Herpes Encephalitis
In adults, herpes simplex virus type 1 (HSV 1) accounts for 95% of all fatal cases of sporadic encephalitis and usually results from reactivation of the latent virus. The clinical findings and neuroimaging appearance are both consistent with spread of the virus from a previously infected ganglion.
In children and neonates, herpes simplex virus type 2 (HSV 2) accounts for 80-90% of neonatal and almost all congenital infections. An isolated case report of an immunocompromised adult patient developing HSV 2 infection has been described. MRI can play an important role in determining the diagnosis and extent of disease.
More recently, sporadic cases of human herpes virus 6 (HHV 6) have been described in immunocompromised patients or those with lymphoproliferative disorders. Herpes encephalitis is the most common cause of sporadic viral encephalitis, with a predilection for the temporal lobes and a range of clinical presentations, from aseptic meningitis and fever to a severe rapidly progressive form involving altered consciousness.
Herpes encephalitis can occur either through hematogenous spread or neuronal transmission. In the typical adult infected with HSV 1, the neuronal spread of the latent virus occurs from the peripheral neuron in retrograde fashion to the brain, usually through the trigeminal or olfactory tract. In addition to retrograde propagation of the latent virus in the peripheral ganglion, reactivation of latent virus within the brain has also been postulated in cases of encephalitis.
Among neonatal patients, the initial infection occurs in the birth canal and spreads hematogenously, with the virus gaining access to the neuronal tissue by diffusing through the blood-brain barrier or by infecting the endothelial cells in the blood vessels. Herpes viruses consist of a double-stranded DNA core with a surrounding envelope of distinguishing glycoproteins.
On pathology, herpes viruses cause a fulminant hemorrhagic and necrotizing meningoencephalitis. Typical gross findings include severe edema and massive tissue necrosis, with petechial hemorrhages and hemorrhagic necrosis. Often, the petechial hemorrhage is not observed on CT or MRI. On microscopy, a focal necrotizing vasculitis is observed with perivascular and meningeal lymphocytic infiltration and eosinophilic intranuclear inclusions in glial cells and neurons.
Although adult herpes encephalitis accounts for 10-20% of viral encephalitis in the United States, the disease is rare. The incidence is 3 cases per 100,000 persons per year. In the United States, millions of women of childbearing age have genital HSV-2. Approximately 1500-2200 neonatal patients with HSV are identified each year.
The risk of HSV in a neonate born to a mother with primary infection is at least 20%, and most often the infection is primary. Neonates born of women with chronic HSV infection have a small risk of recurrent infection, which is estimated to be 1 case per 2000 births. In these patients, passively acquired maternal antibodies may protect against primary infection.
Untreated patients with HSV 1 have a 70% mortality rate. With early treatment, 40% of patients recover without significant neurologic deficits; however, despite appropriate diagnosis and therapy, the mortality rate remains at 30%. Interestingly, HSV does not appear to be more common in immunocompromised patients than in normal hosts.
As new chemical drug options are not viable, alternative antiviral herpes cures are being investigated with great interest. Recent scientific studies of medicinal antiviral plant extracts show very encouraging results for a herpes cure, and have sparked a new methodology for treating herpes.
Studies of these antiviral extracts demonstrate that many of these compounds exhibit significant anti-herpetic activity. Several actually inactivate HSV with great effectiveness. These antiviral extracts represent new effective treatment options for therapeutic use as virucidal agents for recurring herpes infections.
HSVCurative is a potent all natural antiviral cure for herpes, highly effective against HSV1 and HSV2, it has a wide spectrum of antiviral activity against these viruses, even for genital herpes. The cure in this treatment has the ability to inactivate and destroy HSV, which has been established in published clinical trials. It is to be applied directly to an outbreak.
HSVCurative is used specifically to treat HSV1 and HSV2 infections and acts as a curative agent against both these strains of herpes. It exhibits a pronounced anti-herpetic activity against HSV1 and HSV2 and, unlike other cures for herpes, actually kills these viruses upon exposure regardless of location on the body.
Topical application causes herpes outbreaks to dissolve and dry out, with total clearance commonly experienced in 24 to 36 hours. This herpes cure gives immediate results and pain relief are certainly experienced with every application. To learn more, please go to http://www.bcured.net.
In children and neonates, herpes simplex virus type 2 (HSV 2) accounts for 80-90% of neonatal and almost all congenital infections. An isolated case report of an immunocompromised adult patient developing HSV 2 infection has been described. MRI can play an important role in determining the diagnosis and extent of disease.
More recently, sporadic cases of human herpes virus 6 (HHV 6) have been described in immunocompromised patients or those with lymphoproliferative disorders. Herpes encephalitis is the most common cause of sporadic viral encephalitis, with a predilection for the temporal lobes and a range of clinical presentations, from aseptic meningitis and fever to a severe rapidly progressive form involving altered consciousness.
Herpes encephalitis can occur either through hematogenous spread or neuronal transmission. In the typical adult infected with HSV 1, the neuronal spread of the latent virus occurs from the peripheral neuron in retrograde fashion to the brain, usually through the trigeminal or olfactory tract. In addition to retrograde propagation of the latent virus in the peripheral ganglion, reactivation of latent virus within the brain has also been postulated in cases of encephalitis.
Among neonatal patients, the initial infection occurs in the birth canal and spreads hematogenously, with the virus gaining access to the neuronal tissue by diffusing through the blood-brain barrier or by infecting the endothelial cells in the blood vessels. Herpes viruses consist of a double-stranded DNA core with a surrounding envelope of distinguishing glycoproteins.
On pathology, herpes viruses cause a fulminant hemorrhagic and necrotizing meningoencephalitis. Typical gross findings include severe edema and massive tissue necrosis, with petechial hemorrhages and hemorrhagic necrosis. Often, the petechial hemorrhage is not observed on CT or MRI. On microscopy, a focal necrotizing vasculitis is observed with perivascular and meningeal lymphocytic infiltration and eosinophilic intranuclear inclusions in glial cells and neurons.
Although adult herpes encephalitis accounts for 10-20% of viral encephalitis in the United States, the disease is rare. The incidence is 3 cases per 100,000 persons per year. In the United States, millions of women of childbearing age have genital HSV-2. Approximately 1500-2200 neonatal patients with HSV are identified each year.
The risk of HSV in a neonate born to a mother with primary infection is at least 20%, and most often the infection is primary. Neonates born of women with chronic HSV infection have a small risk of recurrent infection, which is estimated to be 1 case per 2000 births. In these patients, passively acquired maternal antibodies may protect against primary infection.
Untreated patients with HSV 1 have a 70% mortality rate. With early treatment, 40% of patients recover without significant neurologic deficits; however, despite appropriate diagnosis and therapy, the mortality rate remains at 30%. Interestingly, HSV does not appear to be more common in immunocompromised patients than in normal hosts.
As new chemical drug options are not viable, alternative antiviral herpes cures are being investigated with great interest. Recent scientific studies of medicinal antiviral plant extracts show very encouraging results for a herpes cure, and have sparked a new methodology for treating herpes.
Studies of these antiviral extracts demonstrate that many of these compounds exhibit significant anti-herpetic activity. Several actually inactivate HSV with great effectiveness. These antiviral extracts represent new effective treatment options for therapeutic use as virucidal agents for recurring herpes infections.
HSVCurative is a potent all natural antiviral cure for herpes, highly effective against HSV1 and HSV2, it has a wide spectrum of antiviral activity against these viruses, even for genital herpes. The cure in this treatment has the ability to inactivate and destroy HSV, which has been established in published clinical trials. It is to be applied directly to an outbreak.
HSVCurative is used specifically to treat HSV1 and HSV2 infections and acts as a curative agent against both these strains of herpes. It exhibits a pronounced anti-herpetic activity against HSV1 and HSV2 and, unlike other cures for herpes, actually kills these viruses upon exposure regardless of location on the body.
Topical application causes herpes outbreaks to dissolve and dry out, with total clearance commonly experienced in 24 to 36 hours. This herpes cure gives immediate results and pain relief are certainly experienced with every application. To learn more, please go to http://www.bcured.net.
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