eMedicine Specialties > Pediatrics: General Medicine > Infectious Disease
Enteroviral Infections
Updated: Jun 5, 2009
Introduction
Background
Enteroviruses, a group of single-stranded sense RNA viruses, are commonly encountered infections, especially in infants and children. They are responsible for a myriad of clinical syndromes, including hand-foot-and-mouth (HFM) disease, herpangina, myocarditis, aseptic meningitis, and pleurodynia.
Patients with enterovirus infections may present with symptoms as benign as an uncomplicated summer cold or as threatening as encephalitis, myocarditis, or neonatal sepsis. Enteroviral infections annually result in a large number of physician and emergency department visits. In 1998, Pichichero et al performed a prospective study and found that nonpolio enteroviral infections resulted in direct medical costs ranging from $69-771 per case.1 In addition, patients with nonpolio enteroviral infections missed a minimum of 1 day of school or camp; some missed as many as 3 days of school or camp. The significant economic and medical impacts of enteroviral infections occur mostly during the peak months of summer and fall. In temperate climates, enteroviral outbreaks occur year-round.
Enteroviruses belong to the Picornaviridae (small RNA viruses) family. The enteroviral group includes coxsackievirus, echovirus, and poliovirus. Enteroviruses are believed to have 2 distinct classes: polioviruses (types 1, 2, and 3) and nonpolioviruses (coxsackievirus, enterovirus, echoviruses, and unclassified enteroviruses). Enteroviral infections consist of 23 coxsackievirus A, 6 coxsackievirus B, 28 echovirus, and 5 unclassified enteroviruses.
More recently, a related genus of viruses, Parechovirus, has been described; two enterovirus species (echovirus types 22 and 23) were reassigned as parechovirus.2 To date, more than a dozen parechovirus strains have been described; however, not all sequences have been published. The clinical appearance of Parechovirus infection can be similar to enteroviral infections, but tests for Parechovirus are mostly confined to research laboratories.
Enterovirus 71 has gained notoriety in recent years for causing a rapidly fatal rhombencephalitis, in association with epidemics of HFM disease in East Asian countries. This appears to be a particularly aggressive neutrophic serotype of enterovirus.
Each virus obtains its antigenicity from the capsid proteins that surround the RNA core. According to the Centers for Disease Control and Prevention (CDC), 65 human serotypes of enteroviruses have been identified; however, a small number cause most outbreaks. Since the implementation of polio vaccines, the incidence of wild-type polio has been eradicated in the western hemisphere.
The most common form of human transmission is the fecal-to-oral route. Although respiratory and oral-to-oral routes are possible, they are more likely to occur in crowded living conditions. Enteroviruses are quite resilient. They remain viable at room temperature for several days and can survive the acidic pH of the human GI tract. The incubation period is usually 3-10 days.
Pathophysiology
The enterovirus enters the human host through the GI or respiratory tract. The cell surfaces of the GI tract serve as viral receptors, and initial replication begins in the local lymphatic GI tissue. The virus seeds into the bloodstream, causing a minor viremia on the third day of infection. The virus then invades organ systems, causing a second viremic episode on days 3-7. This second viremic episode is consistent with the biphasic prodromal illness. The infection can progress to CNS involvement during the major viremic phase or at a later time. Antibody production in response to enteroviral infections occurs within the first 7-10 days.
Coxsackievirus notoriously replicates in the pharynx (herpangina), the skin (HFM disease), the myocardium (myocarditis), and the meninges (aseptic meningitis). It can also involve the adrenal glands, pancreas, liver, pleura, and lung.
Echovirus can replicate in the liver (hepatic necrosis), the myocardium, the skin (viral exanthems), the meninges (aseptic meningitis), the lungs, and the adrenal glands.
After exposure, poliovirus replicates in the oropharynx and GI tissue. Following this replication, polio advances, invading the motor neurons of the anterior horn cells of the spinal cord. It can progress to other CNS regions, including the motor cortex, cerebellum, thalamus, hypothalamus, midbrain, and medulla, causing death of neurons and paralysis. Neuropathy occurs due to direct cellular destruction. Antibody production occurs in the lymphatic system of the GI tract, prior to invasion of the CNS tissue. Infants retain transplacental immunity for the first 4-6 months of life.
The enteroviruses are capable of directing almost all cellular protein translation to viral genes through the modification of host cell translation factors (messenger RNA [mRNA] cap-binding proteins) and using internal ribosome entry sites (IRES) to bypass the crippled host machinery. As such, they are highly damaging to the cells they infect.
Frequency
United States
Nonpolio enteroviral infections cause an estimated 10-15 million symptomatic infections per year in the United States. Many are treated as potential episodes of sepsis, and antibiotics and acyclovir are administered to treat possible bacterial or herpetic infection.
In 1952, an epidemic of polio occurred in the United States, causing 3,000 deaths and 57,879 cases. The vaccine has virtually eliminated wild-type polio in the United States. In 1994, the World Health Organization (WHO) declared the eradication of wild polio in the Western hemisphere. Approximately 6 cases of vaccine-associated paralytic polio (VAPP) occur yearly, leading to the recommendation of inactivated vaccine because the risk of natural disease is so rare in the United States. VAPP is linked to the concomitant administration of live (oral) polio vaccine with intramuscular injections (perhaps allowing the virus better access to myocytes and neuronal axons) and occurs in 1 per 2-4 million vaccinations (paralytic polio occurs in 1 in 200 wild-type infections).
In 1979, an outbreak occurred in numerous Amish communities throughout the United States. A smaller outbreak occurred in 2005 in an Amish community in Minnesota. Genetic sequencing of the virus surprisingly revealed that it was only 2.3% different from the Sabin vaccine strain and was likely acquired from subclinical circulating infections from overseas.
International
Nonpolio enteroviral infections are quite prevalent worldwide. The exact numbers are unavailable.
Poliomyelitis still occurs in many developing countries as a result of poor health care and an inability to access vaccines. The CDC reported 6227 cases in 1998.3 This significant drop from the previous decade, in which 35,251 cases were reported, is due to aggressive vaccination programs. Worldwide eradication is hoped to occur in the near future.
Recently, setbacks have been noted in Nigeria, where suspicion about the motivations of the vaccination program led to a refusal to vaccinate children. One outbreak in 2003 crossed 15 other African countries and even spread as far as Indonesia, resulting in the paralysis of over 200 children. A more recent outbreak in 2006 affected mostly adults who were missed by vaccination campaigns. As of June 2006, 7 people had died and 27 people had been paralyzed. Nigeria had about half of the reported polio infections in the first 3 months of 2009. The data below suggests that the outbreak continues.
Worldwide polio cases from January-March 2009 are reported as follows:4
- Nigeria (endemic) – 51 (801 cases in 2008)
- India (endemic) – 17 (559 cases in 2008)
- Democratic Republic of Congo (importation) – 0 (5 cases in 2008)
- Pakistan (endemic) – 8 (118 cases in 2008)
- Niger (importation) - 3 (12 cases in 2008)
- Afghanistan (endemic) - 4 (31 cases in 2008)
- Angola (importation) - 1 (29 cases in 2008)
- Ethiopia (importation) - 0 (3 cases in 2008)
- Chad (importation) – 0 (37 case in 2008)
- Kenya (importation) - 2 (0 cases in 2008)
- Nepal (importation) - 0 (6 cases in 2008)
- Uganda (importation) - 3 (0 cases in 2008)
- Sudan (importation) - 11 (26 cases in 2008)
- Togo (importation) - 3 (3 cases in 2008)
- Benin (importation ) - 2 (6 cases in 2008)
- Burkina Faso (importation) - 4 (6 cases in 2008)
- Mali (importation) - 1 (1 case in 2008)
- Côte d'Ivoire (importation) - 0 (1 case in 2008)
- Ghana (importation) - 0 (8 cases in 2008)
Some genetic evidence suggests that if the poliovirus is eradicated, genetic recombination between other enteroviruses may result in a phenotypically similar virus. However, this appears to be of academic interest only at this time.
Mortality/Morbidity
The overall mortality rate for nonpolio viruses is extremely low. The patients at greatest risk are those with neonatal sepsis.
Occasionally, enteroviruses cause global encephalitis, which has a good prognosis; however, a few fatalities have been reported. Enterovirus 71 has been linked with a rhombencephalitis (inflammation of the brain stem) in outbreaks of hand-foot-and-mouth disease in the eastern hemisphere (Taiwan, Japan, Malaysia, and Australia). Fatality rates from these outbreaks have been as high as 14%. Myoclonus is a poor prognostic indicator, as are lethargy, persistent fever, and peak temperature higher than 38.5 º C.5
Most cases of myocarditis and pericarditis are self-limited, but a potentially significant mortality rate is associated with myocarditis. Older patients can develop a dilated cardiomyopathy following myocarditis.
The overall mortality rate for paralytic polio is 2-10%. For those who survive, a 6-month period is allowed to predict how much muscle function will return.
Race
Enteroviruses have a worldwide distribution and are not race-specific infections.
Sex
Males and females are equally affected. Males are more likely to be symptomatic.
Age
People of all ages, including adults, elderly people, and young people, are at risk of manifesting symptoms of enteroviruses. Children have a higher rate of infection because of exposure, hygiene, and immunity status. The infection course tends to be benign in older children and more serious in neonates. Unlike most cases of nonpolio enteroviral infections, acute hemorrhagic conjunctivitis occurs most frequently in adults aged 20-50 years.
Clinical
History
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 (HFM) disease that are associated with a serious rhombencephalitis, with significant mortality.
- 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.
Physical
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.
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.
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.
- 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.
- 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.
- 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.
Causes
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.
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Further Reading
Keywords
enteroviral infections, enterovirus, poliovirus, echovirus, coxsackie virus, coxsackievirus, oral polio vaccine, OPV, inactivated polio vaccine, IPV, hand-foot-and-mouth disease, HFM, herpangina, myocarditis, pleurodynia, aseptic meningitis, neonatal sepsis, viremia, biphasic prodromal illness, hepatic necrosis, viral exanthems, vaccine-associated paralytic polio, VAPP, Sabin vaccine, monovalent oral polio vaccine, mOPV, global encephalitis, rhombencephalitis, myoclonus, acute hemorrhagic conjunctivitis, myalgia, orchitis, epididymitis, meningococcemia, neurogenic pulmonary edema, pleurodynia, Bornholm disease, devil’s grippe, bulbar poliomyelitis, auscultatory fiction rub, Hamman crunch, coryza, X-linked agammaglobulinemia, Guillain-Barré syndrome, treatment, diagnosis
