Primary Herpetic Gingivostomatitis
Definition
Primary herpetic gingivostomatitis is a disease that occurs following a primary infection with HSV-1, herpes simplex virus-1, or less commonly HSV-2. The disease primarily affects the oral cavity particularly the oral mucosa and the gingiva. However, it can infect other sites such as perioral skin, buttock, and the scalp (Blevins, 2003).
Aetiology
HSV-1 is the chief cause of primary herpetic gingivostomatitis. HSV-2 can also cause primary herpetic gingivostomattitis; however, it primarily causes lesions in the genital area (George & Anil, 2014). HSV-1 and HSV 2 belong to the human herpes virus family, which is a group of double-stranded DNA viruses. Oral genital contact can cause oral or genital infections by either serotype (George & Anil, 2014). Primary herpetic gingivostomatitis occurs commonly during early childhood years (Faden, 2006). Few patients develop an acute primary infection because the disease self-limiting and often asymptomatic. Primary herpetic gingivostomatitis occurs as a blistering disease of the oral cavity that is transmitted when the shedding virus comes into contact with mucous membranes or broken skin (Blevins, 2003).
Most infections are acquired from other individuals who are shedding the virus although they may not have any visible lesions. Since it is an infectious disease of childhood, infection rates are higher among children who go to day-care facilities (Blevins, 2003). The close proximity of children during various activities and play increases the chances of exchanging oral secretions and viral organisms. Common behaviors that lead to spread of the virus include mouthing toys, sharing of utensils, and thumb sucking (Blevins, 2003).
Epidemiology
HSV-1 and HSV-2 occur everywhere in the world and are not seasonal. Most infected people harbour the virus in its latent form although it can get reactivated and, thus, they can easily infect susceptible individuals (Whitley & Roizman, 2001). Primary herpetic gingivostomatitis peaks at two ages. The first peak is among children aged between 6 months and 5 years (Kolokotronis & Doumas, 2006). The second peak is among young adults during the early 20s. Primary herpetic gingivostomatitis also affects neonates, adults, and elderly people. Socio-economic status and geographic location affect the incidence of the disease (Kolokotronis & Doumas, 2006).
People with low socio economic status in developing countries are more likely to acquire HSV-1 infections compared to those living in developed countries (Kolokotronis & Doumas, 2006). Infection with HSV occurs in early childhood at the age of five years in a third of the children in developing countries while 70-80% of children are affected by adolescent. On the other hand, in developed countries about 20% of children below the age of five years become infected; there is no substantial increase in infection rates during adolescent years until between 20-40 years where there is 40-60% increase in infection rates (Kolokotronis & Doumas, 2006). The prevalence of HSV infections among university students is about 5-10% yearly. Race also seems to affect the prevalence of HSV-1 infections. Approximately 35% of African American children are infected by the age of five years while only 18% of White children are infected with the virus during the same age (Whitley & Roizman, 2001).
Signs and Symptoms
The virus attacks the epithelial cells of the oral mucosa and replicate leading to the breakdown of the cells and spillage of their contents. As a result, the virus is free to attack the adjacent epithelial cells, to spread to other sites, and to infect other people. Despite primary herpetic gingivostomatitis being a self-limiting disease, the virus is transported to the trigeminal ganglia where it remains latent for life (Kolokotronis & Doumas, 2006). Reactivation can occur and is often stimulated by factors such as immune suppression, illness, fever, stress, sun exposure, and menses (Blevins, 2003). If activated again the virus travels from the neural system back to the original site and causes an infection again (Blevins, 2003). In most recurrent infections viral shedding occurs continually although they are asymptomatic. There is an alteration in the magnitude of recurrent infections when compared to the primary infection regardless of whether they become clinically significant. HSV-1 antibodies remain in the circulation thus subsequent infections are weakened. Recurrent infections commonly cause cold sores or sometimes intraoral lesions (George & Anil, 2014).
Primary herpetic gingivostomatitis has an abrupt onset. The severity of symptoms is dependent on the person’s immune system and the virulence of the virus. Symptoms include mild fever, malaise, cervical lymphadenopathy, and presence or absence mucosal lesions. Primary herpetic gingivostomatitis has a general course of 10-14 days which is commonly preceded by an incubation period of about 26 days (George & Anil, 2014). Other symptoms include chills, anorexia, headache, and irritability. Following the onset of the acute phase symptoms such as mouth pain, refusal to drink, salivation, sub-mandibular lymphadenitis, and fetor oris usually occur (Kolokotronis & Doumas, 2006).
Clinical Presentation
Patients typically present with bilateral regionalized lymphadenopathy, malaise and fever of up to 103 Fahrenheit after an incubation period of between three to seven days. Sub-maxillary, sub-mental, and cervical lymph nodes are often enlarged in a number of patients (Blevins, 2003). Many pin-headed vesicles are observable on the mucosa inside the lower lip. The vesicles can also be found on the oral mucosa, gingiva, tongue, hard palate, and the posterior pharynx (Blevins, 2003). The vesicles break down and become many small erythematous lesions which undergo minor enlargement and form central ulcerations covered by yellowish-grey membranes. Neighboring lesions often coalesce to form bigger irregular ulcers. The gingivae commonly have visible erosions along the mid-facial free gingival margins. In a number of patients, lesions are also found in the vermillion and adjacent to the perioral skin (Kolokotronis & Doumas, 2006).
Halitosis is common because of the ulcers. The lesions are very painful thus patients present with difficulty in eating and drinking. As a result, there is excessive pooling of saliva in the mouth due to the difficult swallowing thus children present with drooling (Blevins, 2003). Due to viral shedding following the destruction of epithelial cells, infection to adjacent sites occurs thus lesions are also seen on the chin, lips, or even the cheeks in patients who have had the infection for several days (George & Anil, 2014). The infection can also be spread by the hands to other parts of the body where the skin is broken such as the buttocks or scalp thus causing lesions to appear there. Due to the large number of lesions, the child is usually very restless and irritable.
Diagnosis
Diagnosis of primary herpetic gingivostomatitis is largely dependent on clinical findings. Generally, confirmative tests are not needed. However, there are laboratory investigations available. They include viral culture, direct immunofluorescence, tzanck test, and smears (George & Anil, 2014). Viral culture is the most sensitive diagnostic techniques and is deemed the gold standard but can only be done within the hospital environment. Direct immunofluorescence is also limited to the hospital setting as it is not readily available. Tzanck test show multinucleated giant cells which is characteristic of infections caused by herpes virus. The test detects about 60% of infections caused by herpes virus. Smears distinguish between Varicella zoster virus, HSV-1, and HSV-2 virus (Mohan, Verma, Singh, & Agarwal, 2013). Serological assays are also used to investigate whether there is infection. Tests are positive for herpes IgM alone or for both herpes IgG and IgM in people with recent infections. However, following reactivation of HSV, IgM is usually negative (George & Anil, 2014)
Possible Complications to the Patient
Complications of primary herpetic gingivostomatitis are as minor as cold sores but can be live threatening because they can cause encephalitis. Primary herpetic gingivostomatitis causes morbidity chiefly because of dehydration. Parental fluid is given in severe cases. Bacteraemia can occur due to Kingella kingae; however, it is managed effectively through using antibiotics (Kolokotronis, & Doumas, 2006). Herpes labialis (cold sores) resulting from reactivation of HSV virus in the trigeminal ganglia occurs commonly among adults and is the cause of innocuous morbidity in patients suffering from primary herpetic gingivostomatitis (Kolokotronis, & Doumas, 2006). Recurrences can be as many as 12 annually. HSV-1 infections are the most recurrecent compared to HSV-2.
Burning sensation, excruciating pain, fever blisters, and upper respiratory infections are common due to the blistering caused by the infection (Kolokotronis, & Doumas, 2006). Herpetic glossitis often occurs in immunocompromised patients following HSV-1 infections. The dorsum of the tongue has linear fissures and subdividing dendritic lesions.
Treatment and Management
Systemic antiviral therapy is recommended after early diagnosis to cause faster resolution of the disease. Recurrent infections are commonly managed with topical antiviral drugs. When recurrences become so often or when the infection is superimposed with erythema multiforme, use of long-term antiviral systemic therapy is recommended (George & Anil, 2014). Systemic administration of acyclovir reduces healing time, resolution and minimizes pain dramatically. Patients who are susceptible to complications can be treated with antiviral chemotherapy.
Palliative care and supportive management should be administered and comprises of ensuring hydration, proper care of lesions to accelerate healing, fever and pain control (George & Anil, 2014). Acetaminophen is given at 10-15mg/kg 4 hourly or ibuprofen is given at 10mg/kg 6 hourly for mild to moderate children. Viscous lidocaine (2%) is given for topical application using the Q-tip to provide anaesthesia which can last for about 10 to 15 minutes. Moreover, 20% benzocaine can be found in over the counter gel and is very useful when the lesions are few (George & Anil, 2014). Glyoxide is also available over the counter as a topical solution for soothing the mucous membranes. It contains peroxide and glycerine. Stronger analgesics can be used in cases of severe pain. Intravenous narcotics are sometimes given to hospitalized patients. Antipyretics such as acetaminophen and ibuprofen or either of them are used. Aspirin is not used (Blevins, 2003).
Goldman (2016) recommends using acyclovir to treat children within the first 72 hours when symptoms of primary herpetic gingivostomatitis occur along with symptoms of severe pain or dehydration. The recommended dose of acyclovir presently is 40 to 80mg/kg given in 3 or 4 days for seven days. The adverse effects of acyclovir should be considered during administration. Children with renal failure should be monitored while being treated with acyclovir because acyclovir has nephrotoxic effects at high doses (Goldman, 2016). Acyclovir is given intravenously at 250mg/m2 every 8 hours to children who cannot tolerate oral medication and are dehydrated. Intermittent and diluted infusions should be given over an hour to prevent phlebitis (Blevins, 2003). Faden (2006) seems to favor the use of diphenhydramine and Maalox for managing primary herpetic gingivostomatitis over the use of acyclovir.
References
Blevins, J. (2003). Primary Herpetic Gingivostomatitis in Young Children. Pediatr Nurs, 29(3), 199-202.
Faden, H. (2006). Management of Primary Herpetic Gingivostomatitis in Young Children. Pediatric Emergency Care, 22(4), 268-269. doi.org/10.1097/01.pec.0000218982.46225.f5
George, A., & Anil, S. (2014). Acute Herpetic Gingivostomatitis Associated with Herpes Simplex Virus 2: Report of a Case. Journal of International Oral Health, 6(3), 99-102.
Goldman, R. (2016). Acyclovir for herpetic gingivostomatitis in children. Canadian Family Physician, 62(5), 403-404.
Kolokotronis, A., & Doumas, S. (2006). Herpes simplex virus infection, with particular reference to the progression and complications of primary herpetic gingivostomatitis. Clinical Microbiology and Infection, 12(3), 202-211.doi.org/10.1111/j.1469-0691.2005.01336.x
Mohan, R., Verma, S., Singh, U., & Agarwal, N. (2013). Acute primary herpetic gingivostomatitis. Case Reports, 2013(jul08 1), bcr2013200074-bcr2013200074. doi.org/10.1136/bcr-2013-200074
Whitley, R., & Roizman, B. (2001). Herpes simplex virus infections. The Lancet, 357(9267), 1513-1518. doi.org/10.1016/s0140-6736(00)04638-9
