Medscape is available in 5 Language Editions – Choose your Edition here.



  • Author: Robert A Schwartz, MD, MPH; Chief Editor: Michael Stuart Bronze, MD  more...
Updated: Jun 16, 2016

Practice Essentials

The human enteroviruses are ubiquitous viruses that are transmitted from person to person via direct contact with virus shed from the gastrointestinal or upper respiratory tract. Poliovirus, the prototypical enterovirus, can cause a subclinical or mild illness, aseptic meningitis, or paralytic poliomyelitis. The nonpolio viruses (group A and B coxsackieviruses, echoviruses, enteroviruses) are responsible for a wide spectrum of diseases in persons of all ages, although infection and illness occur most commonly in infants.

For updated epidemiologic information on the 2014 enterovirus 68 outbreak, see Frequency.

See 11 Travel Diseases to Consider Before and After the Trip, a Critical Images slideshow, to help identify and manage several infectious travel diseases.

Signs and symptoms

Clinical manifestations of enteroviral infection differ by viral type. Poliovirus syndromes can be abortive; nonparalytic; or paralytic, including spinal polio, bulbar polio, and polioencephalitis.


  • Abortive polio manifestations include fever, headache, sore throat, loss of appetite, vomiting, and abdominal pain; neurologic symptoms are typically not reported
  • Nonparalytic polio symptoms are similar to those of abortive polio but more intense; also, patients report stiffness of the posterior muscles of the neck, trunk, and limbs
  • Paralytic polio is an acute febrile illness characterized by aseptic meningitis and weakness or paralysis of one or more extremities, along with weakness of one or more muscle groups
  • Spinal polio comprises a prolonged prodrome, with features of aseptic meningitis followed in 1-2 days by weakness and, eventually, paralysis
  • Bulbar polio involves cranial nerves, most commonly IX, X, and XII; patients accumulate pharyngeal secretions, have a nasal twang to the voice, and develop paralysis of vocal cords, causing hoarseness, aphonia, and, eventually, asphyxia
  • Polioencephalitis is principally reported in children; unlike in other forms of polio, seizures are common and paralysis may be spastic

More than 90% of infections caused by nonpolio entero viruses are asymptomatic or result only in an undifferentiated febrile illness.[1] Symptomatic nonpolio virus infections include the following:

  • Pleurodynia
  • Myopericarditis
  • Acute hemorrhagic conjunctivitis (AHC)
  • Nonspecific febrile illness
  • Aseptic meningitis
  • Herpangina
  • Hand-foot-and-mouth disease (HFMD)[2]
  • Encephalitis

Physical examination findings in enteroviral disease vary greatly depending on the type of illness and etiologic agent, as follows:

  • Nonspecific febrile illness – Physical findings are those of general viral illness; mild pharyngeal erythema or conjunctivitis may be present
  • Pleurodynia – Paroxysmal chest pain is characteristic, has no prodrome, and begins with an abrupt onset of spasmodic pain, typically over the lower part of the rib cage or the upper abdominal region; fever often occurs within 1 hour of the onset of pain and subsides as the pain recedes; during paroxysms, respirations are rapid and shallow; the pain is reproducible, and patients appear healthy between paroxysms of pain; auscultation may reveal a pleural friction rub
  • Myopericarditis – The most common symptoms are dyspnea, chest pain, fever, and malaise[3] ; precordial pain may be sharp or dull and is often exacerbated by recumbency; a pericardial friction rub, if present, is transient; signs of congestive heart failure are present in 20% of cases[4]
  • AHC – The hallmark physical findings include ocular erythema and subconjunctival hemorrhage, which seems to be more profuse in young patients[5] ; palpebral edema, chemosis, and ocular discharge may also be noted; preauricular lymphadenopathy is an associated finding
  • Aseptic meningitis – Meningeal signs (nuchal rigidity, bulging fontanelles in infants) may be present; rash may develop; approximately 5%-10% of infants experience complications such as febrile seizures, complex seizures, lethargy, coma, and movement disorders early in the course[6]
  • Encephalitis – Manifestations range from lethargy, drowsiness, and personality change to seizures, paresis, coma, motor seizures, hemichorea, and acute cerebellar ataxia[7]
  • Herpangina – Punctate macular lesions appear the on oral mucosa, most commonly the anterior tonsillar pillar and soft palate; the lesions evolve into vesicles and eventually ulcerate
  • HFMD – Vesicular lesions develop on the hands and feet and in the oral cavity; hands are involved more commonly than feet; the skin lesions consist of mixed papules; clear vesicles appear gray and are surrounded by erythematous rings; lesions are tender and resemble those of herpes simplex or varicella zoster infection; they resolve in approximately 1 week[2]

Nonparalytic polio

  • Signs of meningeal irritation are present
  • Kernig and Brudzinski signs may be present
  • In infants, the head drop sign can be elicited

Paralytic polio

  • In early-stage disease, reflexes are normally active; a change in the character of reflexes precedes paralysis by 12-24 hours
  • Superficial reflexes decrease first, followed in 8-24 hours by loss of deep tendon reflexes
  • Paralysis is flaccid and characteristically asymmetric in distribution, with proximal limb muscles involved more than distal muscles and the lower extremities affected more commonly than the upper extremities

See Clinical Presentation for more detail.


Diagnosis of enterovirus infections is often clinical. Laboratory diagnosis can be achieved with the following:

  • Serological tests – Have multiple drawbacks; infrequently used
  • Viral isolation by cell culture – CSF, blood, or feces can be sampled, depending on the site affected; yield is increased if multiple sites are sampled
  • Polymerase chain reaction (PCR) – Provides rapid results; the best diagnostic test for use in CSF
  • In myopericarditis, chest radiography, echocardiography, and ECG can be used for diagnosis

See Workup for more detail.


Treatment is as follows:

  • Management is supportive and addresses symptoms (eg, bed rest, analgesics)
  • No antiviral medications are currently approved for the treatment of enterovirus infections
  • Immunoglobulins have been used therapeutically and prophylactically for enteroviral CNS infections in neonates and immunocompromised hosts, with mixed results[8]
  • Abortive and nonparalytic polio can be managed at home, but patients with paralytic polio require hospitalization

See Treatment and Medication for more detail.



The human enteroviruses are ubiquitous viruses that are transmitted from person to person via direct contact with virus shed from the gastrointestinal or upper respiratory tract. The enteroviruses belong to the Picornaviridae family of viruses and are traditionally divided into 5 subgenera based on differences in host range and pathogenic potential.[9] Each subgenus contains a number of unique serotypes, which are distinguished based on neutralization by specific antisera. The subgenera include polioviruses, coxsackievirus (groups A and B), and echoviruses.

A total of 72 serotypes were originally identified by conventional methods; 64 serotypes remain after recognition of redundant serotypes. Three serotypes comprise the polioviruses, 23 serotypes comprise coxsackievirus group A, 6 serotypes comprise coxsackievirus group B, and 29 serotypes comprise the echoviruses. A new classification scheme has been adopted that divides all nonpolio enterovirus into 4 groups designated A through D based on the homology within RNA region coding for the VP1 capsid protein.[10] More recently, many new serotypes that are not included in the original classification have been characterized by molecular methods, bringing the number of known serotypes to more than 90.[11, 12]


The enteroviruses are icosahedral nonenveloped viruses that are approximately 30 nm in diameter.

They have a capsid composed of 60 subunits each formed from 4 proteins (VP1 to VP4).

They are stable at a pH from 3-10, distinguishing them from other picornaviruses (including rhinoviruses), which are unstable below pH 6.

A linear, single-strand RNA genome of about 7.5 kb is enclosed by the capsid; the translation product is a single polyprotein that is cleaved after translation by viral-coded proteases into the structural proteins (VP1 to VP4), RNA polymerase, proteases, and other nonstructural proteins.[13]

Enteroviruses resist lipid solvents, ether, chloroform, and alcohol. They are inactivated at temperatures above 50°C but remain infectious at refrigerator temperature.

Molar MgCl2 reduces thermolability at higher temperatures.

The viruses are inactivated by ionizing radiation, formaldehyde, and phenol.

Enteroviruses cause a wide range of infections. Poliovirus, the prototypical enterovirus, can cause a subclinical or mild illness, aseptic meningitis, or paralytic poliomyelitis, a disease that has been eradicated in the United States and other developed countries. The nonpolio viruses (group A and B coxsackieviruses, echoviruses, enteroviruses) continue to be responsible for a wide spectrum of diseases in persons of all ages, although infection and illness occur most commonly in infants.

Coxsackievirus infection is the most common cause of viral heart disease. Group A coxsackieviruses may cause flaccid paralysis, while group B coxsackieviruses cause spastic paralysis. Other diseases associated with group A coxsackievirus infections include hand-foot-and-mouth disease (HFMD) and hemorrhagic conjunctivitis, while group B coxsackievirus is associated with herpangina, pleurodynia, myocarditis, pericarditis, and meningoencephalitis. Aseptic meningitis and the common cold are associated with both groups.

Diseases caused by echoviral infections range from the common cold and fever to aseptic meningitis and acute hemorrhagic conjunctivitis (AHC).



Enteroviruses are transmitted predominantly via the fecal-oral route. However, there are some exceptions, including coxsackievirus A21, which is spread mainly by respiratory secretions,[14] and enterovirus 70, which is shed in tears and spread via fingers and fomites.[15]

Upon entry into the oropharynx, the virus replicates in submucosal tissues of the distal pharynx and alimentary tract.[16] Viral particles are shed in the feces and in upper respiratory tract secretions for days prior to symptom onset. The average incubation period is 3-10 days, during which the virus migrates to regional lymphoid tissue and replicates. Minor viremia results, which is associated with the onset of symptoms and viral spread to the reticuloendothelial system (spleen, liver, bone marrow).[17]

Dissemination to target organs follows, and viral replication in target organs produces the major viremia with possible secondary seeding of the CNS. Potential target organs include the skin and CNS. Infectious virus is shed from the upper respiratory tract for 1-3 weeks and from the feces for 3-8 weeks. Enteroviruses undergoes a high rate of mutation during replication in the gastrointestinal tract, where single-site mutations can occur in the 5' noncoding region of the attenuated polioviruses; this can lead to prolonged excretion and neurovirulence.[18]

The neuropathy of paralytic diseases caused by enteroviruses is due to direct cellular destruction. Neuronal lesions occur mainly in anterior horn cells of the spinal cord. The 3 serotypes of poliovirus all bind to the cell surface receptor CD155.

Immunity and immune response

Immunity to enterovirus is serotype-specific. Intact humoral immunity is required for the control and eradication of enteroviral disease.

T lymphocytes do not contribute to viral clearance and, in coxsackievirus B3 myocarditis, may contribute to myocardial inflammation.[19]

Humoral immunity (antibody-mediated) mechanisms operate both in the alimentary tract (to prevent mucosal infection) and in the blood (to prevent dissemination to target organs).

Secretory immunoglobulin A (IgA) appears in nasal and alimentary secretions 2-4 weeks after the administration of live-attenuated oral poliovirus vaccine (OPV) and persists for at least 15 years.[20] Upon re-exposure to infectious virus, high titers of secretory IgA antibodies prevent or substantially reduce poliovirus shedding; higher secretory IgA titers lead to better immunity.[20]

Immunoglobulin M (IgM) antibodies appear as early as 1-3 days after enteroviral challenge and disappear after 2-3 months.[20]

Immunoglobulin G (IgG) antibody, which is generally detected 7-10 days after infection, is mostly of the IgG1 and IgG3 subtypes. Serum neutralizing IgG antibodies persist for life after natural enteroviral infections.[21]

Macrophage function is also a critical component of the immune response in enteroviral infections; ablation of macrophage function in experimental animals markedly enhances the severity of coxsackievirus B infections.[22]



United States

Nonpolio enteroviruses are responsible for 10-20 million symptomatic infections per year and are more prevalent among children of lower socioeconomic class, probably because of crowding, poor hygiene, and opportunities for fecal contamination.

AHC was first recognized in the United States in 1981 during an epidemic in Florida; few cases have been reported since. The prevalence is higher in southern areas than in northern areas.

Between 2002 and 2004, echoviruses 9 and 30 were the most commonly reported enterovirus serotypes in the United States.[23] In contrast, other enterovirus serotypes (eg, echovirus 1, coxsackievirus B6, and enteroviruses 68 and 69) are rarely reported and appear to have little epidemic potential.[24] However, difficulty in isolation of enterovirus 68 (EV68, EV-D68, EVD-68, HEV68) may bias the data, leading to an underestimation of its prevalence.[25]

A 2014 outbreak of enterovirus 68 (also called enterovirus D68) has been reported in at least six US states, including Colorado, Illinois, Iowa, Kansas, Kentucky, and Missouri, among others. In China, it had been noted since 2016.[26] From mid-August to September 11, 2014, 82 cases of enterovirus 68 infection had been confirmed by the CDC in the outbreak, although the total number of confirmed cases is higher since this figure does not include cases confirmed by individual state laboratories. This outbreak has been notable for its high number of hospitalizations involving infected children.[27] It is probable that there were different EV-D68 strains in China and America with mutations accounting for different prevalence.[26]

Coxsackievirus A is likely underrepresented because only some serotypes are readily isolated in cell culture.[28]

National or regional outbreaks of aseptic meningitis are occasionally reported, such as the echovirus 30 outbreaks in the United States between 1989 and 1992 and in 2003 and echovirus 13 and echovirus 18 outbreaks in 2001. Aseptic meningitis is no longer a nationally notifiable disease in the United States.


Enteroviruses are distributed worldwide and are influenced by season and climate. Infections occur in summer and early fall in temperate areas, while tropical and semitropical areas bear the brunt all year.

AHC occurs as epidemics in tropical countries during the hot and rainy season. It was first recognized in 1969 in Ghana (Apollo disease) and Indonesia. AHC is also epidemic in India and the Far East.

The worldwide prevalence of poliomyelitis has decreased significantly because of improved economic conditions and availability of vaccines. The last case of wild polio in the Americas occurred in Peru in 1991. In 1994, the World Health Organization declared polio eradicated from the Western Hemisphere. In 2000, 7 cases of poliomyelitis due to a mutated polio strain related to oral polio vaccine were reported from Haiti and the Dominican Republic. Polio remains a significant disease in the developing world, and, in 2003, 6 endemic countries were identified: Afghanistan, Egypt, India, Niger, Nigeria, and Pakistan.

In 2008, 1,652 confirmed cases of paralytic polio were reported worldwide. Polio is endemic in 4 countries: Afghanistan, India, Nigeria, and Pakistan. In addition, 14 other previously polio-free countries (Angola, Burkina Faso, Benin, Central Africa Republic, Chad, Côte d'Ivoire, The Democratic Republic of Congo, Ghana, Ethiopia, Nepal, Niger, Sudan, Tango) have reported cases in 2008-2009 (114 cases through August 2009) as a result of importations.[29, 30] As of September 2009, 969 cases of polio (including wild polio strains and oral vaccine–derived) had been reported in endemic and nonendemic countries.[31]

In a Korean study of children during an outbreak of aseptic meningitis, echovirus 6 or 30 infection was the most common manifestation.[32]



More than 90% of infections caused by the nonpolio enteroviruses are asymptomatic or result in only an undifferentiated febrile illness.[1]

Myopericarditis carries a mortality rate of 0%-4%. Myocarditis carries a higher mortality rate than pericarditis. Additionally, murine model studies have suggested that a deficiency of complement receptors 1 and 2 leads to increased morbidity in coxsackie B3 infections, including myocarditis, dilated cardiomyopathy, and fibrosis.[33]

Prior to the vaccine era, the mortality rate in polio epidemics was 5%-7%.

The overall risk of OPV-related disease is estimated to be 1 case per 2.6 million doses of OPV. The inactivated poliovirus vaccine (IPV) was incorporated into the routine polio vaccination in Europe and Canada in the 1980s. IPV has been used in the United States since 2000; OPV is no longer used in the United States.

Despite the risk of OPV-related paralysis, it is still the preferred vaccine for global polio eradication in developing nations (see Deterrence/Prevention).


The male-to-female ratio of myopericarditis is 2:1. The risk of cardiac involvement is higher during pregnancy and immediately postpartum.

The prevalence of polio infection is equal in boys and girls, although paralysis is more common in boys. Among adults, women are at increased risk of infection and the postpolio syndrome.

Aseptic meningitis is approximately twice as common in males as in females.


Enteroviral infections are most common in young children. Herpangina primarily affects children aged 3 months to 16 years. Poliomyelitis is observed in children younger than 15 years. Aseptic meningitis due to enteroviral infection is more common in infants than in adults. Most cases of pleurodynia occur in children and adults younger than 30 years.

Myopericarditis is most prevalent in young adults, especially those who are physically active. AHC is most prevalent in adults aged 20-50 years.

Neonates are at high risk for severe sepsis due to enterovirus infections.

Contributor Information and Disclosures

Robert A Schwartz, MD, MPH Professor and Head of Dermatology, Professor of Pathology, Pediatrics, Medicine, and Preventive Medicine and Community Health, Rutgers New Jersey Medical School; Visiting Professor, Rutgers University School of Public Affairs and Administration

Robert A Schwartz, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, New York Academy of Medicine, American Academy of Dermatology, American College of Physicians, Sigma Xi

Disclosure: Nothing to disclose.


Mark R Wallace, MD, FACP, FIDSA Clinical Professor of Medicine, Florida State University College of Medicine; Clinical Professor of Medicine, University of Central Florida College of Medicine

Mark R Wallace, MD, FACP, FIDSA is a member of the following medical societies: American College of Physicians, American Medical Association, American Society for Microbiology, Infectious Diseases Society of America, International AIDS Society, Florida Infectious Diseases Society

Disclosure: Nothing to disclose.

Pratibha Dua, MD, MBBS Staff Physician, Internal Medicine, United Medical Park

Pratibha Dua, MD, MBBS is a member of the following medical societies: American Medical Association

Disclosure: Nothing to disclose.

Rajendra Kapila, MD, MBBS Professor, Department of Medicine, Rutgers New Jersey Medical School

Rajendra Kapila, MD, MBBS is a member of the following medical societies: American College of Physicians, American Medical Association, Infectious Diseases Society of America, Infectious Diseases Society of New Jersey

Disclosure: Nothing to disclose.

Smeeta Sinha, MD Resident Physician, Department of Dermatology, Rutgers New Jersey Medical School

Smeeta Sinha, MD is a member of the following medical societies: Alpha Omega Alpha, Phi Beta Kappa, Sigma Xi

Disclosure: Nothing to disclose.

Alexander Velazquez, MD Fellow, Department of Infectious Diseases, Orlando Regional Medical Center

Alexander Velazquez, MD is a member of the following medical societies: American College of Physicians, Infectious Diseases Society of America

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

Mary D Nettleman, MD, MS MACP, Professor and Chair, Department of Medicine, Michigan State University College of Human Medicine

Mary D Nettleman, MD, MS is a member of the following medical societies: American College of Physicians, Association of Professors of Medicine, Central Society for Clinical and Translational Research, Infectious Diseases Society of America, Society of General Internal Medicine

Disclosure: Nothing to disclose.

  1. Kogon A, Spigland I, Frothingham TE, Elveback L, Williams C, Hall CE. The virus watch program: a continuing surveillance of viral infections in metropolitan New York families. VII. Observations on viral excretion, seroimmunity, intrafamilial spread and illness association in coxsackie and echovirus infections. Am J Epidemiol. 1969 Jan. 89(1):51-61. [Medline].

  2. Koh WM, Bogich T, Siegel K, Jin J, Chong EY, Tan CY, et al. The Epidemiology of Hand, Foot and Mouth Disease in Asia: A Systematic Review and Analysis. Pediatr Infect Dis J. 2016 Jun 3. [Medline].

  3. Smith WG. Coxsackie B myopericarditis in adults. Am Heart J. 1970 Jul. 80(1):34-46. [Medline].

  4. Koontz CH, Ray CG. The role of Coxsackie group B virus infections in sporadic myopericarditis. Am Heart J. 1971 Dec. 82(6):750-8. [Medline].

  5. Kono R, Uchida Y. Acute hemorrhagic conjunctivitis. Ophthalmol Dig. 1977. 39:14.

  6. Rorabaugh ML, Berlin LE, Heldrich F, et al. Aseptic meningitis in infants younger than 2 years of age: acute illness and neurologic complications. Pediatrics. 1993 Aug. 92(2):206-11. [Medline].

  7. Modlin JF, Dagan R, Berlin LE, Virshup DM, Yolken RH, Menegus M. Focal encephalitis with enterovirus infections. Pediatrics. 1991 Oct. 88(4):841-5. [Medline].

  8. Quartier P, Debre M, De Blic J, et al. Early and prolonged intravenous immunoglobulin replacement therapy in childhood agammaglobulinemia: a retrospective survey of 31 patients. J Pediatr. 1999 May. 134(5):589-96. [Medline].

  9. Melnick JL. The discovery of the enteroviruses and the classification of poliovirus among them. Biologicals. 1993 Dec. 21(4):305-9. [Medline].

  10. Oberste MS, Maher K, Kilpatrick DR, Flemister MR, Brown BA, Pallansch MA. Typing of human enteroviruses by partial sequencing of VP1. J Clin Microbiol. 1999 May. 37(5):1288-93. [Medline]. [Full Text].

  11. Oberste MS, Maher K, Michele SM, Belliot G, Uddin M, Pallansch MA. Enteroviruses 76, 89, 90 and 91 represent a novel group within the species Human enterovirus A. J Gen Virol. 2005 Feb. 86:445-51. [Medline].

  12. Oberste MS, Maher K, Nix WA, et al. Molecular identification of 13 new enterovirus types, EV79-88, EV97, and EV100-101, members of the species Human Enterovirus B. Virus Res. 2007 Sep. 128(1-2):34-42. [Medline].

  13. Rueckert RR. Picornaviridae and their replication. Fields BN, Knipe DM, eds. Virology. 2nd ed. New York: Raven Press; 1990. 507.

  14. Couch RB, Douglas RG Jr, Lindgren KM, Gerone PJ, Knight V. Airborne transmission of respiratory infection with coxsackievirus A type 21. Am J Epidemiol. 1970 Jan. 91(1):78-86. [Medline].

  15. Onorato IM, Morens DM, Schonberger LB, Hatch MH, Kaminski RM, Turner JP. Acute hemorrhagic conjunctivitis caused by enterovirus type 70: an epidemic in American Samoa. Am J Trop Med Hyg. 1985 Sep. 34(5):984-91. [Medline].

  16. Wolf JL, Rubin DH, Finberg R, et al. Intestinal M cells: a pathway for entry of reovirus into the host. Science. 1981 Apr 24. 212(4493):471-2. [Medline].

  17. Horstmann DM, Mccollum RW. Poliomyelitis virus in human blood during the minor illness and the asymptomatic infection. Proc Soc Exp Biol Med. 1953 Mar. 82(3):434-7. [Medline].

  18. Minor PD, John A, Ferguson M, Icenogle JP. Antigenic and molecular evolution of the vaccine strain of type 3 poliovirus during the period of excretion by a primary vaccinee. J Gen Virol. 1986 Apr. 67 ( Pt 4):693-706. [Medline].

  19. Rose NR, Wolfgram LJ, Herskowitz A, Beisel KW. Postinfectious autoimmunity: two distinct phases of coxsackievirus B3-induced myocarditis. Ann N Y Acad Sci. 1986. 475:146-56. [Medline].

  20. Ogra PL, Karzon DT. Formation and function of poliovirus antibody in different tissues. Prog Med Virol. 1971. 13:157.

  21. Torfason EG, Reimer CB, Keyserling HL. Subclass restriction of human enterovirus antibodies. J Clin Microbiol. 1987 Aug. 25(8):1376-9. [Medline]. [Full Text].

  22. Rager-Zisman B, Allison AC. The role of antibody and host cells in the resistance of mice against infection by coxsackie B-3 virus. J Gen Virol. 1973 Jun. 19(3):329-38. [Medline].

  23. Centers for Disease Control and Prevention (CDC). Enterovirus surveillance--United States, 2002-2004. MMWR Morb Mortal Wkly Rep. 2006 Feb 17. 55(6):153-6. [Medline].

  24. Centers for Disease Control and Prevention. Enterovirus surveillance--United States, 2000-2001. MMWR Morb Mortal Wkly Rep. 2002 Nov 22. 51(46):1047-9. [Medline].

  25. 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].

  26. Xiang Z, Xie Z, Liu L, Ren L, Xiao Y, Paranhos-Baccalà G, et al. Genetic divergence of enterovirus D68 in China and the United States. Sci Rep. 2016 Jun 9. 6:27800. [Medline].

  27. Enterovirus D68. Centers for Disease Control and Prevention. Available at Accessed: September 11, 2014.

  28. Lipson SM, Walderman R, Costello P. Sensitivity of rhabdomyosarcoma and guinea pig embryo cell cultures to field isolates of difficult-to-cultivate group A coxsackieviruses. J Clin Microbiol. 1986. 26:1298.

  29. World Health Organization - Regional Office for Eastern Mediterranean. AFP Surveillance, Polio Fax weekly bulletin. World Health Organization - Regional Office for Eastern Mediterranean. 9/7/2009.

  30. Center for Disease Control and Prevention. Glopal Polio Erradication Program. CDC. July 2009.

  31. Global Polio Eradication Initiative. Wild Poliovirus Weekly Update. Sept 8,2009. Available at

  32. Kim HJ, Kang B, Hwang S, Hong J, Kim K, Cheon DS. Epidemics of viral meningitis caused by echovirus 6 and 30 in Korea in 2008. Virol J. 2012 Feb 15. 9:38. [Medline]. [Full Text].

  33. Fairweather D, Frisancho-Kiss S, Njoku DB, Nyland JF, Kaya Z, Yusung SA. Complement receptor 1 and 2 deficiency increases coxsackievirus B3-induced myocarditis, dilated cardiomyopathy, and heart failure by increasing macrophages, IL-1beta, and immune complex deposition in the heart. J Immunol. 2006 Mar 15. 176(6):3516-24. [Medline].

  34. Curnen EC, Shaw EW, Melnick JL. Disease resembling nonparalytic poliomyelitis associated with a virus pathogenic for infant mice. J Am Med Assoc. 1949 Nov 26. 141(13):894-901. [Medline].

  35. Weller TH, Enders JF, Buckingham M, Finn JJ Jr. The etiology of epidemic pleurodynia: a study of two viruses isolated from a typical outbreak. J Immunol. 1950 Sep. 65(3):337-46. [Medline].

  36. Warin JF, Davies JB, Sanders FK, Vizoso AD. Oxford epidemic of Bornholm disease, 1951. Br Med J. 1953 Jun 20. 1(4824):1345-51. [Medline].

  37. Narula J, Khaw BA, Dec GW Jr, et al. Brief report: recognition of acute myocarditis masquerading as acute myocardial infarction. N Engl J Med. 1993 Jan 14. 328(2):100-4. [Medline].

  38. Kono R. Apollo 11 disease or acute hemorrhagic conjunctivitis: a pandemic of a new enterovirus infection of the eyes. Am J Epidemiol. 1975 May. 101(5):383-90. [Medline].

  39. Sklar VE, Patriarca PA, Onorato IM, et al. Clinical findings and results of treatment in an outbreak of acute hemorrhagic conjunctivitis in southern Florida. Am J Ophthalmol. 1983 Jan. 95(1):45-54. [Medline].

  40. Arnow PM, Hierholzer JC, Higbee J. Acute hemorrhagic conjunctivitis: A mixed virus outbreak among Vietnamese refugees on Guam. Am J Epidemiol. 1977. 105:69.

  41. Jacobson LM, Redd JT, Schneider E, et al. Outbreak of lower respiratory tract illness associated with human enterovirus 68 among American Indian children. Pediatr Infect Dis J. 2012 Mar. 31(3):309-12. [Medline].

  42. Marier R, Rodriguez W, Chloupek RJ, Brandt CD, Kim HW, Baltimore RS. Coxsackievirus B5 infection and aseptic meningitis in neonates and children. Am J Dis Child. 1975 Mar. 129(3):321-5. [Medline].

  43. Berlin LE, Rorabaugh ML, Heldrich F, Roberts K, Doran T, Modlin JF. Aseptic meningitis in infants < 2 years of age: diagnosis and etiology. J Infect Dis. 1993 Oct. 168(4):888-92. [Medline].

  44. Huang CC, Liu CC, Chang YC, Chen CY, Wang ST, Yeh TF. Neurologic complications in children with enterovirus 71 infection. N Engl J Med. 1999 Sep 23. 341(13):936-42. [Medline].

  45. Cherry JL, Soriano F, Jahn CL. Search for perinatal enterovirus infection. Am J Dis Child. Sept/1968. 116(3):245-50.

  46. Lukashev AN, Koroleva GA, Lashkevich VA, Mikhailov MI. [Enterovirus 71: epidemiology and diagnostics]. Zh Mikrobiol Epidemiol Immunobiol. 2009 May-Jun. 110-6. [Medline].

  47. Fowlkes AL, Honarmand S, Glaser C, et al. Enterovirus-associated encephalitis in the California encephalitis project, 1998-2005. J Infect Dis. 2008 Dec 1. 198(11):1685-91. [Medline].

  48. Roden VJ, Cantor HE, O'Connor DM, Schmidt RR, Cherry JD. Acute hemiphegia of childhood associated with Coxsackie A9 viral infection. J Pediatr. 1975 Jan. 86(1):56-8. [Medline].

  49. Whitley RJ, Cobbs CG, Alford CA Jr, et al. Diseases that mimic herpes simplex encephalitis. Diagnosis, presentation, and outcome. NIAD Collaborative Antiviral Study Group. JAMA. 1989 Jul 14. 262(2):234-9. [Medline].

  50. Barak Y, Schwartz JF. Acute transverse myelitis associated with ECHO type 5 infection. Am J Dis Child. 1988 Feb. 142(2):128. [Medline].

  51. Rotbart HA, Brennan PJ, Fife KH, et al. Enterovirus meningitis in adults. Clin Infect Dis. 1998 Oct. 27(4):896-8. [Medline].

  52. Mathes EF, Oza V, Frieden IJ, et al. "Eczema coxsackium" and unusual cutaneous findings in an enterovirus outbreak. Pediatrics. 2013 Jul. 132(1):e149-57. [Medline].

  53. Begier EM, Oberste MS, Landry ML, et al. An outbreak of concurrent echovirus 30 and coxsackievirus A1 infections associated with sea swimming among a group of travelers to Mexico. Clin Infect Dis. 2008 Sep 1. 47(5):616-23. [Medline].

  54. Chung WH, Shih SR, Chang CF, et al. Clinicopathologic Analysis of Coxsackievirus A6 New Variant Induced Widespread Mucocutaneous Bullous Reactions Mimicking Severe Cutaneous Adverse Reactions. J Infect Dis. 2013 Aug 30. [Medline].

  55. Pozzetto B, Gaudin OG, Aouni M, Ros A. Comparative evaluation of immunoglobulin M neutralizing antibody response in acute-phase sera and virus isolation for the routine diagnosis of enterovirus infection. J Clin Microbiol. 1989 Apr. 27(4):705-8. [Medline]. [Full Text].

  56. Trabelsi A, Grattard F, Nejmeddine M, Aouni M, Bourlet T, Pozzetto B. Evaluation of an enterovirus group-specific anti-VP1 monoclonal antibody, 5-D8/1, in comparison with neutralization and PCR for rapid identification of enteroviruses in cell culture. J Clin Microbiol. 1995 Sep. 33(9):2454-7. [Medline]. [Full Text].

  57. Rotbart HA, Sawyer MH, Fast S, 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].

  58. Halonen P, Rocha E, Hierholzer J, et al. Detection of enteroviruses and rhinoviruses in clinical specimens by PCR and liquid-phase hybridization. J Clin Microbiol. 1995 Mar. 33(3):648-53. [Medline].

  59. Archimbaud C, Chambon M, Bailly JL, et al. Impact of rapid enterovirus molecular diagnosis on the management of infants, children, and adults with aseptic meningitis. J Med Virol. 2009 Jan. 81(1):42-8. [Medline].

  60. Xiao XL, Wu H, Li YJ, et al. Simultaneous detection of enterovirus 70 and coxsackievirus A24 variant by multiplex real-time RT-PCR using an internal control. J Virol Methods. 2009 Jul. 159(1):23-8. [Medline].

  61. Avner E, Satz J, Plotkin SA. Hypoglycorrhachia in young infants with viral meningitis. J Pediatr. 1975. 87:883.

  62. Garg A, Shiau J, Guyatt G. The ineffectiveness of immunosuppressive therapy in lymphocytic myocarditis: an overview. Ann Intern Med. 1998 Aug 15. 129(4):317-22. [Medline].

  63. Goland S, Czer LS, Siegel RJ, et al. Intravenous immunoglobulin treatment for acute fulminant inflammatory cardiomyopathy: series of six patients and review of literature. Can J Cardiol. 2008 Jul. 24(7):571-4. [Medline]. [Full Text].

  64. Rotbart HA, Webster AD. Treatment of potentially life-threatening enterovirus infections with pleconaril. Clin Infect Dis. 2001 Jan 15. 32(2):228-35. [Medline].

  65. Mason JW, O'Connell JB, Herskowitz A, et al. A clinical trial of immunosuppressive therapy for myocarditis. The Myocarditis Treatment Trial Investigators. N Engl J Med. 1995 Aug 3. 333(5):269-75. [Medline].

  66. Brunetti L, DeSantis ER. Treatment of viral myocarditis caused by coxsackievirus B. Am J Health Syst Pharm. 2008 Jan 15. 65(2):132-7. [Medline].

  67. Kew O, Morris-Glasgow V, Landaverde M, et al. Outbreak of poliomyelitis in Hispaniola associated with circulating type 1 vaccine-derived poliovirus. Science. 2002 Apr 12. 296(5566):356-9. [Medline].

  68. Combined immunization of infants with oral and inactivated poliovirus vaccines: results of a randomized trial in The Gambia, Oman, and Thailand. WHO Collaborative Study Group on Oral and Inactivated Poliovirus Vaccines. J Infect Dis. 1997 Feb. 175 Suppl 1:S215-27. [Medline].

  69. Sutter RW, John TJ, Jain H, et al. Immunogenicity of bivalent types 1 and 3 oral poliovirus vaccine: a randomised, double-blind, controlled trial. Lancet. 2010 Nov 13. 376(9753):1682-8. [Medline].

  70. Wadia NH, Katrak SM, Misra VP, et al. Polio-like motor paralysis associated with acute hemorrhagic conjunctivitis in an outbreak in 1981 in Bombay, India: clinical and serologic studies. J Infect Dis. 1983 Apr. 147(4):660-8. [Medline].

  71. McKinney RE Jr, Katz SL, Wilfert CM. Chronic enteroviral meningoencephalitis in agammaglobulinemic patients. Rev Infect Dis. 1987 Mar-Apr. 9(2):334-56. [Medline].

  72. Hyoty H. Enterovirus infections and type 1 diabetes. Ann Med. 2002. 34(3):138-47. [Medline].

  73. Richer MJ, Horwitz MS. Coxsackievirus infection as an environmental factor in the etiology of type 1 diabetes. Autoimmun Rev. 2009 Jun. 8(7):611-5. [Medline].

  74. Galama JM, de Leeuw N, Wittebol S, Peters H, Melchers WJ. Prolonged enteroviral infection in a patient who developed pericarditis and heart failure after bone marrow transplantation. Clin Infect Dis. 1996 Jun. 22(6):1004-8. [Medline].

  75. Chakrabarti S, Osman H, Collingham KE, Fegan CD, Milligan DW. Enterovirus infections following T-cell depleted allogeneic transplants in adults. Bone Marrow Transplant. 2004 Feb. 33(4):425-30. [Medline].

  76. American Academy of Neurology. Mysterious Polio-Like Illness Found in Five California Children. Available at Accessed: February 26, 2014.

  77. Anderson P. Polio-Like Syndrome Surfaces in California. Available at Accessed: February 26, 2014.

  78. Barnard DL. Current status of anti-picornavirus therapies. Curr Pharm Des. 2006. 12(11):1379-90. [Medline].

  79. Desmond RA, Accortt NA, Talley L, Villano SA, Soong SJ, Whitley RJ. Enteroviral meningitis: natural history and outcome of pleconaril therapy. Antimicrob Agents Chemother. 2006 Jul. 50(7):2409-14. [Medline].

  80. Honeyman M. How robust is the evidence for viruses in the induction of type 1 diabetes?. Curr Opin Immunol. 2005 Dec. 17(6):616-23. [Medline].

  81. Huang YC, Chu YH, Yen TY, et al. Clinical features and phylogenetic analysis of Coxsackievirus A9 in Northern Taiwan in 2011. BMC Infect Dis. 2013 Jan 24. 13:33. [Medline]. [Full Text].

  82. Melnick JL. Enteroviruses: polioviruses, coxsackieviruses, echoviruses, and newer enteroviruses. Fields Virology. 3rd ed. Philadelphia, Pa: Lippincott-Raven; 1996. 655-712.

  83. Modlin JF. Introduction to Enteroviruses. Mandell GL, Bennett JE, Dolin R, eds. Principles and Practice of Infectious Diseases. 6th ed. Churchill Livingstone: New York; 2005.

  84. Pesonen E, Andsberg E, Ohlin H, Puolakkainen M, Rautelin H, Sarna S. Dual role of infections as risk factors for coronary heart disease. Atherosclerosis. 2007 Jun. 192(2):370-5. [Medline].

  85. Racaniello VR. One hundred years of poliovirus pathogenesis. Virology. 2006 Jan 5. 344(1):9-16. [Medline].

  86. Skarsvik S, Puranen J, Honkanen J, Roivainen M, Ilonen J, Holmberg H. Decreased in vitro type 1 immune response against coxsackie virus B4 in children with type 1 diabetes. Diabetes. 2006 Apr. 55(4):996-1003. [Medline].

  87. Webster AD. Pleconaril--an advance in the treatment of enteroviral infection in immuno-compromised patients. J Clin Virol. 2005 Jan. 32(1):1-6. [Medline].

  88. WHO. Resurgence of wild poliovirus type 1 transmission and effect of importation into polio-free countries, 2002-2005. Wkly Epidemiol Rec. 2006 Feb 17. 81(7):63-8. [Medline].

All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.