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Acute Viral EncephalitisApproximately 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
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.
N
• 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)
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.
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: 20-50mg/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.
N
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. 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.