Introduction
Background
Herpangina is an acute febrile illness associated with small vesicular or ulcerative lesions on the posterior oropharyngeal structures. Herpangina typically occurs during the summer and usually develops in children, occasionally occurring in young adults. Various enteroviruses cause the condition.
Pathophysiology
Herpangina is usually caused by coxsackievirus A. Less-common causes of herpangina include coxsackievirus B, echovirus, and enterovirus. Enteroviruses that cause herpangina belong to the Picornaviridae family.
Coxsackievirus B4 virions under electron microscopy. (This image is in the public domain and thus free of any copyright restrictions. Content provider: Centers for Disease Control and Prevention)
A distinct phenotype of enterovirus 71 causes herpangina. This is in contrast to the phenotype of enterovirus 71 that causes encephalitis, myocarditis, poliomyelitislike paralysis, and neonatal sepsis.
Viruses that cause herpangina are typically spread via the fecal-oral route, although they may spread via the respiratory route or through fomites. Freshwater sources (eg, lakes) may act as a reservoir for transmission.
Herpangina typically has an incubation period of 7-14 days. Viremia occurs after inoculation and subsequently results in distant sites of infection. Clinical symptoms at secondary sites of infection occur after viral replication. 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.
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 in at least 5 parts of the world, the most recent being described in Kanagawa Prefecture, Japan, in 2007.1
Mortality/Morbidity
Herpangina is typically a mild and self-limited illness. Although most children who develop herpangina recover, the disease is occasionally complicated by CNS lesions and cardiopulmonary failure. Fatalities associated with herpangina have been reported, primarily in infants aged 6-11 months.
Sex
Herpangina does not have a gender predilection.
Age
Herpangina most commonly affects infants and young children aged 3-10 years. Herpangina is less common in adolescents and adults.
Clinical
History
Approximately 50% of enteroviral infections are asymptomatic. Clinical manifestations may vary, depending on the strain of the virus.
- All enteroviral infections may cause fever, which may be the first apparent symptom. Patients with enteroviral infection typically develop a temperature of 101-104°F
- Most symptomatic patients report malaise.
- Sore throat may develop.
- Persons with enteroviral infection may experience anorexia, emesis, or abdominal pain, which may mimic appendicitis.
- Infants with enteroviral infection may appear listless.
- Exanthem: Characteristics and occurrence rates vary, depending on the viral subtype. Persons with enteroviral infection may develop a rash that is not pruritic and that does not cause skin desquamation. The following are other rash characteristics:
- Macular
- Maculopapular
- Papulopustular
- Papulovesicular
- Vesicular
- Morbilliform
- Urticarial
- Petechial
- Hemangiomalike
Physical
- Oropharyngeal lesions (herpangina)
- In patients with herpangina, lesions characteristically appear as erythematous macules initially. These evolve into vesicles that ulcerate centrally, creating an erythematous halo.
- In most cases, these lesions are the first physical finding of herpangina. The lesions are typically smaller than 5 mm in diameter. Most cases of herpangina involve 2-12 lesions.
- Uninvolved portions of the pharynx usually appear normal. The most commonly affected structures include the anterior pillars of the fauces, posterior pharynx, soft palate, uvula, and tonsils.
- Occasionally, lesions caused by herpangina appear on the tongue and posterior buccal mucosa (see Table 1 for differential diagnoses of oral lesions).
- The ulcers may persist for up to one week, even after the fever has subsided.
- Pharyngitis: Erythema of the pharynx may range from mild to severe. Pharyngitis in enteroviral infections may be associated with pleurodynia, meningitis, and/or exanthem.
- Bilateral, anterior, cervical lymphadenopathy may develop.
Causes
- Coxsackieviruses A 1-10, 16, and 22 represent the most common pathogens that cause herpangina.
- Less-common causes of herpangina include the following:
- Coxsackievirus B 1-5
- Echovirus 3, 6, 9, 11, 16, 17, 22, 25, and 30
- Enterovirus 71 (see Pathophysiology)
More on Herpangina |
 Overview: Herpangina |
| Differential Diagnoses & Workup: Herpangina |
| Treatment & Medication: Herpangina |
| Follow-up: Herpangina |
| Multimedia: Herpangina |
| References |
| Next Page » |
References
Sano T, Saito T, Kondo M, Watanabe S, Onoue Y, Konnai M, et al. Enterovirus detection status of patients with herpangina and hand, foot and mouth disease in epidemic season 2007, Kanagawa Prefecture, Japan. Jpn J Infect Dis. Mar 2008;61(2):162-3. [Medline].
Li C, Wang H, Shih SR, et al. The efficacy of viral capsid inhibitors in human enterovirus infection and associated diseases. Curr Med Chem. 2007;14(8):847-56. [Medline].
Chang LY, King CC, Hsu KH, et al. Risk factors of enterovirus 71 infection and associated hand, foot, and mouth disease/herpangina in children during an epidemic in Taiwan. Pediatrics. Jun 2002;109(6):e88. [Medline].
Chawareewong S, Kiangsiri S, Lokaphadhana K, et al. Neonatal herpangina caused by Coxsackie A-5 virus. J Pediatr. Sep 1978;93(3):492-4. [Medline].
Cherry JD. Herpangina. In: Textbook of Pediatric Infectious Diseases. Vol. 1. 1998:156-7.
Cherry JD. Enteroviruses: Coxsackieviruses, Echoviruses, and Polioviruses. In: Textbook of Pediatric Infectious Diseases. Vol. 2. 1998:1787-1839.
Chole RA, Domb GH. Differential diagnosis of superficial ulcerations of the oral mucosa. Otolaryngol Head Neck Surg. Nov-Dec 1979;87(6):734-40. [Medline].
Christie AB. Enteroviral infections (Coxsackieviruses and echoviruses). In: Infectious Diseases: Epidemiology and Clinical Practice. 1987:753-81.
Haskell R. Oral vesiculo-bullous lesions. J Laryngol Otol. Jan 1976;90(1):101-4. [Medline].
Ho M, Chen ER, Hsu KH, et al. An epidemic of enterovirus 71 infection in Taiwan. Taiwan Enterovirus Epidemic Working Group. N Engl J Med. Sep 23 1999;341(13):929-35. [Medline].
Kung CM, King CC, Lee CN, et al. Differences in replication capacity between enterovirus 71 isolates obtained from patients with encephalitis and those obtained from patients with herpangina in Taiwan. J Med Virol. Jan 2007;79(1):60-8. [Medline].
Lin TY, Chang LY, Hsia SH, et al. The 1998 enterovirus 71 outbreak in Taiwan: pathogenesis and management. Clin Infect Dis. May 1 2002;34 Suppl 2:S52-7. [Medline].
Melnick JL. Enteroviruses: Polioviruses, Coxsackieviruses, Echoviruses, and Newer Enteroviruses. In: Field's Virology. 1990:549-98.
Rosenblatt RM, Domb GH. Herpangina in an anesthesiologist. Anesth Analg. May 1980;59(5):384-5. [Medline].
Further Reading
Keywords
herpangina, enteroviral herpangina, coxsackievirus herpangina, Picornaviridae, coxsackievirus, coxsackievirus A, coxsackievirus B, echovirus, enterovirus, enteroviruses, enteroviral infection, enterovirus 71
