Mumps is an acute, systemic viral infection classically associated with swelling of one or both parotid glands.
Mumps is caused by a paramyxovirus with a negative-strand nonsegmented RNA genome of 15,384 bases encoding nine proteins. The nucleoprotein, phosphoprotein, and polymerase protein participate in viral replication and, together with genomic RNA, form the ribonucleocapsid. The ribonucleocapsid is surrounded by a host-derived lipid bilayer envelope containing the viral hemagglutinin-neuraminidase (HN) and fusion (F) proteins, which are responsible for cell binding by and entry of the virus and are major targets of virus-neutralizing antibodies. The functions of the other virus proteins (small-hydrophobic, matrix, V, and I) are less well understood. The small-hydrophobic gene sequence is highly variable and forms the basis for the 13 genotypes (A through M) used mainly for molecular epidemiologic purposes.
Mumps is endemic worldwide, with epidemics occurring every 3–5 years in unvaccinated populations. The estimated annual global incidence is 100–1000 cases per 100,000 population in countries without national mumps vaccination programs, where virtually the entire population has been infected by adulthood. Following the 1967 introduction of mumps vaccine in the United States, the reported number of cases declined; by 2001, this number had decreased from >150,000 to <300—a 99.8% reduction from prevaccine levels. In 2006, the United States experienced its largest mumps outbreak in more than 20 years, with 6584 reported cases. This outbreak was preceded by outbreaks in the United Kingdom (2004–2005) and followed by outbreaks in Canada. Compelling epidemiologic evidence links the genotype G virus to the outbreaks in all three countries. The majority of cases occurred in college students 18–23 years of age, most of whom had been vaccinated in early childhood. These outbreaks are probably the result of several coincident circumstances, including (1) situations promoting the spread of respiratory viruses among young adults (e.g., residence in college dormitories), (2) waning of vaccine immunity with time, (3) lack of endemically circulating wild-type virus to periodically boost vaccine-induced immune responses, and (4) continuing global epidemics of mumps (due either to lack of mumps vaccination programs or to low rates of mumps vaccination where such programs do exist). Whereas in the pre- and early postvaccine era mumps was historically a disease of childhood, the majority of U.S. cases now occur in previously vaccinated young adults.
Humans are the only natural hosts for mumps virus infection. The incubation period of mumps is ∼19 days (range, 7–23 days). The virus is transmitted by the respiratory route via droplets, saliva, and fomites. Mumps virus is typically shed from 1 week before to 1 week after symptom onset, although this window appears to be narrower in vaccinated individuals. Persons are most contagious 1–2 days before onset of clinical symptoms. Primary replication occurs in the nasal mucosa or upper respiratory mucosal epithelium. Mononuclear cells and cells within regional lymph nodes can become infected; such infection facilitates the development of viremia and poses a risk for a wide array of acute inflammatory reactions. Classic sites of mumps virus replication include the salivary glands, testes, pancreas, ovaries, mammary glands, and central nervous system (CNS).
Little is known of the pathology of mumps since the disease is rarely fatal. The virus replicates well in glandular epithelium, but classic parotitis is not a necessary component of mumps infection. Affected glands contain perivascular and interstitial mononuclear cell infiltrates and exhibit hemorrhage with prominent edema. Necrosis of acinar and epithelial duct cells is evident in the salivary glands and in the germinal epithelium of the seminiferous tubules of the testes. The virus probably enters cerebrospinal fluid (CSF) through the choroid plexus or via transiting mononuclear cells during plasma viremia. Although relevant data are limited, typical mumps encephalitis appears to be secondary to respiratory spread and is probably a parainfectious process, as suggested by perivenous demyelination, perivascular mononuclear cell inflammation, and relative sparing of neurons. Although rare, presumed primary encephalitis has been associated with mumps virus isolation from brain tissue. Evidence of placental and intrauterine spread in pregnancy has been found in both early and late gestation.
Up to half of mumps virus infections are asymptomatic or lead to nonspecific respiratory symptoms. Inapparent infections are more common in adults than in children. The prodrome of mumps consists of low-grade fever, malaise, myalgia, headache, and anorexia. Mumps parotitis—acute-onset unilateral or bilateral swelling of the parotid or other salivary glands lasting >2 days without another apparent cause—develops in 70–90% of symptomatic infections, usually within 24 h of prodromal symptoms but sometimes as long as 1 week thereafter. Parotitis is generally bilateral, although the two sides may not be involved synchronously. Unilateral involvement is documented in about one-third of cases. Swelling of the parotid is accompanied by tenderness and obliteration of the space between the earlobe and the angle of the mandible (Figs. 194-1 and 194-2). The patient frequently reports an earache and finds it difficult to eat, swallow, or talk. The orifice of Stensen's duct is commonly red and swollen. The submaxillary and sublingual glands are involved less often than the parotid gland and are almost never involved alone. Glandular swelling increases for a few days and then gradually subsides, disappearing within 1 week. Recurrent sialadenitis is a rare sequela of mumps parotitis. In ∼6% of mumps cases, obstruction of lymphatic drainage secondary to bilateral salivary gland swelling may lead to presternal pitting edema, associated often with submandibular adenitis and rarely with the more life-threatening supraglottic edema.
Child with mumps. Note the classic submandibular and preauricular enlargement of the parotid gland. (From the Centers for Disease Control and Prevention.)
Schematic drawing of a parotid gland infected with mumps virus (right) compared with ...
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