eMedicine Specialties > Dermatology > Viral Infections

Herpes Simplex: Follow-up

Author: Gisela Torres, MD, Staff Physician, Department of Dermatology, University Hospitals of Cleveland; Senior Instructor in Dermatology, Case Western Reserve University
Coauthor(s): Malcolm Schinstine, MD, PhD, Staff Physician, Department of Pathology and Laboratory Medicine, Dartmouth College Hitchcock Medical Center; Paul Krusinski, MD, Director of Dermatology, Professor, Department of Internal Medicine, Fletcher Allen Health Care, University of Vermont; Stephen K Tyring, MD, PhD, MBA, Founder and Medical Director, Center for Clinical Studies, Clinical Professor, Departments of Dermatology, Microbiology, and Molecular Genetics, and Internal Medicine (Infectious Diseases), University of Texas Health Science Center at Houston
Contributor Information and Disclosures

Updated: Aug 25, 2009

Follow-up

Deterrence/Prevention

  • Herpes simplex virus (HSV) viral shedding is greatest during clinically evident outbreaks; however, transmission from individuals who are seropositive to their partners who are seronegative usually occurs during asymptomatic HSV shedding periods. Therefore, preventing transmission requires more than abstaining from intimate contact during outbreaks.
    • Barrier methods, such as condoms, confer 10-15% protection against the transmission of genital herpes, as transmission can occur to and from uncovered mucocutaneous surfaces or if the integrity of the barrier is compromised. Condoms have also been shown to be more effective in protecting women than men.
    • Various HSV vaccines have been and continue to be under investigation for the treatment and prevention of herpes genitalis, though most have not been shown to be effective. Recently, double-blind randomized trials of a glycoprotein D HSV-2 vaccine revealed that the vaccine conferred protection against the virus in women who were serologically negative for both HSV-1 and HSV-2. However, it did not prevent HSV infection in men despite their serostatus or in women who were positive for HSV-1 but negative for HSV-2.9
    • Long-term suppressive therapy for genital herpes has been shown to decrease asymptomatic HSV shedding, and long-term valacyclovir therapy significantly decreased HSV transmission to susceptible partners of individuals who were HSV-2 positive by 50-77%. Acyclovir and famciclovir have been shown to be as effective as valacyclovir for suppression of recurrences. Considerations for placing a patient on long-term suppressive therapy include frequent and/or severe outbreaks, infection in a patient who is immunocompromised, the patient’s sex, the patient’s HSV serostatus, and the reproductive capability of the patient’s partner.
    • HIV infection of an HSV patient or his or her seronegative partner should also be considered a possible indication for suppression, given the proposed increase in HIV viral load, although HSV suppressive therapy has not been shown to have an effect on HIV-1 viral shedding.
  • Women who are HSV-2 negative should be counseled to abstain from intercourse during the third trimester of pregnancy with partners that could be seropositive because primary HSV infection during this time places the fetus at highest risk of infection.
    • The most common approach in attempting to prevent vertical transmission is to have women with clinically apparent HSV lesions during labor undergo cesarean delivery. However, cesarean delivery does not prevent all cases of neonatal infection because in utero infection occurs and antepartum HSV cultures are not a good predictor of neonatal infections.
    • Use of acyclovir 400 mg PO tid during the third trimester of pregnancy has been proven to be safe and effective in preventing neonatal herpes and in eliminating the need for cesarean deliveries.

Complications

  • The most common complication of HSV infections is bacterial superinfection. In women with primary HSV-2 infection, aseptic meningitis is also common.
  • Significant complications, such as visceral and CNS dissemination and long-term sequelae, are rare and occur in patients who are immunocompromised or in cases of neonatal HSV.

    • Patients with AIDS who are treated with intravenous acyclovir may develop thymidine kinase–negative strains of HSV that are resistant to acyclovir. These patients may be successfully treated with intravenous foscarnet or topical cidofovir.
    • Babies born to mothers with genital HSV infection should be closely monitored for any signs of infection and promptly treated if signs of the disease develop. Neonatal HSV infection has a mortality rate of more than 80% if untreated and a mortality/significant morbidity rate of approximately 50% even when treated.

Prognosis

  • For most people, HSV infections are temporary and resolve without detrimental sequelae; however, recurrence is common.
  • Long-term sequelae (usually CNS) are more common with neonatal HSV infection than with other types of HSV infection. Scarring may occur from severe or superinfected lesions.

Patient Education

Miscellaneous

Special Concerns

  • Women who are pregnant or contemplating pregnancy should receive information regarding neonatal herpes simplex virus (HSV) transmission and the rationale for performing a cesarean delivery and/or for using antiviral therapy if active lesions are present.
 
Acknowledgments

The authors and editors of eMedicine gratefully acknowledge the contributions of previous Chief Editor, William D. James, MD, to the development and writing of this article.



More on Herpes Simplex

Overview: Herpes Simplex
Differential Diagnoses & Workup: Herpes Simplex
Treatment & Medication: Herpes Simplex
Follow-up: Herpes Simplex
Multimedia: Herpes Simplex
References
Further Reading

References

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Keywords

herpes simplex virus, HSV, herpes genitalis, genital herpes, herpes labialis, orolabial herpes, HSV-1, HSV type 1, herpes simplex virus type 1, HSV-2, HSV type 2, herpes simplex virus type 2, localized eczema herpeticum, disseminated eczema herpeticum, Kaposi's varicelliform eruption, Kaposi varicelliform eruption, herpes whitlow, herpes gladiatorum, disseminated HSV infection, neonatal HSV infection, herpetic sycosis

Contributor Information and Disclosures

Author

Gisela Torres, MD, Staff Physician, Department of Dermatology, University Hospitals of Cleveland; Senior Instructor in Dermatology, Case Western Reserve University
Gisela Torres, MD is a member of the following medical societies: American Academy of Dermatology and American Medical Association
Disclosure: Nothing to disclose.

Coauthor(s)

Malcolm Schinstine, MD, PhD, Staff Physician, Department of Pathology and Laboratory Medicine, Dartmouth College Hitchcock Medical Center
Malcolm Schinstine, MD, PhD is a member of the following medical societies: American Society for Clinical Pathology, College of American Pathologists, and United States and Canadian Academy of Pathology
Disclosure: Nothing to disclose.

Paul Krusinski, MD, Director of Dermatology, Professor, Department of Internal Medicine, Fletcher Allen Health Care, University of Vermont
Paul Krusinski, MD is a member of the following medical societies: American Academy of Dermatology, American College of Physicians, and Society for Investigative Dermatology
Disclosure: Nothing to disclose.

Stephen K Tyring, MD, PhD, MBA, Founder and Medical Director, Center for Clinical Studies, Clinical Professor, Departments of Dermatology, Microbiology, and Molecular Genetics, and Internal Medicine (Infectious Diseases), University of Texas Health Science Center at Houston
Disclosure: Nothing to disclose.

Medical Editor

Sungnack Lee, MD, Vice President of Medical Affairs, Professor, Department of Dermatology, Ajou University School of Medicine, Korea
Sungnack Lee, MD is a member of the following medical societies: American Dermatological Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Michael J Wells, MD, Associate Professor, Department of Dermatology, Texas Tech University Health Sciences Center
Michael J Wells, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, and Texas Medical Association
Disclosure: Nothing to disclose.

Managing Editor

Rosalie Elenitsas, MD, Herman Beerman Associate Professor of Dermatology, University of Pennsylvania School of Medicine; Director, Penn Cutaneous Pathology Services, Department of Dermatology, University of Pennsylvania Health System
Rosalie Elenitsas, MD is a member of the following medical societies: American Academy of Dermatology and American Society of Dermatopathology
Disclosure: Nothing to disclose.

CME Editor

Catherine Quirk, MD, Clinical Assistant Professor, Department of Dermatology, Brown University
Catherine Quirk, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Dermatology
Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

 
 
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