Primary herpetic gingivostomatitis in young children.
The human herpes virus family consists of eight currently known pathogens that represent the most frequent isolates in general laboratories (Koneman, Allen, Janda, Schreckenberger, & Winn, 1997). The group includes HSV (types 1 and 2), cytomegalovirus, Epstein-Barr virus, varicella-zoster virus, and human herpes viruses-6, 7, and 8. The HSV is a large, DNA-containing virus that has two serotypes: type 1 (HSV-1) and type 2 (HSV-2). HSV-1 usually affects the oral cavity, whereas HSV-2 infects the genital area; however, there are exceptions to the rule. HSV-1 infections are extremely common.
The majority of primary HSV-1 infections are asymptomatic or mild enough to go unrecognized (Amir, Harel, Smetana, & Varsano, 1997; White, 1998). Mild cases may be confused with teething or other poorly defined illness. When clinically evident, however, the most frequent manifestation of initial HSV-1 disease in young children is primary herpetic gingivostomatitis (PHGS) (Amir et al., 1997; Murph & Grose, 1999). This occurs in 25-30% of affected children (Amir et al., 1997). Pediatric nurses working in both acute and primary care settings will encounter this condition in otherwise healthy young children, yet information about this pediatric infection is extremely limited in the nursing literature. Sheff (2000) highlights HSV as a "microbe of the month," briefly describing type-1 oral infections. Klotz (1990) explores transmission of HSV-1 infections from clients to nurse anesthetists. As an aid to pediatric clinical care, assessment findings, diagnosis, medical management, and nursing implications for PHGS in young children will be examined.
PHGS is a blistering disease of the mouth, easily transmitted when the shedding herpes virus comes in direct contact with mucous membranes or broken skin. Most primary infections are contracted from others who are shedding HSV-1, yet may be free of evident lesions (White, 1998). As is true of other infectious childhood diseases, infection rates for HSV-1 are higher among young children who attend day care centers (Chandrasekar, 1999; Murph, 1999). Close proximity during activities and play increases the likelihood of exchanging oral secretions and viral organisms. Examples of transmission-potential behaviors seen in young children include mouth touching; sharing utensils, cups, and bottles; thumb sucking; and mouthing toys. The virus invades epithelial cells lining the oral cavity of a susceptible host and replicates. Epithelial cells full of the virus break open, spilling their contents. The virus is then free to invade neighboring epithelial cells, be transported to new locations, and infect other people (Crawford, 2000).
Although PHGS is a self-limiting disease, the virus is transported to the trigeminal ganglia, where a latent or dormant infection is established that remains for life (Chandrasekar, 1999; White, 1998). Reactivation of the dormant virus can occur, often precipitated by factors such as sun exposure, stress, illness, menses, fever, or immune suppression. When this happens, the virus travels back along the neural system at or near the original site causing infection again. Most recurrent infections are asymptomatic, yet viral shedding occurs (White, 1998). When clinically evident, these recurrent infections are rarely of the same magnitude as the primary infection. The antibodies specific to HSV-1 will remain in circulation, weakening subsequent infections. Recurrent infections generally cause only single labial lesions (herpes labialis) widely known as fever blisters or cold sores. Repeated intraoral lesions can occur.
Assessment Findings/Physical Exam
Following an incubation period of 3-7 days (Chandrasekar, 1999; White, 1998), a typical syndrome develops abruptly in healthy children. Fever (up to 103[degrees]F); malaise; and bilateral, regionalized lymphadenopathy appear. Cervical, submental, and submaxillary nodes can all be enlarged. White (1998) describes gingivitis followed by the rapid development of fragile vesicles, typically concentrated on the mucosa inside the lower lip (see Figure 1). Vesicles also appear on the gingivae, buccal mucosa, tongue, and hard palate. As underlying epithelial cells are destroyed, the vesicles soon break down into ulcers. Halitosis is present. The oral lesions are very painful and make swallowing, drinking, and eating difficult. The inability to swallow causes excessive saliva to pool in the mouth, and so children drool.
[FIGURE 1 OMITTED]
Viral shedding in the mouth can spread the infection to skin surrounding the mouth, where the process is repeated. Almost three fourths of the children in the study conducted by Amir and colleagues (1999) experienced perioral lesions of the lips, cheeks, or chin after several days of illness. Herpetic whitlow is a direct inoculation into the skin of a finger by HSV-1 (Rosen & Ablon, 1997). This can occur in young children who suck their thumbs during viral shedding. On occasion, the virus has spread by hands to remote sites of the body, such as scalp or buttocks, where skin integrity is disrupted.
The number of lesions and degree of discomfort vary from child to child. Painful lesions make a small child restless and irritable. Illness associated with PHGS is often significant, with persistence of symptoms generally lasting 1 to 2 weeks. Young children are kept out of day care and parents fever, and drooling can all contribute to dehydration. In severe cases, children may require hospitalization due to dehydration.
The majority of PHGS cases are diagnosed based upon the clinical findings. Although clinical diagnosis provides a presumptive diagnosis, this is usually adequate for identifying this infection. The presence of typical intra-oral and extra-oral vesicular lesions is highly indicative of PHGS (Amir, Harel, Smetana, & Varsano, 1999). This characteristic finding can help differentiate PHGS from other blistering mouth diseases that occur in young children. Herpangina (a coxsackie viral disease) characteristically includes vesicles on the back portion of the oral cavity and palate, along with an inflamed pharynx. There are no associated extra-oral lesions with herpangina. Aphthous stomatitis can be mistaken for ulcered herpetic lesions, but the ulcers are not preceded by vesicles, and there are no extraoral lesions. Hand, foot, and mouth disease, another coxsackie viral disease, has both intra-oral and extraoral vesicles. However, the distribution of lesions on the body clearly distinguishes this viral infection from PHGS. Although Stevens-Johnson Syndrome (erythema multiforme) displays oral lesions, the extra-oral manifestations differentiate this disease from PHGS.
In addition to the clinical picture associated with PHGS, a complete blood count may reveal leukocytosis or neutropenia associated with viral infections. In those cases where a definitive and/or early diagnosis is required, lab testing is available. Immunocompromised clients can present with nontypical assessment findings (Chandrasekar, 1999; White, 1998) and benefit from diagnostic labs. Pediatric oncology and HIV/AIDS patients are at increased risk for developing secondary infections, as is any immunosuppressed patient. Infection by the HIV children, and in those undergoing cancer treatments such as chemotherapy and bone marrow transplantation. Radiation mucocitis and the development of opportunistic candidiasis must be ruled out as causes of oral lesions in these populations.
The preferred method of diagnostic confirmation is isolation of the HSV-1 virus using cell culture techniques (White, 1998). HSV-1 is one of the easiest viruses to cultivate (Rosen & Ablon, 1997). Kits containing special swabs and live cell transport medium are commercially available for cell culturing. Swabbing lesions in a young child's mouth can be very difficult and painful. White (1998) reports that fresh vesicular swabs (less than 24 hours old) or saliva can be used for orocutaneous infections. Using newer methods of fluorescent staining or monoclonal antibodies, cell cultures now provide reliable results in less than a day (Chandrasekar, 1999; Lewis, 1999). The cost of viral cultures may range from $60 to $150, depending on whether a specific culture or a comprehensive panel is performed. Virology labs are not widely available, but specimens can be sent out to reference laboratories.
Serology tests can also be performed, primarily checking for the presence of antibodies to the virus. A blood sample is collected in a red top tube for this lab test. Traditional serology methods detect immune status by identifying antibodies in client blood without differentiating between past and present infections, Immunoassay techniques such as enzyme immunoassay (EIA) or enzyme linked immunosorbent assay (ELISA) can identify current infections specific to HSV-1 but may not reliably distinguish the virus from close relatives such as HSV-2 or varicella zoster (Koneman et al., 1997). Newer, DNA specific testing for HSV-1 is available through nucleic acid probes. These viral swabs can be sent to a reference lab and cost approximately $100.
Antiviral therapy with oral acyclovir is recommended in the treatment of PHGS (Amir et al., 1999; Chandrasekar, 1999; Murph & Grose, 1999). Acyclovir interferes with DNA synthesis, thereby inhibiting viral replication. Amir and colleagues (1999) carried out a double blind, placebo controlled study of children under the age of 6 and found acyclovir effectively decreased viral shedding and shortened healing times by several days. The suggested oral dosage for HSV-1 infections is 15 mg/kg, 5 times daily, for a period of 7 days. Having a half life of only 2-3.5 hours, acyclovir requires more frequent administration than oral medications with longer half lives. The oral drug form is available in suspension (200 mg/5 ml) for young children. Side effects of acyclovir may include dizziness, head ache, nausea, vomiting, and diarrhea. The drug can be nephrotoxic with high oral doses or IV administration, so caution should be used in children with renal impairment. Known hypersensitivity to the drug would pose a contraindication. Treatment is usually carried out on an outpatient basis. Children hospitalized with severe cases can receive acyclovir intravenously, since they are unable to tolerate oral medication and have an IV in place for rehydration. The IV dosage of acyclovir is 250 mg/[m.sup.2] every 8 hours. Intermittent infusions should be given over at least 1 hour and be well diluted in order to avoid phlebitis. Intravenous fluids and medication may be needed for several days.
Acetaminophen (10-15 mg/kg every 4 hours) or ibuprofen (10 mg/kg every 6 hours) can be given to children at home for mild to moderate pain. Viscous lidocaine (2%) can be prescribed for topical application using a Q-tip, providing a local anesthetic lasting approximately 10-15 minutes. Over-the-counter topical anesthetics in gel form contain 20% benzocaine and may be helpful for those with a minimal number of lesions. Glyoxide, a topical preparation available over the counter, contains glycerine and peroxide. It is soothing to the mucous membranes. Stronger analgesics can be prescribed for the pain. Hospitalized children may occasionally require intravenous narcotics. Fever can be managed with antipyretics such as acetaminophen and/or ibuprofen. Aspirin is not used since this is a known viral infection.
Supportive nursing care for pain and fever are part of the management process. Nonpharmacologic comfort measures may include age-appropriate distraction techniques, cutaneous stimulation, and the presence of significant caregivers to hold or rock children. For children able to tolerate food and drink, offer a soft, cold diet (applesauce, jello, pudding, etc.) and cool liquids or popsicles. Juices such as pineapple or orange should be avoided due to mucosal irritation from the high acidity. Administering analgesics or topical preparations prior to eating or drinking can enhance food and fluid intake. Monitor hydration status since children are at risk for dehydration. Parents caring for children at home should be informed to report diminishing levels of fluid intake and urination.
Oral care is a problem due to the sensitivity of the mouth. Children should receive oral care if they are able to tolerate it, but gingivitis and hygiene during the acute phase. Some children may tolerate the use of toothettes. Glyoxide can be applied in this manner, and the peroxide content helps to clean the mouth. Drinking clear liquids also helps rinse the mouth.
Infection control is a vital part of nursing care for children with PHGS. Wearing gloves when coming in contact with mucous membranes, saliva, or lesions is mandatory. Prior to the advent of standard precautions and the widespread use of gloves, health care providers such as nurses, nurse anesthetists, and dentists were at increased risk for contracting herpetic whitlow from their patients. Contact precautions should be
instituted for hospitalized children. This includes a private room, use of gloves, and hand washing after glove removal. Gowns may be necessary to protect uniform/clothing when holding a drooling child.
Educating parents or caregivers about transmission is equally vital, whether children are cared for at home or in the hospital. Intrafamilial spread of herpetic infections occurs (Sealander & Kerr, 1998). Younger siblings at home or visiting in the hospital are at risk, as they probably have not yet been infected by HSV-1. Avoiding contact with lesions and thorough hand washing should be emphasized. It is important to control thumb or finger sucking during the course of the illness. Sealander and Kerr (1989) suggest that it may be prudent to inquire whether mothers are breastfeeding. They reported transmission of HSV from a toddler's mouth to his mother's breasts through breastfeeding. The toddler had been infected by his 5-year-old sibling with PHGS.
Parents may have concerns about their child having a "herpes infection," since herpes is so often linked to sexual transmission. The nurse should explain that HSV-1 (rather than HSV2) is considered the infecting organism for their child's condition.
An important primary care issue is informing parents when a child may safely return to daycare or preschool. The American Academy of Pediatrics Red Book recommends that young children infected with PHGS be kept away from childcare facilities if active lesions and drooling are present (Pickering, 2000). Many of these young children will not be able to fully control their oral secretions, as they may engage in activities such as mouthing toys, kissing, spitting, wiping drooled saliva with their hands, or sharing cups and utensils. The Red Book further states that recurrent cold sores should not keep a child from daycare.
Finally, nurses should educate parents about recurrent infections, as acyclovir does not eradicate HSV-1 infections. Caregivers need to be aware of virus latency, which persists life long, and precipitating factors associated with recurrence. Reactivation of the virus in the form of a fever blister is often preceded by sun exposure, illness, or stress. New technology may one day allow for the development of safe and effective HSV vaccines. Vaccine research is currently in progress, but the focus is on genital herpes. Stanberry (1998) supports the need for vaccines to curb common, nongenital infections such as PHGS and recurrent herpetic labialis.
Amir, J., Harel, L., Smetana, Z., & Varsano, I. (1999). The natural history of primary herpes simplex type I gingivostomatitis in children. Pediatric Dermatology, 16(4), 259-263.
Amir, J., Harel, L., Smetana, Z., & Varsano, I. (1997). Treatment of herpes simplex gingivostomatitis with acyclovir in children: a randomized double blind placebo controlled study. British Medical Journal, 314(7097), 1800-1804.
Chandrasekar, P.H. (1999). Identification and treatment of herpes lesions. Advances in Wound Care, 12(5), 254-262.
Crawford, W. (2000). Mucosa: Blistering diseases. Center for Scholarly Technology, University of Southern California. Retrieved December 1, 2000 from www.usc.edu/hsc/dental/opath/Chapters/Chapter 15
Klotz, R.W. (1990). Herpetic whitlow: An occupational hazard. American Association of Nurse Anesthetists Journal, 58(1), 8-13.
Koneman, E.W., Allen, S.D., Janda, W.M., Schreckenberger, P.C., & Winn, C.W. (1997). Color atlas and textbook of diagnostic microbiology. Philadelphia: Lippincott Williams & Wilkins.
Lewis, L. (1999). Viral disease tests: A changing arena. Patient Care, 33(4), 18-31.
Murph, J.R. (Ed.). (1999). Health in day care: A manual for health professionals (2nd ed.). Elk Grove Village, IL: American Academy of Pediatrics.
Murph, J.R., & Grose, C. (1999). Routine acyclovir therapy: Isn't it time? Contemporary Pediatrics, 16(4), 79-91.
Rosen, T., & Ablon, G. (1997). Cutaneous herpesvirus infections update, part 1: Herpes simplex virus types 1 and 2. Consultant, 37(8), 2021-2028.
Pickering, L.K. (Ed.). (2000). Red book: Report of the committee on infectious diseases (25th ed.). Elk Grove Village, IL: American Academy of Pediatrics.
Sealander, J.Y., & Kerr, C.R (1989). Herpes simplex of the nipple: Infant-to-mother transmission. American Family Physician, 39(3), 111-113.
Sheff, B. (2000). Herpes simplex virus. Nursing, 30(3), 30.
Stanberry, L. (1998). Herpes vaccines for HSV. Sexually Transmitted Diseases, 16(4), 811-816.
White, D.K. (1998). Acute viral infections of the oral cavity and parotid gland. Oral and Maxillofacial Surgery Clinics of North America, 10(1), 75-94.
Jo Young Blevins, MSN, RN, CPN, is Professor of Nursing, Somerset Community College, Somerset, KY.
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|Author:||Blevins, Jo Young|
|Date:||May 1, 2003|
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