HSV Infection: Causes and Symptoms

HSV Infection

• Recurrent HSV results from reactivation at latent sites, traveling centripetally to mucosa or skin, causing localized vesicles or ulcers
• Common sites of infection: oral, genital mucosa, and eye; HSV-1 above the waist, HSV-2 below the waist
• Infections can cause:
  • Keratitis (major cause of blindness worldwide)
  • Herpes whitlow (infection of the fingers)
  • Herpes gladiatorum (infections of the skin spread through wrestling)
  • Herpes encephalitis
  • HSV esophagitis and pneumonia
  • Neonatal and disseminated infection
• HSV is an etiologic agent in erythema multiforme
• HSV has been recovered in the endoneurial fluid of patients with Bell palsy

Primary Gingivostomatitis

• Majority of primary HSV-1 infections are subclinical, occurring in children, teenagers, and young adults
• Clinical manifestations:
  • 1-3 day prodrome of fever, loss of appetite, malaise, and myalgia
  • Oral pain leading to poor oral intake, requiring hospitalization for hydration
  • Disease is self-limiting in otherwise normal patients, resolving within 10-14 days
• Oral findings:
  • Erythema and clusters of vesicles/ulcers on keratinized mucosa of hard palate, attached gingiva, and dorsum of the tongue
  • Vesicles break down to form ulcers that coalesce to form larger ulcers with scalloped borders and marked surrounding erythema
  • Gingiva is often erythematous, and the mouth is extremely painful, causing difficulty with eating
  • Pharyngitis causes swallowing difficulties

Recrudescent Oral HSV Infection

• Reactivation of HSV may lead to asymptomatic shedding of HSV in saliva and other secretions, an important risk factor for transmission
• Reactivation of HSV-1 on the oral mucosa is common and usually asymptomatic
• Ulcers are painful and similar to those seen in immunocompetent patients, except that they may be larger and occur on non-keratinized sites
• Presence of 1-2 mm vesicles or satellite ulcers at the edges of the main ulcer is a helpful sign

Laboratory Diagnosis

• HSV isolation by cell culture is the gold standard test for diagnosis
• Single swab of oral ulcers is performed
• PCR from swabs detects HSV antigen 3-4 times more often than culture
• Real-time PCR is highly sensitive and specific
• Primary HSV infection is associated with elevated IgM titers that occur within days
• Followed by permanent IgG titers that indicate previous infection but confer no protection against reactivation
• Recurrent infection is associated with a rise in IgG antibody titer in acute and convalescent sera, but a four-fold rise is seen in only 5% of patients
• Assay for HSV IgM is not particularly reliable for diagnostic purposes

Management

• Primary HSV infection:
  • Directed toward pain control, supportive care, and definitive treatment
• HSV in immunocompromised patients:
  • Should be treated with systemic antivirals to prevent dissemination to other sites (e.g., HSV esophagitis) or systemically
  • Antiviral therapy such as acyclovir or valacyclovir at suppressive doses should be initiated for all patients who are HSV seropositive
  • Acyclovir-resistant HSV is most frequently seen in this group of patients, where the virally derived thymidine kinase that activates acyclovir is mutated
  • In such cases, foscarnet or cidofovir is effective

Varicella-Zoster Virus Infection

• Primary infection with varicella-zoster virus (VZV) leads to varicella (chicken pox)
• The virus then becomes latent, usually in the dorsal root ganglia or ganglia of the cranial nerves
• Reactivation produces herpes zoster infection (HZI), commonly called shingles
• Incidence of HZI increases with age and the degree of immunosuppression
• Involvement of V results in blisters and ulcers on the mandibular gingiva and tongue
• Uncommon complications of HZI:
  • Ramsay Hunt syndrome (Bell palsy, vesicles of the external ear, and loss of taste sensation in the anterior two-thirds of the tongue)
  • Resorption and exfoliation of teeth and osteonecrosis of the jawbones, especially in patients with HIV disease