Herpes simplex virus (HSV) infection, whether primary or recurrent, may "typically" present clinically with grouped vesicles arising on an erythematous base on keratinized skin or mucous membrane. Many HSV infections are "atypical," with patch(es) of erythema, small erosions, fissures, or subclinical lesions that shed HSV. Once an individual is infected, HSV persists in sensory ganglia for the life of the patient, recurring with lessening in immunity. In healthy individuals, recurrent infections are asymptomatic or minor, resolving spontaneously or with antiviral therapy. In the immunocompromised host, mucocutaneous lesions can be extensive, chronic, or disseminate to skin or viscera.
Primary HSV infection occurs through close contact with a person shedding virus at a peripheral site, mucosal surface, or secretion. HSV is inactivated promptly at room temperature; aerosol or fomitic spread unlikely. Infection occurs via inoculation onto susceptible mucosal surface or break in skin. After exposure of skin sites to HSV, the virus replicates in parabasal and intermediate epithelial cells, causing lysis of infected cells, vesicle formation, and local inflammation. After primary infection at inoculation site, HSV ascends peripheral sensory nerves and enters sensory (trigeminal or sacral) or autonomic nerve root ganglia (vagal), where latency is established. Latency can occur after both symptomatic and asymptomatic primary infection. Recurrences result from viral reactivation and synthesis and migration of virus through sensory nerves. Usually occur in the vicinity of the primary infection, may be clinically symptomatic or asymptomatic.
Primary infections are usually severe and are often accompanied by painful, small, fluid-filled blisters; fever; and flu-like symptoms. The blisters may spread extensively. Primary infection may last 2 to 3 weeks.
There are various potential triggers of HSV such as stress, sunlight, changing hormone levels, and illness.
The disease is highly contagious when sores are present.
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