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Pediatric Enteroviral Infections Clinical Presentation

  • Author: Nicholas John Bennett, MBBCh, PhD, MA(Cantab), FAAP; Chief Editor: Russell W Steele, MD  more...
Updated: Sep 23, 2014


Nonpolio enteroviruses cause an astronomical number of infections per year. More than 90% of enteroviral infections are either asymptomatic or cause a nonspecific febrile illness. A wide range of symptoms is observed, but most cases include fever, a viral prodrome, and gastrointestinal symptoms.

  • Patients with nonspecific febrile illness, the most common form of enteroviral infection, present with a sudden onset of fever, temperature ranging from 38.5-40°C. Accompanying symptoms include general upper respiratory and GI complaints. Clinical indicators include a flulike syndrome consisting of malaise, myalgias, sore throat, headache, conjunctivitis, nausea, emesis, and diarrhea. Genitourinary manifestations such as orchitis and epididymitis are possible. Symptoms generally last 3-7 days and are caused by all enteroviral subtypes.
  • Herpangina occurs in children aged 3-10 years. These patients report painful vesicles on the posterior pharynx and tonsils. These lesions are associated with fever, sore throat, odynophagia, and other viral symptoms. Mothers may notice a decreased oral intake by the child due to the painful ulcers. The causative agent is most commonly coxsackievirus group A and, sometimes, coxsackievirus group B. Herpangina is self-limited, and symptoms last 3-7 days.
  • Hand-foot-and-mouth disease is a vesicular eruption in the oropharynx, palms, soles, and interdigits of toddlers and school-aged children. The oral vesicles are not usually painful. Patients often present after 1-2 days of fever and have a characteristic viral exanthem. Lesions are more common on the dorsal surfaces of the hands and feet than in other locations. The most common causative agent is coxsackievirus group A, serotype 16, but strains of enterovirus 71 circulating in East Asia are currently causing outbreaks of hand-foot-and-mouth disease (HFMD) that are associated with a serious rhombencephalitis, with significant mortality.
  • Atypical HFM disease was recently reported around the globe and is caused by coxsackievirus A6.[12] It is characterized by a relatively paucity of oral lesions, but a striking bullous eruption on the extremities. Children with eczema may be more affected and "eczema coxsackium" was coined as far back as 1968 for this condition.[13] Postinfectious loss of the nails is reported frequently.
  • Viral exanthems, a frequent cause of emergency department visits, manifest as rubelliform or roseolalike rashes that occur in the summer months. These exanthems occur in children younger than 5 years and have a benign 3-day to 5-day course. The responsible agents are usually echoviruses.
  • Patients with aseptic meningitis have symptoms that mimic the initial symptoms of nonspecific febrile illnesses, but, as aseptic meningitis progresses, patients report a headache, stiff neck, and photophobia. A nonspecific rash can accompany these symptoms, raising the question of meningococcemia. The clinical course of aseptic meningitis is self-limited and resolves in 1-2 weeks.
    • The coxsackievirus group B and echoviruses are responsible for 80-90% cases in which a causative organism of aseptic meningitis is identified.
    • Neurotropic strains, such as enterovirus 71, can be responsible for more aggressive cases of CNS infections. Ninety percent of some cohorts with enterovirus 71 infection also had rhombencephalitis. This can lead to neurogenic pulmonary edema and has an overall fatality rate of 14%. Early signs of severe infection include myoclonus and sleep disturbance. Fever that lasts longer than 3 days duration, high fevers (>38.5C), and lethargy are predictors of CNS involvement.
  • Patients with myocarditis or pericarditis report chest pain, fatigue, and dyspnea on exertion. These symptoms can progress to dysrhythmia and heart failure. The most common cause of cardiac involvement is coxsackievirus group B5 infection, but echoviruses are also etiologies of infection.
  • Pleurodynia (Bornholm disease, devil's grippe) is an uncommon epidemic that causes severe muscular pains in the chest and abdomen. These sharp pains worsen with breathing or coughing and are associated with profuse sweating. Spasmodic muscular pains last 15-30 minutes in older children and adolescents. The condition can mimic serious surgical conditions and can cause periodic episodes of respiratory difficulty. These symptoms are accompanied by fever, headache, anorexia, nausea, and emesis. Symptoms last for 2 days. Coxsackieviruses B3 and B5 infect the intercostals muscles, causing these frightening but rare outbreaks.
  • Neonates with nonpolio enterovirus infections are at a high risk of developing a sepsislike condition, including meningoencephalitis, myocarditis, and hepatitis. Presenting symptoms include poor feeding, lethargy, fever, irritability, hypoperfusion, and jaundice. Differentiating these infections on clinical grounds from bacterial sepsis is impossible. Infants younger than 10 days are unable to mount a significant immune response and are at a higher risk of a serious infection from echoviruses and coxsackie group B viruses. A history of a mother who had a febrile illness with GI symptoms around the time of birth is often reported; this acute presentation results in exposure to viral shedding without significant transplacental transfer of maternal antibodies.
  • Poliovirus infections are divided into 4 groups of clinical syndromes: asymptomatic, abortive, nonparalytic, and paralytic.
    • Most infections (90-95%) are asymptomatic.
    • Abortive poliomyelitis involves a nonspecific febrile illness that spares the CNS and spontaneously resolves after a few days. Temperature is not higher than 103°F. Patients report a minor febrile upper respiratory infection, such as cough and sore throat, and gastrointestinal infection with nausea and diarrhea.
    • Patients with nonparalytic poliomyelitis (aseptic meningitis) present in the same manner as patients with abortive poliovirus, but nonparalytic poliomyelitis progresses to aseptic meningitis. During the initial flulike illness, patients report stiffness in the posterior neck muscles, limbs, and trunk. This minor viremia is followed by nuchal and spinal rigidity, the hallmark of nonparalytic polio.
    • Paralytic poliomyelitis starts with a nonspecific febrile illness and muscle weakness that resolves after 2-3 days but is followed by a sudden onset of asymmetric flaccid paralysis. Pain, nuchal rigidity, and hypertonia are indicators of brainstem, spinal ganglia, and posterior column involvement. Bulbar poliomyelitis involves the speech and central cardiorespiratory centers of the brain stem and can cause death because of cessation of cardiac and respiratory activity.


Nonspecific febrile illness can include normal findings on physical examination or can include an erythematous pharynx, mild conjunctivitis, and cervical lymphadenopathy.

  • Patients with herpangina present with punctate macules that progress to vesicles that eventually ulcerate. Usually, 3-6 erythematous vesicles about 1-2 mm in size are found on the posterior pharynx, anterior tonsils, and soft palate. The oropharynx may be erythematous, but no exudates are present.
  • Patients with HFM disease present with less painful or painless vesicles that may ulcerate on the buccal mucosa and tongue; the less significant pain differentiates the vesicles of HFM disease from the posterior pharyngeal vesicles of herpangina. See the image below.
    Erosions on the base of the tongue. Erosions on the base of the tongue.
  • In addition to the oral findings, an exanthem of vesicles appears on the palms, soles, and intertriginous digits of the hands and feet. These vesicles heal by resorption of fluid and do not crust over. See the images below.
    A red halo surrounds several vesicles on the fingeA red halo surrounds several vesicles on the finger flexures and palms.
    Small linear vesicle on the thumb. Small linear vesicle on the thumb.
    Vesicle on the dorsal hand of a young adult. Vesicle on the dorsal hand of a young adult.
    See the list below:
    • Occasionally, nonvesicular eruptions are present on the buttocks, proximal extremities, and genitalia. The truncal area is not usually involved, differentiating HFM disease from varicella infections.
    • The absence of gingival erythema, high fevers, and lack of significant cervical lymphadenopathy aid in distinguishing HFM disease from herpetic gingivostomatitis.
      Calf blisters from coxsackievirus A6 as seen in atCalf blisters from coxsackievirus A6 as seen in atypical hand-foot-mouth disease. Courtesy of Elsevier (Feder HM Jr, Bennett N, Modlin JF. Atypical hand, foot, and mouth disease: a vesiculobullous eruption caused by Coxsackie virus A6. Lancet Infect Dis. Jan 2014;14(1):83-6).
  • Viral exanthems appear as a pink, maculopapular, blanching rash that can mimic rubella and roseola. This rash is less commonly vesicular, urticarial, and petechial. Unlike rubella, no significant adenopathy is present. Similar to roseola, it may appear following the cessation of fever.
  • Atypical HFM disease tends to present with bullous lesions on the extremities and may be more severe over areas of preexisting eczema.[12] The lesions are not limited to the hands and feet and may be seen on the arms and legs.
  • Aseptic meningitis reveals physical findings consistent with meningeal irritation, including nuchal rigidity, a bulging fontanel, and, possibly, positive Kernig and Brudzinski signs in children older than 1 year. The accompanying rash is often nonspecific but can occasionally be petechial.
  • Myocarditis and pericarditis symptoms depend on the severity of the disease. The physician should look for signs of congestive heart failure. Patients with pericarditis may have an auscultatory friction rub, Hamman crunch, and poor perfusion.
  • Patients with pleurodynia (Bornholm disease) may present with respiratory distress or in a shocklike state. Patients may localize pain in the abdomen and may have tender abdominal muscular walls. A pleural friction rub may be auscultated during the muscular spasm.
  • Patients with acute hemorrhagic conjunctivitis present with subconjunctival hemorrhage, erythema, lacrimation, chemosis, preauricular lymphadenopathy, and serous eye discharge. Some of these cases may progress to a bacterial conjunctivitis with purulent ocular discharge.
  • Neonatal infections cause the infant to be irritable, lethargic, and inconsolable by the mother. The infection can progress to signs and symptoms that reflect hypoperfusion, such as cool mottled skin, delayed capillary refill, and ashen gray color.
  • Polioviruses should be differentiated into their subtypes.
    • Abortive (nonspecific febrile) illness appears as a general viral upper respiratory and GI infection. Cough, coryza, and pharyngeal exudates are common.
    • Patients with nonparalytic (aseptic meningitis) illness have a nonspecific viral picture, but the physician should recognize symptoms of meningeal irritation. Increase or decrease of the superficial and deep tendon reflex usually occurs prior to onset of weakness. If these reflexes are decreased, the physician should be wary of impending weakness and paralysis. As with all types of polio, sensory examination findings remain intact.
    • The paralytic form is similar to the nonparalytic with the additional classic finding of asymmetric flaccid paralysis. Proximal muscle groups are usually more affected than the distal musculature. Deep tendon reflexes are decreased or absent, and sensory findings are unchanged. Associated symptoms include hypertonia, respiratory and cardiac arrhythmias, and blood pressure and vasomotor changes. Observe for symptoms of respiratory distress, including difficulty speaking, nasal flaring, tachypnea, and immobility of accessory muscles of respiration. Impending respiratory failure may rapidly occur.


Enteroviral risk factors include poor sanitation, crowded living conditions, and lower socioeconomic class status. In addition, children younger than 5 years are more susceptible because of poor hygiene habits and lack of prior immunity.

  • Although debatable, neonatal infections are most likely acquired after birth rather than transplacentally. Exposure from an infected mother or another infant in the nursery during the first 2 weeks of life is the probable mode of transmission. The enteroviral exposure may be perineally acquired during the delivery process.
  • A B-cell response is needed for the host to properly fight off the enteroviral infection and to prevent entry to the CNS. Children who lack a functioning B-cell system, such as those with X-linked agammaglobulinemia, are at risk of serious enteroviral infection, such as meningoencephalitis.
  • Poliovirus is a consideration in all unimmunized or partially immunized children.
Contributor Information and Disclosures

Nicholas John Bennett, MBBCh, PhD, MA(Cantab), FAAP Assistant Professor of Pediatrics, Co-Director of Antimicrobial Stewardship, Medical Director, Division of Pediatric Infectious Diseases and Immunology, Connecticut Children's Medical Center

Nicholas John Bennett, MBBCh, PhD, MA(Cantab), FAAP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics

Disclosure: Received research grant from: Cubist Pharmaceuticals, Durata Therapeutics, and Biota Pharmaceutical<br/>Received income in an amount equal to or greater than $250 from: HealthyCT insurance<br/>Medico legal consulting for: Various.


Joseph Domachowske, MD Professor of Pediatrics, Microbiology and Immunology, Department of Pediatrics, Division of Infectious Diseases, State University of New York Upstate Medical University

Joseph Domachowske, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American Society for Microbiology, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, Phi Beta Kappa

Disclosure: Received research grant from: Pfizer;GlaxoSmithKline;AstraZeneca;Merck;American Academy of Pediatrics<br/>Received income in an amount equal to or greater than $250 from: Sanofi Pasteur;Astra Zeneca;Novartis<br/>Consulting fees for: Sanofi Pasteur; Novartis; Merck; Astra Zeneca.

Mobeen H Rathore, MD, CPE, FAAP, FIDSA Chief of Division of Pediatric Infectious Diseases/Immunology, Associate Chairman of Department of Pediatrics, University of Florida College of Medicine at Jacksonville; Hospital Epidemiologist and Section Chief of Infectious Disease and Immunology, Wolfson Children's Hospital; Director of University of Florida Center for HIV/AIDS Research, Education and Service (UF CARES)

Mobeen H Rathore, MD, CPE, FAAP, FIDSA is a member of the following medical societies: American Academy of Pediatrics, American Society for Microbiology, Florida Medical Association, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, Society for Healthcare Epidemiology of America, Society for Pediatric Research, Southern Medical Association, Southern Society for Pediatric Research, Florida Chapter of The American Academy of Pediatrics, Florida Pediatric Society, European Society for Paediatric Infectious Diseases

Disclosure: Nothing to disclose.

Specialty Editor Board

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 Minnesota American Legion and Auxiliary Heart Research Foundation 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, Society for Pediatric Research

Disclosure: Nothing to disclose.

Chief Editor

Russell W Steele, MD Clinical Professor, Tulane University School of Medicine; Staff Physician, Ochsner Clinic Foundation

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, Southern Medical Association

Disclosure: Nothing to disclose.

Additional Contributors

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

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, Society for Pediatric Research

Disclosure: Nothing to disclose.


The authors and editors of eMedicine gratefully acknowledge the contributions of previous author Michelle Mowad, MD, to the original writing and development of this article.

Figure 5 is a photograph of a case of Atypical HFMD seen by Dr Henry Feder and Dr Nicholas Bennett. Permission to use the photograph was granted by the patient's family. The image is reprinted from The Lancet Infectious Diseases, Vol. 14(1), Feder, Bennett and Modlin, Atypical hand, foot, and mouth disease: a vesiculobullous eruption caused by Coxsackie virus A6, Pages 83-86., Copyright (2014), with permission from Elsevier.

  1. Pichichero ME, McLinn S, Rotbart HA, et al. Clinical and economic impact of enterovirus illness in private pediatric practice. Pediatrics. 1998 Nov. 102(5):1126-34. [Medline]. [Full Text].

  2. Picornaviridae Study Group. New and Re-classified TypesGenus Parechovirus, species Human parechovirus. Available at Accessed: 3/14/09.

  3. Centers for Disease Control and Prevention. Enterovirus D68. Available at Accessed: September 23, 2014.

  4. Lowes R. Enterovirus-D68 Is Now Coast to Coast. Medscape Medical News. Available at Accessed: September 23, 2014.

  5. Tra My PV, Rabaa MA, Vinh H, Holmes EC, Hoang NV, Vinh NT, et al. The emergence of rotavirus G12 and the prevalence of enteric viruses in hospitalized pediatric diarrheal patients in southern Vietnam. Am J Trop Med Hyg. 2011 Oct. 85(4):768-75. [Medline]. [Full Text].

  6. Ikeda T, Mizuta K, Abiko C, Aoki Y, Itagaki T, Katsushima F, et al. Acute respiratory infections due to enterovirus 68 in Yamagata, Japan between 2005 and 2010. Microbiol Immunol. 2012 Feb. 56(2):139-43. [Medline].

  7. Puenpa J, Theamboonlers A, Korkong S, Linsuwanon P, Thongmee C, Chatproedprai S, et al. Molecular characterization and complete genome analysis of human enterovirus 71 and coxsackievirus A16 from children with hand, foot and mouth disease in Thailand during 2008-2011. Arch Virol. 2011 Nov. 156(11):2007-13. [Medline].

  8. Poliovirus. Pediatrics. 2011 Oct. 128(4):805-8. [Medline].

  9. CDC. Enterovirus surveillance--United States, 1997-1999. MMWR Morb Mortal Wkly Rep. 2000 Oct 13. 49(40):913-6. [Medline].

  10. Global Polio Eradication Initiative. Wild Poliovirus Weekly Update. Global Polio Eradication. Available at Accessed: 2-16-2014.

  11. Ooi MH, Wong SC, Mohan A, Podin Y, Perera D, Clear D, et al. Identification and validation of clinical predictors for the risk of neurological involvement in children with hand, foot, and mouth disease in Sarawak. BMC Infect Dis. 2009 Jan 19. 9:3. [Medline]. [Full Text].

  12. Feder HM Jr, Bennett N, Modlin JF. Atypical hand, foot, and mouth disease: a vesiculobullous eruption caused by Coxsackie virus A6. Lancet Infect Dis. 2014 Jan. 14(1):83-6. [Medline].

  13. Nahmias AJ, Froeschle JE, Feorino PM, McCord G. Generalized eruption in a child with eczema due to coxsackievirus A16. Arch Dermatol. 1968 Feb. 97(2):147-8. [Medline].

  14. Chonmaitree T, Menegus MA, Powell KR. The clinical relevance of 'CSF viral culture'. A two-year experience with aseptic meningitis in Rochester, NY. JAMA. 1982 Apr 2. 247(13):1843-7. [Medline].

  15. Singer JI, Maur PR, Riley JP, Smith PB. Management of central nervous system infections during an epidemic of enteroviral aseptic meningitis. J Pediatr. 1980 Mar. 96(3 Pt 2):559-63. [Medline].

  16. Ahmed A, Brito F, Goto C, et al. Clinical utility of the polymerase chain reaction for diagnosis of enteroviral meningitis in infancy. J Pediatr. 1997 Sep. 131(3):393-7. [Medline].

  17. Tan CW, Lai JK, Sam IC, Chan YF. Recent developments in antiviral agents against enterovirus 71 infection. J Biomed Sci. 2014 Feb 12. 21(1):14. [Medline].

  18. Wood DL. Increasing immunization coverage. American Academy of Pediatrics Committee on Community Health Services. American Academy of Pediatrics Committee on Practice and Ambulatory Medicine. Pediatrics. 2003 Oct. 112(4):993-6. [Medline]. [Full Text].

  19. Hyoty H, Hiltunen M, Knip M, et al. A prospective study of the role of coxsackie B and other enterovirus infections in the pathogenesis of IDDM. Childhood Diabetes in Finland (DiMe) Study Group. Diabetes. 1995 Jun. 44(6):652-7. [Medline].

  20. Abzug MJ, Keyserling HL, Lee ML, et al. Neonatal enterovirus infection: virology, serology, and effects of intravenous immune globulin. Clin Infect Dis. 1995 May. 20(5):1201-6. [Medline].

  21. Abzug MJ, Levin MJ, Rotbart HA. Profile of enterovirus disease in the first two weeks of life. Pediatr Infect Dis J. 1993 Oct. 12(10):820-4. [Medline].

  22. Andrus JK, Strebel PM, de Quadros CA, Olive JM. Risk of vaccine-associated paralytic poliomyelitis in Latin America, 1989-91. Bull World Health Organ. 1995. 73(1):33-40. [Medline].

  23. Ballow M. Mechanisms of action of intravenous immune serum globulin in autoimmune and inflammatory diseases. J Allergy Clin Immunol. 1997 Aug. 100(2):151-7. [Medline].

  24. Gaspar BG, Kinnon C. Humoral Immunodeficiency: X-linked agammaglobulinemia. Immunol Allergy Clin North Am. 2001. 21(1):

  25. Huang CC, Liu CC, Chang YC, et al. Neurologic complications in children with enterovirus 71 infection. N Engl J Med. 1999 Sep 23. 341(13):936-42. [Medline].

  26. Jiang P, Faase JA, Toyoda H, et al. Evidence for emergence of diverse polioviruses from C-cluster coxsackie A viruses and implications for global poliovirus eradication. Proc Natl Acad Sci U S A. 2007 May 29. 104(22):9457-62. [Medline]. [Full Text].

  27. Kohler KA, Banerjee K, Gary Hlady W, Andrus JK, Sutter RW. Vaccine-associated paralytic poliomyelitis in India during 1999: decreased risk despite massive use of oral polio vaccine. Bull World Health Organ. 2002. 80(3):210-6. [Medline].

  28. Morag A, Ogra P. Enteroviruses. Nelson Textbook of Pediatrics. 16th ed. Philadelphia, Pa: WB Saunders Co; 2000.

  29. Norris CM, Danis PG, Gardner TD. Aseptic meningitis in the newborn and young infant. Am Fam Physician. 1999 May 15. 59(10):2761-70. [Medline].

  30. Prager P, Nolan M, Andrews IP, Williams GD. Neurogenic pulmonary edema in enterovirus 71 encephalitis is not uniformly fatal but causes severe morbidity in survivors. Pediatr Crit Care Med. 2003 Jul. 4(3):377-81. [Medline].

  31. Prevots DR, Burr RK, Sutter RW, Murphy TV,. Poliomyelitis prevention in the United States. Updated recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR Recomm Rep. 2000 May 9. 49(RR-5):1-22; quiz CE1-7. [Medline]. [Full Text].

  32. Roivainen M. Enteroviruses and myocardial infarction. Am Heart J. 1999 Nov. 138(5 Pt 2):S479-83. [Medline].

  33. Rotbart HA, Sawyer MH, Fast S, Lewinski C, Murphy N, Keyser EF, et al. Diagnosis of enteroviral meningitis by using PCR with a colorimetric microwell detection assay. J Clin Microbiol. 1994 Oct. 32(10):2590-2. [Medline]. [Full Text].

  34. Shechet RJ, Tanenbaum B. Preventing unnecessary hypospadias repair. Am Fam Physician. 1999 Nov 1. 60(7):1933. [Medline].

  35. WHO. Progress towards interruption of wild poliovirus transmission in 2005. Wkly Epidemiol Rec. 2006 Apr 28. 81(17):165-72. [Medline]. [Full Text].

  36. Wilfert CM, Lehrman SN, Katz SL. Enteroviruses and meningitis. Pediatr Infect Dis. 1983 Jul-Aug. 2(4):333-41. [Medline].

  37. Yang TT, Huang LM, Lu CY, et al. Clinical features and factors of unfavorable outcomes for non-polio enterovirus infection of the central nervous system in northern Taiwan, 1994-2003. J Microbiol Immunol Infect. 2005 Dec. 38(6):417-24. [Medline].

  38. Zaoutis T, Klein JD. Enterovirus infections. Pediatr Rev. 1998 Jun. 19(6):183-91. [Medline].

Erosions on the base of the tongue.
A red halo surrounds several vesicles on the finger flexures and palms.
Small linear vesicle on the thumb.
Vesicle on the dorsal hand of a young adult.
Calf blisters from coxsackievirus A6 as seen in atypical hand-foot-mouth disease. Courtesy of Elsevier (Feder HM Jr, Bennett N, Modlin JF. Atypical hand, foot, and mouth disease: a vesiculobullous eruption caused by Coxsackie virus A6. Lancet Infect Dis. Jan 2014;14(1):83-6).
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