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Herpes simplex virus can be divided
into two types on the basis of antigenicity, pathogenicity and genetic
properties.
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Herpes simplex type II is the major
cause of urogenital infections, whereas Herpes simplex type I is more
often isolated from nongenital infections.
Herpes simplex viruses have a worldwide
distribution, and direct contact with infected secretions is the
principal mode of spread.
Visit:
Herpes Zoster(Shingles)
;
Chickenpox
;
Herpes Simplex Pancreatitis
Clinical
presentation:
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Herpes simplex causes disease of the
skin and mucosa such as acute gingivostomatitis, recurrent stomatitis,
oral ulcers (cold sores), herpetic keratoconjunctivitis, herpetic
esophagitis, and genital herpes.
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It also causes systemic disease as in
disseminated herpetic infection of infants, acute necrotizing
encephalitis of the adult, and infections in the immunodeficient host.
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Cytopathologic changes in Herpes infection:
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Two types of cytopathology seen in
herpes simplex infections are rounding and degeneration of the cells
with inclusion body formation and cell fusion with formation of
syncytia.
The intranuclear inclusion is the
characteristic cellular lesion, and it consists of a single,
eosinophilic, well-demarcated inclusion body surrounded by a halo and
marginated chromatin.
By electron microscopy the inclusion
body consists of paracrystalline arrays of viral capsids and
electron-dense glycoprotein.
Herpetic infection of skin and mucosa:
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Herpetic infection of skin and mucosa
is manifested by the appearance of red papules that quickly become
vesiculated.
Histologically there is degeneration of
the cells in the stratum malpighii and the stratified squamous
epithelium.
In early stages one observes ballooning
of the epidermal cells and clearing of the nuclear chromatin.
There is acantholysis and formation of
a unilocular vesicle.
The typical inclusion bodies (Cowdry
type A) can be seen in the epidermal cells.
The upper dermis or submucosal portions
of the affected regions show an inflammatory infiltrate around
capillaries.
The histologic lesion of herpes simplex
in skin and mucosa is practically indistinguishable from that caused
by herpes zoster.
Immunohistochemistry using fluorescent
antibodies or immuno-peroxidase can, however, make the distinction
between these viruses and even allows typing of the herpesvirus.
Disseminated
herpetic disease:
Disseminated herpetic infection of the
newborn affects neonates in the first 4 weeks of life as well as an
older group of infants in whom it causes hepatoadrenal necrosis.
Autopsies of infants dying from
disseminated herpetic disease show multiple military foci of necrosis
surrounded by hemorrhagic borders in the liver, adrenal gland, and
brain.
Microscopically these foci consist of a
zone of central coagulative necrosis surrounded by an area of
hyperemia with a sparse mononuclear inflammatory inflammatory
reaction.
Inclusion bodies characteristic of the
herpetic infection are found in nuclei of the parenchymal cells
surrounding the necrotic zone.
Pathologic combination may be
complicated by the presence of gram-negative septicemia.
Morphologic manifestations of
disseminated intravascular coagulation (DIC) may be also prominent.
The virus can be easily easily
demonstrated in the lesions by electron microscopic examination.
Acute
necrotizing encephalitis:
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Herpes simplex virus has been shown to
be a cause of acute necrotizing encephalitis of the adult.
Patients with this syndrome may display
a picture of encephalitis or a clinical picture of an expanding
lesion, often of the temporal lobe.
In fatal cases the brain shows
asymptomatic necrosis particularly prominent in the temporal lobes but
also involving the hippocampus and the posterior occipital cortex.
Hemorrhage may be prominent. In the
early stages of the disease the histopathologic picture is that of
acute necrosis associated with a diffuse meningoencephalitis.
Inclusion bodies within the nuclei of
neurons and glial cells can be seen but on occasion are difficult to
find.
Reactivation and dissemination of
herpetic lesions are not uncommon in immunocompromised hosts.
Esophageal and upper respiratory tract
lesions are commonly found at autopsy in patients who have undergone
intense chemotherapy.
Dissemination occasionally occurs, and
a picture similar to the disseminated disease in newborns can be seen.
Dissemination with fatal outcome also
occurs in some severely burned patients.
Evidence is
accumulating that herpes simplex virus (HSV) infection is implicated
in oncogenesis. HSV antigens have been observed in some oral cancers.
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