Mumps is caused by a paramyxovirus that typically presents as swelling of the parotid or other salivary glands. It is spread through respiratory droplets and saliva. While most infections are asymptomatic or mild, complications can include orchitis, meningitis, and deafness. Diagnosis is made through PCR detection of viral RNA or serology. Treatment is supportive and includes analgesics. Vaccination with the live attenuated Jeryl Lynn strain as part of the MMR vaccine provides around 90% protection with two doses and has significantly reduced mumps cases worldwide.

1. MUMPS

2. DEFINITION
Mumps is an illness characterized by acute-onset
unilateral or bilateral tender, self-limited swelling of
the parotid or other salivary gland(s) that lasts at least
2 days and has no other apparent cause.

4. ETIOLOGIC AGENT
 Mumps is caused by a paramyxovirus with a negative-strand,
nonsegmented RNA genome.
 12 mumps virus genotypes have been identified.
 The viral genome is surrounded by a host cell–derived lipid
bilayer

6. EPIDEMIOLOGY
 Mumps is endemic worldwide, with epidemics every 3–5
years in unvaccinated populations.
 These epidemics typically occur in locations where children
and young adults congregate, such as schools, military
barracks, and other institutions.
 By 2001, fewer than 300 cases were reported, representing a
99.8% reduction from prevaccineera levels.

8. PATHOGENESIS
 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.

9.  Persons are most contagious 1–2 days before onset of clinical
symptoms.
 Inference from related respiratory diseases indicates that
primary replication likely occurs in the nasal mucosa or upper
respiratory mucosal epithelium.
 Mononuclear cells and cells within regional lymph nodes can
become infected;
 Further such infection facilitates the development of viremia
and poses a risk for a wide array of acute inflammatory
reactions.

10.  Classic sites of mumps virus replication include the salivary
glands, testes, pancreas, ovaries, mammary glands, and central
nervous system (CNS).
 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.

11.  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.
 Evidence of placental and intrauterine spread in pregnancy has
been found in both early and late gestation.
 Disease is rarely fatal.

12. CLINICAL MANIFESTATIONS
 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 that lasts >2 days and
has no other apparent cause—develops in 70–90% of
symptomatic infections.

13.  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
 The patient frequently reports an earache and finds it difficult
to eat, swallow, or talk.

14.  The orifice of the parotid 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.
 In ~6% of mumps cases, obstruction of lymphatic drainage
secondary to bilateral salivary gland swelling may lead to
presternal pitting edema.

17.  Epididymo-orchitis is the next most common manifestation of
mumps, developing in 15–30% of cases in postpubertal males,
with bilateral involvement in 10–30% of those cases.
 Orchitis, accompanied by fever, typically occurs during the
first week of parotitis but can develop up to 6 weeks after
parotitis or in its absence.
 The testis is painful and tender and can be enlarged to several
times its normal size; this condition usually resolves within 1
week.
 Testicular atrophy develops in one-half of affected men.

19.  Sterility after mumps is rare, although subfertility is estimated
to occur in 13% of cases of unilateral orchitis and in 30–87%
of cases of bilateral orchitis.
 Oophoritis occurs in ~5% of women with mumps and may be
associated with lower abdominal pain and vomiting .
 sterility or premature menopause rarely been associated .
 Mumps infection in postpubertal women may also present with
mastitis.

21.  Documented CSF pleocytosis indicates that mumps virus
invades the CNS in ~50% of cases;
 However, symptomatic CNS disease, typically in the form of
aseptic meningitis, occurs in <10% of cases, with a male
predominance.
 CNS symptoms of aseptic meningitis like stiff neck, headache,
and drowsiness.
 Appear ~5 days after parotitis and also occur often in the
absence of parotid involvement.

22.  Within the first 24 h polymorphonuclear leukocytes may
predominate in CSF (1000–2000 cells/μL).
 Second day nearly all the cells are lymphocytes.
 The glucose level in CSF may be low and the protein
concentration high, a pattern reminiscent of bacterial
meningitis.
 Mumps meningitis is a self-limited manifestation without
significant risk of death or long-term sequelae.

23.  Cranial nerve palsies have occasionally led to permanent
sequelae, particularly deafness.
 The reported incidence of mumps-associated hearing loss
varies between 1 in 1000 and 1 in 100,000.
 In ~0.1% of infections, mumps virus may cause encephalitis,
which presents as high fever with marked changes in the level
of consciousness, seizures, and focal neurologic symptoms.
 Electroencephalographic abnormalities may be seen.
 The mortality rate ~1.5%.

24. Other CNS problems occasionally associated with mumps
include;
 Cerebellar ataxia,
 Facial palsy,
 Transverse myelitis,
 Hydrocephalus,
 Guillain-barre syndrome,
 Flaccid paralysis, and
 Behavioral changes.

25.  Mumps pancreatitis, which may present as abdominal pain,
occurs in ~4% of infections.
 Myocarditis and endocardial fibroelastosis are rare and self-
limited but may represent severe complications of mumps
infection.
 However, mumps-associated electrocardiographic
abnormalities have been reported in up to 15% of cases.
 Other unusual complications include thyroiditis, nephritis,
arthritis, hepatic disease, keratouveitis, and thrombocytopenic
purpura.

26.  Abnormal renal function is common, but severe, life-
threatening nephritis is rare.
 It remains at issue whether an excessive number of
spontaneous abortions are associated with gestational mumps.
 Mumps in pregnancy does not appear to lead to premature
birth, low birth weight, or fetal malformations.

28. DIFFERENTIAL DIAGNOSIS
 Infectious causes of parotitis include
Viruses
 HIV
 Coxsackievirus
 Parainfluenza virus type 3
 Influenza A virus
 Epstein-barr virus
 Adenovirus
 Parvovirus B19
 Lymphocytic choriomeningitis virus
 Human herpesvirus 6

29.  Gram-positive bacteria
 Atypical mycobacteria
 Bartonella species
Parotitis can also develop in the setting of
 Sarcoidosis
 Sjogren’s syndrome
 Uremia
 Diabetes mellitus
 Malnutrition
 Cirrhosis
 Drug treatments.
Unilateral parotitis can be caused by ductal obstruction, cysts,
and tumors.

30. LABORATORY DIAGNOSIS
 Laboratory diagnosis is primarily based on detection of viral
RNA by reverse-transcriptase polymerase chain reaction
(RT-PCR) or on serology.
 For RT-PCR-based testing, viral RNA can be extracted either
directly from clinical samples or from cell cultures incubated
with clinical samples.

31.  Buccal swabs appear to be the best specimens for virus
detection, particularly when obtained within 2 days of clinical
onset.
 Mumps virus can also be detected readily in throat swabs and
saliva and, in cases of meningitis, in CSF.
 Mumps virus has rarely been detected in blood.
 The ability to detect viral RNA in clinical samples rapidly
diminishes beyond the first week after symptom onset,

32.  In several studies rates of virus detection were substantially
lower in recipients of two vaccine doses than in unvaccinated
persons or recipients of one dose.
 A serologic diagnosis of mumps is typically made by Enzyme-
linked immunosorbent assay (ELISA). The data must be
interpreted with caution.
 In vaccinated persons with mumps, IgM is typically absent;
thus, a negative IgM result in a vaccinated person does not rule
out mumps.

33.  In addition, regardless of vaccination status, IgM may not be
detectable;
 If serum is assayed too early (prior to day 3 of symptom onset)
or too late (beyond 6 weeks after symptom onset) in the course
of disease.
 Reliance on a rise in IgG titer in paired acute- and
convalescent-phase sera also is problematic: IgG titers in
convalescent-phase sera may be only nominally greater than
those in acute-phase sera.

34.  The main downside to replacement of these functional
serologic assays with the more RAPID ELISA method.
 Is the latter’s detection of all virus-specific antibodies,
including those that are nonneutralizing (i.e., nonprotective).
 Thus, an individual who is seropositive by ELISA may lack
protective levels of antibody.
 While there is a strong association between the presence of
mumps virus neutralizing antibody and protection from
disease.

35. TREATMENT
 Mumps is generally a benign, self-resolving illness.
 Therapy for parotitis and other clinical manifestations is
symptom based and supportive.
 The administration of analgesics and the application of warm
or cold compresses to the parotid area may be helpful.

36.  Testicular pain may be minimized by the local application of
cold compresses and gentle support for the scrotum.
Anesthetic blocks also may be used.
 Neither the administration of glucocorticoids nor incision of
the tunica albuginea is of proven value in severe orchitis.
 Anecdotal information on a small number of patients with
orchitis suggests that SC administration of interferon á2b may
help preserve the organ and fertility.

37.  Lumbar puncture is occasionally performed to relieve
headache associated with meningitis.
 Mumps immune globulin has not been consistently shown to
be effective in preventing mumps and is not recommended for
treatment or postexposure prophylaxis

38. PREVENTION
 Vaccination is the only practical control measure.
 Incidence and morbidity typically exceeding 90% after
vaccination.
 Large mumps outbreaks,young (often unvaccinated) children
in primary;
 Secondary in schools,young adults, particularly on college
and university campuses.

39.  Several mumps virus vaccines are used throughout the world;
the live attenuated JERYL LYNN STRAIN is used.
 Current recommendations are that mumps vaccine be
administered as part of the;
 Combined Trivalent measles-mumps-rubella vaccine (M-M-
R II)
or
 Quadrivalent measles-mumps-rubella-varicella vaccine
(ProQuad ).

40. According to IAP MMR vaccine
 1st doze should be given after 9mts of age/270 days of age
 2nd doze 15mts of age/4-8 week after 1st doze
 3rd doze after 4-6 yrs of age
 Mumps vaccine contains live attenuated virus.
It is not recommended for
 Pregnant women
 Allergic reaction to components of the vaccine
 Primary or secondary immunosuppression.

41.  Immunity to mumps is associated with the development of
neutralizing antibody.
 Seroconversion occurs in ~95% of recipients of the Jeryl Lynn
strain.
vaccine efficacy is
 one dose for ~80%
 two doses for 90%.