Herpes – oral Information | Mount Sinai

Cold sore; Fever blister; Oral herpes simplex; Herpes labialis; Herpes simplex

Oral herpes is an infection of the lips, mouth, or gums due to the herpes simplex virus. It causes small, painful blisters commonly called cold sores or fever blisters. Oral herpes is also called herpes labialis.

This close-up view of an early herpes outbreak shows small, grouped blisters and a lot of redness.

Causes

Oral herpes is a common infection of the mouth area. It is caused by the herpes simplex virus type 1 (HSV-1). Most people in the United States are infected with this virus by age 20.

After the first infection, the virus goes to sleep (becomes dormant) in the nerve tissues in the face. Sometimes, the virus later wakes up (reactivates), causing cold sores.

Herpes virus type 2 (HSV-2) most often causes genital herpes. However, sometimes HSV-2 is spread to the mouth during oral sex, causing oral herpes.

Herpes viruses spread most easily from individuals with an active outbreak or sore. You can catch this virus if you:

• Have intimate or personal contact with someone who is infected
• Touch an open herpes sore or something that has been in contact with the herpes virus, such as infected razors, towels, dishes, and other shared items

Parents may spread the virus to their children during regular daily activities.

Symptoms

Some people get mouth ulcers when they first come into contact with HSV-1 virus. Others have no symptoms. Symptoms most often occur in kids between 1 and 5 years old.

Symptoms may be mild or severe. They most often appear within 1 to 3 weeks after you come into contact with the virus. They may last up to 3 weeks.

Warning symptoms include:

• Itching of the lips or skin around the mouth
• Burning near the lips or mouth area
• Tingling near the lips or mouth area

Before blisters appear, you may have:

• Sore throat
• Fever
• Swollen glands
• Painful swallowing

Blisters or a rash may form on your:

• Gums
• Lips
• Mouth
• Throat

Many blisters are called an outbreak. You may have:

• Red blisters that break open and leak
• Small blisters filled with clear yellowish fluid
• Several smaller blisters that may grow together into a large blister
• Yellow and crusty blister as it heals, which eventually turns into pink skin

Symptoms may be triggered by:

• Menstruation or hormone changes
• Being out in the sun
• Fever
• Stress

If the symptoms return later, they are usually more mild in most cases.

Exams and Tests

Your health care provider can diagnose oral herpes by looking at your mouth area. Sometimes, a sample of the sore is taken and sent to a laboratory for closer examination. Tests may include:

• Viral culture
• Viral DNA test
• Tzanck test to check for HSV

Treatment

Symptoms may go away on their own without treatment in 1 to 2 weeks.

Your provider can prescribe medicines to fight the virus. This is called antiviral medicine. It can help reduce pain and make your symptoms go away sooner. Medicines used to treat mouth sores include:

• Acyclovir
• Famciclovir
• Valacyclovir

These medicines work best if you take them when you have warning signs of a mouth sore, before any blisters develop. If you get mouth sores frequently, you may need to take these medicines all the time.

• Antiviral skin creams may also be used. However, they are expensive and often only shorten the outbreak by a few hours to a day.

The following steps can also help make you feel better:

• Apply ice or a warm washcloth to the sores to help ease pain.
• Wash the blisters gently with germ-fighting (antiseptic) soap and water. This helps prevent spreading the virus to other body areas.
• Avoid hot beverages, spicy and salty foods, and citrus.
• Gargle with cool water or eat fruit-flavored ice pops.
• Rinse with salt water.
• Take a pain reliever such as acetaminophen (Tylenol).

Outlook (Prognosis)

Oral herpes most often goes away by itself in 1 to 2 weeks. However, it may come back.

Herpes infection may be severe and dangerous if:

• It occurs in or near the eye.
• You have a weakened immune system due to certain diseases and medicines.

Possible Complications

Herpes infection of the eye is a leading cause of blindness in the United States. It causes scarring of the cornea.

Other complications of oral herpes may include:

• Return of mouth sores and blisters
• Spread of the virus to other skin areas
• Bacterial skin infection
• Widespread body infection, which may be life threatening in people who have a weakened immune system due to atopic dermatitis, cancer, or HIV infection

When to Contact a Medical Professional

Contact your provider if you have:

• Symptoms that are severe or that don’t go away after 2 weeks
• Sores or blisters near your eyes
• Herpes symptoms and a weakened immune system due to certain diseases or medicines

Prevention

Here are some tips to prevent mouth sores:

• Apply sunblock or lip balm containing zinc oxide to your lips before you go outside.
• Apply a moisturizing balm to prevent the lips from becoming too dry.
• Avoid direct contact with herpes sores.
• Wash items such as towels and linens in boiling hot water after each use.
• Do not share utensils, straws, glasses, or other items if someone has oral herpes.

Do not have oral sex if you have oral herpes, especially if you have blisters. You can spread the virus to the genitals. Both oral and genital herpes viruses can sometimes be spread, even when you do not have mouth sores or blisters.

DinulosJGH. Warts, herpes simplex, and other viral infections. In: Dinulos JGH, ed. Habif’sClinical Dermatology: A Color Guide in Diagnosis and Therapy. 7th ed.Philadelphia, PA: Elsevier; 2021:chap 12.

Schiffer JT,Corey L. Herpes simplex virus. In: Bennett JE, Dolin R, Blaser MJ, eds. Mandell, Douglas, and Bennett’s Principles and Practice of Infectious Diseases.9th ed. Philadelphia, PA: Elsevier; 2020:chap 135.

Whitley RJ,Gnann JW. Herpes simplex virus infections. In: Goldman L, Schafer AI, eds. Goldman-CecilMedicine. 26th ed. Philadelphia, PA: Elsevier; 2020:chap 350.

Last reviewed on: 7/19/2021

Reviewed by: Linda J. Vorvick, MD, Clinical Associate Professor, Department of Family Medicine, UW Medicine, School of Medicine, University of Washington, Seattle, WA. Also reviewed by David Zieve, MD, MHA, Medical Director, Brenda Conaway, Editorial Director, and the A.D.A.M. Editorial team.

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.

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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.

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Doctors not found. Change the filtering options.

Herpes simplex virus type 1 and 2 (HSV 1/2), oropharyngeal DNA qualitative determination; separable blisters and erosive and ulcerative lesions, as well as from the cerebrospinal fluid

PCR can detect even a small amount of viral particles in biological material. It allows you to identify herpes viruses, regardless of the duration of infection, even at a time when antibodies have not yet formed.

The most common are types 1 and 2 of herpes. Both are contagious and contribute to the appearance of small bubbles (vesicles) on the mucous membranes, which burst, forming open sores. In HSV-1, blisters appear 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 when there are vesicles on the skin, and sometimes when there are no visible lesions on the skin. HSV-2 is often referred to as a sexually transmitted disease, 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% – type 2. Because type 2 symptoms are barely noticeable, 90% of those infected with it may not be aware of their infection.

In the case of a 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 experience flu-like symptoms, such as chills and a 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 the infection enters the body and spreads, 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.
Currently, there is no cure for herpes, however, there are antiviral drugs that suppress its spread, as well as shorten the duration of the acute phase of a viral infection and alleviate the symptoms of the disease.

What is research used for?

To detect genital herpes infection in men and women and monitor its treatment.
To test a woman for herpes before and during pregnancy (if there is a risk of infection).
When is the test scheduled?

If necessary, confirm or deny the fact of genital herpes infection.

An important place is occupied by the preparation for the study. To make the result of the analysis as reliable as possible, a smear from the oropharynx is taken under the following conditions:

On an empty stomach (or not earlier than 2-3 hours after a meal).
Before rinsing, mucosal irrigation, drops or lozenges.