Herpes simplex infections are common in daily practice, and often the patient comes to the emergency services. These infections are occasionally recurrent, often painful and associated with systemic symptoms, by which the emergency physician must be familiar with the clinical diagnosis and management.
There are two varieties of the Herpes simplex virus (HSV) capable of causing infection in humans: type 1 (HSV-1) and type 2 (HSV-2) that distinguished by several characteristics, including their behaviors clinical and epidemiological, antigenicity, DNA composition and sensitivity to different physical and chemical agents.
HSV-1 is primarily extragenital location, with a predilection by tissues of ectodermal, whereas HSV-2 for the “Herpes progenitalis†described separately in infections sexual transmission.
The oral regions are a common site of Herpes simplex 1, which is common cause of recurrent orofacial injuries and other diseases (encephalitis). Mouth herpes can be treated with Zovirax.
Humans are the only known natural reservoir of herpes virus simplex, although some experimental animals can be infected with ease although herpes symptoms in men are more common.
Primary infection of HSV-1 occurs mostly during childhood, while type 2 occurs in adolescents and young adults sexually active. Infection rates are inversely proportional to socioeconomic status.
The main mechanism of transmission is direct contact with infected secretions. HSV-1 is transmitted by saliva and HSV-2 via genital herpes. Although viral titers are higher when there are injuries active, is also common in infected asymptomatic viral shedding. Therefore, viral transmission can take place even in the absence of active lesions.
The persistence of infection and recurrences are phenomenon common to both HSV-1 and for HSV-2 and is usually caused by endogenous reactivation. The precipitating factors ranging from sunlight, wind, local trauma, fever, menstruation and even emotional stress.
In an individual who is first infected, the virus replicates in epithelial cells and regional lymph-node, then sensory nerve spreads. A large percentage of these infections are asymptomatic, but the virus remains dormant in the ganglia at 50 to 90% of the adult population, to get back out caused by reactivation factors set out above. Most people over three years carry the virus in a latent form as a result of infection previa.
After replication in the epithelial cells of the site where it entered, it develops a local inflammatory reaction with cytolysis, produced the characteristic lesion, an intra-epidermal vesicle unilocular. It has then spread to local lymph spread via nerve-sensitive, reaching ganglia neurons nearby. Viremia is more frequent in malnourished children, in adults with deficiency of T cell-mediated immunity and occasionally in immunocompetent individuals.
The integrated viral DNA to DNA reactivates neurons under certain stimuli. During reactivation, the virus goes the opposite way to the periphery, following the sensory nerves. Once you reach areas skin, spreads from cell to cell, until the immune system limits the infection again.
Those patients with primary genital infection with pain strong and systemic symptoms (fever, muscle pain) should be hospitalized for observation. It is also indicated the same behavior patients with large lesions that progress rapidly or have important immunological disorders such as immunosuppression for transplant chemotherapy or HIV infection.
In the emergency department be directed to the patient about nature of the disease and if possible be sent to consultation with a dermatologist, infectious disease specialist or gynecologist with experience in treating this condition.