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Chapter 227 – Mumps
Yvonne Maldonado
Mumps is an important childhood disease that was historically widespread but now occurs very infrequently. It is an acute viral infection characterized by painful enlargement of the salivary glands, chiefly the parotids, as the usual presenting sign.
Etiology.
Mumps virus, the cause of mumps, is an RNA virus of the genus Paramyxovirus in the family Paramyxoviridae, which also includes the parainfluenza viruses. Only one serotype is known.
Epidemiology.
Mumps is endemic in most unvaccinated populations; the virus is spread from human reservoir by direct contact, airborne droplets, fomites contaminated by saliva, and possibly by urine. It is distributed worldwide and affects both sexes equally. Before introduction of the vaccine in 1967, the peak incidence of the disease occurred in children 5–9 yr of age; 85% of infections occurred in children younger than 15 yr of age. Now most cases occur in young adults, producing outbreaks in colleges or in the workplace. Outbreaks appear to be primarily related to a lack of immunization, especially in an underimmunized cohort of children born from 1967–1977, rather than to waning to immunity. Epidemics occur at all seasons but are slightly more frequent in late winter and spring.
There has been a dramatic decrease in the incidence of mumps since the introduction of the mumps vaccine in 1968. Except for a small increase in 1987, the incidence of mumps has steadily decreased in the United States. In 2001 there were 226 reported cases of mumps, a greater than 99% reduction from the 152,209 cases reported in 1968.
Virus has been isolated from saliva as long as 6 days before and up to 9 days after appearance of salivary gland swelling. Transmission does not seem to occur more than 24 hr before the appearance of the swelling or later than 3 days after it has subsided. Virus has been isolated from urine from the 1st–14th day after the onset of salivary gland swelling.
Pathogenesis.
After entry into the last and initial multiplication in the cells of the respiratory tract, the virus is bloodborne to many tissues, among which the salivary and other glands are the most susceptible.
Clinical Manifestations.
The incubation period ranges from 14–24 days, with a peak at 17–18 days. Approximately 30–40% of infections are subclinical. In children, prodromal manifestations are rare but may be manifest by fever, muscular pain (especially in the neck), headache, and malaise.
SALIVARY GLANDS.
The onset is usually characterized by pain and swelling in one or both parotid glands. The parotid swells characteristically; it first fills the space between the posterior border of the mandible and the mastoid and then extends in a series of crescents downward and forward, being limited above by the zygoma. Edema of the skin and soft tissues usually extends further and obscures the limit of the glandular swelling, so that the swelling is more readily appreciated by sight than by palpation. Swelling may proceed extremely rapidly, reaching a maximum within a few hours, although it usually peaks in 1–3 days. The swollen tissues push the earlobe upward and outward, and the angle of the mandible is no longer visible. Swelling slowly subsides within 3–7 days but occasionally lasts longer. One parotid gland usually swells a day or two before the other, but in approximately one quarter of cases the disease remains unilateral. The swollen area is tender and painful, pain being elicited especially by tasting sour liquids such as lemon juice or vinegar. Redness and swelling about the opening of the Stensen duct are common. Edema of the homolateral pharynx and soft palate accompanies the parotid swelling and displaces the tonsil medially; acute edema of the larynx has also been described. Edema over the manubrium and upper chest wall may occur, probably because of lymphatic obstruction. The parotid swelling is usually accompanied by low-grade fever, but this may be absent.
Although the parotid glands alone are affected in the majority of patients, swelling of the submandibular glands occurs frequently and usually accompanies or closely follows that of the parotid glands. In 10–15% of patients only the submandibular gland(s) may be swollen. Little pain is associated with the submandibular infection, but the swelling subsides more slowly than that of the parotids. Redness and swelling at the orifice of the Wharton duct frequently accompany swelling of the gland. Least commonly, the sublingual glands are infected, usually bilaterally; the swelling is evident in the submental region and in the floor of the mouth.
Diagnosis.
The diagnosis of mumps parotitis is usually apparent from the clinical symptoms and physical examination. When the clinical manifestations are limited to less common lesions, the diagnosis is less clear but may be suspected during an outbreak.
Routine laboratory tests are nonspecific; usually leukopenia is present with relative lymphocytosis. An elevation in serum amylase levels is common; the rise tends to parallel the parotid swelling and then to return to normal within 2 wk.
The microbiologic diagnosis is by serology or virus culture. Enzyme immunoassay for mumps immunoglobulin (Ig) G and IgM antibodies are most commonly used for diagnosis. IgM antibodies are detectable in the first few days of illness and are considered diagnostic. They may remain elevated for weeks to months. IgG antibodies are directed primarily against the fusion (F) protein; cross reactions with parainfluenza viruses may occur. Seroconversion, or a fourfold increase in IgG titer, is diagnostic.
Mumps virus can be cultured from the saliva, cerebrospinal fluid, blood, urine, brain, and other infected tissues. Primary cultures of human or monkey kidney cells are used for viral isolation. Cytopathic effect is occasionally observed, but hemadsorption is the most sensitive indicator of infection.
The mumps skin test is unreliable for diagnosis of mumps and for determination of susceptibility to infection.
DIFFERENTIAL DIAGNOSIS.
Other viral causes of parotitis include HIV infection, influenza, parainfluenza viruses 1 and 3, cytomegalovirus, and coxsackieviruses. Acute suppurative parotitis is a bacterial infection usually caused by Staphylococcus aureus in which pus can often be expressed from the duct. A salivary calculus obstructing either a parotid or, more commonly, a submandibular duct causes intermittent swelling. Preauricular or anterior cervical lymphadenitis can be differentiated by the well-defined borders of the lymph node and a location that is completely posterior to the angle of the mandible. Orchitis may also be caused by coxsackieviruses.
Treatment.
There is no specific antiviral therapy; treatment is entirely supportive. Antipyretics (acetaminophen or ibuprofen) are indicated for fever. Bed rest should be guided by the patient's needs, but no evidence indicates that it prevents complications. The diet should be adjusted to the patient's ability to chew. Orchitis should be treated with local support and bed rest. Mumps arthritis may respond to a 2-wk course of a nonsteroidal anti-inflammatory agent or corticosteroids. Salicylates do not appear to be effective.
Complications.
Viremia early in the infection probably accounts for the widespread complications. There is no firm evidence that maternal infection is damaging to the fetus; a possible relationship to endocardial fibroelastosis has not been firmly established. Mumps in early pregnancy does increase the chance of abortion.
MENINGOENCEPHALOMYELITIS.
This is the most frequent complication in childhood. Its true incidence is hard to estimate because subclinical infection of the central nervous system, as evidenced by cerebrospinal fluid pleocytosis, has been reported in more than 65% of patients with mumps parotitis. Clinical manifestations occur in more than 10% of patients. The incidence of mumps meningoencephalitis is approximately 250/ 100,000 cases; 10% of these cases occurred in patients older than 20 yr of age. The mortality rate is about 2%. Males are affected three to five times as frequently as females.
The pathogenesis of mumps meningoencephalitis may be either a primary infection of neurons or a postinfectious encephalitis with demyelination. In the first type, parotitis frequently appears at the same time or following the onset of encephalitis. In the latter type, encephalitis follows parotitis by an average of 10 days. Parotitis may in some cases be absent. Aqueductal stenosis and hydrocephalus have been associated with mumps infection. Injecting mumps virus into suckling hamsters has produced similar lesions.
Mumps meningoencephalitis is clinically indistinguishable from meningoencephalitis of other origins (see Chapter 174.2 ). Moderate stiffness of the neck is seen, but the remaining findings on neurologic examination are usually normal. The cerebrospinal fluid may show a lymphocytic pleocytosis of less than 500 cells/ mm3, although occasionally the count may exceed 2,000 cells/mm3.
ORCHITIS AND EPIDIDYMITIS.
These complications rarely occur in prepubescent boys but are common (14–35%) in adolescents and adults. The testis is most often infected with or without epididymitis; epididymitis may also occur alone. Bilateral orchitis occurs in approximately 30% of patients. Rarely, there is a hydrocele. The orchitis usually follows parotitis within 8 days. Orchitis may also occur without evidence of salivary gland infection. The onset is usually abrupt, with a rise in temperature, chills, headache, nausea, and lower abdominal pain; when the right testis is implicated, appendicitis may be suggested as a diagnostic possibility. The affected testis becomes tender and swollen, and the adjacent skin is edematous and red. The average duration of illness is 4 days. Approximately 30–40% of affected testes atrophy, leaving a cosmetic imbalance. Infertility is rare even with bilateral orchitis.
OOPHORITIS.
Pelvic pain and tenderness are noted in about 7% of postpubertal female patients. There is no evidence of impairment of fertility.
PANCREATITIS.
Mild or subclinical pancreatic involvement is common, but severe pancreatitis is rare. It may be unassociated with salivary gland manifestations and may be misdiagnosed as gastroenteritis. Epigastric pain and tenderness, which are suggestive, may be accompanied by fever, chills, vomiting, and prostration. An elevated serum amylase value is characteristically present in patients with mumps, with or without clinical manifestations of pancreatitis.
MYOCARDITIS.
Serious cardiac manifestations are extremely rare, but mild infection of the myocardium may be more common than is recognized. Electrocardiographic tracings revealed changes, mostly depression of the ST segment, in 13% of adults in one series. Such involvement may explain the precordial pain, bradycardia, and fatigue sometimes noted among adolescents and adults with mumps.
ARTHRITIS.
Migratory polyarthralgia and even arthritis are occasionally seen in adults with mumps but are rare in children. The knees, ankles, shoulders, and wrists are most commonly affected. The symptoms last from a few days to 3 mo, with a median duration of 2 wk.
THYROIDITIS.
Although it is uncommon in children, a diffuse, tender swelling of the thyroid may occur about 1 wk after the onset of parotitis; antithyroid antibodies subsequently develop.
DEAFNESS.
Unilateral, rarely bilateral, nerve deafness may occur; although the incidence is low (1/15,000 cases), mumps was historically a leading cause of unilateral nerve deafness. The hearing loss may be transient or permanent.
OCULAR COMPLICATIONS.
Dacryoadenitis may occur with painful swelling, usually bilateral, of the lacrimal glands. Optic neuritis (papillitis) may occur; symptoms vary from loss of vision to mild blurring, with recovery in 10–20 days.
Prognosis.
The prognosis of rubella in childhood is excellent. Infection usually confers permanent immunity, although reinfections have been documented.
Prevention.
Mumps vaccine is derived from the Jeryl Lynn strain of mumps virus, which is attenuated by serial passage in embryonated hens' eggs and chick embryo cell culture. The vaccine induces antibody in 96% of seronegative recipients and has 97% protective efficacy.
The initial mumps immunization, usually as measles-mumps-rubella (MMR) vaccine, is recommended at 12–15 mo of age. A second immunization, also as MMR, is recommended routinely at 4–6 yr of age but may be administered at any time during childhood provided at least 4 wk have elapsed since the first dose. Children who have not previously received the second dose should be immunized by 11–12 yr of age. Women should avoid becoming pregnant for 30 days after monovalent mumps vaccination (3 mo if vaccination was performed with rubella vaccine). Other contraindications to vaccination include allergy to a vaccine component (anaphylaxis to neomycin), moderate or severe acute illnesses with or without fever, immunodeficiency (primary immunodeficiencies, cancer and cancer therapy, long-term high-dose corticosteroid therapy, severely immunocompromised, including those with HIV infection), and recent immune globulin administration (see Chapter 282 ). Rarely, parotitis and low-grade fever can develop 10–14 days after vaccination. Vaccinees do not shed virus.
Persons born before 1957 can be considered immune to mumps. Maternal antibody is protective in the infant in the first 6 mo of life.
Behrman: Nelson Textbook of Pediatrics, 17th ed.
Chapter 368 – MUMPS
John W. Gnann Jr.
Mumps is an acute systemic viral infection that occurs most commonly in children, is usually self-limited, and is clinically characterized by nonsuppurative parotitis.
Virology
Mumps virus is a member of the Paramyxovirus family. Mumps virions are pleomorphic, roughly spherical, enveloped particles with an average diameter of 200 nm. Glycoprotein spikes project from the surface of the envelope, which encloses a helical nucleocapsid composed of nucleoproteins and linear, nonsegmented, single-stranded, negative-sense RNA. Humans are the only natural hosts for mumps virus, although infection can be induced experimentally in a variety of mammalian species. In vitro, mumps virus can be cultured in many mammalian cell lines and in embryonated hens' eggs.
Epidemiology
In unvaccinated urban populations, mumps is a disease of school-aged children (5 to 9 years), and more than 90% have mumps antibodies by age 15 years. Before the mumps vaccine was released in the United States in 1967, mumps was an endemic disease with a seasonal peak of activity occurring between January and May. The largest number of cases reported in the United States was in 1941, when the incidence of mumps was 250 cases per 100,000 population. In 1968, when the mumps vaccine was first entering clinical use, the incidence of mumps was 76 cases per 100,000 population. In 1985, only 2982 cases of mumps were reported, an incidence of 1.1 per 100,000 population, representing a 98% decline from the number of cases reported in 1967. Between 1985 and 1987, the incidence of mumps in the United States increased five-fold to 5.2 cases per 100,000 population. More than one third of the cases reported between 1985 and 1989 occurred in adolescents and young adults, reflecting the slow acceptance of universal mumps vaccination during the 1970s. Epidemiologic studies of mumps epidemics in high schools, colleges, and military units during the 1980s demonstrated that outbreaks were due principally to failure to vaccinate. Renewed emphasis on vaccination resulted in a further decline in the annual incidence of mumps. More recent studies have attributed smaller mumps outbreaks in the 1990s to primary vaccine failure and possibly to waning vaccine-induced immunity. In 1999, the Centers for Disease Control and Prevention reported only 387 cases of mumps in the United States, the lowest annual total ever recorded.
Pathogenesis
Mumps is highly contagious and can be transmitted experimentally by inoculation of virus onto the nasal or buccal mucosa, suggesting that most natural infections result from droplet spread of upper respiratory secretions. The average incubation period for mumps is 18 days. Primary viral replication takes place in epithelial cells of the upper respiratory tract, followed by spread of virus to regional lymph nodes and subsequent viremia and systemic dissemination. Virus can be isolated from saliva for 5 to 7 days before and up to 9 days after the onset of clinical symptoms, meaning that an infected individual is potentially able to transmit mumps for a period of about 2 weeks. An estimated 30% of mumps infections in children are subclinical or associated only with nonspecific upper respiratory infection symptoms. Transient immunoglobulin M (IgM) antibody responses are detected early in the course of mumps infection, followed by the appearance of IgG antibody and cytotoxic T lymphocytes. Mumps-specific IgG can be detected during the first week of acute infection, peaks at 3 to 4 weeks, and persists for decades. Lifelong immunity follows natural infection. Patients who report more than one episode of mumps probably had parotitis of another cause.
Clinical Manifestations
PAROTITIS.
Mumps usually begins with a short prodromal phase of low-grade fever, malaise, headache, and anorexia. Young children may complain initially of ear pain. Patients then develop the characteristic parotid tenderness and enlargement, which lifts the earlobe forward and obscures the angle of the mandible. The parotid glands are involved most commonly, although other salivary glands may occasionally be enlarged. Parotitis may initially be unilateral, with swelling of the contralateral parotid gland occurring 2 to 3 days later; bilateral parotitis eventually develops in 70% of patients with symptomatic salivary gland involvement. Painful parotid gland enlargement progresses over about 3 days, followed by defervescence and resolution of parotid pain and swelling within about 7 days. Long-term sequelae of mumps parotitis are uncommon.
ASEPTIC MENINGITIS.
Symptomatic meningitis occurs in 15% of cases and is the second most common manifestation of mumps. About 50% of patients with mumps parotitis have cerebrospinal fluid (CSF) pleocytosis, although many have no clinical evidence of meningitis. Signs and symptoms of meningeal inflammation (headache, neck stiffness, vomiting, and lethargy) plus high fever usually develop 4 to 5 days after the onset of parotitis, although the meningitis may occasionally precede the parotitis. Indeed, 40 to 50% of all cases of documented mumps meningitis occur in patients who never have clinical parotitis. For unexplained reasons, symptomatic central nervous system (CNS) involvement with mumps is two to three times more common in males than in females. Examination of the CSF usually reveals normal opening pressure and a mononuclear cell pleocytosis with an average cell count of 450/mm3. A polymorphonuclear leukocyte predominance may be seen in some patients early during the course of mumps meningitis. The CSF protein is usually normal or mildly elevated (<100 mg/dL). Hypoglycorrhachia, which is not usually seen in viral meningitis, may be present in 10 to 30% of patients with mumps meningitis. Mumps virus can be recovered from CSF. Whereas the symptoms of mumps meningitis usually resolve within 7 to 10 days, the CSF abnormalities may persist for up to 5 weeks. Mumps meningitis is usually benign, and significant neurologic complications are rare.
ENCEPHALITIS.
The spectrum of mumps-induced CNS disease ranges from mild "aseptic" meningitis (which is common) to severe encephalitis (which is rare). Some cases of encephalitis develop concurrently with the parotitis and are thought to result from direct extension of viral infection from the choroid plexus ependyma into parenchymal neurons. Other cases of mumps encephalitis occur 1 to 2 weeks after the onset of parotitis and may represent a demyelinating postinfectious encephalitis. Clinical findings in mumps encephalitis include obtundation (and less commonly delirium), generalized seizures, and high fever. Other neurologic findings can include focal seizures, aphasia, paresis, and involuntary movements. Recovery from mumps encephalitis is usually complete, although complications such as aqueductal stenosis with hydrocephalus, seizure disorders, and psychomotor retardation have been reported. The overall mortality from mumps encephalitis is 0.5 to 2.3%.
ORCHITIS.
Epididymo-orchitis is rare in boys with mumps but occurs in 15 to 35% of postpubertal men with mumps. Orchitis is most often unilateral (bilateral involvement occurs in 17 to 38% of cases) and results from replication of mumps virus in seminiferous tubules with resulting lymphocytic infiltration and edema. Orchitis typically develops within 1 week of the onset of parotitis, although orchitis (like mumps meningitis) can develop before or even in the absence of parotitis. Mumps orchitis is characterized by marked testicular swelling and severe pain accompanied by fever, nausea, and headache. The pain and swelling resolve within 5 to 7 days, although residual testicular tenderness can persist for weeks. Testicular atrophy may follow orchitis in 35 to 50% of cases, but sterility is an uncommon complication even among men with bilateral orchitis.
OTHER MANIFESTATIONS.
Mumps can cause inflammation of other glandular tissues, including pancreatitis and thyroiditis. Oophoritis and mastitis have been reported in postpubertal women with mumps. Transient renal function abnormalities are common in mumps, and virus can be isolated readily from urine; significant renal damage is rare, however. Other infrequent manifestations of mumps include sensorineural deafness (either transient or permanent), arthritis, myocarditis, and thrombocytopenia. Maternal mumps infection during the first trimester of pregnancy results in an increased frequency of spontaneous abortions, but no clear association between congenital malformations and maternal mumps has been demonstrated.
Diagnosis
The diagnosis of mumps is usually based on clinical findings in a child who presents with fever and parotitis, particularly if the individual is known to be susceptible and has been exposed to mumps during the preceding 2 to 3 weeks. An atypical clinical presentation (e.g., meningitis or orchitis without parotitis) requires laboratory confirmation. Culturing for mumps virus is definitive but not universally available. Testing of acute and convalescent sera should demonstrate a diagnostic four-fold rise in mumps antibody titer. Alternatively, finding mumps IgM antibody provides good evidence of recent infection. About 30% of patients have an elevated serum amylase level that may be due to parotitis or pancreatitis.
The differential diagnosis of parotitis includes infections caused by other viruses such as influenza A, parainfluenza virus, coxsackievirus, or lymphocytic choriomeningitis virus or bacteria such as Staphylococcus aureus. Parotid gland enlargement can also be associated with Sjögren's syndrome, sarcoidosis, amyloidosis, thiazide ingestion, iodine sensitivity, tumor, or salivary duct obstruction. A careful examination should distinguish parotitis from lymphadenopathy.
Treatment
Management of the patient with mumps consists of conservative measures to provide symptomatic relief and to ensure adequate hydration and nutrition. Treatment of orchitis includes bedrest, scrotal support, analgesics, and ice packs. Patients with significant CNS involvement require hospitalization for observation and supportive care. There is currently no established role for antiviral drugs, corticosteroids, or passive immunotherapy in treatment of mumps.
Prevention
The cornerstone of mumps prevention is active immunization using the live attenuated mumps vaccine. In the United States, mumps vaccine is administered in combination with the measles and rubella vaccines (MMR) to children at age 12 to 15 months and produces protective antibody levels in more than 95% of recipients. A second dose of MMR is recommended for children at age 4 to 6 years. The mumps vaccine is also indicated for susceptible adults.
The Jeryl-Lynn strain of attenuated mumps virus used in the United States since 1967 is a very well tolerated vaccine, although rare instances of fever, parotitis, and possibly aseptic meningitis have been reported after immunization. In recent years, an increased frequency of cases of vaccine-related mumps meningitis has been recognized in other countries. These cases occurred after administration of an MMR vaccine that contained the Urabe AM9 mumps virus. In several cases, the vaccine virus was isolated from CSF and positively identified by nucleotide sequencing. This problem has not been recognized in the United States, where the Jeryl-Lynn mumps vaccine continues to be used.
Questions regarding prevention often arise when an individual with no history of mumps (typically an adult male) is exposed to a patient with active mumps. The immune status of the exposed individual can be determined by serologic testing, although this may involve some delay. A variety of serologic tests are available to determine susceptibility to mumps. The neutralizing antibody assay has been considered the "gold standard" test but is technically demanding. The hemagglutination inhibition assay is simple to perform but less specific because of cross-reactivity with other paramyxoviruses. Detection of complement-fixing antibodies against V (hemagglutinin-neuraminidase) and S (nucleocapsid) antigens was previously the routine method for determining immune status but has been replaced by more sensitive and specific enzyme-linked immunosorbent assays. The mumps skin test is not a reliable indicator of immune status. The vast majority of adults born in the United States before 1957 were naturally infected and are therefore immune. Mumps vaccine can be safely administered to an individual of unknown immune status, although vaccine given to a susceptible individual after exposure to mumps may not provide protection.
Highly controversial reports have been published that suggest an etiologic association between administration of MMR vaccine and development of autism. Parental concerns generated by the adverse publicity resulted in lower rates of immunization. However, subsequent large-scale epidemiologic studies conducted in the United States and the United Kingdom have failed to demonstrate any link between the MMR vaccine and childhood autistic disorders.
Goldman: Cecil Textbook of Medicine, 22nd ed.
This post has been edited by Guardian on 7 Jun 2007, 20:37
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