Neurologic Complications in Children with Enterovirus 71 Infection
Update of Enterovirus Infection in Infants and Children
The human enteroviruses are ubiquitous, enterically transmitted viruses that cause a wide spectrum of both common and uncommon illnesses among infants and children. In temperate climates, enterovirus infections occur mainly in the summer and fall. We will discuss enteroviruses other than polioviruses. Enteroviruses are members of the family Picornaviridae. The genus Enterovirus is now divided into five major groups: polioviruses, group A coxsackieviruses, group B coxsackiviruses, echoviruses and (newer) enteroviruses.
Enteroviruses are shed in the upper respiratory tract for 1-3 weeks and in the feces for up to 8 weeks after primary infection. The fecal-oral route is thought to be the predominant mode of enterovirus transmission, although some exceptions occur including coxsackie A21, which is spread mainly by respiratory secretions, and enterovirus 70, which is shed in tears and spread via fingers and fomites.
The majority of enterovirus infections in children are asymptomatic.
NONFOCAL, ACUTE FEBRILE ILLNESS
Prospective studies have shown that the nonpolio enteroviruses are a common cause of fever without an apparent focus among infants seen in the emergency room. During the summer and fall, enteroviruses account for at least 53-63% of these cases. A study in New York showed that infants born during the Enterovirus season acquired an enterovirus infection during the first 3 months of life, and 21% of the infected infants were hospitalized. Fever often is the sole finding,although some infants will also have irritability, lethargy, poor feeding, vomiting, diarrhea, exanthems, or sings of upper respiratory tract infection. Upon evaluation, approximately half of enterovirus-infected infants will have aseptic meningitis, although there are no clinical features that distinguish those with meningitis before performing the lumbar puncture. Infants with enterovirus-induced fever recover within 2-10 days without complications.
A recently completed study in Baltimore has confirmed that more than 90% of community-acquired cases of viral meningitis are caused by the group B coxsackievirus and echoviruses. Coxsackie serotypes B2 and B5, and echovirus 4,6,9,11,16 and 30 are the most frequently implicated as causative agents of aseptic meningitis. The least associated, causing fewer than 5% of cases are the group A coxsackievirus. Naturally occurring (wild type) polioviruses were an important cause of viral meningitis (often called onparalytic poliomyelitis? before the control and ultimate eradication of poliomyelitis in the US. Therefore, it is not surprising that rare cases of viral meningitis are now attributed to the attenuated (oral polio vaccine) polioviruses.
Viral meningitis associated with oral polio vaccine occurs among both recipients of OPV and among children who appear to have acquired infection by contact with an OPV vaccinee. Only a minority of infants younger than 3 months with aseptic meningitis will have clinical manifestations of neurologic disease. Ten percent have acute CNS complications such as seizures, obtundation, or increased intracraneal pressure.
The enteroviruses account for approximately 10% to 20% of cases of frank encephalitis of proven viral etiology. The group A coxsackieviruses have been conspicuous among the agents isolated from infants and children with focal enteroviral encephalitis.
The nonpolio enteroviruses rarely cause a syndrome of acute motor weakness and paralysis that is clinically and pathologically indistinguishable form poliomyelitis, although myelitis caused by the nonpolio enteroviruses is less severe, muscle weakness is less likely to persist and bulbar involvement is less common. Enterovirus 71 is known to have been responsible for large outbreaks of acute paralysis involving hundreds of individuals, mostly children.
The cardiomyotropic nature of the group B coxsackieviruses has been recognized since they were first discovered; they account for one third to one half of all cases of sporadic, acute myopericarditis, and for virtually all cases reported to have occurred during epidemics.
The pathophysiology of group B coxsackievirus myopericarditis has been well studied; viral replication in the myocardium peaks within 3-7 days, depending on the route of infection, and persists for 7-10 days in immunocompetent hosts, and longer in those with compromise. Physically active adolescents and young adults may have the highest risk; males have at least twice the risk of females.
Enteroviral myopericarditis is clinically indistinguishable from disease caused by other cardiotropic viruses, including adenoviruses, influenza A virus, and mumps virus. Two-thirds of patients report a febrile upper respiratory tract infection preceding symptoms of frank myocarditis, which may include fever, substernal chest pain, exercise intolerance and dyspnea. A pericardial friction rub is present in 35-80% of cases, and gallop rhythm or other signs of ventricular failure in about 20%. Echocardiography confirms the diagnosis.
Acute hemorrhagic conjunctivitis (AHC) is a highly contagious infection characterized by eye pain, eyelid swelling, and subconjuntival hemorrhages. Two enterovirus serotypes have been responsible for widespread epidemics of AHC that have occurred throughout the tropics. AHC is transmitted directly form person to person via fingers and fomites.
ENTEROVIRUSES AND DIABETES MELLITUS