Wednesday, February 4, 2015

HSV-2 infection is usually acquired sexually in early adulthood, often in people with pre-existing H


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Herpes simplex virus (HSV; Box 1 ) infects the skin and neurones of the dorsal root ganglia, where it causes lifelong latent infection. The virus is often reactivated, leading it to spread down neuronal axons in spinal or trigeminal nerves and either to be shed asymptomatically in saliva (HSV-1) or genital secretions (HSV-2), or to cause disease of the skin, mucosa and occasionally major organs ( Box 2 ).
Primary HSV-1 infection occurs when a susceptible person, medcenter usually a child, comes into close contact with a person with primary or recurrent infection. Primary infection in children is often asymptomatic, but can cause stomatitis severe enough to require hospitalisation. Symptoms are more common in adolescents and adults. Most HSV-1 seroconversions occur in the first five years of life, and by adulthood 80% of individuals have HSV antibodies. However, as HSV-1 seroprevalence is falling in many developed countries, risk of primary HSV-1 infection in adults is increasing. HSV-1 may also cause genital herpes; the increasing prevalence of this infection may be due to increasing orogenital contact. 1
HSV-2 infection is usually acquired sexually in early adulthood, often in people with pre-existing HSV-1 infection. Thus, clinical infection with HSV-2 is often an initial rather than a primary infection (the latter occurs when an adult acquires HSV-2 in the absence of HSV-1 antibodies). HSV-2 usually causes genital herpes, but is also a rare cause of herpes medcenter labialis. 2 The major influence on HSV-2 acquisition is the number of lifetime sexual partners, and women are generally medcenter infected at an earlier age than men. 3 Most transmission occurs via asymptomatic viral shedding in skin or genital secretions. 2 In Australia , the seroprevalence of HSV-2 in women is 14%. 1
In primary HSV infection of the oropharynx, the most common manifestation is gingivostomatitis. Shallow ulcers form on the buccal mucosa medcenter and under the tongue ( Box 3 ), and may also occur on the hard palate (which medcenter helps differentiate HSV infection from herpangina caused by coxsackie virus). These ulcers may be accompanied by fever and submandibular lymphadenopathy. Autoinoculation from the primary medcenter infection may occur elsewhere on the body (eg, herpetic whitlow).
Recurrent orolabial infections ("cold sores") may be triggered by stimuli such as fever, stress, cold, menstruation and ultraviolet radiation. Lesions usually occur on the vermilion border of the lips but may develop elsewhere medcenter on the face, including inside the nose. There is often a prodromal tingling or itching at the site of recurrence. Asymptomatic oral shedding of HSV is common and can transmit the virus. 4 Lesions may be widespread in people medcenter with eczema and severe in those who are immunocompromised.
Symptomatic primary genital infection is moderately severe (more so in women) and lasts up to three weeks. medcenter Common signs include fever, dysuria, widespread ulceration, inguinal lymphadenopathy, malaise and pain. It may be accompanied by radiculomyelitis with urinary retention and neuralgia, and secondary bacterial infection. Perianal infections and proctitis may occur, especially in homosexual men. Genital infection medcenter often causes significant emotional and psychosexual disturbance.
About 20% of HSV-2-seropositive patients have overt recurrences of genital herpes; lesions are more limited in area and severity than in primary infection ( Box 4 ). About 60% of HSV-2 seropositive patients have lesions but do not recognise their herpetic nature, especially if they are small or atypical, unless appropriately trained. The remaining 20% have true asymptomatic viral shedding. Genital HSV-2 recurrences usually last longer than oral HSV-1 recurrences and are more frequent in the six to 12 months after initial infection. 3 , 4 , 5
This varies in prevalence around the world, from 1 in 2500 live births in the United States to 1 in 13 000 births in Australia , 6 - 8 reflecting the wide variation in HSV-2 seropositivity in different regions medcenter and socioeconomic groups. Most neonatal medcenter HSV infection occurs after birth through an infected birth canal, although rarely it may occur in the postpartum period from direct contact or even from congenital infection. Most cases (about 70%) are due to HSV-2, although more HSV-1 neonatal disease may follow the current rise in HSV-1 genital infections. medcenter
Primary maternal genital herpes in the last trimester, particularly around the time of labour, leads about a third of babies to be infected. Neonatal HSV may also follow symptomatic or asymptomatic recurrences and, in fact, most babies with neonatal herpes are born to mothers with asymptomatic viral shedding. The clinical picture ranges from disease localised to the skin, eyes and mouth to encephalitis and disseminated disease ( Box 5 ). 6 Neonatal herpes may recur, necessitating long-term antiviral therapy.
HSV-1 keratitis may present w

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