HSV has been associated with an infection of oral mucous membranes (gingivostomatitis, herpes labial, and pharyngitis), genital membranes (genital herpes), neonatal and congenital infection, eczema herpeticum (in patients with underlying atopic dermatitis or dariers disease or Sezary syndrome), visceral HSV infection (in immunocompromised hosts), encephalitis, myelitis, meningitis, and ocular complications (Remeijer et al., 2004; Whitley 2004; Kimberlin 2005; Kimberlin and Whitley 2005). Varicella zoster also has been associated with a number of clinical manifestations ranging from a mild illness such as chickenpox to potentially significant complications such as those involving the central nervous system (Koskiniemi et al., 2002; Frenoset et al., 2007).
HSV infects mucosal epithelium or damaged cutaneous epithelium, therefore infection can occur at a variety of sites, but it is more common in oral and genital sites (Miller and Dummer, 2007). Since oral and genital infections are by far the most common, the trigeminal and sacral ganglia are the usual sites of latent infection by HSV (Davison and Clements 2005). Primary infection refers to the persons home first experience of HSV-1 or HSV-2 infection in a completely non-immune persons, however if a person already exposed to HSV-1 become infected with HSV-2 or vies versa, then the infection is described as an initial infection. After infection with either primary or initial infection the virus establishes a latent infection within the sensory nerve, and reactivation of this latent virus results in another round of infection called recurrent infection (Collier et al., 2000). Moreover if the infection of a person occurs by his own strain of virus at another site, then it describes as an endogenous re-infection, and if it is a different strain it describes as exogenous re-infection.
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Primary and Initial Infection
Primary infection with HSV-1 occurs in the early stage of life, in younger age groups infections are asymptomatic, but it can cause a variety of clinical symptoms such as gingivostomatitis and pharyngitis (Whitley 2001). In most patients infection with HSV-1 is self-limited and it last from 10 to 14 days without complication, however in sever cases intraoral lesions and associated swelling can be painful and thus eating become difficult, therefore children home suffer from this may required hospitalisation for dehydration. In younger adults it usually associated with pharyngitis and mononucleosis like syndrome (Annunziato and Gershon 1996). In HSV-1 oral primary infection virus can be isolated from the moth and saliva of asymptomatic children for as long as 23 days with an average of 7 to 10 days (Amir et al., 1997).
As for HSV-1, primary infection with HSV-2 is either asymptomatic or sub-clinical, however it is most sever in genteel infection (Whitley et al 1998). Infection start with the appearance of a small raised macules and papules in the infected area, and then develops into desserts vesicles and papules that progress later to develop ulcers. Symptoms usually last for approximately 3 weeks and it is differ between different sexes. In females it is appears as painful lesions located in vulva and cervix and up to 25% of the infected women will develop aseptic meningitis. Symptoms include a painful micturation with urinary retention. Whereas in males lesions are occur on the glans penis or penile shaft, however other parties of the body such as the buttocks, thighs and perineum may be infected. Symptoms include urinary retention and meningitis or meningoencephalitis.
Initial infection of HSV-1 or HSV-2 occurs when a person whom have antibody to either HSV-1 or HSV-2 and re-infected by the other virus. In this case symptoms are less severe and heal rabidly. Furthermore the course of infection will tack les than 3 weeks and the severity of the lesions are reduced.
Recurrent infection with HSV-1 appears as cold sores and/or recurrent keratoconjunctivitis, however, it may occur with the absence of the clinical symptoms. Recurrence is triggered by a variety of stimuli, including sunlight, physical trauma, stress, respiratory infections and hormonal change, however it is not known whether these stimuli act by a common pathway. Recurrent infection is usually starts with pain, burning, tingling and itching at the site of the primary infection and/or in adjacent areas, this duo to either centrifugal spread via peripheral nerves or contiguous spread to new epithelial cells (Steiner 1996). This will be flowed by the appearance of blisters or vesicles after 24h at the mucocutaneous junction of the lip and sometimes inside the mouth, however, it can be found in other sites innervated by the affected neurone such as the chin and inside the nose (Figure 1.5). Vesicles usually crust over within 72 h, however complete heeling will takes from 8 to 10 days. During that time the virus is shed from the vesicles and the amount of shedding decreases as the lesion crusts over (Scott et al., 1997; Liljeqvist et al., 2009). The frequency of recurrence is variables between different individuals, where is it can be once a month (24%) or twice a year (19%) (Spruance et al., 1977). In genital herpes recurrent infection in female has a minor vulvar irritation, whereas in males it characterised by the appearance of a number of vesicles in the penis. The clinical course is mild with duration from 7 to 10 days and rare secondary symptoms, however the major problem with recurrent infection is that it can occur in a frequent event.
HSV Clinical Manifestation
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The classically primary oral infection with HSV-1 usually presents as multiple painful sores in the tongue, nose, lips and on the skin around the mouth, in pre-school children it causes gingivostomatitis. In addition, the child usually feels sick and has a fever, a headache, and the mouth sores last 7 to 10 days and are often very severe, making eating and drinking extremely uncomfortable. However, most of primary infection goes unrecognized. Unlike the first oral infection, recurrences manifest around the mouth as a cluster of vesicles (3-5), which are milder, more localized and often of shorter duration than primary or initial infection (Collier et al., 2000). Before a cold sore appears, the child usually feels a tingling at the site, lasting from minutes to a few hours, followed by redness and swelling. Usually, fluid-filled blisters form and break open, leaving sores. The sores quickly form a scab. After about a week, the scab falls off and the episode ends. Less often, tingling and redness occur without blister formation. Sometimes small clusters of sores develop on the gums or the roof of the mouth. These sores also last about a week and then go away.
Skin infection by HSV can occur at any sites of the body as a crop of classic herpetic vesicles; however, it is most common by found on the head and the neck. Children who are thumb-sucking may develop herpes on their finger. Healthcare workers, such as doctors and dentists, may also infect their fingers (digits) from patients with cold sores or oral viral shedding. It's has been known since 1909 and called herpetic whitlow and it is an occupational hazard among professional's doctors and dentists (Cleator and Klapper, 1994). Gill et al., (1988) has estimated the incidence among health care professionals by 2.4 cases per 100.000 individuals per year, and may be caused either to be HSV-1 or HSV-2. In Skaraborg, Sweden the prevalence of HSV skin infection among 7500 individuals over the age of 7 was reported to be 1%. However, in another Swedish study it was reported to be 2% of men and 1.5% of women attending in dermatology clinics through a period of 6 years. In most cases, lesions will heal within a few weeks, unless there is a complication with a bacterial infection. Another severe form of cutaneous herpes may occur in patients suffering from atopic dermatitis; vesicles can be either localized like those of VZV with a dermatomal distribution, or disseminated like those in Kaposi's varicella like eruption (Roizman et al., 2007).
HSV infection of the eye is less common than oral and genital infection; it can occur as endogenous reification or recurrent infection. Eye infection is usually caused by HSV-1 (Roizman et al., 2007). Most HSV infection of the eye are thought to be caused by another infection from another site e.g. cold source following endogens reinfection latent HSV infection is probably established in the trigeminal ganglion and neural tissues connected to it, it is suggested that the cornea may support a neural type of HSV-1 latency (Perng et al., 1994).
Latency provides a viral reservoir that allow for spontaneous and recurrent reactivation of the disease (Liesegang, 1989). Ocular infection with HSV-1 can cause disease ranging from blepharitis, conjunctivitis, epithelial keratitis and stromal keratitis (Liesegang, 1999). HSV-1 ocular infection is an important cause of blindness that is serious viral eye infectious in the United States (Liesegang, 2001). It was estimated that HSV-1 ocular infection occurs annually in up to 20.7 per 100000 populations in all countries (Elnifro et al., 1999).
Genital herpes is one of the most common sexually transmitted disease (STDs) (Stanberry et al., 1999). Historically, HSV-2 has been associated with genital infection, but recent reports suggest that an increasing share of genital herpes is caused by HSV-1 (Ribes et al., 2001; Scoular et al., 2002). Primary genital herpes infections are usually more sever than recurrent infections, although primary infection may be asymptomatic. Primary genital HSV-1 infection is less likely than HSV-2 infection to result recurrent disease (Benedetti et al., 1994; Engelberg et al., 2003). Although the clinical course of primary genital herpes infections among patients with HSV-1 and HSV-2 is similar, there are difference in the epidemiology and natural history of the disease caused by the two viral subtypes (Kinghorn, 1994). Genital HSV-1 infections are characterised by less asymptomatic shedding (Kinghorn, 1996), a lower transmission frequency to new partner, longer time between recurrence, and lower clinical recurrence rates (Mindel et al., 1986). Infection with HSV-1 in childhood may protect adults from most genital HSV-1 infections. Socioeconomic condition improvement, the increase in orogenital sexual practice and a decline in age specific may be lead to change in the epidemiology of genital HSV-1 infections. A change in the epidemiology of genital HSV-1 infection has been recognised for several years. HSV-1 is an increasingly important cause of genital herpes. Moreover, an increasing proportion of genital infection is attributable to HSV-1 rather than to HSV-2 (Corey et al., 1999; Whitley et al., 1998).
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