Pathophysiology of Viral Encephalitis
Viral infection of the central nervous system can be in several ways:
1 Invasion directly through anatomical barrier.
a. Scalp, skull and dura mater forming an effective barrier against infection directly from the surrounding environment. Infection with the direct path is usually due to trauma or surgery wounds.
2. axonal transport by neurons of the peripheral.
a. Neurons can be road traffic from and to the "Cell Body" and antegrade and retrograde transport systems, such as rapid retrograde transport an average of 200-300 mm / day, for example, the herpes simplex virus and varicella zozter are transported of replication in skin and mucosa by sensory fibers to the dorsal nerve roots.
3 The entrance of respiratory tract pass through the olfactory epithelium.
a. How to enter the organism in the olfactory mucosa through the apical process of nerve cell receptors that stand out on the edge of the epithelium as "olfactory rads", so that the particle is placed on the olfactory mucosa can be taken by pinocytic vesicles and transported to the olfactory bulb.
4 Infection through blood vessels pass through the capillary endothelium or epithelial plexus choroideus.
Viral infection of the central nervous system can be in several ways:
1 Invasion directly through anatomical barrier.
a. Scalp, skull and dura mater forming an effective barrier against infection directly from the surrounding environment. Infection with the direct path is usually due to trauma or surgery wounds.
2. axonal transport by neurons of the peripheral.
a. Neurons can be road traffic from and to the "Cell Body" and antegrade and retrograde transport systems, such as rapid retrograde transport an average of 200-300 mm / day, for example, the herpes simplex virus and varicella zozter are transported of replication in skin and mucosa by sensory fibers to the dorsal nerve roots.
3 The entrance of respiratory tract pass through the olfactory epithelium.
a. How to enter the organism in the olfactory mucosa through the apical process of nerve cell receptors that stand out on the edge of the epithelium as "olfactory rads", so that the particle is placed on the olfactory mucosa can be taken by pinocytic vesicles and transported to the olfactory bulb.
4 Infection through blood vessels pass through the capillary endothelium or epithelial plexus choroideus.
When viral pathogen entry into the nervous system of unique resistance will occur. The brain does not have the intrinsic system to produce antibodies, has no good lymphatic system, and just has few phagocytic cells. Blood-brain barrier (BBB), which prevents the entry of the virus, also inhibit the entry of leukocytes and therapeutic ingredients. Lack of antigen "Histocompatibility complex" limit the effectiveness of the cellular immune response. These things make the central nervous system into place for latent infection. Organisms that enter the brain not all can affect the CNS. The virus can be about almost all neuronal cells, full peripheral depends also on the kind of virus. Some viruses only attack neurogen cells that cause headache, hot, and stiff neck. While other viruses that attack the neurons and glial cells that promote focal infection in the brain, such as herpes simplex encephalitis in adults.
Infections caused by viruses, causing mononuclear cell response. The basic components of an immunological reaction consisting of T cells, B cells and antigen presenting cells (cells such as macrophages and dendritic cells) which are in peripheral lymphoid tissues. Early phase of T cell activation occurs in peripheral, perhaps in limfo nodi near the site of virus entry and viral replication. In the CNS, the T cells to produce cytokines can menstimulais. Cytokines will stimulate cell proliferation and differentiation and release it into the CNS during inflammation. The ability of T cells in the CNS that interact with antigen presenting cells led to the emergence of MMC class II antigens (CD4-T) or in infected cells also occur MMC antigen class I (CD8 + T). both class I and II antigens normally present in the CNS. Both can occur in microglia funds occasionally in endothelial cells, oligodendrocyte, and artrosit at the time of virus infection. At week 2 of inflammatory cells B be an important component of local inflammation because B cells produce immunoglobulin. Antiibodi contained in the normal CNS is derived from the serum and the levels of IgA and IgG in the cerebrospinal fluid ranges are 0.2-0.4% of plasma levels. IgM was also found although the levels are lower due to the entry of proteins into the cerebrospinal fluid depends on the size and payload. Intrathecal production of antibodies against the organism that causes inflammation is a common situation encountered in viral infections of the CNS.
In encephalitis there is damage to neurons and glia where there intraceluler inclusion bodies, inflammation of the brain, spinal cord and brain edema. Also there is inflammation of the small blood vessels pambuluh, thrombosis and proliferation of astrocytes and microglia. Damaged neurons eaten by macrophages or microglia, known as neuronophagia is something that is typical for primary encephalitis. In the spinal cord, the virus spreads through the endoneurium in the interstitial space on the nerves as occurs in rabies and herpes simplex. In encephalitis, neuronal cells and glia, were damaged.
Neurological damage in encephalitis caused by:
1. direct invasion and destruction of nerve tissue by actively proliferating virus
2 Reaction neural network to viral antigens
Viral encephalitis usually divided into 3 groups:
1 Primary Encephalitis can be caused by infection with herpes simplex virus groups, influenza viruses, ECHO, Coxsackie and arbo virus.
2 primary encephalitis of unknown cause
3 para-infectious encephalitis, which arise as a complication of encephalitis virus disease known as rubeola, varicella, herpes zoster, epidemic parotitis, infectious mononucleosis and vaccination.
Encephalitis Primary Herpes Simplex
There are two main lines (port d'entree) to enter the host (the host), ie from the oral mucosa and vaginal mucosa. After entering the body of the host, the virus multiplies locally and in other secondary places, causing viremia. In experiments have demonstrated that HSV spread to the central nervous system (CNS) involve olfactory neurons in the nasal mucosa, and cells of the central processes of neurons was due to a gap in the cribriform plate and synapse with the olfactory bulb. Another potential pathway is through trigeminalis nerve and ganglion gasseri. Hematogenous spread can also occur, the virus passes the blood brain barrier and plexus choroideus, along with the migration of lymphocytes into glial and vascular regions, which should be sterile. In the cellular mechanisms of viral infection, there is necrosis of the white matter and gray matter, particularly in the inferomedial temporal lobe. At the network level, meningeal congestion and infiltration of mononuclear, perivascular necrosis with myelin damage and neuronal cell transmission interference. Some literature also says can damage the basal ganglia, thalamus, and subthalamic nucleus, causing permanent movement disorders.
In children and adults, herpes simplex virus encephalitis is a manifestation of the re-activation of latent infection. In this case, the herpes simplex virus herpes dwells in the endosymbiotic brain tissue, probably in the ganglion gasseri and encephalitis have only risen. Reactivity of herpes simplex virus can be caused by factors - factors which once mentioned above, namely ultraviolet radiation, and hormonal disorders. Ultraviolet irradiation can occur at any iatrogenic or travel to high places located.
Damage to brain tissue in the form of necrosis in the white matter and gray matter as well as ischemic infarction with limpositer infiltration around blood vessels intracerebral. In the nucleus of nerve cells are "inclusion body" which is typical for herpes simplex virus. Picture of herpes simplex virus encephalitis is not much different from other primary encephalitis others. But that is characteristic for herpes simplex virus encephalitis is the way the disease progression. Start with a headache, fever and vomiting. Then comes the "acute organic brain syndrome" which quickly deteriorated into a coma. Before the coma can be found hemiparesis or aphasia. And epileptic seizures can occur from the beginning of the disease. At lumbar puncture found pleiositosis limpositer with erythrocytes.
There are two main lines (port d'entree) to enter the host (the host), ie from the oral mucosa and vaginal mucosa. After entering the body of the host, the virus multiplies locally and in other secondary places, causing viremia. In experiments have demonstrated that HSV spread to the central nervous system (CNS) involve olfactory neurons in the nasal mucosa, and cells of the central processes of neurons was due to a gap in the cribriform plate and synapse with the olfactory bulb. Another potential pathway is through trigeminalis nerve and ganglion gasseri. Hematogenous spread can also occur, the virus passes the blood brain barrier and plexus choroideus, along with the migration of lymphocytes into glial and vascular regions, which should be sterile. In the cellular mechanisms of viral infection, there is necrosis of the white matter and gray matter, particularly in the inferomedial temporal lobe. At the network level, meningeal congestion and infiltration of mononuclear, perivascular necrosis with myelin damage and neuronal cell transmission interference. Some literature also says can damage the basal ganglia, thalamus, and subthalamic nucleus, causing permanent movement disorders.
In children and adults, herpes simplex virus encephalitis is a manifestation of the re-activation of latent infection. In this case, the herpes simplex virus herpes dwells in the endosymbiotic brain tissue, probably in the ganglion gasseri and encephalitis have only risen. Reactivity of herpes simplex virus can be caused by factors - factors which once mentioned above, namely ultraviolet radiation, and hormonal disorders. Ultraviolet irradiation can occur at any iatrogenic or travel to high places located.
Damage to brain tissue in the form of necrosis in the white matter and gray matter as well as ischemic infarction with limpositer infiltration around blood vessels intracerebral. In the nucleus of nerve cells are "inclusion body" which is typical for herpes simplex virus. Picture of herpes simplex virus encephalitis is not much different from other primary encephalitis others. But that is characteristic for herpes simplex virus encephalitis is the way the disease progression. Start with a headache, fever and vomiting. Then comes the "acute organic brain syndrome" which quickly deteriorated into a coma. Before the coma can be found hemiparesis or aphasia. And epileptic seizures can occur from the beginning of the disease. At lumbar puncture found pleiositosis limpositer with erythrocytes.
Arbovirus Encephalitis
Arbo-virus or full "arthropod-borne virus" is sometimes a cause of febrile illness and primary encephalitis. Tersebur virus spread throughout the world. Ticks and mosquitoes spread the virus into the vector. Belong to the arbo-virus is a virus that causes dengue, St. Louis encephalitis, yellow fever, Colorado tick fever, and hemorrhagic fever.
Characteristic of primary arbo-virus encephalitis is a biphasic disease course. In the first wave of influenza-like illness illustration which can last 4-5 days. After which the person was already healed. In the third week the fever can recur. And the fever is a symptom of the rise of the precursor neurologic manifestations, such as headache, nystagmus, diplopia, convulsions and "acute organic brain syndrome".
Arbo-virus or full "arthropod-borne virus" is sometimes a cause of febrile illness and primary encephalitis. Tersebur virus spread throughout the world. Ticks and mosquitoes spread the virus into the vector. Belong to the arbo-virus is a virus that causes dengue, St. Louis encephalitis, yellow fever, Colorado tick fever, and hemorrhagic fever.
Characteristic of primary arbo-virus encephalitis is a biphasic disease course. In the first wave of influenza-like illness illustration which can last 4-5 days. After which the person was already healed. In the third week the fever can recur. And the fever is a symptom of the rise of the precursor neurologic manifestations, such as headache, nystagmus, diplopia, convulsions and "acute organic brain syndrome".
Parainfectious Encephalitis
Arising as a complication of encephalitis virus disease epidemic parotids, mononucleosis, varicella and herpes zoozter called para-infectious encephalitis. But this is actually not a pure encephalitis. The symptoms of meningitis, myelitis, cranial neuritis, radiculitis and peripheral neuritis can coexist with a picture of encephalitis. Even sometimes a primary complication of Guillain-Barre type radiculitis or transverse myelitis, while very mild manifestations ensefalitisnya or does not mean. So for some types of encephalitis parainfectious, mieloencephalitis more precise diagnosis than encephalitis. One type mielo-viral encephalitis, is rabies.
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