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Practice Essentials

Mumps is an acute, self-limited, systemic viral illness characterized by the swelling of one or more of the salivary glands, typically the parotid glands. The illness is caused by the RNA virus, Rubulavirus. Rubulavirus is within the genus Paramyxovirus and is a member of the family Paramyxoviridae. This virus contains a single-stranded, negative-sense RNA surrounded by a glycoprotein envelope. Of 2 glycoproteins on the surface of the RNA viral envelope, one mediates neuraminidase and hemagglutination activity, whereas the other is responsible for fusion to the lipid membrane of the host cell.

Rubulavirus can be isolated in viral culture from saliva, urine, and cerebrospinal fluid (CSF). Chemical agents (ie, ether, formalin, chloroform), heat and ultraviolet light can inactivate this virus.

Serologic assays determine the presence of an antibody response and assess differences between acute and convalescent titers. Affected salivary glands show edema and lymphocytic infiltration. (See the image below.) (See Workup.)

Child with mumps.

Child with mumps.

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Even though the mumps virus, Rubulavirus, shares similar morphologic features to human parainfluenza viruses (known as hPIVs, as part of the Paramyxovirus genus), no cross-immunity between these viruses is known. The mumps virus does share various epidemiologic characteristics with other well-known viral pediatric diseases, such as measles (RNA virus, of the genus Morbillivirus, in the Paramyxoviridae family) and rubella (RNA virus, of the genus Rubivirus, in the Togaviridae family).

Mumps occurs worldwide. Humans are the only known natural hosts. This Paramyxovirus is highly infectious to nonimmune individuals and is the only cause of epidemic parotitis. (See Epidemiology.) Although mumps cases occur at any time of year, an increase in case number is noted during late winter and early spring.

(Also see Management of Acute Presentation of Mumps.

Mumps and SARS

During the 2003 epidemic of severe acute respiratory syndrome (SARS), it was thought that the SARS-causing virus belonged to the Paramyxoviridae family. However, current case criteria have determined that SARS follows the clinical, laboratory, and transmission characteristics of an RNA coronavirus named SARS-associated coronavirus (SARS-CoV).

Vaccination history and timeline

The monovalent live, attenuated mumps vaccine was licensed in the United States in December 1967, and the Advisory Committee on Immunization Practices (ACIP) recommended that its use be considered for children nearing puberty, for adolescents, and for adults. At this time, the public health community considered mumps vaccination a low priority; as such, the ACIP believed that mumps immunization should not compromise the effectiveness of established immunization public health programs. By 1972, the ACIP recommendations were changed to indicate that mumps vaccination was particularly important for the initially targeted teenage and adult age groups. Hence, in 1977, routine vaccination was recommended for all children age 12 years and older. (See Treatment)

In 1980, further recommendations called for mumps vaccination of susceptible children, adolescents, and adults, unless it was medically contraindicated. Following these comprehensive recommendations and enactment of state laws requiring mumps vaccination for school entry and attendance, the reported incidence of mumps steadily declined.

However, in 1986 and 1987, large outbreaks of mumps occurred among under-immunized cohorts of people born between 1967 and 1977, as based on a single-dose mumps vaccine regimen. This caused a shift in peak incidence from persons age 5-9 years to those age 10-19 years.
 In 1989, the ACIP recommended that a second dose of mumps-containing vaccine be given to children age 4-6 years (at time of entry to kindergarten or first grade) and designated MMR as the vaccine of choice.

Over the next decade (1988-1998), the incidence of mumps decreased among all age groups. The greatest decrease occurred among persons aged 10-19 years. This age group had reversed the trend seen in 1986 and 1987, when a resurgence of outbreaks had occurred among susceptible adolescents and young adults.

Subsequent outbreaks have occurred among well-vaccinated populations. During 1989-1990, a large outbreak occurred among students in a primary and a secondary school. Most students in these schools had been vaccinated, suggesting that a vaccination failure (in addition to failure to vaccinate) might have contributed to the outbreak. Another mumps outbreak occurred a year later, in a secondary school where most of the students had been vaccinated; this outbreak was mostly attributed to primary vaccination failure.

The shift in higher risk for mumps to these other age groups (ie, from younger school-aged children to older children, adolescents, and young adults), which occurred after the routine use of the mumps vaccine was initiated, has persisted despite minimal fluctuations in disease incidence that have occurred among the various age groups.

Transmission, course, and symptoms

Humans are the sole reservoir for the mumps virus. The transmission mode is person to person via respiratory droplets and saliva, direct contact, or fomites. (See Etiology.) The presence of maternal antibodies typically protects infants younger than 12 months old from the disease. Infections can be a symptomatic in 20-30% of persons. Of those with symptomatic infection, adults tend to be more severely affected when compared to children. Lifelong immunity usually follows clinical or subclinical mumps infection, although second infections have been documented.

Mumps has an incubation period of 16-18 days; however, cases can arise 12-25 days after exposure. After this period, prodromal symptoms (such as low-grade fever, malaise, myalgias, headache, and anorexia) occur; these symptoms can last 3-5 days.

After this prodromal period (about 48 h), the clinical path of the virus depends on which organ is affected. The most common presentation is a parotitis, which occurs in 30 to 40% of all patients and in 95% of those who are symptomatic. Parotitis is caused by direct viral infection of the ductal epithelium and presents with localized gland inflammation. Other reported sites of infection are the central nervous system (CNS), eyes, pancreas, kidneys, testes, ovaries, and joints.

Mumps is the only known cause of epidemic parotitis; as such, parotitis is used as a clinical parameter of maximum communicability of the mump virus. A patient is considered infectious from about 3 days before the onset of, and up to 4 days after, the start of active parotitis (although it has been suggested that the communicable period is actually longer, lasting from 6 days before, to 9 days after, facial swelling is apparent).

After the prodromal period, one or both parotid glands begin to enlarge. Initially, local parotid tenderness and same-sided earache can occur. Ordinarily, the parotid glands are not palpable; but in patients with mumps, parotid swelling increases rapidly over several days. Seventy to 80% of symptomatic cases are bilateral with unilateral swelling occurring first, followed by bilateral parotid involvement. Occasionally, simultaneous involvement of both glands occurs. Edema over the parotid gland presents with non-discrete borders, pain with pressure, and obscures the angle of the mandible. The opening of the parotid duct (also known as Stensen’s duct) appears erythematous and enlarged. Parotid swelling can last for 10 days. Serologically, this inflammatory process can be confirmed with an elevated salivary amylase (s-amylase) level.

Despite the classic correlation of mumps and parotitis, mumps is no longer the most common cause of parotid swelling. Other viral causes include cytomegalovirus, parainfluenza virus 1 and 3, influenza A, and HIV. Bacterial infections, drug reactions, and metabolic disorders can also cause parotitis. Refer to the Medscape article on Parotitis for further information.

Other sites of viral infection

Central nervous system

CNS involvement is the most common extrasalivary complication of mumps. Its presentation is most often as aseptic meningitis rather than as a true encephalitis. This complication occurs up to 3 times more often in males when compared with females.
 It may precede parotitis or occur in its absence, but it usually presents within the first week after parotid swelling.

Aseptic meningitis has been seen in up to 10% of patients with history of parotitis. This percentage increases to 50% in those patients without parotid gland swelling. Salient clinical indicators of CNS involvement include headache, fever, nausea, vomiting, and nuchal rigidity. Marked changes in sensorium, convulsions, paresis, and/or paralysis present in patients with encephalitis, not typically in aseptic meningitis.

In clinically diagnosed aseptic meningitis or encephalitis, the CSF profile is similar. A CSF mononuclear pleocytosis occurs, as does normal glucose; although hypoglycorrhachia has been reported. Pleocytosis has a wide range of WBCs per microliter (10-2000 WBCs/µL), with a lymphocytic predominance, although an early polymorphonuclear predominance has been reported. CSF total protein is usually normal or can be mildly elevated.
 In addition, the mumps virus can be isolated from CSF early in the illness. Pleocytosis in the CSF has also been shown to occur in persons without clinical signs of CNS involvement.

CNS involvement (meningitis or encephalitis) carries a good prognosis and is usually associated with a complete recovery.

Neuritis of the auditory nerve may cause sensorineural deafness.
. A sudden onset of tinnitus, ataxia, and vomiting precedes a permanent hearing loss. Other neurologic complications include facial nerve neuritis and myelitis.


Another clinical manifestation of mumps is acute pancreatitis. Pancreatitis presents with mid-abdominal pain and distention, fever (typically low grade), nausea, and vomiting. An elevated serum lipase value supports this diagnosis.


Approximately one third of post-pubertal male patients develop unilateral orchitis. Orchitis is the most common complication of mumps infection in adult males. This inflammation usually follows parotitis but may precede or occur in the absence of parotid gland swelling. Orchitis usually appears during the first week of parotitis, but it can occur in the second or third week. Bilateral orchitis occurs less frequently (about 10% of cases). Gonadal atrophy may follow orchitis and poses a greater risk with bilateral involvement; however, sterility is rare.
 Prepubertal boys may develop orchitis, but it is uncommon in boys younger than 10 years old.

Orchitis presents with high fevers (39-41°C), severe testicular pain accompanied by swelling, and erythema of the scrotum. Nausea, vomiting, and abdominal pain are often present. Fever and gonadal swelling usually resolve in 1 week, but tenderness may persist.

Retrospective case studies have investigated a possible link between mumps orchitis and the subsequent development of testicular cancer; no increased risk has been shown to date.

Oophoritis occurs in about 7% of postpubertal female patients.

A more complete list of complications appears below. (See also Prognosis.)


A list of potential complications from mumps infection is cited below:

Aseptic meningitis/encephalitis

Sensorineural hearing loss/deafness

Transverse myelitis


Guillain-Barré syndrome

Cerebellar ataxia (with encephalitis)











Thrombocytopenia purpura

Mumps in infancy

Maternal transplacental antibodies protect infants up to 12 months of age. Infants born to mothers who have had mumps a week prior to delivery, may have clinically apparent mumps at birth or develop illness in the neonatal period.

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