Tuberculous meningoencephalitis is an infection of the meninges and brain caused by Mycobacterium tuberculosis. It can cause inflammation of the brain and meninges, as well as the formation of tuberculomas in the brain. On microscopy, there are inflammatory infiltrates containing lymphocytes, plasma cells, and macrophages, with caseous necrosis and granulomas sometimes visible. Acid-fast staining can identify the infectious agent.

3. Meningoencephalitis
Greek: 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.

4. (
.

5. Tuberculous Meningoencephalitis
T

6. contains a
at
the
There may be
scattered over the
The most
common pattern of involvement

7. 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.

8. 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 .

9. ;
and
, arterial occlusion and infarction.
When the process involves
, may also be
affected.
and

10. .
• Also at risk for infection by
.
• These lesions typically contain
with little or associated granulomatous
reaction.

11. (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.

12. 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

13. by
associated 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

14. 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.

15. ( )
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
(

16. A parenchymal infection of the brain associated
with .
Types:
Arthropod-Borne Viral Encephalitis
Herpes Simplex Virus Type 1
(

17. 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.

18. 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.

19. Characteristic findings of viral encephalitis include
perivascular cuffs of lymphocytes (A) and microglial
nodules (B).
Characteristic findings of viral encephalitis include
(A) and
(B).

20. 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.

21. 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

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

23. 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

24. ( )
In Herpes zoster reactivation there may be a
persistent postherpetic
particularly 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

26. Subacute encephalitis, CMV inclusion-
bearing cells.
severe hemorrhagic necrotizing
ventriculoencephalitis choroid plexitis.
painful radiculoneuritis
light microscopy confirmed as
CMV by immunohistochemistry

27. 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

28. 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

29. .
Because of the destruction of motor neurons,
paresis or paralysis follows; when it involves the
innervation of the diaphragm and intercostal
muscles, severe respiratory compromise may
occur and cause long-term morbidity

30. Can develop in patients 25 to 35
years after the resolution of the
initial illness.
It is characterized by

31. • Rabies is a transmitted to
humans by the bite of a
that form natural
reservoirs.
.

32. 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.

33. The pathognomonic microscopic finding, are
cytoplasmic, round to oval,
that can be found in
and
sites usually devoid of
inflammation.
•

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

35. 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
;

36. There is
and, as the disease progresses,
. Periods of
progress to coma and death from
respiratory center failure.

37. 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, perivascular
inflammation, and some myelin loss in the
hemispheres.

38. 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

39. 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.

40. 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

41. HIV . Note the
and

42. , 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

43. caused by the ; is its
principal pathologic effect. The disease occurs
almost exclusively in immunosuppressed
individuals
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 cerebellar
white matter.

44. destruction of
the white matter
.
On microscopic examination the typical lesion consists of
At the edge of the lesion are greatly enlarged oligodendrocyte
nuclei with glassy amphophilic viral inclusions ,which contain
viral antigens by immunohistochemistry.

45. Progressive multifocal leukoencephalopathy. Section stained for
myelin showing irregular, poorly defined
, which become confluent in places. Inset,
represents the effect of
viral infection.

46. 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.

47. 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 ;