Herpes simplex is caused by the herpes viruses I and II. Both are DNA viruses.
HSV I: is the common form.
HSV II: requires sexual transmission and produces the sexual form of the disease.
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.
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 same pattern.
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 infection.
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 patient population.
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 patients.
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