Herpes Labialis (Cold Sore) General Info

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Herpes Labialis (Cold Sore) General InfoHerpes Labialis (Cold Sore)
The Herpes virus has always been a notorious one when causing infection, primarily because of how difficult it is to treat. Herpes simplex in particular is rather stubborn, with a majority of the population having suffered from it at one point in their life. It can affect the mouth, genitals and even cause encephalitis.

In this article, we will discuss Herpes labialis in a bit more detail.

Epidemiology
Also called a cold sore, Herpes labialis is a rather common clinical condition, with reports of an annual incidence of 1.6 per 1000 patients per year.1 Classically, herpes labialis is characterised by a superficial rash on the skin or mucus membrane, particularly on the lip. It is considered cosmetically unpleasant but usually resolves itself in around a week to 10 days.

Herpes Labialis is caused by Herpes Simplex Virus 1 and 2, more often though by the former. Studies have shown a higher prevalence of the HSV virus in developing countries when compared to the developed part of the world. 2

Etiology
Herpes labialis is caused by HSV-1 primarily, though in the recent years HSV-2 has also been identified as a common cause. It is usually acquired in childhood or during adolescence through non-sexual contact, such as drinking from the same water bottle as someone who already suffers from herpes labialis.

However, in the recent past, improvement in socio-economic conditions has led to a shift in the time of onset of the disease, and these days patients are usually affected during adolescence rather than at childhood. As a result, it is not uncommon for the primary infection to manifest as genital herpes first due to oro-genital contact.3*

Pathophysiology
When infected by HSV-1 and 2, the virus enters the sensory nerves and migrates up to the sensory ganglion, where it remains dormant for long periods of time. During times of stress such as fever, menstruation, exposure to ultraviolet light (from sunlight), psychological stress and even chest infections, the virus can migrate back through the sensory nerves to the epithelial cells on the skin surface.4,5,6

The ganglion that is commonly affected is the trigeminal ganglion, and as a result infection is most often seen on the lip, though they can occur on the hard palate as well.

Triggers of latent Herpes Labialis

• Fever
• Psychological stress
• Menstruation
• Exposure to ultraviolet light
• Fatigue
• Trauma

Clinical features
Classically, patients are unaware of when they might have acquired the virus. Clinical features include a prodromal phase, where patients can experience burning and itching sensations on the lip or hard palate associated with development of erythema and papules along the vermilion border. This is usually a symptom of reactivation of the virus, and can last for 12 to 36 hours.

Shortly after, patients will notice a 4-stage process of transformation of the lesion, characterised by vesicle formation, postulation, ulceration on the surface and eventually ending with scab formation. Scarring rarely occurs at the site of the lesion.7

In children, infection can sometimes be a bit more severe, with multiple blister formation around the mouth and on the tongue. However, in adults, features are as described above, and may be associated with cervical lymphadenopathy and a sore throat.

Diagnosis
Diagnosis of herpes labialis is primarily clinical. The lesion has a characteristic appearance and location. Most cases of primary herpes labialis are asymptomatic. However, in some cases, further confirmation of the diagnosis may be required (such as in immunocompromised patients). In such cases, tissue culture may be required, which on microscopy can show ballooning of the cells and apoptosis. HSV 1 and 2 can also be diagnosed and differentiated using immunoflourescence.

Other more advanced techniques such as polymerase chain reaction and Tzank smears may also be performed to confirm the diagnosis.

References
1. Van der Linden MW, Westert GP, De Bakker DH, Schellevis FG. Second national study into diseases and actions in general practice. Utrecht, Bilthoven: Netherlands Institute for Health Services Research (NIVEL), National Institute of Public Health and the Environment (RIVM); 2004.
2. Xu F, Sternberg MR, Kottiri BJ, McQuillan GM, Lee FK, Nahmias AJ, et al. Trends in herpes simplex virus type 1 and type 2 seroprevalence in the United States. JAMA. 2006;296:964–73.
3. Scoular A, Norrie J, Gillespie G, Mir N, Carman WF. Longitudinal study of genital infection by herpes simplex virus type 1 in Western Scotland over 15 years. BMJ. 2002;324(7350):1366–7.
4. Stock C, Guillén-Grima F, de Mendoza JH, Marin-Fernandez B, Aguinaga-Ontoso I, Krämer A. Risk factors of herpes simplex type 1 (HSV-1) infection and lifestyle factors associated with HSV-1 manifestations. Eur J Epidemiol. 2001;17:885–90.
5. Spruance SL, Kriesel JD, Evans TG, McKeough MB. Susceptibility to herpes labialis following multiple experimental exposures to ultraviolet radiation. Antiviral Res. 1995;28:57–67.
6. Lorette G, Crochard A, Mimaud V, Wolkenstein P, Stalder J-F,, El Hasnaoui A. A survey on the prevalence of orofacial herpes in France: the INSTANT Study. J Am Acad Dermatol. 2006;55:225–32.
7. Fatahzadeh M, Schwartz RA. Human herpes simplex virus infections: epidemiology, pathogenesis, symptomatology, diagnosis, and management. J Am Acad Dermatol. 2007;57:737–63.

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