningoencephalitis

Multiple foci of necrosis of gray and white matter single-cell neuronal necrosis with phagocytosis of the debris (neuronophagia).

Microglial cells form small aggregates around foci of necrosis, called microglial nodules.

In severe cases there may be a with associated .

• The is by a combination , , and methods.

Characteristic findings of viral encephalitis include perivascular cuffs of lymphocytes (A) and microglialnodules (B).

Characteristic findings of viral encephalitis include

(A) and

(B).

Herpes Simplex Virus Type 1

Most common in . Only about 10% of the affected individuals have a history of prior herpes. Symptoms are

In some individuals, HSV-1 encephalitis follows a with clinical manifestations (

) that evolve during a more protracted period (4 to 6 weeks).

DIGNOSIS: PCR-based methods for virus detection in CSF samples have increased the ease of diagnosis and the recognition of a subset of patients with less severe disease.

Treatment: Antiviral agents now provide effective treatment in many cases, with a significant reduction in the mortality rate.

most severely involves .

The infection is

are usually present, and may be found in both and .

In individuals with slowly evolving HSV-1 encephalitis, there is

A, Herpes encephalitis showing extensive destruction of inferior frontal and anterior temporal lobes. B,

characterizes acute herpes encephalitis.

in adults it causes ,

born by vaginal delivery to women with active primary HSV genital infections acquire the infection during passage through the birth canal and develop

.

In the face of active HIV infection, HSV-2 may cause an

( )

In Herpes zoster reactivation there may be a persistent postherpeticparticularly after age 60, including both

as well as following nonpainful stimuli.

Herpes zoster has been associated with a

In immunosuppressed individuals, herpes zoster may cause with numerous

characterized by followed by

Subacute encephalitis, CMV inclusion-bearing cells.

severe hemorrhagic necrotizing ventriculoencephalitis choroid plexitis.

painful radiculoneuritis

light microscopy confirmed as CMV by immunohistochemistry

Secondarily invades the nervous system.

Acute cases show mononuclear cell perivascular cuffs and neuronophagia of the anterior-horn motor neurons of the spinal cord.The inflammatory reaction is usually confined to the anterior horns but may extend into the posterior horns, and the damage is occasionally severe enough to produce

In situ reverse transcriptase–PCR has shown poliovirus RNA in anterior-horn cell motor neurons.

The cranial motor nuclei are sometimes involved.

Postmortem examination in long-term survivors of symptomatic poliomyelitis shows and in the affected anterior horns of the spinal cord, some

.

Because of the destruction of motor neurons, paresis or paralysis follows; when it involves the innervation of the diaphragm and intercostalmuscles, severe respiratory compromise may occur and cause long-term morbidity

Can develop in patients 25 to 35 years after the resolution of the initial illness.

It is characterized by

• Rabies is a transmitted to humans by the bite of a

that form natural reservoirs.

.

GROSS: The brain shows intense edema and vascular congestion.

MICROSCOPY: There is widespread neuronal degeneration and an inflammatory reaction that is The basal ganglia, spinal cord, and dorsal root ganglia may also be involved.

The pathognomonic microscopic finding, are cytoplasmic, round to oval,

that can be found in and

sites usually devoid of inflammation.

•

The diagnostic histologic finding in rabies is the , as seen here in a (arrows).

commonly between 1 and 3 months depends on the distance between the wound and the brain. of malaise, headache, and fever, but the conjunction of these symptoms with local around the wound is diagnostic. As the infection advances, the affected individual exhibits

;

There is and, as the disease progresses,

. Periods of progress to coma and death from

respiratory center failure.

occurs within 1 to 2 weeks of seroconversion in about 10% of patients;

HIV invasion of the nervous system have shown a mild lymphocytic meningitis, perivascularinflammation, and some myelin loss in the hemispheres.

Among the cell types of the CNS, only have the appropriate combination of CD4 and a chemokine receptor (CCR5 or CXCR4) to allow for efficient infection by HIV.

During the chronic phase, an is commonly found when symptomatic individuals come to

chronic inflammatory reaction with infiltrates of microglial nodules, sometimes with associated foci of tissue necrosis and reactive gliosis.

. These changes occur especially in the subcortical white matter, diencephalon, and brainstem.

An important component of the microglial nodule is the macrophage-derived multinucleated giant cell.

HIV can be detected in CD4+ mononuclear and multinucleated macrophages and microglia by

HIV . Note the and

, both mild and severe (HIV-associated .

This disorder is related to the extent of activated microglia in the brain, not all of which are necessarily HIV-infected.

A wide range of possible mechanisms for neuronal dysfunction and injury in this setting have been proposed, including actions of cytokines and activation of an inflammatory cascade as well as a cavalcade of toxic effects of HIV-derived proteins;

has a contributory role in

caused by the ; is its principal pathologic effect. The disease occurs almost exclusively in immunosuppressedindividuals

Although most people have serologic evidence of exposure to JC virus by the age of 14 years, no clinical disease has been associated with primary infection by the virus.

It is thought that PML results from the

Clinically, affected individuals develop focal and relentlessly progressive neurologic symptoms and signs, and imaging studies show extensive, often multifocal, lesions in the hemispheric or cerebellarwhite matter.

destruction of the white matter

.On microscopic examination the typical lesion consists of

At the edge of the lesion are greatly enlarged oligodendrocytenuclei with glassy amphophilic viral inclusions ,which contain viral antigens by immunohistochemistry.

Progressive multifocal leukoencephalopathy. Section stained for myelin showing irregular, poorly defined

, which become confluent in places. Inset, represents the effect of

viral infection.

Characterized by cognitive decline, spasticity of limbs, and seizures.

.

The disease represents infection of the CNS by an altered measles virus; changes in several viral genes have been associated with the disease.

MICROSCOPY

Gliosis and myelin degeneration;

argely within the nuclei of oligodendrocytes and neurons;

variable of white and gray matter; and .

Ultrastructural study shows that the inclusions contain nucleocapsids ;