Mumps

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.)

View Image

Child with mumps.

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.^[1]

(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).^{[2, 3]}

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.^[4]  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.^{[4, 5]}

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.^[6]  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.^[7]  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.^[8] . A sudden onset of tinnitus, ataxia, and vomiting precedes a permanent hearing loss. Other neurologic complications include facial nerve neuritis and myelitis.

Gastrointestinal

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.

Genitourinary

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.^[9]  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.^{[10, 11]} .

Oophoritis occurs in about 7% of postpubertal female patients.

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

Complications

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

• Aseptic meningitis/encephalitis
• Sensorineural hearing loss/deafness^[8]
• Transverse myelitis
• Polyneuritis
• Guillain-Barré syndrome
• Cerebellar ataxia (with encephalitis)
• Keratouveitis
• Thyroiditis
• Myocarditis
• Mastitis
• Pneumonia
• Pancreatitis
• Nephritis
• Orchitis
• Oophoritis
• Arthritis
• 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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Etiology

After the initial entry into the respiratory system, the virus replicates locally. Viremic dissemination then occurs to target tissues, such as the salivary glands (parotid glands) and extrasalivary locations (CNS). These findings are based on experimentally induced mumps infection by Henly et al in 1948.

A secondary phase of viremia that occurs before the immune response is due to the replication of the virus at the target organs. Viruria is also common, via blood transmission of the virus into the kidneys, where active replication occurs. Therefore, impaired renal function (glomerulonephritis) may occur.

Cell necrosis and inflammation with mononuclear cell infiltration is the tissue response. Salivary glands show edema and desquamation of necrotic epithelial cells lining the ducts. Focal hemorrhage and destruction of germinal epithelium may occur, leading to duct plugging.

Risk factors

Lack of immunization, international travel, and immune deficiencies are all factors that increase risk of infection by the Paramyxovirus mumps virus.

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Epidemiology

Incidence and prevalence in the United States

After licensure of the mumps vaccine in the United States in December 1967 and the subsequent introduction of state-mandated immunization laws in an increasing number of states, the reported incidence of mumps substantially decreased. There were 666 cases of mumps reported in 1998. This number is in marked contrast to 152,209 cases reported in 1968, 30 years earlier.

Although incidence decreased in all age groups, the largest decreases (>50% reduction in incidence rate per 100,000 population) occurred in persons aged 10 years or older. Overall, the incidence of mumps was lowest in US states with comprehensive school immunization laws requiring mumps vaccination for entry.

Presently, the prevalence of mumps is at record low levels because of the recommendation of 2 doses of MMR vaccine and its high coverage rate in the United States. During the 1990s, mumps cases continued to substantially decline, from 5,292 reported cases in 1990 to 266 reported cases in 2001, meeting the Healthy People 2000 Objective of less than 500 cases per year. In 2003, the Centers for Disease Control and Prevention (CDC) reported a total of 231 cases.^[12]

However, in July 2005, an epidemic occurred in Sullivan County, New York at a summer camp.^[13] An investigation conducted by the New York State Department of Health (NYSDOH) identified 31 cases of mumps, likely introduced by a camp counselor who had traveled from the United Kingdom and had not been vaccinated for mumps. The United Kingdom reported an epidemic of mumps this year, with 56,390 cases reported in persons aged 15-24 years who were not vaccinated.^[14]

Even though 96% of the participants at this summer camp had been vaccinated for mumps, a mumps outbreak can result from exposure to virus imported from a country with an ongoing mumps epidemic (as in this outbreak). The likelihood of disease in US residents caused by imported virus from areas with mumps epidemics remains high.

International status

The mumps virus is present throughout the world and hence, risk of exposure to mumps outside the United States may be high. In many countries worldwide, mumps remains endemic. The mumps vaccine is in use in only 57% of countries belonging to the World Health Organization (WHO), predominantly those countries with more developed economies.^[15]

Worldwide variations in the number of persons who receive the mumps vaccination make it difficult to estimate the number of cases. The incidence varies markedly from region to region.

Race predilection

During 1990-1998, race and ethnicity were reported for approximately two thirds of cases in each of 28 states and the District of Columbia. Mumps incidence decreased for people of all races during this period. However, for each year, incidence was highest among black persons, ranging from 1.2-8.2 times the incidence of any other racial group. Moreover, this higher incidence was found to occur within each age grouping; this observation was most notable for persons age 5-19 years.

Although incidence rates for Hispanics exceeded the rates for non-Hispanics in every age group, differences in rates were minimal for children younger than 5 years and for persons aged 20 years or older. The greatest difference in incidence rates between Hispanics and non-Hispanics was in persons aged 5-19 years.

Sex predilection

Males and females are affected equally with parotitis.

CNS involvement has shown a male-to-female ratio of 3:1.

Age predilection

Today, most reported mumps cases occur in school-aged children (age 5-14 y). This was also the case in the prevaccine era. An average of 75% of mumps cases were reported from 1967-1971, whereas 60% of mumps cases occurred in this same age population from 1985-1987, within the first 5-year period post licensure. For 2 consecutive years, 1986 and 1987, the reported peak incidence rate shifted from children, 5-9 years old, to older age groups.

Persons aged 15 years or older accounted for more than 33% of the reported total from 1985-1987. During the earlier years, 1967-1971, an average of only 8% of reported mumps cases occurred among this population group. From 1985-1987, the incidence of reported mumps increased in all age groups. The most dramatic increases were noted among adolescents aged 10-14 years (almost a 7-fold increase) and young adults aged 15-19 years (more than an 8-fold increase).

Increased occurrence of mumps in susceptible adolescents and young adults has been documented by several outbreaks in high schools, on college campuses, and in occupational settings.^[16] Nonetheless, despite this age shift in reported mumps, the overall reported risk of disease in persons aged 10-14 years and those aged 15 years or older is still lower risk than that seen in the prevaccine and early postvaccine eras.

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Prognosis

The prognosis for patients with uncomplicated mumps is excellent.

For patients with encephalitis, the prognosis is generally favorable. Reported rates of mumps encephalitis cite 5 cases per 1000 reported mumps cases. Permanent sequelae are rare; however, neurologic damage and death can occur with the average encephalitis case-fatality rate of 1.4%. Approximately 10% of patients develop a mild form of aseptic meningitis, which can be confused with bacterial meningitis. Transient myelitis or polyneuritis is also uncommon.

Sensorineural deafness is a serious complication involving the CNS.^[8] It occurs infrequently, with an estimated frequency of 0.5-5 cases per 100,000 reported mumps cases. Permanent deafness after mumps is rare and, if it occurs, primarily affects unilateral hearing (only 20% bilateral). Transient sensorineural hearing loss occurs in 4% of adults with mumps. Minor degrees of hearing loss are more likely to occur with higher incidence and are most likely reversible.

Pancreatitis occurs in 5% of persons infected with mumps. The hyperglycemia that results is usually transient, but a few cases of diabetes mellitus have occurred as a post complication. Limited experimental, clinical, and epidemiologic data suggest permanent pancreatic damage may result from injury caused by direct viral invasion. At present, it is unclear if the mumps virus is responsible.^[17]

Orchitis (usually unilateral) has been reported as a complication in 20-50% of clinical mumps cases in postpubertal males. A degree of testicular atrophy occurs in about 35% of cases of mumps orchitis. Complete sterility is rare. Impaired fertility occurs in 13% of patients.

Oophoritis is a benign inflammation of the ovaries and occurs in about 5% of postpubertal females. Compromised fertility has not been shown.

Other rare complications include myocarditis, thyroiditis, mastitis, viral pneumonia nephritis, arthritis, and thrombocytopenia purpura. These complications usually resolve within 2-3 weeks without sequelae. Thirteen percent of adults with myocarditis had significant electrocardiographic findings of depressed ST segments and bradycardia. The incidence of myocarditis is 15%, but typically it is asymptomatic.^[18] However, death due to myocarditis has been reported.

Mumps infection in pregnant women increases the risk of embryonic loss, spontaneous fetal loss, and fetal death, especially during the first trimester of pregnancy (reported to be as high as 27%). No association has been found between mumps and congenital anomalies. Studies relating maternal mumps infection to endocardial fibroelastosis in the fetus are inconclusive. Mumps during pregnancy was rare prior to immunization recommendations and is now even less common with the widespread use of mumps vaccination programs.

Death due to mumps is rare; the majority of fatalities (>50 %) occur in patients older than 19 years.

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Patient Education

Advise parents and educators to exclude infected children from large-population facilities until 9 days after parotid swelling begins or until this swelling subsides.

Advise all children and adults to follow good hand washing practices.

For patient education information, see the Children's Health Center and the Infections Center, as well as Mumps and Immunization Schedule, Children.

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History

Symptoms in the patient’s history consist mostly of fever, headache, and malaise. Within 24 hours, patients may report ear pain localized near the ear lobe that is aggravated by a chewing movement of the jaw. Older children may describe a swelling sensation at the mandibular angle and an associated sour taste in the mouth. Fever usually subsides within 7 days, notably before parotid gland edema disappears. Sudden hearing loss may occur due to a vestibular reaction.

Diffuse, tender swelling of the thyroid gland (thyroiditis) may occur about 1 week after parotitis. Antithyroid antibodies are detected in the serum.

Pancreatitis is a severe but, fortunately, rare complication. A sudden onset of mid-epigastric pain and tenderness occurs, accompanied by fever, chills, nausea, and vomiting. Patients generally recover within 1 week with appropriate supportive treatment.

Orchitis can occur in up to 50% of postpubertal males, and as many as 30% have bilateral involvement.^[17] Orchitis presents acutely with fever, chills, nausea, vomiting, and lower abdominal pain. After the fever, the testes begin to swell rapidly. Increase in testicular size can be minimal or as much as 4 times normal size. As the fever decreases, the accompanying testicular pain and edema subside. Loss of turgor is noticed, with up to 50% of cases demonstrating atrophy.

Oophoritis in postpubertal females is associated with abdominal and/or pelvic pain and tenderness.

Mumps can also cause aseptic meningitis, a CNS complication which usually is indistinguishable from other viral etiologies, such as enteroviruses, herpesviruses, or poxviruses. CSF analysis reflects less than WBC 500 cells/µL with a lymphocytic predominance. 

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Physical Examination

Parotid glands are not palpable in the craniofacial exam of a healthy patient. But for patients with mumps, the parotid glands rapidly progress to maximum swelling over several days. Patients may have trismus.

Submaxillary gland edema, palpable underneath and anterior to the angle of the mandible, may be accompanied by edema spreading onto the cheek and downward onto the neck. These clinical findings can make it difficult for the examiner to differentiate from cervical adenitis. The opening of the submandibular duct (also known as Wharton duct) may be erythematous and edematous.

Sublingual gland involvement, most commonly bilateral, is a less common finding in mumps. The sublingual gland is palpated on the floor of the mouth and submental area. In severe and extensive cases, the edema may extend to the presternal area due to obstruction of lymphatic vessels from compression by enlarged salivary glands. Submandibular glands may also be involved and swollen.

The opening of Stensen's duct can be enlarged, edematous, and erythematous.

In addition, a morbilliform rash may be present.

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Approach Considerations

Mumps is a clinical diagnosis. A study investigated the difficulty of medical professionals to diagnose mumps, noting that only 14% of 2082 cases occurring during an outbreak could be confirmed by laboratory sera testing.^[19] This study concluded that the examiner's ability to diagnosis mumps as based solely on clinical presentation was low.

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Laboratory Studies

Serum amylase is elevated in mumps parotitis (amylase-S) and in pancreatitis (amylase-P). Serum lipase is elevated in pancreatitis.

A complete blood cell (CBC) count reveals a normal, decreased, or elevated white blood cell (WBC) count, with the differential reflecting a relative lymphocytosis. Sera inflammatory markers, such as C-reactive protein or erythrocyte sedimentation rate (ESR), can be elevated to reflect a nonspecific systemic inflammatory response.

Viruria is present, even in uncomplicated cases, with the mumps virus detected in urine within the first 2 weeks of illness.^[20]

Mumps virus can be isolated from nasopharyngeal swabs, blood, and fluid from the buccal cavity typically within the window of 7 days before, up until 9 days after, the onset of parotitis. The virus can also be isolated in a cell culture inoculated with throat washings, urine, or spinal fluid. CNS involvement usually shows a lymphocytic pleocytosis. Polymerase chain reaction (PCR) assay of the CSF can be used to detect viral mumps RNA and fosters a rapid confirmation modality for the diagnosis.

Mumps infection can be confirmed by a positive mumps-specific immunoglobulin M (IgM) titer or by demonstration of a significant rise in mumps-specific immunoglobulin G (IgG) antibody titers between acute and convalescent sera specimens.  IgG titers can be detected by complement fixation, hemagglutination inhibition, or enzyme immunoassay. Interpretation of titer rise may have limitations due to potential mumps cross-reaction with other parainfluenza viruses.^[21]

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Imaging Studies

No specific imaging studies are diagnostic for mumps infection.

Imaging studies may be needed to further evaluate certain complications associated with mumps infection. If concern exists for meningitis or encephalitis, head computed tomography (CT) scanning without contrast should be considered, prior to lumbar puncture procedure to obtain CSF.

Scrotal ultrasonography must be performed when orchitis is clinically suspected, with specific focus to rule out testicular torsion.

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Other Tests

Complicated cases may require further testing to determine additional organ involvement.

Given the association between mumps infection and sensorineural hearing loss, auditory testing is indicated to assess for development of a hearing impairment.

If diagnostic clues for meningitis or encephalitis are present, a lumbar puncture to obtain CSF must be strongly considered to clarify cause. 

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Approach Considerations

Mumps without associated major complications can be managed on an outpatient basis with supportive health guidance and continuity of care. Patients diagnosed with mumps should be isolated for 5 days from the onset of symptoms to minimize the risk of infecting others.

Also see Management of Acute Presentation of Mumps.

Medical care

Conservative, supportive medical care is indicated for patients with mumps. No antiviral agent is indicated for treatment of this viral illness, as mumps is a self-limited disease.

Encouraging oral fluid intake is essential, as maintenance of adequate hydration and alimentation of patients is important. Refrain from acidic foods and liquids as they may cause swallowing difficulty, as well as gastric irritation.

Prescribe analgesics (acetaminophen, ibuprofen) for headaches or discomfort due to parotitis. Topical application of warm or cold packs to the swollen parotid area may soothe the region.

Stronger analgesics may be required for patients with orchitis. Bed rest, scrotal support, and ice packs are recommended.

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Inpatient Care

Patients with specific complications may require inpatient care for intravenous fluid stabilization, pain management and continuous close observation.

Patients with meningitis, encephalitis, myocarditis, nephritis, or severe pancreatitis require a higher level of inpatient supportive care.

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Consultations and Transfer

Consultation may be considered in complicated cases involving multiple organ systems. Medical and treatment guidance from specialists in critical care, infectious disease, neurology, cardiology, gastroenterology and urology may be indicated.

Transfer to a medical facility with a higher level of care is rarely indicated. This action is warranted, if major complications are present and the current medical facility cannot properly support the patient's treatment needs.

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Diet and Activity

A light diet with generous fluid intake is recommended and best tolerated.

Avoidance of acidic foods (eg, tomato, vinegar-containing food additives) and liquids (eg, orange juice) is beneficial to lessen oral pain and discomfort.

Bed rest is recommended to foster a speedy recovery and is indicated for patients with complicated cases.

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Deterrence and Prevention

The principal strategy to prevent mumps is to achieve and maintain high immunization levels, primarily in infants and young children. Universal immunization, as part of preventative good health care, should be routinely carried out in physicians' offices and public health clinics. Programs aimed to vaccine children with MMR should be established and maintained in all communities. In addition, all other persons thought to be susceptible should be vaccinated, unless otherwise contraindicated. Reaching adolescents and young adults is especially important, due to the past observed increased risk of disease in these populations.

If a case of mumps occurs in a childcare facility, immediately notify the local health department and parents/caregivers. Make sure all children and adults continue to follow good handwashing practices. In large facilities, follow appropriate group separation guidelines. Review the immunization records of all children in the facility to assure that they have received their first mumps vaccination. Those not adequately vaccinated should be referred to their health care provider. Continue to closely observe all children for symptoms and refer anyone developing symptoms to his or her primary care provider.

Initially, children with mumps were excluded from school and childcare centers for 9 days following the onset of parotid gland swelling. However in 2007, the American Academy of Pediatrics (AAP), the Centers for Disease Control and Prevention (CDC), and the Healthcare Infection Control Practices Advisory Committee (HICPAC) modified their recommendation from 9-day isolation guidance (standard precautions and droplets precautions) to 5 days after the onset of clinical symptoms (eg, parotitis) based on current medical evidence.^[22] . Children who have not been vaccinated due to medical or religious reasons should be excluded from school or daycare for at least 26 days after the onset of parotitis, beginning from the date of the last person with mumps in the affected facility.

Despite these isolation guidelines, spread of the infection can be difficult to control as the virus is present in saliva days prior to the onset of parotid swelling, and viral shedding does occur in asymptomatic persons.

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Vaccination

Susceptible children, adolescents, and adults should be vaccinated against mumps, unless vaccination is contraindicated. Mumps vaccine is important for children approaching puberty and for adolescents and, adults who have not had mumps. The MMR vaccine is the vaccine of choice for routine administration and should be used in all situations in which recipients are also likely to be susceptible to measles, rubella, or both. A favorable benefit-to-cost ratio for routine mumps immunization is better achieved when the MMR vaccine or the MMRV vaccine is given.

Persons are susceptible to mumps, unless they have documentation of the following:

• Physician-diagnosed mumps
• Adequate immunization with live attenuated mumps virus vaccine on or after their first birthday
• Laboratory evidence of immunity

Prior to 1977 in the US, the live attenuated mumps vaccine was not used routinely and the peak age incidence of disease in children was age 5-9 years; as such, most persons born before 1957 are likely to have been naturally infected with the mumps virus between 1957 and 1977. Therefore, most are considered to be immune, even in cases without clinically recognizable mumps disease. However, this cutoff date for susceptibility is arbitrary. Although outbreak control efforts should be focused on persons born after 1956, these recommendations do not preclude vaccination of possibly susceptible persons born before 1957, who currently may be exposed in outbreak settings.

Persons who are unsure of their mumps disease history, mumps vaccination history, or both should be vaccinated. Persons who have previously either received mumps vaccine or had mumps, do not have an increased risk of local or systemic reactions from receiving live attenuated mumps vaccine. Testing for susceptibility prior to vaccination, especially among adolescents and young adults, is not necessary. In addition to the expense, some tests (eg, mumps skin test, complement-fixation antibody test) may be unreliable, and tests with established reliability (eg, neutralization test, enzyme immunoassay, single-radial hemolysis antibody test) are not easily available.

A single dose of vaccine in the volume specified by the manufacturer (standardly 0.5 mL) should be administered subcutaneously (SC). Although not routinely recommended, intramuscular (IM) vaccination is effective and safe.

Administration of the live attenuated mumps virus vaccine as either MMR (measles-mumps-rubella) or MMRV (measles-mumps-rubella-varicella) is recommended at any age on or after the first birthday for all susceptible persons, unless a contraindication is present. It should not be administered to infants younger than 12 months because persisting maternal antibody might interfere with seroconversion. To ensure immunity, all infants vaccinated too early (before their first birthday), should be revaccinated on or after their first birthday.^{[23, 24]}  This action properly covers them for their first dose. A second dose is then, administered at age 4-6 years, to serve as a safeguard to ensure immunity against possible initial vaccine failure.

ACIP recommends a third dose of MMR vaccine for those previously vaccinated with two doses and identified as being at higher risk for acquiring mumps because of an outbreak.^{[34, 35]}

If the vaccine is administered after an exposure to the mumps virus, it may not provide adequate protection from disease development. However, if the exposure does not result in infection, vaccination should induce protection against infection from subsequent exposures. The risk of vaccine-associated adverse events does not increase, if the vaccine is administered to persons who are incubating disease at that time.

Immunoglobulin (IVIG) has not shown benefit to patients as treatment for post-exposure prophylaxis and hence, is not recommended. In the United States, mumps IVIG is no longer available or licensed for use. Vaccination post-exposure is not harmful and may possibly avert later disease.

A study published in 2011 evaluated MMR vaccine effectiveness in persons who received 1 or 2 doses of this vaccine during a mumps outbreak that occurred between September 1, 2009 and June 10, 2010 in Ontario, Canada. This study also aimed to estimate the coverage level required to achieve “herd” immunity and to interrupt community transmission. Using data from Ontario's Public Health Information System, 134 confirmed cases were identified; 114 of those reported receiving the MMR vaccine. Of those, 63 received 1 dose (49.2-81.6% effectiveness), while 32 received 2 doses (66.3-88% effectiveness). The authors concluded that if the assumed vaccine effectiveness after receiving 2 doses of MMR is 85%, then the populace vaccine coverage of 88.2% and 98% would be needed to interrupt community transmission of mumps. This study reemphasizes the need for routine vaccination and warns against complacency in vaccination programs.^[25]

Cardemil et al evaluated the effectiveness of a third dose of the MMR vaccine in a study that included 20,496 university students, of which 259 were diagnosed with mumps during an outbreak. The study reported the attack rate was lower among the 4783 students that received the third dose than those who had received two (6.7 vs 14.5 cases per 1000 population, P< 0.001). The third dose was associated with a 78.1% lower risk of mumps compared to the second dose at 28 days post vaccination (adjusted hazard ratio, 0.22; 95% confidence interval, 0.12 to 0.39).^[26]

Another mumps outbreak was reported in September 2011 on a university campus in California. The California Department of Public Health (CDPH) confirmed using PCR, 3 cases of mumps in college students who were recently evaluated at the university's student health services with symptoms suggestive of mumps. An investigation by CDPH, student health services, and the local health department identified a total of 29 mumps cases. The index patient was an unvaccinated student with history of recent travel to Western Europe, where mumps infection was circulating. Additional knowledge in regard to the date of onset of this index case, clarified that two generations of transmission had occurred before public health authorities were properly alerted. This mumps outbreak illustrates the value of requiring MMR vaccination (including documentation of immunization or other evidence of immunity) prior to college enrollment, the need for heightened clinical awareness, and timely reporting of suspected mumps cases to public health personnel.^[27]

Children age 12-23 months who are vaccinated with the combination MMRV vaccine have a slightly higher risk of febrile seizures, when compared to those children who are vaccinated separately, with the MMR and the VZV (varicella vaccine). The risk period for febrile seizures is 5-12 days after receipt of MMRV. However, the risk for febrile seizures is not increased among the older children aged 4-6 years receiving the MMRV. In response to this observation, the AAP has recommended that for the first dose given at age 12-48 months, the child can receive either MMR and VZV vaccines separately, or the MMRV. For children 48 months of age or older, both recommended vaccinations are for the inclusive MMVR.^[28]

A published 2015 study by Siberry et al compared the immunity response to MMR vaccination of children who contracted perinatal HIV (PHIV), to those children who were perinatally HIV-exposed but uninfected (HEU). The children in the PHIV group lacked serologic evidence of immunity to MMR, despite proper documented immunization and current treatment with sustained combination antiretroviral therapy (cART). The study found that among 428 children with PHIV, and 221 children with HEU, the immunity protection of the participants was significantly lower in children who contracted perinatal HIV (PHIV), for measles seroprotection (57% vs 99%), rubella seroprotection (65% vs 98%), and mumps seropositivity (59% vs 97%).^[29]

Adverse effects of vaccine use

Reports of adverse effects following mumps vaccination have cited low-grade fever and parotitis. Allergic reactions, presenting as a pruritic rash, have been temporally associated with mumps vaccination, but are uncommon. If allergic reactions occur, they are usually mild and of brief duration.

Encephalitis occurring within 30 days after receipt of a mumps-containing vaccine has been reported to be 0.4 cases per million doses. This incidence is not greater than the observed background incidence rate for encephalitis in healthy populations. Other indicators of CNS involvement, such as febrile seizures and sensorineural deafness, have been infrequently reported.^[30]  Reports of CNS illness in patients following administration of the mumps vaccination, do not necessarily indicate an etiologic relationship between the CNS complication and the vaccine.

Contraindications to vaccine use in pregnancy

Although the live attenuated mumps vaccine does infect the placenta and fetus, no evidence indicates that this infection causes congenital malformations in the fetus. Due to the theoretical risk of fetal damage, avoiding administration of live virus vaccine to pregnant women is prudent. Women of child-bearing age are recommended to avoid pregnancy for 3 months postvaccination of the live attenuated mumps vaccine.

Routine precautions prior to vaccinating women of child-bearing age are to inquire if they are, or may be pregnant. Of those who say they are or may be, it is important to explain the theoretical risk to those women who plan to receive this vaccine.

Vaccination during pregnancy should not be considered an indication for termination of pregnancy. However, discussion to take this action rests between the patient and her physician.

Severe febrile illness

Vaccine administration should not be postponed due to a minor febrile illness, such as a mild upper respiratory infection. MMR vaccination scheduled for those persons who have a severe febrile illness should be deferred, until health is restored.

Allergies

The live attenuated mumps vaccine is produced in chick embryo cell culture; hence persons with a history of anaphylactic reactions (i.e., hives, swelling of the mouth and throat, difficulty breathing, hypotension, shock) after egg product ingestion should be vaccinated with caution, using published protocols. Evidence indicates that persons are not at increased risk, if their egg allergy response is not of an anaphylactic nature. Vaccination can proceed in the usual manner for these patients. As a precaution, patients with known egg allergy should be observed for a minimum of 20 minutes post receiving the vaccine, at the medical facility. 

No evidence indicates that persons with allergies to chickens or feathers are at increased risk of reaction to the vaccine.

Mumps vaccine does contain trace amounts of neomycin (25 mcg). As such, persons who have experienced anaphylactic reactions to topically or systemically administered neomycin should not receive the mumps vaccine. Patients who have a neomycin allergy presenting as a contact dermatitis without systemic involvement can receive the vaccine, as its administration is not contraindicated in this situation.

Recent immunoglobulin (IVIG) injection

Passively acquired antibody can interfere with the response to live attenuated virus vaccines because antibody in these products neutralizes the vaccine virus and interferes with successful immunization. Therefore, the MMR vaccine should be administered at least 2 weeks before, or deferred until 3 months after the administration of IVIG or blood product transfusion.

Exceptions

Recommendations for live attenuated vaccine administration differ for children with immunodeficiency diseases or for those receiving immunosuppressive therapy (e.g., patients with HIV or oncologic disease, or treatment with high dose corticosteroids). All HIV-infected patients who are not severely immune compromised (age-specific CD4⁺ T-lymphocyte counts of ≥15%) should receive MMR vaccination as scheduled.

Patients with leukemia in remission, whose chemotherapy ended at least 3 months earlier, can receive live attenuated mumps virus vaccine (as MMR). Vaccination of close susceptible contacts to immunocompromised patients is very important as to minimize risk of mumps exposure. Immunized patients cannot transmit the mumps vaccine virus to others.

• References

Medication Summary

Treatment of mumps is usually supportive care. Vaccine pharmacotherapy is used to immunize the child.

• References

Ibuprofen (Advil, Motrin, NeoProfen)

• Dosing, Interactions, etc.

Clinical Context:  This is the drug of choice for patients with mild to moderate pain and fever. It inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.

• References

Acetaminophen (Tylenol, Aspirin Free Anacin, FeverAll)

• Dosing, Interactions, etc.

Clinical Context:  This is the drug of choice for pain in patients with documented hypersensitivity to nonsteroidal anti-inflammatory drugs (NSAIDs), with upper GI disease, or who are taking PO anticoagulants. Acetaminophen reduces fever by acting directly on hypothalamic heat-regulating centers, which increases dissipation of body heat via vasodilation and sweating.

• References

Class Summary

These agents may be prescribed for severe headaches or discomfort and pain due to parotitis. For patients with orchitis, stronger analgesics may be needed.

• References

Measles-mumps-rubella vaccine, live (MMR)

Clinical Context:  Live virus vaccine. Combined MMR vaccine is recommended for the prevention of mumps, measles, and rubella. For children, the typical recommended 2-dose schedule is administered at age 12-15 months for the 1st dose and age 4-6 years for the second dose.

• References

Class Summary

Prevention of mumps through immunization cannot be overemphasized. All children younger than 7 years should receive the mumps vaccine. In the United States, mumps vaccine is recommended and is usually combined with MMR.

The combined measles-mumps-rubella-varicella (MMRV) vaccine (ProQuad) has been shown to be associated with an increased risk of febrile seizure occurring 5-12 days following vaccination at a rate of 1 in 2300-2600 children, aged 12-23 months, compared with separate MMR vaccine and varicella vaccine administered simultaneously.^{[31, 32]} As a result, the CDC Advisory Committee on Immunization Practices (ACIP) recommends that separate MMR and varicella vaccines be used for the first dose, although providers or parents may opt to use the combined MMRV vaccine for the first dose after counseling regarding this risk.^[33] MMRV is preferred for the second dose (at any age) or for the first dose if given at age 48 months or older.

Data from postlicensure studies did not suggest that children aged 4-6 years who received the second dose of MMRV vaccine had an increased risk for febrile seizures after vaccination compared with children the same age who received MMR vaccine and varicella vaccine administered as separate injections at the same visit.^[33]

• References