Mumps is an acute, generalized viral disease in which painful enlargement of the salivary glands, chiefly the parotids, is the usual presenting sign.
The virus is a member of the paramyxovirus group, which also includes the parainfluenza, measles, and
disease viruses. Only one serotype is known. 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. Virus has been isolated from saliva, cerebrospinal fluid, blood, urine, brain, and other infected tissues. Newcastle
Mumps is endemic in most urban populations; the virus is spread from a human reservoir by direct contact, airborne droplets, fomites contaminated by saliva, and possibly by urine. It is distributed worldwide and affects both sexes equally; 85% of infections occurred in children younger than 15 yr prior to widespread immunization. Now disease often occurs in young adults, producing epidemics in colleges or in the work place. Epidemics appear to be primarily related to lack of immunization rather than to waning of immunity. Epidemics occur at all seasons but are slightly more frequent in late winter and spring. Sources of infection may be difficult to trace because 30–40% of infections are subclinical. There has been a decrease in the incidence since the introduction of mumps vaccine 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 longer than 24 hr before 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.
Lifelong immunity usually follows clinical or subclinical infection, although second infections have been documented. Transplacental antibodies seem to be effective in protecting infants during their first 6–8 mo. Infants born to mothers who have mumps in the week prior to delivery may have clinically apparent mumps at birth or experience illness in the neonatal period. Severity ranges from mild parotitis to severe pancreatitis. The serum neutralization test is the most reliable method for determining immunity but is cumbersome and expensive. A complement-fixing antibody test is available (see Diagnosis). The presence of V antibodies alone suggests previous mumps infection.
After entry and initial multiplication in the cells of the respiratory tract, the virus is blood-borne to many tissues, among which the salivary and other glands are the most susceptible.
The incubation period ranges from 14–24 days, with a peak at 17–18 days. In children, prodromal manifestations are rare but may be manifest by fever, muscular pain (especially in the neck), headache, and malaise. 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 ear lobe 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 swelling limited to one gland is common. 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 moderate fever; normal temperatures are common (20%), but temperatures of 40º C (104º F) or more are rare.
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.
A maculopapular erythematous rash, most prominent on the trunk, occurs infrequently; rarely it is urticarial.
OTHER ORGANS DAMAGE
Meningoencephalomyelitis. This is the most frequent complication in childhood. The 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 parotitis. Clinical manifestations occur in over 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. The mortality rate is about 2%. Males are affected three to five times as frequently as females. Mumps is one of the most common causes of aseptic meningitis
The pathogenesis of mumps meningoencephalitis has been described as (1) a primary infection of neurons and (2) 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. Moderate stiffness of the neck is seen, but the remainder of the neurologic examination is usually normal. The cerebrospinal fluid (CSF) usually contains fewer than 500 cells/mm3, although occasionally the count may exceed 2,000. The cells are almost exclusively lymphocytes, in contrast to enteroviral aseptic meningitis, in which polymorphonuclear leukocytes often predominate early in the disease. Mumps virus can be isolated from cerebrospinal fluid early in the illness.
Orchitis, 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. Rarely, there is a hydrocele. The orchitis usually follows parotitis within 8 days or so; it may also occur without evidence of salivary gland infection. In about 30% of patients both testes are affected. 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 is 4 days. Approximately 30–40% of affected testes atrophy. Impairment of fertility is estimated to be about 13%, but absolute infertility is probably rare.
Oophoritis. Pelvic pain and tenderness are noted in about 7% of postpubertal female patients. There is no evidence of impairment of fertility.
Pancreatitis. Severe involvement of the pancreas is rare, but mild or subclinical infection may be more common than is recognized. It may be unassociated with salivary gland manifestations and 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 with mumps, with or without clinical manifestations of pancreatitis.
Nephritis. Viruria has been reported frequently. In one study of adults, abnormal renal function occurred at some time in every patient, and viruria was detected in 75%. The frequency of renal involvement in children is unknown. Fatal nephritis, occurring 10–14 days after parotitis, has been reported.
Thyroiditis. Although uncommon in children, a diffuse, tender swelling of the thyroid may occur about 1 wk after the onset of parotitis with subsequent development of antithyroid antibodies.
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.
Mastitis. This is uncommon in each sex.
Deafness. Unilateral, rarely bilateral, nerve deafness may occur; although the incidence is low (1:15,000), mumps is a leading cause of unilateral nerve deafness. The hearing loss may be transient or permanent.
Ocular Complications. These include dacryoadenitis, painful swelling, usually bilateral, of the lacrimal glands; optic neuritis (papillitis) with symptoms varying from loss of vision to mild blurring with recovery in 10–20 days; uveokeratitis, usually unilateral, with photophobia, tearing, rapid loss of vision, and recovery within 20 days; scleritis; tenonitis, with resultant exophthalmos; and central vein thrombosis.
Arthritis. Arthralgia associated with swelling and redness of the joints is an infrequent complication; complete recovery is the rule.
Thrombocytopenic Purpura. This sign is infrequent.
Mumps Embryopathy. There is no firm evidence that maternal infection is damaging to the fetus; a possible relationship to endocardial fibroelastosis has not been established. Mumps in early pregnancy does increase the chance of abortion.
The diagnosis of mumps parotitis is usually apparent from the symptoms and physical examination. When the clinical manifestations are limited to those of one of the less common lesions, the diagnosis is not so clear but may be suspected, especially during an epidemic. The routine laboratory tests are nonspecific; there is usually leukopenia with relative lymphocytosis, but complications often result in polymorphonuclear leukocytosis of moderate degree. An elevation of serum amylase is common; the rise tends to parallel the parotid swelling and then to return to normal within 2 wk or so. The etiologic diagnosis depends on isolation of the virus from the saliva, urine, spinal fluid, or blood or the demonstration of a significant rise in circulating complement fixation antibodies during convalescence. Serum antibodies to the S antigen reach their peak early in about 75% of patients and are detectable at the time of the presenting symptoms. They gradually disappear within 6–12 mo; antibodies against the V or viral antigen usually reach a peak titer in about 1 mo, remain stationary for about 6 mo, and then slowly decline during the ensuing 2 yr to a low level, at which they persist. The presence of a high anti-S titer and a low anti-V titer during the acute stage of an otherwise undiagnosed meningoencephalitis, for example, strongly suggests a mumps infection, which would be confirmed if a convalescent serum (taken 14–21 days later) revealed a fourfold rise of anti-V antibodies accompanied by little change in the titer of anti-S antibodies.
This includes parotitis of other origin, as in viral infections including human immunodeficiency virus (HIV) infection, influenza, parainfluenza 1 and 3, cytomegalovirus, or the rare instances of coxsackievirus A and lymphocytic choriomeningitis infections. These infections can be distinguished by specific laboratory tests; suppurative parotitis, in which pus can often be expressed from the duct; recurrent parotitis, a condition of unknown origin, but possibly allergic in nature, which has frequent recurrences and a characteristic sialogram; salivary calculus, obstructing either a parotid or, more commonly, a submandibular duct, in which the swelling is intermittent; preauricular or anterior cervical lymphadenitis from any cause; lymphosarcoma or other rare tumors of the parotid; orchitis resulting from infections other than mumps, for example, the rare infections by coxsackievirus A or lymphocytic choriomeningitis viruses; and parotitis caused by cytomegalovirus in immunocompromised children.
Treatment of parotitis is entirely symptomatic. Bed rest should be guided by the patient's needs, but no statistical 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 corticosteroids or a nonsteroidal anti-inflammatory agent. Salicylates do not appear to be effective.
Passive. Hyperimmune mumps gamma globulin is not effective in preventing mumps or decreasing complications.
Active. The routine administration of live, attenuated mumps vaccine is discussed in Chapter 247. Vaccinated children usually do not experience fever or other detectable clinical reactions, do not excrete virus, and are not contagious to susceptible contacts. Rarely, parotitis can develop 7–10 days after vaccination. The vaccine induces antibody in about 96% of seronegative recipients and has a protective efficacy of about 97% against natural mumps infection. The protection appears to be long lasting. In one outbreak of mumps, several children who had been immunized with mumps vaccine in the past experienced an illness characterized by fever, malaise, nausea, and a red papular rash involving the trunk and extremities but sparing the palms and soles. The rash lasted about 24 hr. No virus was isolated from these children, but increases in the titer of mumps antibody were demonstrated.
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