The human enterovirus genus is a member of the Picornaviridae family of small, icosahedral, single-stranded, positive-sense RNA viruses. More than 100 serotypes are currently recognized by the International Committee on Taxonomy of Viruses classification,  as follows:
Human enterovirus type A (20 serotypes): These include coxsackie A virus types 2-8, 10, 12, 14, 16 and enterovirus types 71, 76, 89-92, 114, 119-121. 
Human enterovirus type B (61 serotypes): These include coxsackie A virus type 9; coxsackie B virus types 1-6; echovirus types 1-7, 9, 11-21, 24-27, 29-33; and enterovirus types 69, 73-76, 77-88, 93, 97, 98, 100, 101, 106, and 107. 
Human enterovirus type C (16 serotypes): The most well known are coxsackie A virus types 1, 11, 13, 15, 17, 19-22, and 24. Human enterovirus types 95, 96, 99, 102, 104, 105, 109, 116, and 118 and poliovirus types 1-3 have been included in this group. 
Human enteroviruses are distributed worldwide, with two major patterns of infections, endemic and epidemic, within a given geographical area. 
Enteroviruses usually cause transient, often subclinical, infections. Enteroviruses are also responsible for a wide variety of syndromes, including exanthematic fever, enteritis, encephalitis, aseptic meningitis, myocarditis, and respiratory tract infections. Coxsackieviruses, echoviruses, and enterovirus type 71 are also significant causes of cutaneous disease. Enteroviruses cause outbreaks that range from small, community clusters due of acute hemorrhagic conjunctivitis to large, nationwide human enterovirus 71 epidemics.  A relationship between enterovirus RNA and chronic fatigue syndrome has been described,  and these viruses could initiate and perpetuate the immunological response seen in chronic fatigue syndrome.
Coxsackieviruses are separated into 2 groups, A and B. Group A consists of 23 serotypes (1-22, 24) and group B consists of six serotypes (1-6). Coxsackie A viruses are the primary etiologic agents of herpangina and hand-foot-and-mouth disease (HFMD). Coxsackie B viruses are associated with epidemic pleurodynia (ie, Bornholm disease), epidemic myalgia, myocarditis, and pericarditis. Bowles et al suggest that coxsackie B virus may be an etiologic agent of juvenile dermatomyositis. 
Zahorsky first described the clinical spectrum of herpangina in 1920. Later, coxsackie A virus was isolated from pharyngeal washings and stool samples of patients with herpangina. Subsequently, many reports have confirmed this association. Robinson et al first isolated the coxsackie A virus type 16 serotype in 1957 during a Canadian epidemic of exanthema and stomatitis.  Two years later, Alsop et al used the term hand-foot-and-mouth disease to describe a similar eruption in England. 
Echoviruses include 34 distinct serotypes, and at least half can cause a rash. The two skin diseases specifically associated with echoviruses are Boston exanthem disease (BED), caused by echovirus type 16, and eruptive pseudoangiomatosis, (EP) caused by echovirus types 25 and 32.
Enteroviral infection occurs primarily in the summer and early fall. Infants are highly susceptible to enteroviruses.
Enteroviruses are spread from person to person by oral-oral and fecal-oral routes and, because the virus can be isolated from cutaneous and ocular lesions, presumably, may also be transmitted through direct contact with fluid from these cutaneous and ocular lesions.
Another important route of enterovirus transmission is inhalation of airborne viruses in respiratory droplets. 
Another possible route is from fomites, because enterovirus RNA has been found on objects in a pediatric office.  Similarly, nosocomial infection of enteroviruses in neonatal intensive care units has also been described. 
Another source of infection could be swimming pools because enteroviruses are easily detectable in natural and treated water sources.
It has been suggested that enteroviruses can be transmitted antenatally, either transplacentally or potentially via ascending infection. When maternal enterovirus infection is acquired during late pregnancy, vertical transmission has been shown to be relatively common. 
The viral incubation period is usually 2-5 days. The viruses are highly contagious, and they are a common cause of widespread outbreaks. After the ingestion of infectious material, enteroviruses are implanted and replicated in the alimentary tract (nasopharynx and ileum). If local replication is limited, the disease remains asymptomatic. If the virus passes into the regional lymphatic nodes and the reticuloendothelial system organs, minor or nonspecific disease may develop. Virus may also spread by the hematologic route, which results in a more severe and characteristically systemic illness.
Immune activation by the enterovirus leads to the production of immunoglobulin M (IgM) type-specific antibodies, which may be detected in the serum 1 week after infection. They are responsible for neutralization and rapid elimination of the virus from the blood and other sites of implantation. Serum IgM antibodies can be detected for 6 months after the patient's recovery, and convalescent immunoglobulin G can be detected for 1-2 years. Most enteroviral infections confer lifelong immunity to the serotype-specific agent. In addition, antibodies to these related viruses are known to cross-react, and they do so in different patterns, based on the country, serotype, and specific population, making comparisons of disease-based studies amongst these groups difficult.
Although enteroviruses are responsible for an estimated 50 million infections and 30,000-50,000 hospitalizations each year, note that less than 1% of infections result in significant symptomatic illness and the vast majority of hospitalizations are for aseptic meningitis. 
The US Centers for Disease Control and Prevention (CDC) reported from mid August 2014 to January 15, 2015 an outbreak of enterovirus 68 (also called enterovirus D68) and a total of 1,153 people in 49 states were affected.  However, in the last 2 years, the number of confirmed new cases felt abruptly to zero in 2015 and to four cases as of June 3, 2016. 
Although the frequency is not known, a sentinel surveillance system was established at the Taiwan Center for Disease Control (CDC, Taiwan) in 1998 to assess the epidemiologic features of enterovirus type 71 infection. It registered 1571 severe cases of hand-foot-mouth disease/herpangina from 1998-2007. 
In China, a total of 852,925 cases of HFMD, including 77 deaths, were reported as of May 31, 2016. 
The overall number has been estimated at 1 billion or more annually worldwide.
Some authors suggest a slight male predominance, but this has not been confirmed.
Enteroviral infections mainly affect children younger than 10 years, probably because they lack cross-reacting immunity resulting from repeated exposures, but they are not uncommon in adults.
In general, the systemic and cutaneous manifestations of enteroviruses in immunocompetent individuals are self-limited. Cutaneous lesions heal without scarring. Mortality rates ranging between 0-42% in the neonatal period. Risk factors for severe infection are as follows:
Maternal viral symptoms at delivery
Symptoms in the first week of life
No specific antibodies (acquired by placental transfer) of the infecting serotype in the neonate 
A few cases of prolonged or recurrent HFMD have been reported. In 1964, Evans and Waddington  reviewed a large outbreak in South Wales. They described a relapsing course occurring over 2 years in one patient.
Some postinfection sequelae have been described. Some evidence suggests that enterovirus 71 CNS involvement can cause not only acute and severe complications with higher mortality, but also long-term neurologic and psychiatric disorders. 
Occasionally, cardiac and neurological complications occur. Deaths in neonates infected with enteroviruses have been reported. They are usually the result of fulminant myocarditis.
When viral transmission is antenatal, neonatal enterovirus infection is very severe and has a poor outcome.