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 1). 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. Poliovirus, the prototypical enterovirus, can cause a subclinical or mild illness, aseptic meningitis, or paralytic poliomyelitis. Non-polio enteroviruses (group A and B coxsackieviruses, echoviruses, enteroviruses) cause about 10 to 15 million infections and tens of thousands of hospitalizations each year in the United States and are more prevalent among children of lower socioeconomic class, probably because of crowding, poor hygiene, and opportunities for fecal contamination 2). Most people who get infected with non-polio enteroviruses do not get sick or they only have mild illness, like the common cold. But some people can have serious complications, especially infants and people with weakened immune systems.

Between 2002 and 2004, echoviruses 9 and 30 were the most commonly reported enterovirus serotypes in the United States. 3). 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 4). However, difficulty in isolation of enterovirus 68 (EV68, EV-D68, EVD-68, HEV68) may bias the data, leading to an underestimation of its prevalence 5).

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 6). From mid-August to September 11, 2014, 82 cases of enterovirus 68 infection had been confirmed by the Centers for Disease Control and Prevention (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 7). It is probable that there were different EV-D68 strains in China and America with mutations accounting for different prevalence 8). Foster et al 9) have suggested that DV-68 infection may act as a trigger for childhood asthma.

Coxsackievirus A is likely underrepresented because only some serotypes are readily isolated in cell culture 10).

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 transmitted predominantly via the fecal-oral route. However, there are some exceptions, including coxsackievirus A21, which is spread mainly by respiratory secretions 11) and enterovirus 70, which is shed in tears and spread via fingers and fomites (objects or materials which are likely to carry infection, such as clothes, utensils, and furniture) 12).

Upon entry into the oropharynx, the virus replicates in submucosal tissues of the distal pharynx and alimentary tract 13). Enteroviruses 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) 14).

Dissemination to target organs follows, and viral replication in target organs produces the major viremia with possible secondary seeding of the central nervous system (CNS). Potential target organs include the skin and CNS (central nervous system). 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 15).

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 16).

Human enteroviruses 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 central nervous system (CNS) infections in neonates and immunocompromised hosts, with mixed results 17)
  • Abortive and nonparalytic polio can be managed at home, but patients with paralytic polio require hospitalization

Enterovirus causes

Enteroviruses cause a wide range of infections. The most common mode of transmission of enteroviruses is via the fecal-oral route. Poor sanitation, low socioeconomic status, and crowded living conditions all facilitate the spread of infection. Direct contact with feces occurs with activities such as diaper changing. Indirect transmission due to poor sanitary conditions may occur via numerous routes, including via contaminated water, food, fingers, fomites, or contaminated ophthalmological instruments (eg, acute hemorrhagic conjunctivitis).

Respiratory-oral spread may also be the mode of transmission for coxsackievirus A21 and other coxsackievirus serotypes.

Transmission of enteroviruses has been described among travelers swimming in sewage-contaminated seawater 18).

Enteroviruses belong to the Picornaviridae family of viruses and are traditionally divided into 5 subgenera based on differences in host range and pathogenic potential 19). 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 20). 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 21).

Enteroviruses are inactivated by ionizing radiation, formaldehyde, and phenol.

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. Prior to the polio vaccine era, the mortality rate in polio epidemics was 5%-7%. The overall risk of oral polio vaccine (OPV)-related disease is estimated to be 1 case per 2.6 million doses of oral polio vaccine (OPV). The inactivated poliovirus vaccine (IPV) was incorporated into the routine polio vaccination in Europe and Canada in the 1980s. Inactivated poliovirus vaccine (IPV) has been used in the United States since 2000; oral polio vaccine (OPV) is no longer used in the United States. Despite the risk of oral polio vaccine (OPV)-related paralysis, it is still the preferred vaccine for global polio eradication in developing nations.

The nonpolio enteroviruses (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. More than 90% of infections caused by the nonpolio enteroviruses are asymptomatic or result in only an undifferentiated febrile illness 22).

Coxsackievirus infection is the most common cause of viral heart disease. 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 23).

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 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.

Human enterovirus 68 infection in children may produce a respiratory outbreak characterized by pneumonia and wheezing 24).

Polio enteroviruses

Disease due to wild-type poliovirus infection no longer occurs in the Western Hemisphere, and a World Health Organization (WHO) international eradication program is making significant progress in the rest of the world 25).

Non-polio enteroviruses

More than 90% of infections caused by the nonpolio enterovirus are asymptomatic or result only in an undifferentiated febrile illness 26).

Nonspecific febrile illness

This is the most common presentation of enterovirus infection.

More than 90% present with a nonspecific febrile illness that manifests as sudden fever (temperature, 101-104°F). The fever may last for as long as a week and may show a biphasic pattern 27).

Patients may also report myalgia, headache, sore throat, nausea, vomiting, mild abdominal discomfort, and diarrhea.

Pleurodynia (Bornholm disease, devil’s grippe)

Group B coxsackieviruses, particularly B3 and B5, are the most important causes of epidemic pleurodynia. Multiple family members may be affected 28).

Pleurodynia manifestations include a sudden onset of fever accompanied by muscular pain in the chest and abdomen 29). The pain is spasmodic in nature, with spasms lasting 15-30 minutes and worsening during inspiration or coughing. This paroxysmal pain is characteristically associated with fever, peaking within 1 hour after onset of each paroxysm and subsiding with the subsequent paroxysm. Headache, nausea, and vomiting are also frequently reported.


Enteroviruses appear to be the most common viral cause of myopericarditis and account for at least half of all cases of acute myopericarditis.

Neonatal infections typically develop within the first week of life, and involvement is predominantly myocardial. In contrast, older children and adults usually present with symptoms of pericarditis.

The typical presentation in adolescents and adults is shortness of breath, chest pain, and fever 1-2 weeks following an upper respiratory tract infection. Chest pain may be dull or sharp; it is worsened by inspiration and may improve with sitting and leaning forward. It can be differentiated from angina by lack of response to nitroglycerin.

Enteroviral myocarditis can present as acute myocardial infarction associated with arrhythmias and heart failure. Some patients with myocardial infarction who have normal findings on coronary angiographic studies have been shown to have myocarditis by radiolabeled antimyosin antibody cardiac scanning 30).

Acute hemorrhagic conjunctivitis

This highly contagious ocular infection can cause large-scale epidemics. Acute hemorrhagic conjunctivitis was first described in 1969. Enterovirus 70 is the most common etiology in epidemics. Coxsackievirus A24 causes a similar disease. Acute hemorrhagic conjunctivitis was initially recognized in Ghana and Indonesia and is now epidemic in India and the Far East 31).

The first reported outbreak of acute hemorrhagic conjunctivitis in United States was Key West, Florida, in 1981; subsequently, 2,500 cases were reported in Miami. Since then, with the exception of few imported cases, acute hemorrhagic conjunctivitis activity has not been reported in the United States 32).

The mode of transmission is from finger or fomite to eye. Acute hemorrhagic conjunctivitis is highly contagious, and crowding and unsanitary conditions favor spread. Reuse of water for bathing and sharing of towels have been implicated as factors contributing to the spread of infection 33).

Onset is abrupt, and the most common symptoms include ocular pain and burning, swelling of the eyelids, and the sensation of a foreign body in the eye. Patients may also experience photophobia and watery discharge. The other eye becomes involved within hours of the first eye.

Nonspecific symptoms such as fever, malaise, and headache may be present. The symptoms typically improve by the second or third day of infection, and recovery is complete within 7-10 days.

Aseptic meningitis

Enteroviral infections (group B coxsackievirus and echovirus) account for 90% of cases of aseptic meningitis in patients younger than one year and 50% of cases in older children and adults 34).

The clinical presentations of aseptic meningitis vary greatly. Prodromal symptoms include fever, chills, headache, photophobia, and nuchal rigidity. Rash and upper respiratory tract symptoms may also occur. In infants, fever and irritability are the most common symptoms 35).

Fever and meningeal signs subside within 2-7 days.

Enterovirus 71, which causes hand-foot-and-mouth disease, has also been associated with a particularly more aggressive and, in some instances, fatal CNS infection in children. It manifests as flaccid motor paralysis and brain stem encephalitis. Large outbreaks were reported in the late 1990s in Eastern Europe, Russia, Thailand, and Taiwan 36).

Most of the enterovirus-positive 758 children in a Korean outbreak experienced fever, headache, vomiting, and neck stiffness, although some also showed cold symptoms, sore throat, altered mental status, and seizures 37). More than 80% of these had either echovirus types 6 or 30. The majority recovered uneventfully.


Coxsackie A virus is the main etiologic agent of herpangina, described as a vesicular enanthem of the tonsillar fauces and soft palate that principally affects children aged 3-10 years 38). Other serotypes have been isolated including enterovirus 71 (EV71), which has cause recent outbreaks and epidemics in South-East Asia 39).

Symptoms include sudden onset of fever, sore throat, and difficulty swallowing, followed a day later by a painful vesicular eruption of the oral mucosa. The posterior pharynx and tonsils may also be involved. Most disease occurs in the summer.

Patients may report anorexia, malaise, irritability, headache, backache, and diarrhea. Symptoms resolve in 3-4 days.

Hand-foot-and-mouth disease

This is mainly a disease of children; most patients are younger than 10 years. Epidemics of hand-foot-and-mouth disease occur approximately every 3 years.

Coxsackievirus A16 is the most common etiologic agent, although enterovirus 71 and numerous other coxsackievirus serotypes may also cause the disease 40).

Following an incubation period of 3-6 days, patients experience prodromal symptoms such as fever, cough, sore throat, malaise, and anorexia. The prodrome lasts from 12-36 hours; afterward, vesicular eruptions of the hands, feet, and oral cavity develop. This may cause decreased oral intake in young children. The lesions self-resolve within 5-7 days.

Infection with enterovirus 71 may be accompanied by severe neurologic disease including encephalitis, meningitis, and poliolike paralysis 41).


Frank encephalitis is an unusual manifestation of enterovirus infection 42).

Echovirus 9 is the most common etiologic agent.

Clinical manifestations have ranged from lethargy, drowsiness, and personality change to seizures, paresis, and coma. Children with focal encephalitis present with partial motor seizures, hemichorea, and acute cerebellar ataxia; this may mimic herpes simplex encephalitis 43).

Nonpoliovirus paralytic disease

Enterovirus 71 and coxsackievirus A7 have been associated with large outbreaks of poliomyelitislike disease in Russia, Eastern Europe, Thailand, and Taiwan 44). Some cases have manifested as brainstem encephalitis or noncardiogenic pulmonary edema, with some having a fatal course.

Paralytic disease caused by nonpolioviruses other than enterovirus 71 is usually less severe and is associated with paralysis. It manifests as muscle weakness and complete unilateral oculomotor palsy.

Guillain-Barré syndrome and transverse myelitis has been reported in a small number of patients infected with coxsackievirus serotypes A2, A5, A9, and B4 and with echovirus serotypes 5, 6, and 22 45).

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 46).

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 47). 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 48).

Immunoglobulin M (IgM) antibodies appear as early as 1-3 days after enteroviral challenge and disappear after 2-3 months 49).

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 50).

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 51).

Enterovirus symptoms

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

Polio enterovirus

Disease due to wild-type poliovirus infection no longer occurs in the Western Hemisphere, and a World Health Organization (WHO) international eradication program is making significant progress in the rest of the world 52).

Patients with abortive polio present with symptoms similar to those of other viral infections, including 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.

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

Paralytic polio presents similarly to nonparalytic polio. It 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. Exercise increases the severity of paralytic polio, especially during the first 3 days of the major illness. Intramuscular injections or skeletal muscle injury predisposes to localization of polio to that extremity (termed provocation poliomyelitis).

  • 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

Non-polio enteroviruses

More than 90% of infections caused by nonpolio enteroviruses are asymptomatic or result only in an undifferentiated febrile illness 53). Symptomatic nonpolio enterovirus infections include the following:

  • Pleurodynia
  • Myopericarditis
  • Acute hemorrhagic conjunctivitis
  • Nonspecific febrile illness
  • Aseptic meningitis
  • Herpangina
  • Hand-foot-and-mouth disease
  • Encephalitis

Physical examination findings in enterovirus infection 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 54); 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 55)
  • Acute hemorrhagic conjunctivitis – The hallmark physical findings include ocular erythema and subconjunctival hemorrhage, which seems to be more profuse in young patients 56); 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 57)
  • Encephalitis – Manifestations range from lethargy, drowsiness, and personality change to seizures, paresis, coma, motor seizures, hemichorea, and acute cerebellar ataxia 58)
  • 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
  • Hand-foot-and-mouth disease – 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 59).
  • The coxsackievirus A6 (CVA6)–associated North American enterovirus outbreak of 2011-2012 was evaluated 60). Atypical hand-foot-and-mouth disease was noted as a vesiculobullous and erosive eruption, with 61% of patients having the rash involving more than 10% body surface area in a perioral, extremity, and truncal distribution in addition to palms, soles, and buttocks. In half the patients, there was an accentuation in areas of eczematous dermatitis. Other morphologic patterns included those of Gianotti-Crosti disease in 37% and petechial/purpuric eruptions in 17%.
  • Orchitis: In some remote cases, the presentation of coxsackievirus B infection clinically resembles mumps orchitis.

Enterovirus diagnosis

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 – cerebrospinal fluid (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 (cerebrospinal fluid)
  • In myopericarditis, chest radiography, echocardiography, and electrocardiogram (ECG) can be used for diagnosis


The microneutralization test is the most widely used method for detecting antibodies to enteroviruses. Serological examination reveals a 4-fold increase in antibodies to enteroviruses between the acute and convalescent phases of illness 61). This diagnostic modality is infrequently used since it is serotype-specific, relatively insensitive, poorly standardized, labor intensive, and too slow for clinical purposes.

Viral isolation

The virus can be isolated from CSF (cerebrospinal fluid), blood, or feces, depending on the site affected, and the yield is increased if multiple sites are sampled. Enterovirus produces a characteristic cytopathic effect in cultured cells. Poliovirus is easily cultured from stool and nasopharyngeal secretions, but isolation from the CSF is more difficult. The cytopathic effect is confirmed by indirect immunofluorescence using a broadly specific monoclonal antibody. The sensitivity of viral culture ranges from 60%-75% 62).

Polymerase chain reaction

This rapid test is highly sensitive and specific for detecting enteroviral RNA in CSF specimens, with a sensitivity of 100% and specificity of 97% 63). PCR provides rapid results and is the best diagnostic test for use in CSF but is limited by availability in some areas and cost in underdeveloped regions 64).

In 2008, a multiplex real-time PCR (RT-PCR) assay was developed for simultaneous detection, identification, and quantification of enterovirus 70 and a coxsackievirus A24 variant. The novel technique is used as a rapid diagnostic method to evaluate for enterovirus-related acute hemorrhagic conjunctivitis 65).

Cardiac enzyme levels

Cardiac enzyme levels may be elevated in persons with myopericarditis, indicating myocardial damage.

CSF analysis

The CSF profile in patients with aseptic meningitis usually reveals a mildly elevated white blood cell count, and the differential invariably shifts to a predominance of lymphocytes during the initial 1-2 days of illness. Glucose levels are normal or mildly decreased 66), while the protein level is normal or slightly increased.

Imaging studies

  • Chest radiography: In patients with myopericarditis, chest radiography may reveal cardiomegaly secondary to pericardial effusion or cardiac dilation. In pleurodynia, chest radiographic findings are normal.
  • Echocardiography: Transient wall motion abnormalities may be detectable in mild cases. Severe cases may demonstrate acute ventricular dilation and reduced ejection fraction.

Other tests

  • ECG (electrocardiogram): Nonspecific ST-T changes may be observed in persons with myopericarditis. Severe disease may cause Q waves, ventricular tachyarrhythmias, and heart block. ECG findings may demonstrate evolution through several stages of myopericarditis, as follows:
    • Stage I – Diffuse ST elevation with PR depression
    • Stage II – Normalization of ST and PR segments
    • Stage III – Deep symmetric inversion of T waves
    • Stage IV – May revert to normal or permanent T-wave inversions
  • Electroencephalography: This test may be useful for evaluating the extent and severity of illness in patients with encephalitis.

Ophthalmic slit-lamp examination: In persons with acute hemorrhagic conjunctivitis, corneal erosions may be visualized using a fluorescein stain. Enterovirus 70 and coxsackievirus A24 can often be recovered from conjunctival swabs during the first 3 days of infection.

Enterovirus treatment

Enterovirus treatment depends on the type of enterovirus infection and symptoms you have.


Polio management is supportive in nature, as follows:

  • Abortive polio: Treatment with bed rest and minimal exertion may be done at home. Supportive treatment with analgesics and sedatives may be used.
  • Nonparalytic polio: Management is similar to that of abortive polio. Combine analgesic therapy with hot packs for pain relief.
  • Paralytic polio: In contrast to abortive and nonparalytic polio, which can be managed at home, patients with paralytic polio require hospitalization.
  • Bed rest is required during the early stages of the disease because exertion may worsen the paralysis.
  • Applying hot packs to affected muscles may alleviate pain.
  • Align the body in a neutral position to minimize deformity. Patients should start physical therapy soon after the resolution of pain. Physical therapy should include both active and passive exercises.
  • Mechanical ventilation may be required if respiratory muscles are affected.
  • Postural drainage and suction should be implemented in mild bulbar polio.
  • Patients with weakness or paralysis of the bladder may be treated with cholinergic agents, the sound of running water, or catheterization.


  • Treatment is symptomatic, using analgesics and heat application for pain relief. Severe pain may require opiate analgesics.

Aseptic meningitis

  • Treatment is symptomatic, with analgesics for headache relief. Headache is often severe and prolonged in adults; potent analgesics should be administered, when necessary.


Treatment is mainly supportive in nature and involves management of pericardial pain, pericardial effusion, arrhythmias, and heart failure.

Bed rest is important since exercise can increase the degree of myocardial necrosis.

Intravenous immunoglobulin (IVIG) therapy has shown some benefit in small case-control studies. Nevertheless, most reports lack statistical significance, and randomized trials are needed 67).

Capsid-binding inhibitors belong to a class of drugs that have shown benefit in some immunosuppressed patients with myocarditis. However, these drugs are not available for use in the United States 68).

Corticosteroids yield little or no benefit, and immunosuppressive therapy is contraindicated during the acute phase of viral myocarditis because they have been shown to cause clinical deterioration 69).

Cardiac transplantation may be required in severe cases of dilated cardiomyopathy due to enteroviral infection.

Acute hemorrhagic conjunctivitis

Treatment is primarily symptomatic in nature.

Antimicrobial agents are not indicated unless bacterial superinfection occurs. Corticosteroids are contraindicated.

Cold compresses may be used, along with antihistamine/decongestant eye drops.

Herpangina and hand-foot-and-mouth disease

Symptomatic treatment for sore throat is the mainstay of treatment, including analgesics, topical anesthetics, mouth wash, and saline rinses.

Viscous lidocaine (2% solution) may be helpful.

References   [ + ]