Pediatric Herpes Simplex Virus Infection Clinical Presentation

  • Author: Swetha G Pinninti, MD; Chief Editor: Russell W Steele, MD   more...
 
Updated: Mar 5, 2012
 

History

Herpes simplex virus (HSV) causes myriad clinical presentations. The course depends on the age of the patient, the immune status of the host, the site of infection, the individual's previous immunity to autologous or heterologous viruses, and the antigenic type of the virus. Herpes simplex virus type 1 (HSV-1) typically causes infection above the waist and the infections are localized to mouth and oropharynx, whereas herpes simplex virus type 2 (HSV-2) usually causes genital infections and can also cause CNS or disseminated disease in neonates.[27]

Compared with latent infection, primary infection with either virus is typically associated with systemic signs, increased severity of symptoms, and increased rates of complications. Upon reactivation, both viruses establish latent infections in sensory neurons and cause recurrent disease at or near the entry site into the body.

Orolabial infection

Primary infection

Most infections are caused by HSV-1 and are localized to the mouth and oropharynx. Only 10-30% of orolabial infections are symptomatic.

The most common clinical presentation of first-episode, primary herpes simplex virus infection in children (usually aged 6 mo to 5 y) is acute herpetic gingivostomatitis, as is shown in the image below.

Primary herpes simplex virus (HSV) gingivostomatitPrimary herpes simplex virus (HSV) gingivostomatitis in an infant is shown. This same patient also had concomitant herpes whitlow as shown in Media file 2.

Clinical features include the following[28] :

  • Abrupt onset of illness
  • Fever
  • Listlessness or irritability
  • Inability to eat and/or drink
  • Gingivitis (with markedly swollen, erythematous, and occasionally bleeding gums)
  • Increased drooling in infants due to pain on swallowing
  • Vesicular lesions on the tongue, buccal mucosa, and palate with extension, at times, to the lips and face (These may rupture and coalesce to form large, ulcerated areas.)
  • Tender submandibular or cervical adenopathy

The lesions can be quite painful and symptoms may persist for 10-14 days. Primary herpes simplex virus infection of the oropharynx may be associated with viral shedding for as long as 23 days.

Primary HSV-1 infection of the oropharynx in adolescents and adults usually manifests as pharyngotonsillitis rather than gingivostomatitis. Patients usually present with fever, malaise, odynophagia, and headache with vesiculoulcerative lesions on the tonsils.

Primary HSV-2 infection can have a presentation similar to this after orogenital contact and it may occur concurrently with genital herpes simplex virus infection.

Reactivation

Reactivation of herpes simplex virus from the trigeminal ganglion may follow oral trauma or dental procedures but is usually asymptomatic.

A mild prodrome of localized pain, tingling, burning, or itching is followed by eruption of vesicular lesions. The prodrome may occur 6-53 hours before the first vesicular lesions appear.

The most common site of recurrent orolabial lesions is the vermilion border. On occasion, vesicles may be noted on other areas of the face or in the nares, often at sites contaminated by infected saliva during the initial infection. The pattern of recurrent disease varies greatly from one person to the other. However, specific triggers may be fairly predictable for individual patients and the lesions tend to recur at the same site as the original lesions.

HSV-1 orolabial infections recur at a rate of approximately 0.1 episode per month or 1.2 per year.

Genital infections

Primary infection occurs in the absence of preexisting antibodies to herpes simplex virus, either HSV-1 or HSV-2. First episode nonprimary infections occur in the absence of any previous signs or symptoms of genital herpes but in the presence of preexisting heterologous antibodies.

Primary infection

Primary, first-episode genital infections are characterized by severe constitutional symptoms, including fever, malaise, and myalgias.[29] Itching and pain usually are the initial symptoms, followed in 24-48 hours by more troublesome signs and symptoms.

Lesions evolve from vesicles to pustules to wet ulcers and heal by crusting. New lesions develop over 7-8 days. Lesions occur on the labia majora, labia minora, mons pubis, vaginal mucosa, and cervix and on the shaft of the penis. Painful inguinal lymphadenopathy, dysuria, and vaginal discharge are frequent complaints. Complications in both sexes include paresthesias of the legs and perineum. Urinary retention, more common in women than in men, may be reported. Mean duration of viral shedding is 12 days.

Preexisting antibodies to HSV-1 have an ameliorating effect on the severity of disease caused by HSV-2. Previous orofacial infection with HSV-1 generally protects a person against infection with HSV-1 but not HSV-2.

Most primary genital herpes simplex virus infections are asymptomatic, and 70-80% of seropositive individuals have no history of symptomatic genital herpes. Periodic subclinical recurrences with viral shedding make them sources of infection.[30]

Nonprimary first episode infections have lower frequencies of systemic symptoms, fewer lesions and more rapid healing than in patients with primary infections, presumably due to preexisting heterologous antibodies.

Reactivation

Recurrences are more common with HSV-2 infections than with HSV-1 infections (5 vs 1 per y). Individuals with HSV-2 infection generally have high rates of recurrence in the first and second years followed by a substantial decrease in subsequent years (median, 2 per y). About 25% of individuals have at least one recurrence in 5 years. Recurrences often follow stressful events, illness, trauma, and menstruation.

Most reactivations are asymptomatic (1% of individuals with previous HSV-2 infection have asymptomatic viral shedding on any given day).[31]

When symptomatic reactivation occurs, genital lesions are typically few. Tender lymphadenopathy, dysuria, vaginal discharge, and systemic symptoms are less common.

Intrauterine and perinatal infections

Congenital herpes simplex virus infection is a very rare entity and has been infrequently reported in the literature.[32, 33] Manifestations include skin lesions and scars, chorioretinitis, and microcephaly.

Most neonatal herpes simplex virus infections occur at the time of delivery through the genital tract of a woman asymptomatically shedding virus. History of previous infection and presence of maternal antibody are protective, as approximately half of neonates exposed to maternal primary herpes simplex virus infection contract the virus as opposed to less than 5% of those exposed to recurrent herpes simplex virus disease.[2, 34, 35]

Herpes neonatorum can be categorized as follows[34, 35, 36, 37, 38] :

  • Skin, eye, and mucous membrane (SEM) disease: Infection with herpes simplex virus limited to SEM historically accounts for about 20% of all neonatal herpes simplex virus infections. Infants with SEM infections generally present at age 10-12 days. Skin lesions tend to appear at the site of trauma. Many newborns with herpes simplex virus–related SEM disease do not present with symptoms of systemic illness. Outcome of SEM disease is excellent with prompt antiviral therapy; however, 75% of the cases progress to disseminated disease without treatment.
  • Disseminated infection: Disseminated infection now accounts for approximately 25% of herpes simplex virus infections in newborns. The recognition and treatment of herpes simplex virus–related SEM disease early has resulted in lower rates of progression to disseminated disease than in years past. It usually presents during the first few days of life as severe bacterial infection, often with hepatic, pulmonary, and neurologic dysfunction or failure. In the absence of prompt recognition and early institution of antiviral treatment, the disease has a high mortality rate.
  • CNS infection: Nearly one third of infants with neonatal herpes simplex virus infection have encephalitis as the sole manifestation of disease. Patients usually present with symptoms and signs of illness at 2-3 weeks of age. Initial manifestations include lethargy, irritability, and focal seizures. Without treatment, most children with CNS disease die and survivors sustain severe neurologic impairment.

Herpes simplex virus CNS infection

Herpes simplex virus is the most common cause of sporadic encephalitis in the United States.[39, 40, 41] One third of all cases of herpes simplex virus encephalitis are believed to occur in the pediatric population.

Herpes simplex virus encephalitis may be a manifestation of primary or recurrent infection with the virus. The infection may have an insidious or an abrupt onset. Patients present with headache, altered consciousness, and focal neurological abnormalities (often consistent with temporal lobe involvement).

Aseptic meningitis caused by herpes simplex virus can occur after primary genital HSV-2 infection. Patients with herpes simplex virus meningitis present with headache, fever, stiff neck, and photophobia. Symptoms usually begin 3-12 days after the onset of genital lesions. They reach maximum severity by 2-4 days into the illness, and gradually diminish over 2-3 days.

Dysfunction of the autonomic nervous system and transverse myelitis has been associated with genital herpes simplex virus infection. Symptoms may include hyperesthesia or anesthesia of the lower back, perineum, or sacral region. Urinary retention and constipation are other associated symptoms.

Infection in immunocompromised hosts

Severe herpes simplex virus infection in immunocompromised children is similar to that in adults.[42, 43] Infection is a frequent source of morbidity but is rarely fatal. The severity of disease is proportional to the deficiency of cellular immune responses.

It is characterized by the presence of oral and genital lesions that progress slowly to involve contiguous mucosal surfaces and cause esophageal, tracheal or pulmonary involvement, leading to disseminated infection.

Other herpes simplex virus infections

Herpes simplex virus infection of the tip of the finger is referred to as herpetic whitlow.[44] It presents much as other infections of the fingertip. Associated fever and enlarged regional adenopathy are common. An example is shown in the image below.

Herpes whitlow in an infant. Herpes whitlow in an infant.

Herpes gladiatorum is a manifestation of herpes disease seen in wrestlers.[45] It results in painful herpes simplex virus lesions, frequently with numerous cutaneous vesicles. An example is shown in the image below.

Herpes gladiatorum in an adolescent wrestler. Herpes gladiatorum in an adolescent wrestler.

Keratoconjunctivitis manifests with acute onset of pain, watery discharge, itching, blurred vision, lid swelling, and conjunctival injection.[46] Acute retinal necrosis can result in blindness.

Mollaret meningitis, a recurrent aseptic meningitis is rarely associated with herpes simplex virus.[47] Low-grade fever, headache, and myalgias may occur with these episodes. Approximately 50% of patients have transitory neurologic symptoms of meningeal irritation. The disease usually spontaneously remits over days.

Herpes simplex virus is one of the most common precipitating factors for erythema multiforme (EM).[48] Approximately 15% of patients with EM provide a history of recurrent herpes simplex virus infections before the characteristic skin lesions erupt.

Next

Physical

Neonatal infections

Skin lesions in SEM disease appear as macules which progress rapidly to vesicles on an erythematous base in areas of trauma, most commonly the site of insertion of a fetal scalp electrode (but also the oropharynx, circumcision site, or the presenting part).[2] Vesicular scalp lesions are shown in the image below.

Vesicular scalp lesions caused by herpes simplex vVesicular scalp lesions caused by herpes simplex virus (HSV) in a 7-day-old infant.

Herpes simplex virus CNS disease presents usually between age 2-3 weeks with lethargy and focal seizures[37] . Skin lesions are present in about 50% of patients. Cerebrospinal fluid (CSF) examination reveals pleocytosis and modestly elevated protein. The electroencephalogram is diffusely abnormal.

Disseminated herpes simplex virus disease in neonates usually mimics severe bacterial infection, often presenting within the first few days of life. Skin lesions are often absent at the onset of illness but 70% of the patients demonstrate skin lesions at some point during the illness. Disease manifestations may include vascular instability, jaundice, hepatomegaly, and pneumonitis.[42]

Orolabial herpes simplex virus infections [49]

Primary herpetic gingivostomatitis results in vesicles and ulcers involving the hard and soft palate, gingiva, tongue, and lips. These lesions are initially vesicular, but rupture fairly rapidly, leaving 1-3 mm, shallow, gray-white ulcers on erythematous bases. Fever and cervical and/or submandibular adenopathy are common.

Patients with herpes simplex virus pharyngotonsillitis typically present with ulcers and exudates on the posterior pharynx and tonsillar area. Lesions may also be noted on the tongue, buccal mucosa, or gingiva. Fever may last 2-7 days. Cervical adenopathy is common.

Recurrent orolabial herpetic infection is preceded by a prodrome of pain, burning, tingling, and itching. The prodrome is followed by the emergence of painful vesicles 24-48 hours later. The vesicles evolve into pustules and heal by crusting. Lesions typically appear on the vermillion border of the lip.

Genital infections

Primary genital herpes appears as macules and papules, followed by vesicles, pustules, and ulcers. Fever and localized inguinal adenopathy are frequently noted. Lesions are typically observed on labia major, labia minora, and mons pubis in females and on the shaft of the penis in males.[50]

The painful and tender lesions are associated with dysuria and may involve the buttocks, perineum, and vagina. Urinary retention is observed in 10-15% of female patients.

As many as 25% of women with genital herpes simplex virus have findings suggestive of meningitis.

Recurrent herpes simplex virus infection causes ulcerating vesicular lesions or merely irritation of the vulva in women.

Herpes simplex virus CNS disease

Disease occurs in those aged 5-30 years and older than 50 years.

Patients typically have malaise, irritability, and nonspecific symptoms lasting 1-7 days followed by acute onset of fever and focal neurologic signs.[39]

CSF analysis reveals pleocytosis with lymphocytic predominance and an increased number of RBCs.

Electroencephalography may demonstrate paroxysmal lateralizing epileptiform discharges (PLEDs) but more commonly shows focal spike and slow-wave abnormalities.

Edema with hemorrhagic necrosis is observed on MRI of the brain.

Herpes simplex virus in the immunocompromised patient

Patients with primary immunodeficiencies, AIDS, malignancy, malnutrition, burns, and transplant recipients (eg, bone marrow, organs) receiving immunosuppressive therapy can have unusually severe herpes simplex virus infections.

Severe orolabial infections may begin as typical herpes simplex virus lesions in or around the mouth. Over several days, the papules and vesicles can progress to bullae, frequently with hemorrhagic fluid. These bullae then may evolve into large, chronic, bloody lesions that coalesce and erode into the subcutaneous tissue or deeper tissues.

Orolabial herpes simplex virus infection may involve contiguous mucosal surfaces to cause herpes simplex virus esophagitis, tracheitis, pneumonitis, or disseminated infection. Patients with esophagitis typically present with fever, retrosternal pain, and odynophagia and patients with pneumonitis present in respiratory failure.

Other herpes simplex virus infections

Herpes simplex virus infection of the eye presents as blepharitis, follicular conjunctivitis, or keratoconjunctivitis. Signs include corneal or conjunctival injection, watery discharge, lid swelling, and preauricular adenopathy.

Patients with Mollaret meningitis present with fever, nuchal rigidity, and transitory neurologic findings that accompany meningeal irritation.

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Contributor Information and Disclosures
Author

Swetha G Pinninti, MD  Fellow in Pediatric Infectious Diseases, Department of Pediatrics, University of Alabama at Birmingham School of Medicine

Swetha G Pinninti, MD is a member of the following medical societies: American Academy of Pediatrics, Infectious Diseases Society of America, and Pediatric Infectious Diseases Society

Disclosure: Nothing to disclose.

Coauthor(s)

Robert W Tolan Jr, MD  Chief, Division of Allergy, Immunology and Infectious Diseases, The Children's Hospital at Saint Peter's University Hospital; Clinical Associate Professor of Pediatrics, Drexel University College of Medicine

Robert W Tolan Jr, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, Phi Beta Kappa, and Physicians for Social Responsibility

Disclosure: Novartis Honoraria Speaking and teaching

Specialty Editor Board

Leonard R Krilov, MD  Chief of Pediatric Infectious Diseases and International Adoption, Vice Chair, Department of Pediatrics, Professor of Pediatrics, Winthrop University Hospital

Leonard R Krilov, MD is a member of the following medical societies: American Academy of Pediatrics, American Pediatric Society, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, and Society for Pediatric Research

Disclosure: Medimmune Grant/research funds Cliinical trials; Medimmune Honoraria Speaking and teaching; Medimmune Consulting fee Consulting

Mary L Windle, PharmD  Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Mark R Schleiss, MD  American Legion Chair of Pediatrics, Professor of Pediatrics, Division Director, Division of Infectious Diseases and Immunology, Department of Pediatrics, University of Minnesota Medical School

Mark R Schleiss, MD is a member of the following medical societies: American Pediatric Society, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Robert W Tolan Jr, MD  Chief, Division of Allergy, Immunology and Infectious Diseases, The Children's Hospital at Saint Peter's University Hospital; Clinical Associate Professor of Pediatrics, Drexel University College of Medicine

Robert W Tolan Jr, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, Phi Beta Kappa, and Physicians for Social Responsibility

Disclosure: Novartis Honoraria Speaking and teaching

Chief Editor

Russell W Steele, MD  Head, Division of Pediatric Infectious Diseases, Ochsner Children's Health Center; Clinical Professor, Department of Pediatrics, Tulane University School of Medicine

Russell W Steele, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Immunologists, American Pediatric Society, American Society for Microbiology, Infectious Diseases Society of America, Louisiana State Medical Society, Pediatric Infectious Diseases Society, Society for Pediatric Research, and Southern Medical Association

Disclosure: Nothing to disclose.

Additional Contributors

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous author Sherman Alter, MD, to the original writing and development of this article.

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Primary herpes simplex virus (HSV) gingivostomatitis in an infant is shown. This same patient also had concomitant herpes whitlow as shown in Media file 2.
Herpes whitlow in an infant.
Cutaneous herpes simplex virus (HSV) lesions in a child in whom sexual abuse is suspected.
Vesicular scalp lesions caused by herpes simplex virus (HSV) in a 7-day-old infant.
Herpes gladiatorum in an adolescent wrestler.
MRI shows abnormal signal intensity in the left temporal lobe of an 18-year-old man with herpes simplex virus (HSV) encephalitis.
 
 
 
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