Cold sores – fact versus fiction Print E-mail
Written by GlaxoSmithKline   
Cold sores, also known as herpes labialis, affect approximately one in three people at some time in their life.1,2 The sores can appear unsightly and can even be disfiguring. There is also a certain social stigma attached and sufferers may feel self-conscious and embarrassed. As a pharmacist, you will probably see a large number of customers with cold sores. Although there is no cure as such, cold sores are entirely treatable. Yet, despite the availability of effective medications, one-fifth of sufferers do not treat at all.[3]

This article gives a brief overview of the causes and triggers of cold sores and discusses the various treatment options available. One aim is to attempt to dispel some of the myths and misconceptions to help combat the stigma.

What is a cold sore?


Caused by the herpes simplex virus (HSV), a cold sore appears as a small cluster of blisters, usually on the lip or adjacent to the lip or nose. There are about 100 different herpes viruses, but only some of these can cause infection in humans.4 HSV itself has two serotypes: HSV-1 and HSV-2. HSV-1 is mostly associated with orofacial infections5 (e.g. cold sores), while HSV-2 is more frequently associated with genital infections.[6]

Herpes is one of the most common viral infections. Studies have shown that in the Western world, about 70 per cent of adults will become infected with HSV-1 and carry antibodies to the virus in their bloodstream.[7] The primary infection is usually acquired in the first decade of life through close physical contact with parents, siblings or friends.[1] However, only a small number of these individuals will develop significant symptoms.[8]

The virus first infects the mouth, before travelling to nerves in and around the face, where it remains indefinitely. Between cold sore attacks, the virus lies dormant and inaccessible to the body’s immune system. Once reactivation is triggered, the virus travels down the nerve to the skin’s surface (epidermis) where it replicates and multiplies, leading to the tingling or burning sensation that often signals the start of a cold sore attack.

Around one in three people with HSV-1 experience recurrent cold sores.[9] These recurrent infections vary in severity between individuals and can occur up to once every month.[1]

Triggers and prevention


We don’t really know what causes outbreaks of HSV-1, but it is thought that certain trigger factors provoke recurrent cold sores (see box “Common cold sore triggers”). Most sufferers can identify everyday events that trigger virus reactivation and lead to the development of a cold sore. Knowing these triggers is important to prevent an outbreak. If patients are not aware of their triggers, they should be encouraged to begin treatment as soon as they feel the first tingling sensations.

Application of therapy during the prodrome, or tingle, stage can prevent or reduce the severity of the cold sore outbreak.[10] However, the virus continues to be present throughout the cold sore cycle, from tingle to blister, right up until crust, so therapy should not be stopped sooner than recommended.
    

The cold sore cycle


Cold sores follow a natural cycle from first tingle through to painful blister and final healing. If untreated, a typical cold sore lasts about 10 days and progresses through five distinct stages:[7,11]

1. Tingling/prodromal phase (a few hours to one day)[7]
At first, the area gets warm and painful; tingling sensations may occur. However, 46–60 per cent of patients notice cold sore recurrences developing during this stage.

2. Blister phase (one to two days)[7]
The area becomes red and small bumps form, often accompanied by a throbbing pain. Colourless, clear fluid-filled blisters then start to develop, most often on the lips. These blisters can be painful and contain millions of HSV-1 viruses, which are highly contagious.

3. Ulcer phase (one day)[7]
The blisters burst to produce an ulcer, which is itchy, painful and often cracks or bleeds. This stage is a major cause of discomfort.

4. Scab phase (five to six days)[7]
Eventually, the ulcer becomes dry and itchy as the scab forms. This brittle layer may crack and bleed. The risk of infection is low.

5. Healing (one to two days )[7]
Finally the scab turns into dry flaky skin and falls off. There is residual redness until a return to normal skin with no scarring.[7,11] The pain disappears. Symptoms disappear until the virus is reactivated.

Stopping the spread of infection


Cold sores are highly infectious and capable of spreading to other parts of the body. Indeed ‘self-infection’ – spreading the virus (usually with the hands) to another location – is just as common as the risk of passing the virus to another person. Infection is possible from the beginning of the first symptoms until a hard crust has formed and the scabs have dried up.

ImageHSV-1 can be transmitted in a number of ways, including kissing and close physical contact, oral sex, contamination of drinking cups, eating utensils and towels, and contact with fluid produced by the cold sore. Sufferers should also remember to wash their hands thoroughly after touching a cold sore – for example, after applying treatment.

 

 

Treatments


There is currently no cure for cold sores – once HSV enters the body it stays there indefinitely. However, a number of symptomatic and antiviral treatments are available over the counter in pharmacies to treat an attack.

Symptomatic treatments
These include astringents and antiseptics (ammonia solution, phenol), surface protectors (dimeticone and zinc sulphate), analgesics (paracetamol and aspirin) and herbal remedies or nutritional products (extract of melissa and zinc). Although these treatments may relieve the pain or itching and aid healing, they do not target the underlying cause of the cold sore – the HSV-1 virus – and therefore provide only temporary symptom relief.

Antiviral agents
These are now considered central to the treatment of cold sores as they can provide symptom relief and targeted antiviral activity. The active ingredient in many antiviral brands is aciclovir. In the 1970s, pioneering work showed that aciclovir was a potent inhibitor of HSV replication, work that led two researchers to win the Nobel Prize. Aciclovir selectively enters infected cells, inhibiting HSV replication by inactivating the enzyme DNA polymerase. Administered in an inactive form, aciclovir only takes effect once it interacts with these specific viral enzymes, so it does not affect healthy cells. Following aciclovir treatment, HSV-1 fails to replicate and the cold sore outbreak is shortened.[1]

ImageThere are now over 100 generic topical aciclovir creams available over the counter in Europe, but there is wide variation in the formulations and the efficacy of skin penetration is not equal across all of them.[12] As aciclovir is poorly absorbed by the skin, cold sore formulations often contain propylene glycol to help them penetrate more effectively. A recent study has shown that 40 per cent propylene glycol is the optimum level for skin penetration.[12]

References

1.     Spruance S. Herpes simplex labialis. In Sacks S (ed). Clinical Management of Herpes Viruses. pp3–42. Amsterdam: IOS Press, 1995.
2.     Lamey P, Lewis M. Viral Infection. In Lamey P (ed). A Clinical Guide to Oral Medicine. London: British Dental Association, 1997.
3.     Hall and Partners, October 2000.
4.     www.micro.msb.le.ac.uk/3035/Herpesviruses.html
5.     Spruance S, Kriesel J. Treatment of herpes simplex labialis. Herpes 2002; 9(3): 64–69.
6.     www.emedicine.com/MED/topic1006.htm
7.     Lewis M. Int Dent J 2004; 54(2): 103–111.
8.     Scully C. Oral Surg Oral Med Oral Pathol 1989; 68:         701–710.
9.     Van Straten M et al. A review of antiviral therapy for herpes labialis. Arch Dermatol 2001; 137: 1232–1235.
10.     Biagioni PA et al. Acyclovir cream prevents clinical and thermographic progression of recrudescent herpes labialis beyond the prodromal stage. Acta Derm Venereol 1998; 78(1): 46–47.
11.     Gross E & Patz B. Deutsche Apotheker Zeitung. 13 April 2006.
12.     Trottet L et al. Are all aciclovir cream formulations bioequivalent? Int J Pharm 2005; 304: 63–71.
 
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