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Herpes simplex is caused by the herpes viruses I and II. Both are DNA
The herpes virus enters the body through an abrasion in the skin or mucosa.
It replicates there until there are sufficient amounts of the virus present
to infect either sensory or autonomic nerve endings. Once the virus infects
the nerves its nucleus (nucleocapsid) is carried in the axon of the nerve
to the nerve cell bodies in the ganglia. Once there the virus enters a period
known as latency in which the virus remains dormant and does not replicate
or further infect the body. Later in life and due to external factors, such
as lowered immunity, the disease undergoes reactivation. During this stage
the virus replicates (actually the human nerve cells start 'mass producing'
the virus. They then migrate through the nerve axon back to the skin or
mucous membranes and produce the disease lesions.
Like all other members of the herpes family once infected the person
remains infected his whole life with the virus present in the nerve cells.
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HSV has been isolated from nearly all visceral or mucocutaneous sites.
The clinical manifestations and course of HSV infection depend on the anatomic
site involved, the age and immune status of the host, and the antigenic
type of the virus.
Oral-Facial infections: Both viral subtypes can cause oral-facial
infections, and the infections caused by the two subtypes are clinically
indistinguishable. Gingivostomatitis and pharyngitis are the most frequent
clinical manifestations of first-episode HSV-1 infection, while recurrent
herpes labialis is the most frequent clinical manifestation of reactivation
HSV infection. Conversely, oral-labial HSV-1 infection recurs more frequently
than oral-labial HSV-2 infection. Asymptomatic shedding rates follow the
Genital Infections: Both viral subtypes can cause genital and
oral-facial infections, and the infections caused by the two subtypes are
clinically indistinguishable. Genital HSV-2 infection is twice as likely
to reactivate and recurs 8 to 10 times more frequently than genital HSV-1
Herpetic Whitlow: HSV infection of the finger may occur as a complication
of primary oral or genital herpes by inoculation of virus through a break
in the epidermal surface or by direct introduction of virus into the hand
through occupational or some other type of exposure.
Herpes Gladiatorum: HSV may infect almost any area of skin. Mucocutaneous
HSV infections of the thorax, ears, face, and hands have been described
among wrestlers. Transmission of these infections is facilitated by trauma
to the skin sustained during wrestling.
Eye Infection: HSV keratitis presents with an acute onset of pain,
blurring of vision, chemosis, conjunctivitis, and characteristic dendritic
lesions of the cornea. Use of topical glucocorticoids may exacerbate symptoms
and lead to involvement of deep structures of the eye. Debridement, topical
antiviral treatment, and/or interferon therapy hastens healing.
Central and Peripheral Nervous System Infections: HSV accounts
for 10 to 20% of all cases of sporadic viral encephalitis in the United
States. The clinical hallmark of HSV encephalitis has been the acute onset
of fever and focal neurologic (especially temporal-lobe) symptoms. Clinical
differentiation of HSV encephalitis from other viral encephalitides, focal
infections, or noninfectious processes is difficult. The most sensitive
noninvasive method for early diagnosis of HSV encephalitis is the demonstration
of HSV DNA in cerebrospinal fluid (CSF) by PCR.
Autonomic nervous system dysfunction, especially of the sacral region,
has been reported in association with both HSV and varicella-zoster virus
infections. Numbness, tingling of the buttocks or perineal areas, urinary
retention, constipation, CSF pleocytosis, and (in males) impotence may occur.
Visceral Infections: HSV infection of visceral organs usually
results from viremia, and multiple-organ involvement is common. Occasionally,
however, the clinical manifestations of HSV infection involve only the esophagus,
lung, or liver (especially in immunocompromised individuals.
Neonatal HSV Infection: Neonates (infants younger than 6 weeks)
have the highest frequency of visceral and/or CNS infection of any HSV-infected
A clinical diagnosis can be made accurately when characteristic multiple
vesicular lesions on an erythematous base are present. Umbulication of vesicles
is almost pathognomonic. HSV infection is best confirmed in the laboratory
by isolation of virus in tissue culture or by demonstration of HSV antigens
or DNA in scrapings from lesions.
All three compounds -- acyclovir, valacyclovir, and famciclovir -- have
proven effective in shortening the duration of symptoms and lesions of mucocutaneous
as well as systemic HSV infections in both immunocompromised and immunocompetent