Diagnosis and management of recurrent herpes simplex infections
MICHAEL A. SIEGEL, D.D.S., M.S.
 |
ABSTRACT
|
|---|
Background. Dentists are frequently asked by patients to diagnose and treat recurrent herpetic infections, which are painful and disfiguring. The author explores the diagnosis and treatment of these commonly encountered viral conditions.
Overview. Herpetic infections represent a reactivation of the herpes simplex virus, which is highly infectious to patients, their families, dentists and staff members. The diagnosis of these conditions usually is based on case-specific historical findings, the characteristic clinical appearance and the location of the lesions.
Conclusions. Dentists often treat patients with a history of recurrent herpetic infections. Currently used topical antiviral agents, when used in a timely manner, are well-absorbed and quite effective in decreasing the severity and duration of herpetic episodes.
Clinical Implications. Until the herpetic lesions are completely healed, the dental team and patient should use management strategies to prevent spread of the virus, ensure adequate nutrition and maintain appropriate oral hygiene practices.
Herpes simplex virus, or HSV, is responsible for the most commonly occurring viral infections of the mouth and perioral soft tissues.1 HSV has two distinct serotypes: HSV type 1, or HSV-1, which primarily is associated with oral and labial lesions, and HSV type 2, or HSV-2, which usually is associated with genital lesions. Studies have shown that the predilection of a specific viral serotype to an anatomic site is changing, in part owing to varying sexual practices.
When used in a timely manner, topical antiviral agents are well-absorbed and quite effective in decreasing the severity and duration of herpetic episodes.
Ribes and colleagues2 reported that although HSV-2 remained the predominant type of genital herpes, during the period from 1994 through 1999, a trend developed toward increasing proportions of HSV-1 genitalis, affecting 31.8 percent of male patients and 44.8 percent of female patients who were tested from 4,498 cultures. These authors also reported that HSV-1 was the predominant type of herpes in patients with HSV in nongenital sites. HSV-2 was isolated from only 9.4 percent of patients with nongenital HSV infections. This study, as well as the study by Langenberg and colleagues,3 clearly suggests that this trend is ongoing and that sexually active people should receive counseling about the risk of oral-genital contact, especially during pregnancy.
Exposure to HSV-1 is widespread in the United States. HSV-1 serum antibodies can be found in up to 90 percent of Americans who have been tested.4 Primary herpetic infections develop in people who have not been previously exposed to the virus. They are seen most often in children and adolescents. Primary herpetic infections do occur in adults, but are often misdiagnosed by health care professionals.
Most often, exposure to HSV in children results in a subclinical infection. The child may complain of a mild flulike condition that is commonly overlooked by parents and the patient’s pediatrician. Only a small percentage of patients (approximately 1 percent) will develop clinical manifestations of primary herpetic gingivostomatitis, pharyngitis or both. Use of aspirin and nonsteroidal anti-inflammatory medications should be avoided for patients with acute, systemic viral infections, especially for children because of the risk of development of Reye’s syndrome.5 Primary herpetic gingivostomatitis is seldom encountered by practicing dentists and will not be discussed further.
|
RECURRENT HERPES SIMPLEX VIRUS
|
|---|
Approximately 30 to 40 percent of patients who have been exposed to HSV will develop recurrent infections. Recurrent HSV infections can occur as either recurrent herpes labialis, or RHL, or recurrent intraoral herpes, or RIH. These recurrent infections represent reactivation and not reinfection of HSV, which persists in a latent state in the trigeminal (semilunar) ganglion.6 Recurrent HSV infections are characterized by a mild clinical course, and have been associated with exposure to sunlight, as well as stress, fatigue, menstruation and oral trauma.7
RHL.
RHL (that is, a cold sore or a fever blister) is preceded by prodromal signs or symptoms such as burning, tingling, soreness or swelling at the site where the lesions will develop. Within hours, small vesicles develop in clusters along the vermilion border of the lips. The vesicles quickly rupture, resulting in erosions that can coalesce to form larger irregular lesions with a crusted surface (Figure 1
).
In an otherwise healthy person, the lesions heal without scarring within seven to 14 days. Lesions of recurrent extraoral herpetic infections can develop anywhere along the affected sensory division of the trigeminal nerve (Figure 2). The diagnosis of RHL is based on its characteristic clinical appearance. Diagnostic tests such as viral isolation in tissue culture and direct immunofluorescent antibody testing are available to confirm the diagnosis, but they are not routinely used in an otherwise healthy patient.
View larger version (116K):
[in this window]
[in a new window]
|
Figure 2. Vesicles on the tip of the nose caused by shedding of recurrent herpes simplex virus along the second division of the trigeminal nerve.
| |
The treatment for RHL is primarily symptomatic. Ice, ether, chloroform and rubbing alcohol have been used as topical agents with mixed results. Lysine tablets also have been used, with varying degrees of success. Griffith and colleagues8 reported that lysine resulted in milder episodes of RHL if taken in high doses (that is, 2 to 3 grams). Single or multiple daily doses of lysine can be administered, and treatment should be initiated at the first prodromal signs and continued until the lesion has completely healed. Griffith and colleagues8 also reported that lysine was effective in preventing recurrences in some patients if the patient continued to take 1,000 milligrams per day as a nutritional supplement.
Historically, topical antiviral agents such as acyclovir ointment or vidarabine (3 percent) ophthalmic ointment also have been used with limited success, primarily because of poor transcutaneous absorption.9 Penciclovir (1 percent) topical cream is available by prescription for the treatment of RHL10 (Table11). It has been shown to reduce the severity and duration of the viral outbreak by inhibiting viral replication.
Spruance and colleagues12 reported that penciclovir (1 percent) cream decreased the healing time of classical lesions of RHL by between one-half and one day, while decreasing pain and promoting earlier cessation of viral shedding. In addition, penciclovir has been shown to increase healing and decrease pain whether patients apply it initially during their prodromal symptoms or after the lesion is clinically present.12
Recently, docosanol (10 percent) cream became available as an over-the-counter treatment for RHL.13 The mechanism of action of docosanol is via alteration of healthy cell membranes to prevent viral entry. Systemic antiviral agents, such as acyclovir, are used primarily in severe cases of mucocutaneous or ophthalmologic herpes simplex infections in immunocompromised patients.14 However, in patients known to have RHL induced by exposure to sunlight, a prophylactic regimen of acyclovir (400 mg twice daily) may be used if prolonged actinic exposure is anticipated (Table
11).15 Because sunlight is a known trigger of RHL, prevention of lesions may be enhanced by using a sunscreen with a sun protection factor of 15 or greater.16
RIH.
In a systemically healthy patient population, RIH occurs less frequently than does RHL. Lesions of RIH may be triggered by dental therapy; local, thermal or chemical injury; or trauma from mastication. Lesions of RIH begin as clusters of tiny vesicles that rupture rapidly, leaving small discrete erosions or superficial ulcerations of the keratinized oral tissues (Figure 3). These erosions or ulcers are superficial and coalesce to form larger, irregular lesions. RIH develops primarily on oral tissues that are firmly bound down to the underlying bone (that is, the hard palate, attached gingiva and edentulous alveolar ridges).
View larger version (116K):
[in this window]
[in a new window]
|
Figure 3. Localized erosions of the keratinized palatal soft tissues resulting from ruptured vesicles of recurrent intraoral herpes after a palatal injection of local anesthetic.
| |
This is in direct contrast to recurrent aphthous ulcerations, which, in the immunocompetent patient, usually are singular and round to ovoid and develop on mucosal tissues (such as the buccal mucosa and tongue) that are not bound down to underlying bone.17 However, because recurrent aphthous ulcerations and herpetic lesions can be confused when their presentations are atypical, the astute clinician should inquire whether the erosive or ulcerative lesions were preceded by a vesicular stage, prodromal symptoms or both, which would suggest a viral etiology.
The diagnosis of RIH is based on the clinical appearance of the lesions and their location. The amount of discomfort associated with these lesions varies and they heal without scarring in seven to 14 days. Advising patients of the benign and self-limiting nature of these lesions will help allay apprehension.
Patients must be informed of the infectious nature of recurrent oral herpetic conditions. The vesicles of oral herpetic infections are extremely contagious, so care must be exercised to avoid autoinoculation of other mucosal sites, as well as transmission to others. The vesicular stage of these lesions is the most contagious, but all stages of these viral lesions are potentially infectious until complete re-epithelialization has occurred.
|
DISCUSSION
|
|---|
Treatment of recurrent oral herpetic infections is usually topical in nature. Therapy should address cleanliness to prevent autoinoculation and spread to others, nutrition and hydration, oral discomfort and oral hygiene, and local control of the disease process. Hand washing must be stressed to prevent spread of the virus to the eyes or genitals of the affected patient, as well as to minimize spread of the virus to others. Patients must be told to refrain from kissing their loved ones. Eating utensils should be placed in the dishwasher or cleaned by hand with hot, soapy water.
Topical medications should be dabbed on rather than rubbed in to minimize mechanical trauma to the lesions. Mechanical stimulation, especially while the virus is actively shedding, will increase the duration and severity of the recurrent herpetic lesions. Clinicians must advise patients to apply these medications at the earliest possible time, which usually is at the first sign of prodromal symptoms. Once the virus has been shed, these medications are less effective in producing the desired results. Researchers are evaluating novel medication carriers aimed at improving the efficacy of topical antiviral drugs in the treatment of RHL.18,19
If the oral lesions are painful enough to limit normal dietary intake, nutritional supplementation and adequate hydration must be stressed to the patient. When necessary, a protein-vitamin-mineral food supplement serves this purpose in a convenient, cost-effective manner. Cold beverages or ice chips may provide temporary relief of oral pain. Citrus fruits, carbonated beverages and other acid-containing foods or spicy foods will exacerbate oral discomfort, so they should be avoided. Topical anesthetics such as lidocaine (viscous 2 percent) may be prescribed to further reduce discomfort.
Mouthrinses containing a hydroalcoholic vehicle should be avoided because of the oral discomfort that will result. The amount of oral discomfort experienced by patients with oral herpetic lesions varies and often can be controlled with acetaminophen, if necessary.
|
DENTAL CARE
|
|---|
Dentists must decide on an individual basis whether to treat a patient who has an active recurrent herpetic infection since there are no universally accepted standards governing these circumstances. The dentist should consider whether the dental treatment is emergent and must be performed, or is elective in nature and might be easily rescheduled. The stage of the lesion may help the dentist decide whether to treat, since early fluid-filled vesicles are more infectious than late lesions, which are almost healed.
All stages of recurrent herpes virus infections are potentially contagious and, therefore, must be viewed as an infectious, potentially transmissible disease. Universal precautions, including gloves, masks and eye protection, must be used if the patient is to be treated. Trauma to the lesion must be avoided so that healing will not be retarded. Because the lesion is transmitted via direct contact (thigmotaxis), care must be taken not to spread the virus to other mucous membranes, such as the eyes or nasal mucosa. For this reason, air-water sprays should be avoided unless a rubber dam can be used to isolate the lesion.
Clinicians should instruct patients to perform regular oral hygiene during the time in which lesions are present. Patients must be encouraged to brush and floss their teeth after meals in a gentle, yet efficient manner. Recurrent oral herpetic infections in the nonimmunocompromised patient are self-limiting, so complete resolution of the lesions should be expected within two weeks. Lesions persisting after this time warrant further investigation.
|
CONCLUSION
|
|---|
Dentists frequently treat patients with a history of recurrent herpetic infections, which are painful and disfiguring. When used in a timely manner, topical antiviral agents are well-absorbed and quite effective in decreasing the severity and duration of herpetic episodes. Until the herpetic lesions are completely healed, the dental team and patient should use management strategies to prevent spread of the virus, ensure adequate nutrition and maintain appropriate oral hygiene practices.
View larger version (127K):
[in this window]
[in a new window]
|
Dr. Siegel is an associate professor, Department of Oral Medicine and Diagnostic Sciences, Dental School, and an associate professor, Department of Dermatology, Medical School, University of Maryland, 666 W. Baltimore St., Baltimore, Md. 21201-1586, e-mail "mas001@dental. umaryland.edu". He also is chairman-elect of the ADA Council on Scientific Affairs. Address reprint requests to Dr. Siegel.
| |
|
FOOTNOTES
|
|---|
Although the Practical Science feature is developed in cooperation with the ADA Council on Scientific Affairs and the Division of Science, the opinions expressed in this article are those of the author and do not necessarily reflect the views and positions of the Council, the Division or the Association.
|
REFERENCES
|
|---|
- Miller CS, Redding S. Diagnosis and management of orofacial herpes simplex virus infections. Dent Clin North Am 1992;36:879–95.[Medline]
- Ribes JA, Steele AD, Seabolt JP, Baker DJ. Six-year study of the incidence of herpes in genital and nongenital cultures in a cental Kentucky medical center patient population. J Clin Microbiol 2001;39: 3321–5.[Abstract/Free Full Text]
- Langenberg AG, Corey L, Ashley RL, Leong WP, Straus SE. A prospective study of new infections with herpes simplex virus type 1 and type 2. N Engl J Med 1999;341:1432–8.[Abstract/Free Full Text]
- Regezi JA, Sciubba JJ. Vesiculobullous diseases. In: Oral pathology: Clinical pathologic correlations. 2nd ed. Philadelphia: Saunders; 1993:1–33.
- Ward MR. Reye’s syndrome: an update. Nurse Pract 1997;22(12):45–53.[Medline]
- Miller CS, Danaher RJ, Jacob RJ. Molecular aspects of herpes simplex virus I latency, reactivation and recurrence. Crit Rev Oral Biol Med 1998;9:541–62.[Abstract/Free Full Text]
- Logan HL, Lutgendorf S, Hartwig A, Lilly J, Berberich SL. Immune, stress and mood markers related to recurrent oral herpes outbreaks. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1998;86:48–54.[Medline]
- Griffith RS, Norins AL, Kagan C. A multi-centered study of lysine therapy in herpes simplex infection. Dermatologica 1978;156: 257–67.[Medline]
- Little JW, Falace DA, Miller CS, Rhodus NL. Sexually transmitted diseases. In: Dental management of the medically compromised patient. 5th ed. St. Louis: Mosby–Year Book; 1997:308–24.
- Wynn RL. New drug approvals in 1996. Gen Dent 1997;45:224–7.[Medline]
- Siegel MA. Strategies for management of commonly encountered oral mucosal disorders. J Cal Dent Assoc 1999;27:210–27.
- Spruance SL, Rea TL, Thoming C, Tucker R, Saltzman R, Boon R. Penciclovir cream for the treatment of herpes simplex labialis: a randomized, multicenter, double-blind, placebo-controlled trial. JAMA 1997;277:1374–9.[Abstract]
- Pope L, Marcelletti J, Katz L, et al. The anti-herpes simplex virus activity of n-docosanol includes inhibition of the viral entry process. Antiviral Res 1998;40:85–94.[Medline]
- Physicians’ desk reference. 55th ed. Montvale, N.J.: Medical Economics; 2001.
- Scully C. Orofacial herpes simplex virus infections: current concepts in the epidemiology, pathogenesis, and treatment, and disorders in which the virus may be implicated. Oral Surg Oral Med Oral Pathol 1989;68: 701–10.[Medline]
- Siegel MA, Silverman S, Sollecito TP. Clinician’s guide to treatment of common oral conditions. 5th ed. New York: American Academy of Oral Medicine; 2001:17–9.
- Eisen D. The clinical characteristics of intraoral herpes simplex virus infection in 52 immunocompetent patients. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1998;86:432–7.[Medline]
- Horowitz E, Pisanty S, Czerninski R, Helser M, Eliav E, Touitou E. A clinical evaluation of a novel liposomal carrier for acyclovir in the topical treatment of recurrent herpes labialis. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1999;87:700–5.[Medline]
- Cassady KA, Whitley RJ. New therapeutic approaches to the alphaherpesvirus infections. J Antimicrob Chemother 1997;39:119–28.[Abstract/Free Full Text]
TOP
ABSTRACT
RECURRENT HERPES SIMPLEX VIRUS
