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Herpangina

  • Author: Sandra G Gompf, MD, FACP, FIDSA; Chief Editor: Michael Stuart Bronze, MD  more...
 
Updated: Sep 02, 2015
 

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).[1, 2] Enterovirus 71 has emerged as an important public problem, causing severe clinical illness, encephalomyelitis, and potentially death in young children.[3] . Enteroviruses that cause herpangina belong to the Picornaviridae family.

Coxsackievirus B4 virions under electron microscop 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, aseptic meningitis, myocarditis, poliomyelitis-like paralysis, and neonatal sepsis. 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.[4, 5, 6]

While herpangina is generally a mild disease in adults, infection during pregnancy has been associated with a herpangina associated with a 2.29- (95% confidence interval [CI], 1.42-3.69), 1.67- (95% CI, 1.04-2.68), and 1.63-fold (95% CI, 1.14-2.33) increased risk of low birth weight, preterm delivery, and small-for-gestational-age infants, respectively.[7]

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 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 in at least 5 parts of the world, the most recent being described in Kanagawa Prefecture, Japan, in 2007.[8]

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.

Notably, herpangina has been associated with the potential for adverse pregnancy outcomes. 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.[9]

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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Contributor Information and Disclosures
Author

Sandra G Gompf, MD, FACP, FIDSA Associate Professor of Infectious Diseases and International Medicine, University of South Florida College of Medicine; Chief, Infectious Diseases Section, Director, Occupational Health and Infection Control Programs, James A Haley Veterans Hospital

Sandra G Gompf, MD, FACP, FIDSA is a member of the following medical societies: American College of Physicians, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Coauthor(s)

Burke A Cunha, MD Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital

Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Beata Catherine Casanas, DO Associate Professor, Department of Internal Medicine, Division of Infectious Diseases and International Medicine, University of South Florida College of Medicine

Beata Catherine Casanas, DO is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, American Medical Association, American Osteopathic Association, Florida Medical Association, Infectious Diseases Society of America

Disclosure: Received honoraria from ViiV for speaking and teaching; Received honoraria from Pfizer for speaking and teaching.

Moise Carrington, MD Physician, Internal Medicine, Infectious Diseases Specialty

Moise Carrington, MD is a member of the following medical societies: American College of Physicians

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

Michael Stuart Bronze, MD David Ross Boyd Professor and Chairman, Department of Medicine, Stewart G Wolf Endowed Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center; Master of the American College of Physicians; Fellow, Infectious Diseases Society of America

Michael Stuart Bronze, MD is a member of the following medical societies: Alpha Omega Alpha, American Medical Association, Oklahoma State Medical Association, Southern Society for Clinical Investigation, Association of Professors of Medicine, American College of Physicians, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Additional Contributors

Thomas E Herchline, MD Professor of Medicine, Wright State University, Boonshoft School of Medicine; Medical Director, Public Health, Dayton and Montgomery County, Ohio

Thomas E Herchline, MD is a member of the following medical societies: Alpha Omega Alpha, Infectious Diseases Society of Ohio, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

References
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  2. Cherry JD, et al. Herpangina. Textbook of Pediatric Infectious Diseases. 6th ed. 2009. Vol 1: Chap 11.

  3. Chen KT, Chang HL, Wang ST, Cheng YT, Yang JY. Epidemiologic features of hand-foot-mouth disease and herpangina caused by enterovirus 71 in Taiwan, 1998-2005. Pediatrics. 2007 Aug. 120(2):e244-52. [Medline].

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  8. 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. 2008 Mar. 61(2):162-3. [Medline].

  9. Chen YH, Lin HC, Lin HC. Increased risk of adverse pregnancy outcomes among women affected by herpangina. Am J Obstet Gynecol. 2010 Jul. 203(1):49.e1-7. [Medline].

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  28. Miyazawa I, Azegami Y, Kasuo S, Yoshida T, Kobayashi M, Shiraishi T. Prevalence of enterovirus from patients with herpangina and hand, foot and mouth disease in Nagano Prefecture, Japan, 2007. Jpn J Infect Dis. 2008 May. 61(3):247-8. [Medline].

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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)
Table 1. Clinical Manifestations of Herpangina, Herpes Simplex Virus (HSV), and Hand-Foot-and-Mouth Disease
Clinical Manifestations Herpangina HSV Hand-Foot-and-Mouth Disease
 



Causative organism



 



Enteroviruses



 



HSV-1 and HSV-2



 



Enteroviruses



 



Oral vesicular/ulcerative lesions



 



+



 



+



 



+1



 



Anterior pharynx



 



-



 



+



 



+



 



Posterior pharynx



 



+



 



+/-



 



-



 



Gingivostomatitis



 



-



 



+/-



 



-



1 Lesions may also occur on the buccal



mucosa



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