MODULE: PAROTITIS

I. Contributor : dr. Irene Ratridewi, Sp.A (K). M.Kes

II. Learning objective
At the end of this module, student should be able to know :
1. definition of parotitis
2. the causes of parotitis
3. pathogenesis of parotitis
4. clinical manifestations of parotitis
5. complication of parotitis
6. diagnosis of parotitis
7. management of parotitis
III. Method
This module is designed for medical students at six semester, and will be processed by
combines lectures and small group discussion.
IV. Overview
A. Introduction
The mumps virus causes an acute, self-limited, viral syndrome. Prior to the
widespread use of an effective vaccine, mumps primarily occurred in young children
attending primary grade school; mumps was also a leading cause of viral meningitis
and the most common cause of unilateral acquired sensorineural deafness in
children.
B. Epidemiology
Mumps epidemics have occurred worldwide with school-aged children
generally serving as the vector for horizontal spread to household family members.
Data from the National Health and Nutrition Examination Study (NHANES) from 1999
to 2004 demonstrated that the seroprevalence of antibody to mumps virus is 90
percent, which is at the low end of the estimated seroprevalence rates needed for
herd immunity (ie, 92 percent). Mumps seroprevalence was significantly lower in the
1967 to 1976 birth cohort (86 percent), suggesting that these individuals may be at
increased risk of mumps infection upon exposure.
Mumps is highly infectious and spreads rapidly among susceptible people
living in close quarters. Mumps virus is typically transmitted by respiratory droplets,
direct contact, or fomites. Infants less than one year rarely acquire mumps due to
passage of maternal antibodies.
The incubation period is usually 14 to 18 days from exposure to onset of
symptoms. Viral shedding in respiratory secretions precedes the onset of
symptomatic illness and the period of peak contagion is just before the onset of
parotitis (approximately three days)
A committee composed of members from the CDC, the American Academy of
Pediatrics, and the Healthcare Infection Control Practices Advisory Committee
reviewed data on viral isolation and shedding during infection to determine the
optimal number of days of required isolation. Based on these data, the guideline
committee recommended that the isolation duration be shortened from nine days to
five days since the risk of transmission after this time is low.
Prior to the introduction of vaccination in the United States, the peak
incidence of mumps was typically in the late winter to early spring, although sporadic
outbreaks have occurred throughout the year. Cases of mumps in the United States
declined 99 percent from 1968 to 1993 (152,209 versus 1,692 reported cases)
following the approval and introduction of a live, attenuated mumps vaccine in 1967.
C. Etiology and Pathonegesis
Mumps virus is a single-stranded RNA virus and is a member of the
Paramyxovirus genus, which also includes human parainfluenza virus. Humans
serve as the only natural host for mumps virus.
The mumps virion possesses a helical core containing the genomic
nucleocapsid portion, which is surrounded by an external glycoprotein envelope. The
major surface glycoproteins provide two discrete functions: hemagglutination-
neuraminidase activity and cell fusion activity. Only one mumps serotype has been
identified. Primary viral isolation culture techniques use a number of cell types,
including monkey kidney cell lines; mumps may be isolated from saliva,
cerebrospinal fluid, and urine.
D. Clinical Features
Mumps infection is frequently accompanied by a nonspecific prodrome
consisting of low-grade fever, malaise, headache, myalgias, and anorexia. These
symptoms are generally followed within 48 hours by the development of parotitis, a
classic feature of mumps infection. Symptomatic infection in adults is usually more
severe than in children.
Parotitis Parotid swelling is present in 95 percent of symptomatic cases of mumps.
Parotitis is due to direct infection of ductal epithelium and local inflammation.
Local parotid tenderness and occasionally earache precedes the onset of parotid
swelling. Enlargement of the contralateral parotid gland occurs in 90 percent of
patients, but may be delayed by several days. On physical examination, parotid
swelling may obscure the angle of the mandible and the orifice of Stensen's duct is
erythematous and enlarged.
Parotid swelling can last up to 10 days. Increased serum amylase supports the
clinical diagnosis.
E. Complication
The more serious complications of mumps, such as meningitis, encephalitis, and
orchitis, may occur in the absence of parotitis , which can delay accurate diagnosis of the
clinical syndrome.
Orchitis Epididymoorchitis, the most common complication of mumps infection in
the adult male, may develop in up to 38 percent of infected postpubertal males.
Symptoms are characterized by the abrupt onset of fever from 39 to 41C and
severe testicular pain, accompanied by swelling and erythema of the scrotum. The
following case series illustrates the range of findings:
In a descriptive series of 67 male patients with orchitis that occurred during a mumps
outbreak in the Gran Canaria Island from 2000 to 2001, nearly all patients had onset
of fever and parotitis that preceded orchitis by approximately five days. Orchitis was
unilateral in approximately 90 percent and bilateral in 10 percent of cases. Fifty-six
patients required hospitalization; nine patients also had mumps meningitis. During
the follow-up period, a high incidence of sperm abnormalities was observed.
While testicular atrophy has been documented in as many as 30 to 50 percent of
patients following mumps orchitis and impaired fertility in approximately 13 percent,
sterility is estimated to be rare. The risk of sterility is higher in men who have bilateral
orchitis.
Oophoritis Oophoritis occurs in approximately 7 percent of post-pubertal girls.
Aseptic meningitis Aseptic meningitis is the most frequent extrasalivary
complication of mumps virus infection . Asymptomatic CSF pleocytosis was
documented in more than 50 percent of patients with clinical mumps, in one series,
while clinical aseptic meningitis due to mumps ranged from 4 to 6 percent in larger
clinical series of mumps outbreaks. Cases of mumps aseptic meningitis occur three
times more often in males than in females.
The onset of meningitis is variable and can occur before, during, or after an episode
of mumps parotitis; aseptic meningitis has been reported in 1 to 10 percent of
patients with mumps parotiti. In some series, up to 50 percent of patients present
with mumps meningitis in the absence of parotitis. The most frequent manifestations
are headache, low grade fever, and mild nuchal rigidity.
The CSF profile may have 10 to 2000 white blood cells (WBC)/microL . The
predominating cells are usually lymphocytes, but an early polymorphonuclear
predominance can occasionally be seen. The CSF total protein is generally normal or
mildly elevated. CSF glucose levels can be mildly depressed, but values below 30 to
40 mg/dL (1.7 to 2.2 mmol/L) have been reported..
Other neurologic complications Encephalitis, deafness, Guillain-Barr syndrome,
transverse myelitis, and facial palsy are other, less frequent, neurologic
complications of mumps.
Encephalitis In the pre-vaccine era, the incidence of mumps encephalitis was
estimated to be approximately 1 in 6000 cases; through the 1960s, mumps was the
most frequent cause of confirmed viral encephalitis cases in the United States.
However, since the implementation of the MMR vaccination program, this incidence
has dramatically decreased. In 1981, mumps accounted for only 0.5 percent of
cases of viral encephalitis in the United States. Similar findings were noted in a
review from Finland . After widespread use of MMR vaccine in 1982, mumps
encephalitis virtually disappeared.
Patients with mumps encephalitis typically present with fever, altered level of
consciousness, seizures, paresis and/or paralysis. As many as one-third of patients
present without parotitis; as a result, the absence of parotitis does not exclude the
diagnosis of mumps. The CSF profile is similar to that seen with mumps aseptic
meningitis which, as noted above, can occasionally mimic those with bacterial
meningitis rather than viral infection.
Deafness In the pre-vaccine era, mumps infection was a prominent cause of
sensorineural hearing loss in children. The onset of deafness was often abrupt but
occasionally exhibited a more gradual clinical course; bilateral involvement has
been reported. Permanent deafness attributable to mumps infection has been
documented .Some patients with sensorineural hearing loss during mumps infection
have concurrently developed prominent vestibular symptoms. Labyrinthitis and
endolymphatic hydrops (Mnires syndrome) also developed subsequently in a
patient with prior acute deafness due to mumps infection.
Arthritis Mumps-associated arthropathy is a relatively infrequent complication but
affects males more often than females; monoarticular large joint (knee, hip)
involvement has been reported in addition to a polyarticular syndrome.
Pancreatitis Acute pancreatitis has occasionally been reported in both children
and adults with mumps infection. The clinical course is typically benign, with the
majority of cases resolving with conservative management; rarely, pseudocyst
formation requiring surgical drainage has occurred.
F. Diagnosis
When the patient has parotitis, the diagnosis of mumps is based upon the
characteristic clinical features. Leukopenia, with a relative lymphocytosis, and an elevated
serum amylase may be noted on routine blood testing.
Specific assays for the diagnosis of mumps are more often used in the setting of prominent
extrasalivary gland involvement or during a mumps outbreak, when laboratory criteria are
necessary to establish accurate incidence figures.
Laboratory evidence supportive of a mumps diagnosis include:
A positive IgM mumps antibody
Significant rise in IgG titers between acute and convalescent specimens
Isolation of mumps virus or nucleic acid from a clinical specimen
In patients with classic symptoms of mumps, laboratory confirmation is not required. In
patients with more atypical presentations (eg, mumps meningitis) polymerase chain reaction
testing of the appropriate fluids enables a rapid diagnosis. Targeted serologic testing may be
recommended by the public health department in the setting of a localized outbreak.
Serology Serum IgM antibody testing should be obtained as soon as mumps infection is
suspected . A second convalescent phase serum sample obtained about two to three weeks
after the first sample should be collected. A fourfold or greater increase in IgG titer is
considered a positive diagnostic result for mumps. In vaccinated persons with breakthrough
disease, IgG titers may rise rapidly and precipitously, which can impair the ability to capture
a fourfold rise in serum antibodies. Thus, it is important to obtain the first serum sample soon
after clinical presentation.
Serum IgM antibody to mumps typically remains positive for up to four weeks but may be
negative in up to 50 to 60 percent of specimens from individuals with acute disease who
were previously immunized . A negative mumps IgM titer in vaccinated individuals, therefore,
does not rule out mumps.
A positive mumps IgG serology is expected among previously immunized persons; however,
the level of neutralizing antibody that is needed for protection against mumps is not known.
Serologic tests cannot differentiate between prior exposure to mumps virus or mumps
vaccine.
Viral culture In patients with aseptic meningitis due to mumps, the virus can frequently be
isolated from the CSF during the first three days of clinical symptoms. Virus is present in
saliva for approximately one week, starting two to three days before the onset of parotitis.
Virus is also excreted in urine for the first two weeks of illness. However, the selective viral
isolation culture techniques are time consuming and may require days to yield a positive
identification of mumps virus, thus delaying the diagnosis.
Polymerase chain reaction assays The use of an IgM antibody capture immunoassay or
a nested polymerase chain reaction (PCR) assay enables more rapid confirmation of mumps
in the CSF. A nested mumps reverse transcriptase (RT) PCR assay using a specific 122 bp
fragment proved capable of detecting 0.001 plaque forming units (PFU)/mL of mumps virus
in one study. Mumps virus RNA was detected in all 18 CSF samples confirmed by viral
isolation techniques. Overall, PCR confirmed mumps virus RNA in the CSF of 96 percent of
patients compared to 39 percent for CSF culture alone.
The RT-PCR assay has enhanced characterization of genomically discrete mumps strains
associated with sporadic outbreaks and serves as a particularly useful tool when applied to
epidemiologic surveillance. Use of mumps RT-PCR assay in various clinical specimens (ie,
saliva, urine, CSF) provides an efficient method to differentiate distinct mumps strains
circulating during a given outbreak and also facilitates distinguishing wild-type stains from
vaccine-derived mumps strains.

G. Management
Therapy for mumps parotitis is symptomatic and includes analgesics or antipyretics,
such as aspirin or acetaminophen. Topical application of warm or cold packs to the
parotid may also be soothing.
Patients who have meningitis or pancreatitis with nausea and vomiting may require
hospitalization for intravenous fluids.
Patients with orchitis are also treated symptomatically with bed rest, nonsteroidal
antiinflammatory agents, support of the inflamed testis, and ice packs.

Case
Boy 7 years old, Class 2 of Elementary school Come to hospital with swelling in the neck 1
day ago with and febris 3 days ago. The child also sore throat and got cough

Question :
1. What the diagnose for this child
2. What the management for this patient
3. What the monitoring should be do for this child
Modul Task
Suggested Reading
1. Albrecht, M.A. Epidemiology, clinical manifestations, diagnosis and management of
mumps
2. Centers for Disease Control and Prevention (CDC). Exposure to mumps during air
travel--United States, April 2006. MMWR Morb Mortal Wkly Rep 2006; 55:401.
3. Centers for Disease Control and Prevention (CDC). Updated recommendations for
isolation of persons with mumps. MMWR Morb Mortal Wkly Rep 2008; 57:1103.
4. Dayan GH, Rubin S. Mumps outbreaks in vaccinated populations: are available
mumps vaccines effective enough to prevent outbreaks? Clin Infect Dis 2008;
47:1458.
5. Gupta RK, Best J, MacMahon E. Mumps and the UK epidemic 2005. BMJ 2005;
330:1132.
6. Kutty PK, Kruszon-Moran DM, Dayan GH, et al. Seroprevalence of antibody to
mumps virus in the US population, 1999-2004. J Infect Dis 2010; 202:667.
7. Okafuji T, Yoshida N, Fujino M, et al. Rapid diagnostic method for detection of
mumps virus genome by loop-mediated isothermal amplification. J Clin Microbiol
2005; 43:1625.
8. Polgreen PM, Bohnett LC, Cavanaugh JE, et al. The duration of mumps virus
shedding after the onset of symptoms. Clin Infect Dis 2008; 46:1447.