What is herpetic gingivostomatitis. How is it caused. What are the symptoms of herpetic gingivostomatitis. How is herpetic gingivostomatitis diagnosed and treated. What are the complications of untreated herpetic gingivostomatitis. How can herpetic gingivostomatitis be prevented. What is the long-term outlook for people with herpetic gingivostomatitis.

Understanding Herpetic Gingivostomatitis: An Overview of Oral Herpes Simplex Virus

Herpetic gingivostomatitis is a painful oral condition caused by the herpes simplex virus type 1 (HSV-1). It primarily affects young children but can also occur in adolescents and adults. This condition is characterized by high fever and painful lesions in the mouth and gums. HSV-1 is highly contagious and spreads through direct contact with infected saliva or lesions.

Is herpetic gingivostomatitis the same as cold sores? While both are caused by HSV-1, herpetic gingivostomatitis is typically the first occurrence of the infection, affecting the entire mouth. Cold sores, also known as herpes labialis, are recurrent outbreaks that usually appear on the lips or around the mouth.

The Viral Culprit: Herpes Simplex Virus Type 1 (HSV-1)

HSV-1 belongs to the alphaherpesvirus family and is characterized by its enveloped structure and linear double-stranded DNA genome. This virus has a particular affinity for oral epithelium, which explains its prevalence in oral infections. While HSV-1 is the primary cause of herpetic gingivostomatitis, in rare cases, especially in adults, HSV-2 has been isolated from oral lesions.

How does HSV-1 cause infection? The virus enters the body through small breaks in the skin or mucous membranes. Once inside, it replicates rapidly, causing cell lysis and tissue destruction. This process leads to the formation of painful blisters and ulcers characteristic of herpetic gingivostomatitis.

Key Biological Properties of HSV-1

• Neurovirulence: The ability to invade and replicate in the nervous system
• Latency: The capacity to maintain a dormant infection in nerve cells
• Reactivation: The potential to replicate and cause recurrent disease when triggered by specific stimuli

Epidemiology: Who is at Risk for Herpetic Gingivostomatitis?

Herpetic gingivostomatitis primarily affects children under the age of 5, but it can occur at any age. By the age of 35, an estimated 90% of the world’s population is seropositive for HSV-1. This high prevalence is due to the ease of transmission through oral secretions and close personal contact.

Are certain populations more susceptible to herpetic gingivostomatitis? The condition does not discriminate based on gender or race and shows no particular seasonal or geographic distribution. However, individuals with weakened immune systems, such as those with HIV or undergoing immunosuppressive therapy, may be more susceptible to severe infections or atypical presentations.

Global Prevalence of HSV-1

• 90% of adults worldwide are seropositive by age 35
• 50% of infected individuals experience reactivation as herpes labialis
• Infection rates are similar across genders and racial groups

The Pathophysiology of Herpetic Gingivostomatitis: From Infection to Symptoms

The development of herpetic gingivostomatitis involves a complex interplay between the virus and the host’s immune system. When HSV-1 comes into contact with abraded surfaces in the mouth, it quickly enters and replicates within epidermal and dermal cells. This rapid replication leads to cell destruction and the formation of characteristic lesions.

What happens after the initial infection? Following sufficient viral replication, HSV-1 enters sensory and autonomic ganglia, traveling intra-axonally to the ganglionic nerve bodies. The virus most commonly infects the trigeminal ganglia, where it establishes latency. This latent infection can later reactivate, typically manifesting as herpes labialis or cold sores.

Stages of HSV-1 Infection

1. Initial contact and entry into oral epithelial cells
2. Rapid viral replication and cell lysis
3. Formation of oral lesions and blisters
4. Viral entry into sensory ganglia
5. Establishment of latent infection
6. Potential for future reactivation

Clinical Presentation: Recognizing the Signs and Symptoms of Herpetic Gingivostomatitis

Herpetic gingivostomatitis typically begins with a prodromal phase characterized by fever, which can be quite high in children. This is followed by the appearance of painful oral lesions. The condition can cause significant discomfort and may lead to dehydration due to difficulty in eating and drinking.

What are the hallmark symptoms of herpetic gingivostomatitis? The most common signs include:

• High-grade fever (often exceeding 39°C or 102°F)
• Painful ulcerative lesions on the gingiva and oral mucosa
• Yellowish, perioral vesicular lesions
• Swollen, erythematous gums
• Excessive salivation and foul breath
• Cervical lymphadenopathy
• Irritability and lethargy, especially in young children

In some cases, patients may experience difficulty swallowing, leading to poor oral intake and potential dehydration. The lesions typically heal within 7-14 days without scarring, but the virus remains latent in the body.

Diagnosis and Differential Considerations: Identifying Herpetic Gingivostomatitis

Diagnosing herpetic gingivostomatitis is primarily based on clinical presentation. The combination of high fever and characteristic oral lesions often provides sufficient evidence for a clinical diagnosis. However, in atypical cases or when confirmation is necessary, laboratory tests can be performed.

How can healthcare providers definitively diagnose herpetic gingivostomatitis? Several diagnostic methods are available:

• Viral culture: The gold standard for diagnosis, but results may take several days
• PCR (Polymerase Chain Reaction): Highly sensitive and specific, providing rapid results
• Direct fluorescent antibody testing: Can provide results within hours
• Tzanck smear: A quick but less specific cytologic test

It’s important to consider other conditions that may present similarly to herpetic gingivostomatitis. These include:

• Aphthous stomatitis
• Hand, foot, and mouth disease
• Streptococcal pharyngitis
• Oral candidiasis
• Stevens-Johnson syndrome

Treatment Approaches: Managing Herpetic Gingivostomatitis Effectively

The management of herpetic gingivostomatitis focuses on symptom relief and prevention of complications. While the condition is self-limiting, treatment can significantly reduce discomfort and speed recovery.

What are the primary treatment strategies for herpetic gingivostomatitis? The main approaches include:

1. Antiviral therapy: Acyclovir, valacyclovir, or famciclovir can be prescribed, especially if started early in the course of the infection
2. Pain management: Over-the-counter pain relievers like acetaminophen or ibuprofen can help reduce pain and fever
3. Oral care: Maintaining good oral hygiene and using topical anesthetics can alleviate discomfort
4. Hydration: Ensuring adequate fluid intake is crucial, especially in children
5. Nutritional support: Offering cold, soft foods and avoiding acidic or spicy items

In severe cases or in immunocompromised patients, hospitalization may be necessary for intravenous fluid administration and more intensive management.

Antiviral Medications for Herpetic Gingivostomatitis

• Acyclovir: 15 mg/kg orally 5 times daily for 7 days (pediatric dosing)
• Valacyclovir: 1 gram orally twice daily for 7-10 days (adult dosing)
• Famciclovir: 500 mg orally twice daily for 7-10 days (adult dosing)

Prevention and Long-term Management: Controlling HSV-1 Infections

While it’s challenging to prevent initial HSV-1 infection completely, certain measures can reduce the risk of transmission and recurrence. Education about the virus and its modes of spread is crucial in prevention efforts.

How can individuals reduce their risk of contracting or spreading HSV-1? Key preventive measures include:

• Avoiding direct contact with active lesions or infected saliva
• Practicing good hand hygiene
• Not sharing personal items like toothbrushes or eating utensils
• Avoiding triggers that may lead to recurrent outbreaks (stress, UV exposure, etc.)

For individuals with recurrent outbreaks, long-term suppressive therapy with antiviral medications may be considered. This can significantly reduce the frequency and severity of recurrences.

Complications and Special Considerations: Beyond Typical Herpetic Gingivostomatitis

While herpetic gingivostomatitis is generally a self-limiting condition, it can lead to complications, especially in certain populations. Understanding these potential issues is crucial for comprehensive patient care.

What complications can arise from herpetic gingivostomatitis? Some potential concerns include:

• Dehydration: Particularly in young children who may refuse to eat or drink due to pain
• Herpetic keratitis: Spread of the infection to the eyes, potentially threatening vision
• Encephalitis: Rare but serious complication involving brain inflammation
• Autoinoculation: Spread of the virus to other parts of the body through touching

Special considerations are necessary for immunocompromised patients, pregnant women, and neonates. These groups may experience more severe infections or atypical presentations and may require more aggressive management.

High-Risk Groups for HSV-1 Complications

• Immunocompromised individuals (e.g., HIV patients, organ transplant recipients)
• Neonates and young infants
• Pregnant women, particularly those nearing term
• Individuals with eczema or other skin conditions

Future Directions: Research and Emerging Therapies for HSV-1

As our understanding of HSV-1 and its impact on human health continues to evolve, researchers are exploring new avenues for prevention and treatment. These efforts aim to reduce the global burden of HSV-1 infections and improve outcomes for affected individuals.

What are some promising areas of research in HSV-1 management? Current focuses include:

• Development of HSV vaccines: Both preventive and therapeutic approaches are under investigation
• Novel antiviral agents: Targeting different stages of the viral life cycle
• Immunomodulatory therapies: Enhancing the body’s natural defense against the virus
• Gene editing techniques: Exploring the potential to eliminate latent virus from ganglia

While these research areas show promise, it’s important to note that bringing new therapies to market involves extensive testing and regulatory approvals. In the meantime, ongoing public health efforts focus on education, prevention, and optimizing current treatment strategies.

Potential Future Therapies for HSV-1

1. Subunit vaccines targeting specific viral proteins
2. mRNA-based vaccines for both prevention and treatment
3. CRISPR-Cas9 gene editing to disrupt latent viral genomes
4. Combination therapies targeting multiple aspects of viral replication

As research progresses, the management of herpetic gingivostomatitis and other HSV-1 related conditions is likely to become more effective and personalized. This ongoing work offers hope for improved quality of life for the millions of individuals affected by HSV-1 worldwide.

Herpetic Gingivostomatitis – StatPearls – NCBI Bookshelf

Minira Aslanova; Rimsha Ali; Patrick M. Zito.

Author Information and Affiliations

Last Update: March 7, 2023.

Continuing Education Activity

Herpetic gingivostomatitis is a manifestation of herpes simplex virus type 1 (HSV-1) and is characterized by high-grade fever and painful oral lesions. While herpetic gingivostomatitis is the most common cause of gingivostomatitis in children before the age of 5, it can also occur in adults. The condition is characterized by a prodrome of fever followed by an eruption of painful, ulcerative lesions of the gingiva and mucosa, and often, yellow, perioral, vesicular lesions. HSV-1 is usually spread from direct contact or via droplets of oral secretions or lesions from an asymptomatic or symptomatic individual. Once a patient is infected with the herpes simplex virus, the infection can recur in the form of herpes labialis with intermittent re-activation occurring throughout life. This activity reviews the presentation, evaluation, and management of herpes gingivostomatitis and emphasizes the role of the interprofessional team in the care of affected patients.

Objectives:

• Identify the epidemiology of herpes gingivostomatitis.

• Describe the presentation of a patient with herpes gingivostomatitis.

• Outline the management options available for herpes gingivostomatitis.

• Review interprofessional team strategies for improving care coordination and communication to advance the treatment of herpes gingivostomatitis and improve outcomes.

Access free multiple choice questions on this topic.

Introduction

Herpetic gingivostomatitis is a manifestation of herpes simplex virus type 1 (HSV-1) and is characterized by high-grade fever and painful oral lesions. While herpetic gingivostomatitis most commonly occurs in children from ages 6 months to 5 years, it may also occur in adults. [1] HSV-1 is usually spread from direct contact or via droplets of oral secretions or lesions from an asymptomatic or symptomatic individual. Once a patient is infected with the herpes simplex virus, the infection can recur in the form of herpes labialis (cold sores) with intermittent re-activation occurring throughout life.[2]

Etiology

The causative agent is Herpes simplex virus type 1 (HSV-1), which belongs to the alphaherpesvirus group.  The virus is enveloped and has a linear double-stranded DNA genome. HSV-1 is mostly responsible for oral, ocular, and facial infections as it has a tropism for oral epithelium. While most cases of herpetic gingivostomatitis are associated with HSV-1 infection, some adult cases have been reported where HSV-2 was isolated from the oral lesions. Oral infection with HSV-2 is probably transmitted through orogenital contact and has also been observed in HIV-positive patients and patients undergoing immunosuppressive therapy.[3]

Epidemiology

Primary herpetic gingivostomatitis typically occurs in children younger than the age of 5 years, but can also occur in adolescents and adults. HSV-1 is usually acquired in childhood by coming into contact with oral secretions. It is estimated that almost 90% of the world’s population is seropositive for HSV-1 by 35 years of age, and half of the individuals carrying the virus will experience reactivation in the form of herpes labialis. Herpetic gingivostomatitis is equally distributed amongst gender and race groups and is not found to have a particular seasonal or geographic distribution.[4][5]

Pathophysiology

Both HSV-1 and HSV-2 have three major biological properties that play an important role in disease pathogenesis. These include neurovirulence, latency, and reactivation. Neurovirulence is the ability to invade and replicate in the nervous system, and latency is the ability to maintain the latent infection in the nerve cell. Reactivation is the ability to replicate and cause the disease process again, once induced by specific stimuli. HSV-1 causes herpes gingivostomatitis and eventually herpes labialis using the same biological properties. The pathogenesis of herpes gingivostomatitis involves the replication of the herpes simplex virus, cell lysis, and eventual destruction of mucosal tissue. Exposure to HSV-1 of the abraded surfaces allows the virus to enter and rapidly replicate in epidermal and dermal cells. This results in the clinical manifestation of perioral blisters, erosions of the lips and mucosa, and eventual hemorrhagic crusting. Sufficient viral inoculation and replication allow the virus to enter sensory and autonomic ganglia, where it travels intra-axonally to the ganglionic nerve bodies. HSV-1 most commonly infects the trigeminal ganglia, where the virus remains latent until reactivation, most commonly in the form of herpes labialis.[2]

Histopathology

Histological appearance of a mucosal herpetic infection includes degeneration of stratified squamous epithelial cells, acantholysis, and formation of an inflammatory infiltrate around the capillaries of the dermis. The characteristic intranuclear inclusion bodies known as Cowdry type A are found on light microscopy showing arrays of viral capsids and electron-dense glycoproteins. [6] Cowdry type A bodies are eosinophilic inclusion bodies that are also found in varicella-zoster, making the histologic lesions of herpetic gingivostomatitis and varicella indistinguishable. Direct immunohistochemistry using fluorescent antibodies can be used to further distinguish between the herpes virus and the varicella virus.[7]

History and Physical

Primary herpes gingivostomatitis usually occurs in children who have not been previously exposed to the virus. It may be asymptomatic in some cases, but most cases develop a prodrome of fever, anorexia, irritability, and the development of painful oral lesions. Associated symptoms include malaise, lethargy, and cervical or submandibular lymphadenopathy.[8]

The initial sign of herpetic gingivostomatitis is hyperemia of the oral and perioral mucosa, followed by rapidly spreading vesicular lesions on the gingiva, palate, buccal, and labial mucosa. The lesions may ulcerate and then eventually rupture. On physical examination, they may appear flat, yellowish in color, and approximately 2 to 5 mm in size. The ulcers are quick to bleed and typically heal without scarring in 2 to 3 weeks.

Recurrent herpes lesions commonly develop in one-third of the patients who have experienced primary herpetic gingivostomatitis. The patient’s symptoms include burning and itching, followed by the formation of vesicular lesions in a localized area. The lesions mostly develop on keratinized skin such as the vermillion border of the lips, perioral skin, or the hard palate. The lesions may develop when the patient is under physical or emotional stress or systemic illness. Other triggers include sunlight exposure and trauma. The lesions occur in the same area during every episode of recurrence, and systemic manifestations such as malaise and lymphadenopathy are mild.[9]

Evaluation

The diagnosis of herpetic gingivostomatitis is usually clinical, based on the patient’s history and physical examination. The appearance of the oral vesicular and ulcerative lesions is sufficient for the diagnosis. However, if additional testing is required, herpetic gingivostomatitis can be confirmed using a direct immunofluorescent examination of ulcer scrapings or blister fluid. Another test that can be used but is not entirely reliable for diagnosis is the Tzanck smear, which shows the cytologic changes induced by the herpes virus. The Tzanck smear will confirm the presence of a virus in the active lesions but fails to distinguish between HSV-1, HSV-2, and varicella-zoster virus.[10] The gold standard for diagnosis is the isolation of the virus in tissue culture. Antibody testing can help demonstrate seroconversion but does not yield a diagnosis.

Treatment / Management

Herpes gingivostomatitis is generally a mild and self-limited condition, and supportive care is generally adequate. Barrier lip creams such as petroleum jelly have been suggested to prevent adhesions in patients with active herpetic gingivostomatitis. The most important component in the management of herpetic gingivostomatitis is hydration. Adequate hydration is often achieved with pain control; thus, analgesics such as oral acetaminophen and oral rinses are encouraged to make the patient more comfortable and promote fluid intake. It is important to note that patients who are unable to drink to maintain proper hydration should be hospitalized. Other indications for hospitalization include immunocompromised children, patients who develop eczema herpeticum, and HSV spread that results in encephalitis or pneumonitis.[11]

Several studies suggest the usage of acyclovir cream or oral suspension in a rinse and swallow technique.[7] Immunocompetent patients with significant pain or refusal to drink can be administered oral acyclovir if they present within the first 72 hours of disease onset.[12]

Differential Diagnosis

Despite the largely based clinical diagnosis of herpetic gingivostomatitis, it is important first to rule out other diseases that present similarly, keeping in mind the age group and past medical history of the patient. Table 1 explains the differences in causation and clinical presentation of several childhood disorders that may be confused with herpes gingivostomatitis. Some of the differential diagnoses to keep in mind when considering herpetic gingivostomatitis include:

• Herpes zoster

• Primary chickenpox

• Behcet disease

• Herpetiform aphthae

• Erythema multiforme

• Acute necrotizing gingivostomatitis

• Reactive arthritis

• Cytomegalovirus ulceration

• Traumatic ulcers

• Burns, chemical and thermal

• Factitial injuries

• Vesiculobullous disease

Complications

Complications of herpetic gingivostomatitis may include:[13]

1. Dehydration

2. Herpes labialis

3. HSV encephalitis

4. Herpetic whitlow

5. Herpetic keratitis

6. Eczema herpeticum[14]

Deterrence and Patient Education

The patients and their families should be informed that the disease is generally mild and self-limited. They should be told about the appropriate management strategy that includes supportive care with pain control, adequate hydration, and a healthy diet. The patients should be managed at home but should be monitored closely for the development of any complications, such as difficulty in eating or drinking, or worsening of lesions. The patients and their families (especially in the case of young children) should be in regular contact with the primary treating physician. The patient should also be educated about the recurrence of the oral lesions (herpes labialis or cold sores) that may develop in one-third of the patients who develop primary herpetic gingivostomatitis.

Enhancing Healthcare Team Outcomes

Herpes gingivostomatitis is a viral infection characterized by high-grade fever and painful oral lesions, occurring most commonly in children from ages 6 months to 5 years. Out-patient management is sufficient in most situations, but hospital admission may be warranted if the patient develops complications. The disease is best managed by an interprofessional team that includes a primary care provider, an internist, a pediatrician, a nurse practitioner, an emergency department physician, an infectious disease specialist, and a pharmacist. Coordination by different health care experts is necessary to improve patient outcomes and enhance patient care.

Review Questions

• Access free multiple choice questions on this topic.

• Comment on this article.

Figure

Differential diagnosis of pediatric oral lesions. Contributed by Rimsha Ali, MD

References

1.

Tovaru S, Parlatescu I, Tovaru M, Cionca L. Primary herpetic gingivostomatitis in children and adults. Quintessence Int. 2009 Feb;40(2):119-24. [PubMed: 19169443]

2.

Arduino PG, Porter SR. Herpes Simplex Virus Type 1 infection: overview on relevant clinico-pathological features. J Oral Pathol Med. 2008 Feb;37(2):107-21. [PubMed: 18197856]

3.

George AK, Anil S. Acute herpetic gingivostomatitis associated with herpes simplex virus 2: report of a case. J Int Oral Health. 2014 Jun;6(3):99-102. [PMC free article: PMC4109238] [PubMed: 25083042]

4.

Taieb A, Body S, Astar I, du Pasquier P, Maleville J. Clinical epidemiology of symptomatic primary herpetic infection in children. A study of 50 cases. Acta Paediatr Scand. 1987 Jan;76(1):128-32. [PubMed: 3031926]

5.

Cataldo F, Violante M, Maltese I, Traverso G, Paternostro D. [Herpetic gingivostomatitis in children: the clinico-epidemiological aspects and findings with acyclovir treatment. A report of the cases of 162 patients]. Pediatr Med Chir. 1993 Mar-Apr;15(2):193-5. [PubMed: 8321723]

6.

Leinweber B, Kerl H, Cerroni L. Histopathologic features of cutaneous herpes virus infections (herpes simplex, herpes varicella/zoster): a broad spectrum of presentations with common pseudolymphomatous aspects. Am J Surg Pathol. 2006 Jan;30(1):50-8. [PubMed: 16330942]

7.

Mohan RP, Verma S, Singh U, Agarwal N. Acute primary herpetic gingivostomatitis. BMJ Case Rep. 2013 Jul 08;2013 [PMC free article: PMC3736476] [PubMed: 23839615]

8.

Yarom N, Buchner A, Dayan D. Herpes simplex virus infection: part I–Biology, clinical presentation and latency. Refuat Hapeh Vehashinayim (1993). 2005 Jan;22(1):7-15, 84. [PubMed: 15786655]

9.

Leung AKC, Barankin B. Herpes Labialis: An Update. Recent Pat Inflamm Allergy Drug Discov. 2017;11(2):107-113. [PubMed: 28971780]

10.

Mortazavi H, Safi Y, Baharvand M, Rahmani S. Diagnostic Features of Common Oral Ulcerative Lesions: An Updated Decision Tree. Int J Dent. 2016;2016:7278925. [PMC free article: PMC5066016] [PubMed: 27781066]

11.

Faden H. Management of primary herpetic gingivostomatitis in young children. Pediatr Emerg Care. 2006 Apr;22(4):268-9. [PubMed: 16651921]

12.

Amir J, Harel L, Smetana Z, Varsano I. Treatment of herpes simplex gingivostomatitis with aciclovir in children: a randomised double blind placebo controlled study. BMJ. 1997 Jun 21;314(7097):1800-3. [PMC free article: PMC2126953] [PubMed: 9224082]

13.

Amir J, Harel L, Smetana Z, Varsano I. The natural history of primary herpes simplex type 1 gingivostomatitis in children. Pediatr Dermatol. 1999 Jul-Aug;16(4):259-63. [PubMed: 10469407]

14.

Tamay Z, Ozcekert D, Onel M, Agacfidan A, Guler N. A child presenting with primary gingivostomatitis and eczema herpeticum. Minerva Pediatr. 2016 Feb;68(1):72-3. [PubMed: 26864720]

Disclosure: Minira Aslanova declares no relevant financial relationships with ineligible companies.

Disclosure: Rimsha Ali declares no relevant financial relationships with ineligible companies.

Disclosure: Patrick Zito declares no relevant financial relationships with ineligible companies.

Cold sore (herpes simplex virus)

Cold sores are small blisters that develop on the lips or around the mouth. They’re caused by the herpes simplex virus. Cold sores usually clear up without treatment within 10 to 14 days.

About cold sores

Cold sores that keep coming back (recurrent) are shorter and less severe than a first infection.

Most people with recurrent herpes lip infections have two or more outbreaks (episodes) per year.

 A minority of people can have six or more outbreaks per year. Infections in the mouth can be more severe and last two to three weeks. 

Symptoms of cold sores

You may not have any symptoms when you first become infected with the virus (the primary infection). An outbreak of cold sores may occur some time later and keep coming back (recurrent infection).

If the primary infection does cause symptoms, they can be quite severe.

Herpes simplex virus primary infection

In children

Symptoms of the primary infection are most likely to develop in children younger than five years old. Symptoms include:

• swollen and irritated gums with small, painful sores in and around the mouth – this is known as herpes simplex gingivostomatitis
• sore throat and swollen glands
• producing more saliva than normal
• high temperature (fever) of 38C (100.4F) or above
• dehydration
• feeling sick (nausea)
• headaches 

Herpes simplex gingivostomatitis usually affects young children, but adults can also develop it. It can last 10 to 14 days, with the sores taking up to three weeks to heal. Gingivostomatitis doesn’t usually recur after the primary infection.

In adults

Primary herpes simplex viruses are rare in adults. But the symptoms are similar to those experienced by children.

Symptoms include:

• you’ll usually have a sore throat with or without swollen glands
• you may also have bad breath (halitosis) and painful sores in and around your mouth – these can develop into ulcers with grey or yellow centres

If you develop the herpes simplex virus at an early age, it may be triggered from time to time in later life. It can cause recurring bouts of cold sores. 

After the primary infection, the symptoms are usually reduced to just the cold sores themselves.

Recurrent infections (cold sores)

Recurrent infections:

• usually last for less time and are less severe than the primary infection
• the only symptom is an outbreak of cold sores, although you may also have swollen glands
• an outbreak of cold sores usually starts with a tingling, itching or burning sensation around your mouth
• small fluid-filled sores then develop, usually on the edges of your lower lip
• if you have frequent recurrent infections, you may develop cold sores in the same place every time – they may grow in size and cause irritation and pain
• to start with they may ooze before crusting or scabbing over within 48 hours of the initial tingling sensation

Most cold sores, in a recurrent infection, disappear within 7 to 10 days without treatment and usually heal without scarring.

When to visit your GP

You only need to visit your GP if:

• you’re unsure whether it’s a cold sore
• it’s severe and spreading further than just the lip
• a cold sore hasn’t healed after 10 to 14 days for a first episode, or seven to 10 days for a recurrence

Treating cold sores

Recurrent cold sores usually clear up by themselves without treatment within 7 to 10 days.

Antiviral creams and other treatments are available over the counter from pharmacies without a prescription.

If used correctly, these can help ease your symptoms and speed up the healing time.

To be effective, these treatments should be applied as soon as the first signs of a cold sore appear. This is when you feel a tingling, itching or burning sensation around your mouth. Using an antiviral treatment after this initial period is unlikely to have much of an effect.

Ask your pharmacist if you need information about treatments for cold sores.

If your GP thinks it is necessary, antiviral tablets may be prescribed for severe cases.

Complications of cold sores

Cold sores are usually mild, but may cause complications in rare cases. People with weak immune systems caused by illness or treatments such as chemotherapy are particularly at risk of complications.

If the infection affects the mouth or throat, dehydration sometimes occurs if drinking fluids becomes painful. Young children are particularly at risk of becoming dehydrated.

Preventing infection

The herpes simplex virus – or “cold sore virus” – is highly contagious. It can be easily passed from person to person by close direct contact.

After someone has contracted the virus, it remains inactive (dormant) most of the time.

It’s not possible to prevent infection with the virus or prevent outbreaks of cold sores. But you can take steps to minimise the spread of infection.

Cold sores are at their most contagious when they burst (rupture). They stay contagious until they’re completely healed. Avoid close contact with others until your cold sore has completely healed and disappeared.

There’s no need to stay away from work or miss school if you or your child have a cold sore.

You can help minimise the risk of the cold sore virus spreading and cold sores recurring by:

• avoid touching cold sores unless you’re applying cold sore cream – creams should be dabbed on gently rather than rubbed in, as this can damage your skin further
• always wash your hands before and after applying cold sore cream and after touching the affected area
• don’t share cold sore creams or medication with other people as this can cause the infection to spread
• don’t share items that come into contact with the affected area, such as lipsticks or cutlery
• avoid kissing and oral sex until your cold sores have completely healed
• be particularly careful around newborn babies, pregnant women and people with a low immune system, such as those with HIV or those having chemotherapy
• if you know what usually triggers your cold sores, try to avoid the triggers – for example, a sun block lip balm (SPF 15 or higher) may help prevent cold sores triggered by bright sunlight

• Find out more about cold sores on the NHS website

More useful links

• How to use your health services

Help improve this page – send your feedback

Herpes Simplex Virus 1/2, IgG

General information about the study

The first and second types of the virus are most common. They are contagious and contribute to the formation of small bubbles on the mucous membranes that burst, forming open wounds. In HSV-1, vesicles appear mainly around the mouth and in the oral cavity, while HSV-2 usually affects areas in the genital area.

The herpes simplex virus can be transmitted through skin contact, contact with blisters, and sometimes even in the absence of visible lesions.

Sexually transmitted HSV-2 is more common, but infection with HSV-1 herpes can also occur, for example, through oral sex. According to WHO, from 50% to 80% of the adult population of developed countries is infected with herpes of the first type and about 20% of herpes of the second type. Since the symptoms are often subtle, 90% may not even be aware of their infection.

In the case of primary infection, painful blisters usually form at the site of infection after two weeks, which usually disappear after four weeks. They appear on the genitals, around the anus, on the buttocks or on the thighs, after which they can burst. You may also have flu-like symptoms, such as chills and sore throat.

However, herpes vesicles do not always form. Sometimes the manifestations of the disease are so mild that they go unnoticed or are mistaken for something else, such as insect bites or allergies. After entering the body and spreading, the herpes virus is in a latent form. With stress or other diseases that lead to a decrease in immunity, it can be activated again. In most cases, herpes simplex is not dangerous to health, but it can cause serious illnesses: neonatal herpes (if a child becomes infected during childbirth from a mother infected with genital herpes) and encephalitis. They can lead to serious incurable neurological diseases and even death.

The following factors increase the risk of contracting herpes:

• diseases that suppress the immune system (eg HIV/AIDS),
• organ transplant.

There are antiviral drugs that suppress the spread of herpes, as well as shorten the duration of the acute phase of a viral infection and alleviate the symptoms of the disease.

Antibodies are produced to fight infection. The formation of IgG to the herpes simplex virus begins a few days after the appearance of IgM. The concentration of IgG in the blood first rises for several weeks, then falls, and then stabilizes. With repeated infection with herpes, it increases much faster – already in the first days of infection. After a disease, small amounts of IgG remain in a person until the end of life, which, however, does not provide one hundred percent protection against re-infection.

What is research used for?

• As an auxiliary test to confirm the diagnosis of symptoms of herpetic lesions (ulcers, vesicles on the mucous membranes) or neonatal herpes.
• To screen certain groups of people, such as those who are sexually active, potential recipients infected with the AIDS virus, or those who have been exposed to HSV infection.

When is the test ordered?

• When examining persons who have been in contact with patients with HSV.
• During pregnancy preparation and monitoring.

Herpes virus type 1, IgG antibodies – Protos Medical Center

General information about the study

The most common are the first and second types of the virus. They are contagious and contribute to the formation of small bubbles (vesicles) on the mucous membranes, which burst, forming open sores. In HSV-1, vesicles appear mainly around the mouth and in the oral cavity, while HSV-2 usually affects areas in the genital area.
Herpes simplex virus can be transmitted through skin contact, contact with vesicles, and sometimes even in the absence of visible virus lesions.
Sexually transmitted HSV-2 is more common, but HSV-1 herpes infection can also occur, for example, through oral sex. According to WHO, from 50% to 80% of the adult population of developed countries is infected with herpes type 1 and about 20% with herpes type 2. Because symptoms are often subtle, 90% of those infected with HSV-2 may not even be aware of their infection.
Infection with HSV type 1 often occurs in childhood or adolescence as a result of direct contact with the saliva of a virus carrier (through kisses, shared utensils and toys). The penetration of HSV 1 into the epithelium of the oral mucosa, and then into the nerve cells, leads to the development of a latent infection, which occurs in the form of orolabial herpes or, more often, asymptomatic virus carriage and virus shedding. Another route of infection with HSV 1 is sexual. Although much less common than HSV 2, HSV type 1 can also cause asymptomatic or symptomatic genital herpes. For any route of infection with HSV type 1, antibodies to this virus can be detected in the patient’s blood 4 to 8 weeks after infection. Thus, the determination of antibodies to HSV type 1 in the patient’s blood does not make it possible to judge the localization of a herpes infection: the result of the study will be positive both in orolabial and genital herpes or in combination. For this reason, the clinical significance of testing for antibodies to HSV type 1 is much narrower than testing for antibodies to HSV 2.
The analysis for specific antibodies to HSV 1 allows you to identify patients who are immune or, conversely, susceptible to this infection. This is of particular importance when examining pregnant women. Primary infection with HSV in late pregnancy is extremely unfavorable. Studies have shown that primary infection with HSV type 1 or 2 in the third trimester of pregnancy increases the risk of developing neonatal herpes to 30-50%. Most of these cases are caused by the fact that a pregnant woman becomes infected and is an asymptomatic carrier of HSV, including at the time of childbirth. A study for antibodies to HSV type 1 allows you to identify pregnant women who are at risk for primary infection with HSV. The test for antibodies to HSV 1 should be carried out together with the test for antibodies to HSV 2.

How should one prepare for this analysis?

Result interpretation

• HSV 1 antibody negative / HSV 2 antibody negative
If the pregnant woman has neither HSV type 1 nor HSV 2 antibodies (HSV seronegative) while her sexual partner is seropositive for at least one of the types of virus, measures to prevent primary HSV infection, i. e. protected sex (including oral) or abstinence, should be strongly recommended.

• Anti-HSV 1 positive / Anti-HSV 2 negative
The detection of antibodies to HSV 1 in the blood of a pregnant woman indicates that she has a herpes infection and at the same time that she is immune to HSV type 1. At the same time, as mentioned above, it is not possible to judge the localization of the infection (orolabial or genital herpes). It should be remembered that immune immunity to HSV 1 does not guarantee immune immunity to HSV 2, and cases of infection with HSV type 2 in the presence of genital herpes caused by HSV type 1 have been described. Therefore, in this case, if an HSV-1-seropositive / HSV-2-seronegative pregnant woman has a sexual partner seropositive for HSV 2, measures to prevent primary infection with HSV should be recommended. If her sexual partner is only HSV 1 seropositive and not HSV 2 seropositive, primary infection with HSV type 1 is impossible by definition and measures to prevent primary infection with HSV 1 are not carried out.