Herpangina

Updated: Apr 11, 2024
  • Author: Sandra G Gompf, MD, FACP, FIDSA; Chief Editor: Michael Stuart Bronze, MD  more...
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Overview

Practice Essentials

Herpangina is a very contagious acute viral infection characterized by small ulcerative or vesicular lesions in the posterior oropharynx. It primarily is seen in children but also affects newborns, adolescents, and young adults. Herpangina mostly occurs during the summer months. It is caused by 22 enterovirus serotypes, and most often is linked to the Coxsackie B virus serotype in the United States. Herpangina may occur along with an enteroviral exanthem and a number of neurological conditions, including aseptic meningitis, acute flaccid paralysis, and encephalitis. [1]

 

 

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Background

Herpangina is an acute febrile illness associated with small vesicular or ulcerative lesions on the posterior oropharyngeal structures (enanthem). Herpangina typically occurs during the summer and usually develops in children, occasionally occurring in newborns, adolescents, and young adults. Herpangina is one of many manifestations of enterovirus infection and can occur in association with enteroviral exanthem, aseptic meningitis, encephalitis, acute flaccid paralysis, and other clinical syndromes.

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Pathophysiology

Herpangina is a pharyngeal infection typically caused by various enteroviruses. In recent years, coxsackievirus A16, enterovirus 71, and coxsackievirus B have been implicated most often. Less-common causes include echovirus, parechovirus 1, adenovirus, and herpes simplex virus (HSV). [2, 3] Enterovirus 71 has emerged as an important public problem, causing severe clinical illness, encephalomyelitis, and potentially death in young children, particularly in Southeast Asia. [4, 5, 40, 41]  Enteroviruses that cause herpangina belong to the Picornaviridae family.

Coxsackievirus B4 virions under electron microscop Coxsackievirus B4 virions under electron microscopy. Courtesy of Centers for Disease Control and Prevention (CDC).

EV-71 genotypes B4, B5, and C4 in Southeast Asia emerged in the early 2000s as causing pediatric encephalitis, aseptic meningitis, myocarditis, poliomyelitis-like paralysis, and neonatal sepsis with neurogenic cardiopulmonary collapse.

The severity of hand-food-and-mouth-disease (HFMD) can be graded from 1 to 4 based on a Taiwanese system. [40, 41]  Grades 2b-4 are indicators of severe disease warranting hospitalization:

  • Grade 1 - Uncomplicated illness with fever, vesicles in the oral mucosa, and vesicles or papules on hands, feet, and buttocks.
  • Grade 2 - Central nervous system involvement, beginning with myoclonus observed in the fingers
    • Grade 2a - Myoclonus reported by the caregiver.
    • Grade 2b - Myoclonus is observed by a physician. 
  • Grade 3 - Autonomic dysfunction manifesting with fever unresponsive to antipyretics, hypertension, and persistent tachycardia.
  • Grade 4 - Cardiopulmonary dysfunction manifesting with pulmonary edema or hemorrhage, cytokine storm, and cardiorespiratory collapse.

Risk factors for postinfectious neurologic sequelae appear to include myoclonic jerks over 4 times per night. Age younger than 3 years and fever lasting 3 days or longer have been associated with encephalitis in enterovirus 71 infection. [6, 7, 8]

Although herpangina generally is a mild disease in adults, infection during pregnancy has been associated with a herpangina associated with a 2.29-, 1.67-, and 1.63-fold increased risk for low birth weight, preterm delivery, and small-for-gestational-age infants, respectively. [9]

Viruses that cause herpangina typically are spread via the fecal-oral route, although they may spread via the respiratory route or through fomites. Freshwater sources (eg, lakes) may act as reservoirs for transmission.

Herpangina typically has an incubation period of 4-14 days. Viremia occurs after inoculation and subsequently results in distant sites of infection. Viral replication at these secondary sites leads to characteristic clinical symptoms and oropharyngeal lesions. Bilateral, anterior, cervical lymphadenopathy may occur, resulting from infection of the posterior oropharynx. Coxsackievirus A may be recovered from the nasopharynx, feces, blood, urine, and cerebrospinal fluid (CSF). After clinical symptoms have resolved, asymptomatic enteroviral infection may persist in the gastrointestinal tract.

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Epidemiology

Frequency

United States

Enteroviral infections are most common during the summer and fall in temperate climates and occur year-round in tropical climates.

International

Enteroviral infections occur worldwide. Acute fatal epidemics have been reported predominantly in Asia. [10]

Mortality/Morbidity

Herpangina typically is a mild and self-limited illness. [5] Although most children who develop herpangina recover, the disease sometimes is complicated by central nervous system involvement and cardiopulmonary failure. Fatalities associated with herpangina have been reported, primarily in infants aged 6-11 months.

Notably, herpangina has been associated with the potential for adverse pregnancy outcomes. [5] A Taiwanese population-based study of 242 pregnant women with herpangina found an associated 2.29-fold greater risk for low birth weight, 1.67-fold greater risk for preterm delivery, and 1.63-fold greater risk for small-for-gestational-age infants, after adjustment for income, maternal, and fetal characteristics. [11]

Sex

Herpangina does not have a sexual predilection.

Age

Herpangina most commonly affects infants and young children aged 3-10 years. Herpangina is less common in adolescents and adults.

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