Download Acute Viral Encephalitis and Brain abscess

Acute Viral
Encephalitis and Brain
Abscess
Acute Viral Encephalitis
Approximately 20,000 cases of encephalitis occur in
USA each year mostly by viruses.
CNS infectious diseases occur in two forms:
o Neuronal transmission (limited to the CNS).
o Hematogenous dissemination with multi-organ
involvement.
Causes of acute viral encephalitis:
• Herpes simplex 1.
• Rabies Virus infection.
• Arboviruses.
• Enterovirus infection.
Herpes simplex virus-1 (HSV-1)
• Common etiology of sporadic viral encephalitis.
• Associated with 70% mortality rate if untreated.
• Classification:
o Family: Herpesviridae.
o Subfamily: - Alphaherpesvirinae; rapid
growth cycle with cell death.
• General properties:
– Icosahedral enveloped
– Double stranded DNA virus.
– Latency in nerve ganglia.
N
N
Pathogenesis of HSV-1:
• Primary infection of upper respiratory tract
epithelial cells; mild pharyngitis, or
gingivostomatitis.
• Virus transported up peripheral nerve to
sensory neuron in trigeminal ganglion and
establish latent infection their.
• Fibers emerging from the trigeminal
ganglion innervate the dura of the middle
and anterior cranial fossa, and meningeal
arteries.
• Spread from the meninges and meningeal
arteries to the contiguous cortex (temporal and
frontal lobe).
• Destruction of neurons causes mononuclear
infiltration from the perivascular sheaths
(Virchow-Robin spaces).
• None-effective immune response; lymphocytic
infiltration; severe destruction of brain tissue.
• Result: Focal cerebral cortical encephalitis.
• Symptoms: fever, headache and altered mental
status (disorientation, behavioral disturbance,
hallucination e.g. smell hallucination)
N
Rabies Virus infection: Zoonosis:
• Classification:
– Family: Rhabdoviridae.
– Genera: Lyssavirus.
– Species: Rabies.
• General properties:
• Helical enveloped Ss RNA virus.
• Surface glycoproteins are antigenic for
production of neutralizing antibodies.
• Neurotropism: Entry into the neuron by receptor
mediated endocytosis.
N
Pathogenesis of Rabies:
-Bite of an infected animal, or exposure of mucous
membrane or non-intact skin to animal saliva.
-Incubation period (1 to 3 months) .
-Local replication, neuromuscular junction,
infection of peripheral nerves.
-The virus ascend within the peripheral nerves to
the spinal cord to brainstem, cerebellum, and other
brain parenchymal tissue (diffuse encephalitis).
-From brain tissue, the virus descend along
autonomic nerves to skin, cornea, and salivary
glands.
Pathogenesis of Rabies:
N
Arboviruses: (Arthropod-born Viruses)
• Transmitted by insects; mosquitoes, or ticks.
A-Togaviridae and Bunyaviridae: in USA.
B-Flaviviridae Family:
– General properties of flaviviruses: Icosahedral
enveloped single stranded RNA viruses.
– Examples:
• West Nile virus: Encephalitis in America,
Africa, Middle East, and Europe.
• Japanese encephalitis virus: Asia, India,
Australia.
• Ticknborne encephalitis virus: Russia, Europe.
Pathogenesis of Flaviviridae:
• Mosquito bite; skin inoculation; infection of
endothelial cells of small blood capillaries and
skin dendritic cells.
• Invade the blood (primary viremia).
• Infection of reticuloendothelial system
(macrophages of the liver and spleen and
endothelial cells).
• Secondary viremia; the virus cross the BBB
through the choroid plexus to infect the brain
tissues.
• Subcortical white matter encephalitis.
•
•
•
•
Enterovirus infection:
Classification: Picornaviridae.
Etiology: Coxsackievirus A and B, Poliovirus,
and Echovirus.
General properties: Icosahedral non-enveloped
single-stranded RNA virus.
Pathogenesis:
– Viral replication in oropharynx and intestinal
mucosa.
– Intestinal lymphoid tissue infection; viremia.
– Meninges infection; aseptic meningitis.
N
• Coxsackievirus A and B encephalitis is
established from meningitis.
• Poliovirus is transferred by retrograde axonal
transport to infect the neurons of the gray matter
of both the brain and spinal cord; then destroy
them by lysis.
• Result: Acute encephalomyelitis and paralytic
poliomyelitis.
Diagnosis of Viral Encephalitis:
CSF abnormalities are similar to those found in viral
meningitis.
Hematological analysis:
• Leukocytes count in CSF: 10-500 cell/mm3.
• Differential count: Neutrophils: predominate
in first 24 hours, then decreased. Lymphocytes
increases.
• Red blood cells per mm3: 10-500 cells (HSV
infection). RBCs are not present in other CNS
infections.
Biochemistry analysis:
• Glucose concentration mg/dL: 40-80 (normal).
• Protein concentration: mg/dL: 50-100
(Slightly elevated) normal protein: 2050mg/dl.
Molecular detection of virus genes by PCR.
Brain Abscess:
Brain abscess is a focal infection (pus
collection) of the brain parenchyma, caused by
bacteria, fungi, or parasites.
Types of brain abscess:
-Acute brain abscess.
-Chronic brain abscess.
N
Microorganisms that cause brain abscess reach
the brain by:
• Direct extension from a contiguous focus of
infection: (otitis media, sinusitis or mastoiditis;
veins that bridge the surrounding bony structures
and cerebral cortex can become infected (septic
thrombophlebitis).
• Hematogenous dissemination: acute bacterial
endocarditis, septicemia,…
• Direct penetration: Skull fractures or surgical
procedures.
Acute brain abscess:
-Causative agents: Staphylococci , group A and D
Streptococci and mixed anaerobic and aerobic
bacteria.
-The mixture of aerobic and anaerobic bacteria is
similar to the combination of bacteria found in the
mouth, external ear canal or a parameningeal
infection such as otitis media, sinusitis and
mastoiditis.
Treatment:
Drainage and broad-spectrum antibiotics:
Vancomycin, metronidazole, and ceftriaxone.
N
Quinolones or macrolides work effectively at acidic pH.
N
Chronic Brain Abscess:
(located in either meninges or brain tissues).
The most common causative agents are:
-Bacteria: Mycobacterium tuberculosis.
-Fungi: Cryptococcus neoformans, or other fungi.
Other causes of brain Abscess:
-Parasites:
A -Taenia solium (Cysticercosis).
B - Toxoplasma species.
C -Entamoeba histolytica: extraintestinal
amoebiasis: rare.