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Enteroviruses include
Enteroviruses, along with rhinoviruses (see Respiratory Viruses: Common Cold) and human parechoviruses, are picornaviruses (pico, or small, RNA viruses). Human parechoviruses types 1 and 2 were previously named echovirus 22 and 23 but have now been reclassified. All enteroviruses are antigenically heterogeneous and have wide geographic distribution.
Enteroviruses are shed in respiratory secretions and stool and sometimes are present in the blood and CSF of infected patients. Infection is usually transmitted by direct contact with respiratory secretions or stool but can be transmitted by contaminated environmental sources (eg, water). Enteroviral diseases or epidemics in the US occur in summer and fall. Infection transmitted by a mother during delivery can cause severe disseminated neonatal infection, which may include hepatitis or hepatic necrosis, meningoencephalitis, myocarditis, or a combination.
Intact humoral immunity and B-cell function are required for control of enteroviral disease. Severe enteroviral infections (often manifesting as a slowly progressive meningoencephalitis) occur in patients with agammaglobulinemia but usually not in those with other immune deficiencies.
Diseases Caused by Enteroviruses
Enteroviruses cause various syndromes (see Table 1: Enteroviruses: Syndromes Caused by Enteroviruses ). Epidemic pleurodynia, hand-foot-and-mouth disease, herpangina, and poliomyelitis are caused almost exclusively by enteroviruses. Other disorders (eg, aseptic meningitis, myopericarditis) may be caused by enteroviruses or other organisms.
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Table 1
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| Syndromes Caused by Enteroviruses |
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Syndrome
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Serotypes Most Often Implicated
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Aseptic meningitis
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Coxsackieviruses A2, 4, 7, 9, and others and B2–5
Poliovirus types 1–3
Echoviruses 4, 6, 7, 9, 11, and others
Human parechoviruses 1 and 2
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Aseptic meningitis with rash
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Coxsackieviruses A9 and B4
Echoviruses 4 and 16
Enterovirus 71
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Conjunctivitis (hemorrhagic)
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Enterovirus 70
Coxsackievirus A24
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Epidemic pleurodynia (Bornholm disease)
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Coxsackieviruses B1–6
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Hand-foot-and-mouth disease
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Coxsackieviruses A9, 16, and others
Coxsackieviruses B2–5
Enterovirus 71
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Herpangina
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Coxsackieviruses A2, 4–6, 8, and 10
Probably coxsackieviruses B3 and others
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Myopericarditis
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Coxsackieviruses A4 and 16 and B1–5
Echoviruses 9 and 22
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Paralysis
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Polioviruses 1–3
Coxsackieviruses A7 and others
Echoviruses 4, 6, 9, and others
Enterovirus 71
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Rash
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Coxsackieviruses A9 and B1, 3, 4, and 5 (also implicated, A4–6 and 16)
Echoviruses 9 and 16 (also implicated 2, 4, 11, 14, 19, and 25)
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Respiratory disease
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Echoviruses 4, 8, 9, 11, 20, and others
Coxsackieviruses A21 and 24 and B1 and 3–5
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Aseptic meningitis:
Aseptic meningitis is most common among infants and children. In infants and young children, the cause is frequently a group A or B coxsackievirus, an echovirus, or a human parechovirus. In older children and adults, other enteroviruses as well as other viruses may cause aseptic meningitis.
The course is usually benign. A rash may accompany enteroviral aseptic meningitis. Rarely, encephalitis, which may be severe, also occurs.
Although rarely clinically necessary, the causative virus can often be isolated in a sample from the throat, stool, or CSF or be identified by reverse transcriptase–PCR.
Hemorrhagic conjunctivitis:
Rarely, this disorder occurs in epidemics in the US. Importation of the virus from Africa, Asia, Mexico, and the Caribbean may make outbreaks more common.
The eyelids rapidly swell. Hemorrhagic conjunctivitis, unlike uncomplicated conjunctivitis, often leads to subconjunctival hemorrhages or keratitis, causing pain, tearing, and photophobia. Systemic illness is uncommon. However, when hemorrhagic conjunctivitis is due to enterovirus 70, transient lumbosacral radiculomyelopathy or poliomyelitis-like illness (with paralysis) can occur but is rare. Recovery is usually complete within 1 to 2 wk of onset.
Coxsackievirus A24 also causes hemorrhagic conjunctivitis, but subconjunctival hemorrhage is less frequent, and neurologic complications have not been described. Most patients recover in 1 to 2 wk.
Myopericarditis:
Cardiac infection may occur at any age, but most patients are 20 to 39 yr old. Patients may present with chest pain, arrhythmias, or heart failure. Recovery is usually complete, but some patients develop dilated cardiomyopathy. Diagnosis may require PCR of myocardial tissue.
Myocarditis neonatorum (cardiac infection at birth) is caused by group B coxsackieviruses and some echoviruses. It causes fever and heart failure and has a high mortality rate.
Neonatal infection:
Usually, several days after birth, the neonate suddenly develops a syndrome resembling sepsis with fever, lethargy, disseminated intravascular coagulation, bleeding, and multiple organ (including heart) failure. CNS, hepatic, myocardial, pancreatic, or adrenal lesions may occur simultaneously. Recovery may occur within a few weeks, but death may result from circulatory collapse or, if the liver is involved, liver failure.
Rashes:
Certain coxsackieviruses and echoviruses may cause rashes, often during epidemics. Rashes are usually nonpruritic, do not desquamate, and occur on the face, neck, chest, and extremities. They are sometimes maculopapular or morbilliform but occasionally hemorrhagic, petechial, or vesicular. Fever is common. Aseptic meningitis may develop simultaneously. The course is usually benign.
Respiratory infections:
These infections may result from enteroviruses. Symptoms include fever, coryza, pharyngitis, and, in some infants and children, vomiting and diarrhea. Bronchitis and interstitial pneumonia occasionally occur in adults and children. The course is usually mild.
Diagnosis
Diagnosis of enteroviral diseases is clinical. Laboratory diagnosis is usually unnecessary but can often be made by culturing the virus, by detecting viral RNA using reverse transcriptase–PCR or, less commonly, by demonstrating seroconversion. Enteroviruses that cause aseptic meningitis can be cultured in a sample from the throat, stool, blood, or CSF.
Treatment
Treatment of enteroviral disease is supportive. Patients with agammaglobulinemia are treated with IV immune globulins with variable success.
Last full review/revision December 2009 by Mary T. Caserta, MD
Content last modified February 2012
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