on 20-Dec-2024 (Fri)

Our first case had a history of mumps following which he noticed patchy hyperhidrosis on the face, which gradually progressed to involve other body parts associated with hypohidrosis and dryness. Even though a review of literature by Rajput et al.[8]

Definition Mumps is an acute viral infection that most commonly manifests as nonsuppurative swelling and tenderness of the parotid or other salivary glands caused by the mumps virus. Less common manifestations of mumps include meningitis, encephalitis, epididymo-orchitis, oophoritis, and pancreatitis

Epidemiology Mumps is endemic throughout the world, and humans are the only natural hosts for the virus. Incubation period is usually 16 to 18 days, with a range of 2 to 4 weeks. Before the introduction of the mumps vaccine in the United States in 1967, epidemics occurred every 2 to 5 years, with peak incidence between January and May. Since 1967 there has been greater than a 99% decline in the annual US incidence of mumps. Outbreaks of mumps have been reported throughout the world, including the United States, even in populations who have received the recommended two-dose measles-mumps- rubella (MMR) series.

Microbiology Mumps is an enveloped, single-stranded RNA virus. Only one serotype of mumps virus exists, but there are 13 genotypes

Diagnosis The clinical diagnosis is made on the basis of a history of exposure and of parotid swelling and tenderness. The diagnosis is confirmed by isolation of mumps virus or detection of mumps nucleic acid by polymerase chain reaction from clinical specimens or the presence of mumps-specific immunoglobulin M (IgM) antibodies or a fourfold rise in mumps IgG antibodies in serum

Therapy Therapy for mumps is symptomatic and supportive.

Prevention Immunization with live-attenuated mumps virus vaccine as part of the standard MMR vaccine at 12 months and 4 to 6 years of age is recommended for all children; a two-dose series of MMR is recommended for individuals beyond childhood who have not received the childhood series. The Advisory Committee on Immunization Practices recommended that a third dose of MMR be administered to individuals at increased risk of mumps during an outbreak (2018)

The most prominent mani- festation of this disease is nonsuppurative swelling and tenderness of the salivary glands, with one or both parotid glands involved in most cases.

The disease is benign and self-limited, with one-third of affected persons having subclinical infection

Meningitis and epididymo-orchitis represent the two most important of the less frequent manifestations of this disease.

As is characteristic of many viral infections, mumps is usually a more severe illness in persons past the age of puberty than in children and more commonly leads to extrasalivary gland involvement in these older patients.

Hippocrates described mumps and its contagious characteristics in the fifth century bce. In the late 1700s Hamilton emphasized the occurrence of orchitis as a manifestation of mumps

The experimental production of the disease in monkeys by Johnson and Goodpasture in 19341 provided the evidence that a filterable virus was present in the saliva of patients with mumps. In 1945 Habel reported the cultivation of mumps virus in the chick embryo.2 Enders and colleagues3 described the skin test and development of complement-fixing antibodies after mumps in humans

A killed-virus vaccine used in the early 1950s on human subjects achieved limited success,4 and in 1966 Buynak and Hilleman5 reported the development of an effective live-virus vaccine

The etymology of the word mumps is unclear. It may arise from the English noun mump, meaning a lump, or from the English verb to mump, defined as “to be sulky”—a description of the characteristic facial expression.

In the older literature mumps may have been called “epidemic parotitis.”

Mumps virus is a member of the Paramyxoviridae family, which includes the following genera: Rubulavirus (mumps virus, New Castle disease virus, human parainfluenza virus types 2, 4a, and 4b); Paramyxovirus (human parainfluenza virus types 1 and 3); Morbillivirus (measles); and Pneumovirus (human respiratory syncytial virus).

The external surface is regularly studded with glycoproteins possessing hemagglutinin, neuraminidase, and cell fusion activity.

The genome codes for eight proteins—the hemagglutinin-neuraminidase protein (HN), fusion protein (F), nucleocapsid protein (NP), phosphoprotein (P), matrix protein (M), hydrophobic protein (SH), and L proteins.7

Antibodies to the F and HN proteins appear to be the most prominent determinants of immunity.

Although only one serotype of mumps virus is known, there are 13 genotypes (A–M) that have been determined on the basis of sequencing of the SH protein, which is the most variable protein among mumps strains.8–10

Mumps virus is ether sensitive by virtue of its lipid envelope. It is stable at 4°C for several days and at −65°C for months to years; however, repeated freezing and thawing may diminish viral activity.

For primary viral isolation, monkey kidney, human embryonic kidney, or HeLa cell cultures are used for primary isolation

Cytopathic effects, such as the appearance of intracytoplasmic eosinophilic inclusions, rounding of cells, or the fusion of cells into giant multinucleate syncytia, may be noted.12

The presence of mumps virus is usually confirmed by the hemagglutination inhibition (HAI) test, which uses convalescent serum after mumps infection to inhibit the adsorption of chick erythrocytes added to mumps-infected epithelial cells

Mumps is endemic throughout the world.

In the United States, before the licensing of live-attenuated mumps vaccine in 1967, epidemics occurred every 2 to 5 years.13

Although the disease occurred throughout the year, the peak incidence was between January and May.14

There has been more than a 99% decline in the annual US incidence of mumps since 1967, with an average of only 265 cases/year reported to the Centers for Disease Control and Prevention (CDC) from 2001–05; the seasonal variation that was evident in earlier years is no longer apparent.18

Meyer demonstrated that mumps is spread throughout the community by children in schools, with secondary spread to family members.17

In the 2006 outbreak in the United States, 6584 cases of mumps were detected; 85% of patients were in Iowa and the seven contiguous states; the highest attack rate was for the age group of 18 to 24 years, which comprised 29% of all cases, and 83% of this group attended college.20 The outbreak virus was of genotype G, the same virus genotype that had caused an outbreak in the United Kingdom during 2004–06.19 Surprisingly, for those patients with known vaccine status, only 13% had not received vaccine, and 63% had received two or more doses of mumps containing vaccine. The reasons for the outbreaks and the apparent vaccine failures are not clear and may have been multiple.21,22 These include possible waning immunity and exposure pressure from crowded conditions in dormitories, where susceptible individuals may have gathered.

Genotypic differences between the vaccine Jeryl Lynn strain (A) and the circulating mumps strain in outbreaks in the United States and United Kingdom (G) were present. Genotype G has been the predominant circulating mumps strain in the United States since 2006.25

Investigators demonstrated that in the Iowa outbreak, preoutbreak mumps antibody titers were lower among mumps case patients than in exposed but asymptomatic classmates.23,24

However, the genotype A virus vaccines were apparently effective in controlling genotype G outbreaks, so the role of genotype differences in vaccine failure, if any, is unclear.

In the New York outbreak, most of the cases had previously received two doses of measles-mumps-rubella (MMR) vaccine; a third dose of MMR vaccine resulted in a rapid decline of the epidemic, suggesting that waning immunity could be bolstered even in populations with high two-dose coverage of MMR.28

A study of 15 clusters of mumps in France in 2013 indicated that the “odds” of mumps increased for twice-vaccinated individuals by 10% for every year that had passed since the second dose.29 On the basis of this and other studies, the French High Council of Public Health recommended that a third dose of MMR be given during outbreaks of mumps for individuals who had received their second dose more than 10 years before the outbreak

A recent study of outbreaks of mumps in Ireland in 2008–09 showed that immunoglobulin G (IgG) levels to the circulating genotype G5 mumps strain needed to be greater than 40 relative units/mL to be correlated with anti-G5 neutralization activity in vitro.30 Lower titers of serum neutralizing activity were seen in males compared with females with acute mumps infection. This is consistent with previous observations that males are more likely to be infected in such outbreaks

Mumps is uncommon in infants younger than 1 year. Resistance to infection in this age group is based on passive immunity acquired by the placental transfer of maternal antibody.

In the prevaccine era, greater than 50% of cases occurred in the 5- to 9-year-old age group, and 90% of the cases occurred in children younger than 14 years. In 2001 49% of infections were reported in persons older than 15 years

Men and women have the same frequency of development of parotitis with mumps infection.33

Although persistent infections in cultured cells are commonly established by mumps virus,34 a carrier state is not known to exist in humans.

Humans are the only known natural host; however, monkeys and other laboratory animals have been experimentally infected.1

The virus is naturally transmitted via direct contact, droplet nuclei, or fomites and enters through the nose or mouth

More intimate contact is necessary to transmit mumps than for measles or varicella.

The period of peak contagion is just before or at the onset of parotitis

It has been suggested that, during the incubation period, the virus proliferates in the upper respiratory tract epithelium and viremia ensues, with secondary dissemination and localization to glandular and neural tissue.35,36

Experimental mumps infection has been produced in humans and monkeys by direct instillation of the virus into the Stensen duct.1 However, the incubation period in this experimental model is shorter than in naturally occurring disease, and initial infection of the parotid gland does not explain the fact that meningitis or other manifestations of mumps infection may occur before the onset of parotitis.

When parotid glands have been examined, diffuse interstitial edema has been found, along with a serofibrinous exudate consisting primarily of mononuclear leukocytes. Neutrophils and necrotic debris accumulate within the ductal lumen, and the ductal epithelium shows degenerative changes. The glandular cells are relatively spared but may also be involved with edema and overflow of the inflammatory reaction from the interstitial tissues.

The multinucleate syncytia and intracytoplasmic eosinophilic inclusions that are occasionally seen in mumps-infected tissue culture are not present in vivo.

The description of brain involvement in mumps encephalitis has most often been that of postinfectious encephalitis characterized by perivenous demyelinization, perivascular mononuclear cuffing, and a generalized increase in microglial cells, with relative sparing of neurons.37 However, descriptions of what appears to be primary mumps encephalitis that show widespread neuronolysis but no evidence of demyelinization have been reported.38

The incubation period of mumps averages 16 to 18 days, with a range of 2 to 4 weeks.

Characteristically, the prodromal symptoms are non- specific and include low-grade fever, anorexia, malaise, and headache

Within 1 day the nature of the illness becomes apparent when the patient complains of an earache, and tenderness can be elicited by palpation of the ipsilateral parotid. The involved gland is soon visibly enlarged and progresses to a maximum size over the next 2 to 3 days. The most severe pain accompanies the period of rapid enlargement

At its height, parotitis results in lifting of the ear lobe upward and outward. Lesser degrees of enlargement can more readily be appreciated by viewing the patient from behind. The enlarged parotid gland obscures the angle of the mandible, whereas cervical adenopathy does not hide this anatomic landmark

Usually, one parotid gland enlarges 1 or 2 days after the other; however, mumps results in unilateral parotitis alone in one-quarter of patients with salivary gland involvement.

The orifice of the Stensen duct is frequently edematous and erythematous.

Trismus may result from the parotitis, and the patient may have difficulty with pronunciation and mastication

Ingestion of citrus fruits or juices typically exacerbates the pain

During the first 3 days of illness the patient’s temperature may range from normal to 40°C

After parotid swelling has reached its peak, pain, fever, and tenderness rapidly resolve, and the parotid gland returns to normal size within 1 week

Complications of parotitis are rare but are reported to include sialectasia resulting in recurrent acute and chronic sialadenitis.39

Involvement of the other salivary glands may occur in conjunction with parotitis in up to 10% of cases but is rare as the sole manifestation of mumps infection (Table 157.1)

Submandibular gland involvement mimics signs of anterior cervical lymphadenopathy.

The sublingual glands are the least frequently inflamed during mumps infection; when involvement occurs, it is usually bilateral and may be associated with swelling of the tongue.

Presternal pitting edema develops in 6% of patients with mumps, most commonly in those who have submandibular adenitis.40 The proposed mechanism for the involvement of the tongue and presternal area is obstruction of the lymphatic drainage of those regions by enlarged salivary glands

Pharyngolateral edema with dyspnea is a rare complication of mumps and may result in airway stenosis.41 It is most often associated with submandibular gland swelling and is thought to be caused by local inflammation and circulatory disturbance of lymphatic flow. Cases generally respond to administration of steroids, but some cases have required tracheotomy.41

Central nervous system (CNS) involvement is the most common extrasalivary gland manifestation of mumps

Bang and Bang42 reported the presence of cerebrospinal fluid (CSF) pleocytosis in 51% of 255 patients with mumps but without other evidence of meningitis.

Clinical meningitis occurs in 1% to 10% of persons with mumps parotitis,43 but, on the other hand, only 40% to 50% of patients with mumps meningitis, confirmed by serology or viral isolation, have parotitis.43–46

Meningeal symptoms, like any of the other manifestations of mumps infection, may occur before, during, after, or in the absence of parotitis. Its onset averages 4 days after the appearance of salivary gland involvement but may be as early as 1 week before or as late as 2 weeks after parotitis.42–45 Men are afflicted three times as often as women,43–46 but the age distribu- tion is the same as for uncomplicated mumps.

Ritter has noted that mumps meningitis with parotitis is most frequent in the spring, whereas meningitis without parotitis is most frequent in summer.44

The typical clinical features associated with viral meningitis are present—that is, headache, vomiting, fever, and nuchal rigidity.

Lumbar puncture yields CSF containing 10 to 2000 white blood cells (WBC)/mm3. The pre- dominating cells are usually lymphocytes, but 20% to 25% of patients have a polymorphonuclear leukocyte predominance.45 Protein levels are normal to mildly elevated, and 90% to 95% of patients have a CSF protein content less than 70 mg/dL.45,46 Hypoglycorrhachia (CSF glucose concentration <s.

These CSF abnormalities may persist for 5 weeks or longer.44,47

Abatement of fever by lysis and resolution of symptoms generally occur 3 to 10 days after the onset of illness.

The meningitis is benign, with complete recovery and an absence of sequelae

Before the introduction of the live-attenuated mumps vaccine in 1967, mumps accounted for approximately 10% of cases of aseptic meningitis in the United States. At present aseptic meningitis is rarely attributed to mumps.

Encephalitis is reported to occur in from 1 in 600048 to 1 in 40049 cases of mumps. The former ratio probably represents a more accurate estimate. There appears to be a bimodal distribution of cases according to the time of onset—an early group in which onset coincides with the presence of parotitis and a larger late group in which the condition develops 7 to 10 days after the onset of parotitis

As noted earlier in the section “Pathology,” early-onset encephalitis represents direct damage to neurons as a result of viral invasion, whereas late-onset disease is a postinfectious demyelinating process related to the host response to infection. These two processes probably represent the ends of a continuum of disease. Some patients die after the primary viral invasion of the brain, and some of those who survive produce antibodies to the virus or neural breakdown products and develop an “autoimmune” reaction.

The clinical features are generally those of nonfocal encephalitis; in addition to marked changes in the level of consciousness, neurologic findings may include convulsions, paresis, aphasia, and involuntary movements. CSF values are similar to those in uncomplicated meningitis. Fever is high and, characteristically, temperatures of 40° to 41°C are present. Neurologic manifestations and fever gradually resolve over a period of 1 to 2 weeks. Sequelae such as psychomotor retardation and convulsive disorders are reported,44–46 but their frequency cannot be determined from the available data. Death occurs in 1.4% of reported cases.49

However, by 1981 it represented only 0.5% of cases of viral encephalitis nationwide, and by the 1990s mumps encephalitis was rare.

The term meningoencephalitis is frequently used when describing patients with various degrees of CNS involvement.38,43,44,47,50 This term should be eliminated in reference to mumps because it confuses a common and essentially benign condition (meningitis) with a relatively uncommon and serious illness (encephalitis) that might result in neurologic residua or death. Clearly, many patients with mumps meningitis may have lethargy, as may a large percentage of those with any viral infection, such as influenza. However, the presence of profound changes in the level of consciousness or other findings suggestive of supratentorial involvement indicates the clear diagnosis of encephalitis as distinct from the ambiguous designation of meningoencephalitis

Although nuchal rigidity and CSF pleocytosis may be present in patients with encephalitis, the meningeal component is a trivial aspect of this illness

Transient high-frequency-range deafness has been reported in 4.4% of cases of mumps in a military population.51 Permanent unilateral deafness occurs in 1 in 20,000 cases of mumps.52 The onset of otologic symptoms may be gradual or abrupt; vertigo is frequently present. On subsequent testing vestibular function has been normal.

Epididymo-orchitis is the most common extrasalivary gland mani- festation in the adult. It develops in 20% to 30% of postpubertal male adolescents with mumps infection and is bilateral in one of six of those with testicular involvement.64,65 Although it has been reported in infancy, it is rare before puberty.

Two-thirds of cases occur during the first week of parotitis and another 25% arise during the second week.64 However, gonadal involvement may precede parotitis or occur as the only manifesta- tion of mumps

The onset is abrupt, with temperatures in the range of 39° to 41°C, chills, headache, vomiting, and testicular pain. Genital examination reveals warmth, swelling, and tenderness of the involved testicle and erythema of the scrotum. Epididymitis is present in 85% of cases and usually precedes the orchitis, but it is rare without orchitis. The testis may be enlarged to three to four times its normal size.

Constitutional complaints and fever generally parallel the severity of gonadal involvement. Fever resolves in 84% of patients within 5 days. Pain and swelling resolve shortly after defervescence. However, tenderness may persist for longer than 2 weeks in 20% of the cases.64 Early in convalescence a loss of turgor may be appreciated.

When testes are examined months to years later, some degree of atrophy is noted in 50% of patients

Clearly, most men who have unilateral orchitis need fear nothing other than a possible cosmetic imbalance. Even those with bilateral involvement should be assured that impotence (other than psychogenic) is not a sequela and that sterility is rare.

Twenty-eight cases of testicular malignancy in men with atrophy of the testis due to mumps orchitis have been reported.66

Oophoritis develops in 5% of postpubertal women with mumps. Symptoms include fever, nausea, vomiting, and lower abdominal pain. Impaired fertility and premature menopause have been reported as a consequence of ovarian involvement but must be considered to be rare.67

Joint involvement during mumps is noted infrequently in adults and rarely in children.68,69 Migratory polyarthritis is the most frequently described clinical form. Monarticular arthritis and arthralgia have also been reported; both large and small joints are involved. Symptoms most commonly start 10 to 14 days after the onset of parotitis and may last up to 5 weeks. The process resolves spontaneously without residual joint damage

Pancreatitis is manifested by severe epigastric pain and tenderness accompanied by fever, nausea, and vomiting. It is uncommon as a severe illness; however, many affected persons may complain of mild degrees of upper abdominal discomfort

Electrocardiographic changes appear in up to 15% of patients with mumps; the most common abnormalities are depressed ST segments, flattened or inverted T waves, and prolonged P-R intervals.70,71 Clinically manifested myocarditis is rare; however, deaths associated with myocarditis have been reported during the acute illness and after a chronically progressive deteriorating course.70,71

Hughes and colleagues73 have reported two deaths related to mumps-associated nephritis

Gestational viral infections were extensively investigated in a controlled cohort study by Siegel and colleagues.79–81 They observed excess fetal deaths when mumps developed during the first trimester; second- and third-trimester mumps infections were not associated with increased fetal mortality.79

Although the number of cases was small, when the data were analyzed with respect to the onset of infection, the effect on birth weight was greatest when mumps occurred in the first trimester.80

As reported by Siegel and colleagues,81 occurrence rates of major congenital defects were equal in both mumps and control newborn populations; even when the data were analyzed by trimester, no trends could be established

St. Geme and colleagues84 have suggested an “embryopathic” relation- ship between intrauterine mumps infection and endocardial fibroelastosis (EFE) on the basis of the presence of skin test reactivity to mumps antigen in a high percentage of the EFE patients.

A similar controversy exists over the possible role of mumps in the etiology of juvenile diabetes mellitus. Diabetes, transient or permanent, which developed soon after mumps, has been the subject of a number of case reports.88,89 However, it is not clear whether this is simply coincidental. Epidemiologic studies have demonstrated a 7-year periodic- ity in the incidence of both mumps and childhood diabetes, with a 3- to 4-year lag time between their respective peaks.90 Coxsackievirus B4 has also been epidemiologically linked to diabetes.91

Although the frequency of EFE has declined in recent years, there has not been a decline in the frequency of juvenile diabetes mellitus coincident with the decreasing frequency of mumps after introduction of the mumps vaccine.

Complement-fixing antibodies directed against the NP protein (historically, S antigen) appear rapidly; sometimes they are present at the onset of clinically apparent illness. Antibody titers against the HN protein (historically, V antigen) rise more slowly and peak at about 2 to 4 weeks after the beginning of disease.92

However, anti-NP antibody titers decline rapidly over a period of several months to undetectable levels, whereas anti-HN antibody titers drop more slowly and persist for years. This pattern of response provides the possibility of a serologic diagnosis of mumps from a single serum specimen.

An acute-phase serum demonstrating a high anti-NP and low anti-HN titer or a high anti-NP and high anti-HN titer can be interpreted as evidence of current or recent infection, respectively.

IgM antibodies to mumps are the earliest humoral responses and usually fall within 2 to 6 months. IgM anti-NP antibodies detected by capture or enzyme-linked immunosorbent assay (ELISA) are the most sensitive early serologic responses and are used by the CDC to detect acute or recent infection (see later).

Neutralizing antibodies appear during convalescence. They are directed against HN and F proteins, and detectable titers persist for years. Although assays for these antibodies constitute the most reliable test to determine whether a person is immune to mumps, such assays are cumbersome and not routinely performed

Assays for HAI antibodies, which also develop after the onset of mumps, are the simplest of the serologic studies, but results are unreliable because of potential cross- reaction with other paramyxoviruses. ELISAs for antibody to mumps have been developed93,94 and are widely available

Delayed hypersensitivity to an intradermally administered mumps skin test antigen develops between 3 weeks and 3 months after mumps.3 The skin test was widely used as a measure of immunity to mumps and as a test for the competence of delayed hypersensitivity.

Neutralizing antibodies persist for several months and account for the rarity of mumps in young infants and for the lack of response to immunization in this age group

Transplac ental tra nsfe r of mater na l mumps co mpl ement-fixing, HAI, and neutralizing antibodies has been demonstrated.95 Titers in maternal and cord serum are almost identical.

One attack of mumps, whether inapparent or clinically manifested, confers lifelong immunity

When meningitis, orchitis, or pancreatitis is present, leukocytosis with a shift to the left is most commonly encountered.

The serum amylase level is elevated in the presence of parotitis and may remain abnormal for 2 to 3 weeks. Serum amylase levels may also be elevated in the absence of clinical salivary gland involvement

The typical CSF findings in mumps meningitis have been described previously. Similar, although less marked, CSF abnormalities are present in half of patients with mumps parotitis but without apparent CNS involvement

In a patient with aseptic meningitis an elevated serum amylase level should suggest mumps infection

Laboratory confirmation of typical mumps is unnecessary. However, when parotitis is absent or recurrent, when extrasalivary gland manifesta- tions are prominent, or when documentation of the presence of a specific viral disorder is desired, a variety of diagnostic aids can be used

The presence of IgM antibodies, as determined by ELISA or a fourfold rise between acute and convalescent sera on complement fixation, HAI, ELISA, or neutralization testing, confirms the diagnosis

Immunity to mumps is usually assessed by ELISA. This assay combines ease of performance with reliability.

Reverse transcriptase PCR assays that are highly sensitive and specific have been developed and appear to be significantly more sensitive than tissue culture isolation methods.7,97,98

Virus is usually present in saliva for about 1 week, from 2 to 3 days before to 4 to 5 days after the onset of parotitis.99

A recent review of viral shedding data by the CDC, American Academy of Pediatrics, and Healthcare Infection Control Practices Advisory Committee has concluded that virus shedding is relatively low by 5 days after onset of parotitis and recommended that isolation of patients is not necessary for more than 5 days after clinical illness in the hospital or community setting.101

The virus is frequently isolated from the CSF in patients with clinical meningitis during the first 3 days of meningeal symptoms43 and is present as late as the sixth day of CNS disease.

Viruria has been detected during the first 2 weeks of illness; in one study 72% of urine specimens during the first 5 days of illness yielded a positive culture.72

Viremia has rarely been detected and has been found only during the first 2 days of illness.35,36

Mumps viral RNA has been detected by PCR assay in clinical specimens from patients with mumps infection and in throat swabs of healthy children after administration of mumps vaccine.102–104

However, virus has been isolated from saliva as early as 6 days before and as late as 9 days after the first signs of salivary gland involvement.

In addition, virus may be recovered from the saliva of persons with inapparent infection or those who manifest only extrasalivary gland signs.100

Parainfluenza 3 virus, coxsackieviruses, and influenza A viruses have been reported to cause acute parotitis.96,105,106 These entities can be differentiated from mumps only by viral culture or serology.

In a study of 101 cases of sporadic nonoutbreak cases of parotitis in the United States from 2009–11, no specimen was positive for mumps virus; 38 specimens were positive for other viruses, including Epstein-Barr virus, human herpesvirus 6, and parainfluenza; and 17% of cases tested were positive for mumps IgM antibody.107

Bilateral parotid swelling is often seen in children with human immunodeficiency virus (HIV) infection

Suppurative parotitis, most often caused by Staphylococcus aureus or gram-negative organisms, usually occurs in the postoperative period, in premature newborns, or in debilitated patients with poor oral intake. The gland is warm, hard, and extremely tender; the overlying skin is ery- thematous. Massage of the parotid expresses purulent drainage from the Stensen duct

Parotid enlargement caused by drugs or metabolic disorders is usually bilateral and asymptomatic. Phenylbutazone, thiouracil, iodides, and phenothiazines have been implicated in this condition.76

Diabetes mellitus, malnutrition, cirrhosis, and uremia are among the metabolic disorders that can cause parotid swelling.76

Rare conditions that may mimic mumps include Mikulicz syndrome, Parinaud syndrome, uveoparotid fever of sarcoidosis, and Sjögren syndrome.

Therapy for mumps parotitis is symptomatic and supportive

Topical application of warm or cold packs to the parotid may also relieve discomfort

Management of orchitis is purely symptomatic. Bed rest, narcotic analgesics, support of the inflamed testis with a “bridge,” and ice packs make the patient feel more comfortable

An anesthetic block of the spermatic cord with 1% procaine hydrochloride may alleviate severe pain.108

Interferon- α2b administered to four men with bilateral mumps orchitis resulted in prompt resolution of symptoms, with no evidence of testicular atrophy or oligospermia during follow-up study.109

There is no convincing evidence that the use of steroids or diethylstilbestrol or incision of the tunica albuginea produces more rapid resolution of the orchitis or prevents subsequent atrophy.

Gellis and colleagues110 have shown that 20 mL of mumps immune globulin administered intramuscularly to adult men with mumps reduces the incidence of orchitis from 27.4% to 7.8%. However, mumps immune globulin is no longer commercially available

As noted, recommendations for the management of patients with mumps include isolation for 5 days after the onset of parotid swelling to prevent the spread of infection to susceptible persons.101 This measure may be of little value, particularly in closed populations, such as schools or hospitals,111 because virus is present in saliva days before parotitis develops and because those with clinically inapparent infection can shed virus

Passive protection to exposed susceptible persons may have been afforded by mumps immune globulin, available in the past. However, Reed and colleagues16 reported that use of mumps immune globulin during an epidemic in Alaska did not reduce clinical parotitis or inap- parent infection rates and did not diminish the incidence of meningitis and orchitis

Active immunization with the Jeryl Lynn strain of attenuated mumps virus vaccine has been available in the United States since December 1967. The vaccine is prepared in chick embryo cell culture.5

A single subcutaneous immunization produces protective levels of mumps- neutralizing antibodies in greater than 95% of vaccinees.5 Although the antibody levels produced are lower than after natural infection, adequate titers are maintained for at least 10.5 years.112

Adverse reactions to the vaccine are uncommon; transient suppression of tuberculin-delayed hypersensitivity has been reported, and parotitis and orchitis have been recognized rarely.

Vaccine virus is not present in secretions of immunized children

In Japan aseptic meningitis associated with mumps vaccine virus occurred in 0.05% to 0.3% of recipients of the Urabe AM 9 mumps vaccine; manifestations began 2 to 4 weeks after immunization.113,114 US studies did not reveal evidence of an increased risk of aseptic meningitis after administration of the Jeryl Lynn strain of mumps vaccine.115

All children older than 12 months should be immunized. Vaccination should take place at 12 to 15 months and again at 4 to 6 years of age, as part of immunization with the combined live measles-mumps-rubella (MMR) virus vaccine.

A two-dose immunization regimen is recommended for all adolescents and health care personnel without evidence of mumps immunity. Other adults should receive at least one dose of vaccine. Immunization after exposure may not provide protection from natural infection

Based on the results of a study on the effectiveness of a third dose of MMR vaccine to control a mumps epidemic at the University of Iowa in 2015–16, where 98.1% of students had previously received two doses of MMR,116 the Advisory Committee on Immunization Practices recommended in 2018 that a third dose of MMR vaccine be administered to persons at increased risk of mumps during an outbreak.25

As with other live-virus vaccines, mumps vaccine should not be administered to pregnant women, patients receiving immunosuppressive therapy, or those with severe febrile illnesses, advanced malignancies, or congenital or acquired immunodeficiencies

Serious reactions to the mumps component of MMR have not been reported in limited studies in HIV-infected patients. However, a fatal case of measles pneumonitis occurred in a 21-year-old man with advanced HIV disease who was vaccinated with MMR vaccine; therefore it should not be administered to such patients (see Chapter 316).117 Individuals with HIV infection who are not severely immunocompromised may be immunized with MMR vaccine

From year to year in the United States, mսmpѕ cases can range from a few hundred to a few thousand (figure 1) [3-5]. The number of cases reported in 2016 and 2017 (6369 and 5629, respectively) were the highest in a decade [6].

The incubation period is usually 16 to 18 days (range 12 to 25 days) from exposure to onset of symptoms [8-11].

In one review including 15 studies monitoring mսmрs infectivity over time, infectivity could be detected as early as seven days onset to eight days after onset of раrοtitiѕ [12]. The highest rate of infectivity (highest titer of virus) was present immediately preceding the onset of рarotitis, with rapid decrease of virus shedding over the next five days. By days 6 to 9 following onset of раrοtitis, virus titers and infectivity were very low

Several sporadic mսmps outbreaks (the occurrence of ≥3 cases linked by place and time) have occurred since 2006 among susceptible individuals in a variety of settings in the United States and the United Kingdom, including military posts [13], schools [14-16], colleges and universities [17-22], and summer camps [23,24]

The shift in mսmpѕ epidemiology in the United States from a childhood disease (prior to routine vаϲϲiոаtioո) to a disease primarily affecting vaccinated young adults raises the possibility that waning immunity may be a factor in outbreaks [22]. However, high vаϲϲiոatiоn coverage helps limit the size, duration, and spread of mumрѕ.

During outbreaks, mսmрs cases have occurred among vaccinated individuals [35]

The incubation period is usually 16 to 18 days (range 12 to 25 days) from exposure to onset of symptoms [8-11]

Μumрs typically begins with a few days of fever, headache, myalgia, fatigue, and anorexia; these manifestations are usually followed by development of salivary gland swelling within 48 hours

Ρarοtitis occurs most commonly among children between two and nine years of age; tenderness, occasionally associated with earache, typically precedes parotid swelling [36,37].

Раrotitis may be unilateral or bilateral; initial unilateral involvement is followed by contralateral involvement a few days later in 90 percent of cases [ 1]. Parotid swelling can last up to 10 days

On physical examination, parotid swelling may obscure the angle of the mandible (picture 1), and the orifice of Stensen's duct is erythematous and enlarged (figure 2)

Μսmpѕ is usually self-limited; most individuals recover completely within a few weeks

Asymptomatic infection occurs in 15 to 20 percent of cases; it is more common in adults than in children. Adults who do have symptomatic infection are more likely to have severe manifestations than children with symptomatic infection.

There is no firm evidence for an association between mսmpѕ infection during pregnancy and complications [1,39-42]

Complications of mumpѕ may include оrсhitis and neurologic manifestations (including mеningitiѕ, еոϲeрhalitiѕ, and ԁеаfոеѕs); these may occur even among vaccinated individuals who develop mսmps [43]

Complications of mսmpѕ may occur in the absence of рarotitis [ 15,44,45]