The incubation period is 16 - 18 days but may vary from 14 -
25 days. Parotid swelling develops in 95% of those with clinical
illness. The rate of subclinical infection varies with age, but
is on average 30%. In a small proportion of patients, the
symptoms may resemble mild URTI. Typically, a prodromal illness
consisting of headache, malaise, myalgia and low grade fever
occurs 1 - 2 days before the onset of parotid enlargement.
Patients with classic mumps develop enlargement of one parotid
gland, followed 1 - 5 days later by enlargement of the
contralateral gland. The patient complains of pain and tenderness
in the area of the gland. The submandibular and sublingual glands
may occasionally be involved. The parotid swelling starts to
subside after 4 to 7 days. Virus shedding into the saliva begins
a couple of days before the onset of parotitis and ends 7 to 8
days later.
Complications
All the other manifestations of mumps can be regarded as
systemic complications of mumps rather than as true
complications.
Meningitis ;- Aseptic meningitis occurs in 10% of
patients with mumps but as many as 50% show abnormalities
in the CSF. Mumps is the most frequent causative agent of
aseptic meningitis, in many countries being responsible
for 10 - 15% of all cases. Symptoms are indistinguishable
from other types of aseptic meningitis and can start one
week before parotid swelling before parotid swelling to 3
weeks after it. The CSF reveals a lymphocytosis of
usually below 500 lymphocytes/mm3, normal or
elevated protein. Virus can be isolated from the CSF
during the first 2 to 3 days after onset. Later, specific
antibodies can demonstrated in the CSF. Symptoms of
meningitis subside 3 to 10 days after onset and recovery
is usually complete. A study suggests that the majority
of cases of meningitis occur without apparent
parotiditis.
Encephalitis ;- encephalitis occurs rarely as a
complication of mumps, where lesions are found in the
brain and spinal cord. The incidence of encephalitis is
around 1 in 6000 cases of mumps. Probably both direct
viral invasion and allergic inflammatory reactions lie
behind the nervous tissue damage. Clinical features
suggesting encephalitis are convulsions, focal
neurological signs, movement disorder and changes in
sensory perception. Sometimes polio-like paralysis ensues
and fatalities have been reported.
Hearing Loss ;- before vaccinations, mumps used to
be one of the leading causes of hearing loss in children
and young adults. In most cases, the hearing loss is
transient but permanent dysfunction may occur. Hearing
problems did not correlate with meningitis and appears to
be due to direct damage tothe cochlea. The incidence of
hearing loss is estimated to be in the region of 1 per
15,000 cases.
Orchitis and oophoritis ;- orchitis and oophoritis
are more likely to occur after puberty where the
incidence is 20 - 30%, and in 20 - 40% of cases, there is
bilateral involvement. Men are much more likely to be
affected than women.
Pancreatitis ;- the exact incidence of
pancreatitis is hard to determine but is thought to be as
high as 5%.
Arthralgia ;- arthralgia affecting a large joint
may develop 2 weeks after parotitis. They are more
frequent in young male adults.
Myocarditis ;- this can usually only be found on
ECG examination in 10 - 15% of patients. Rarely,
congestive heart failure and deaths have been reported.
Transient Renal Dysfunction ;- this is a frequent
complication of clinical mumps. Cases of symptomatic
nephritis following mumps are unusual.
Insulin Dependent Diabetes ;- there is some
epidemiological evidence to suggest that mumps may be a
triggering mechanism for IDDM. It is thought that
immunological mechanisms may be involved and certain
HLA-D haplotypes are particularly susceptible.
Abortion ;- if a pregnant woman contracts mumps
during her pregnancy, there is increased risk for
abortion. This is thought to be due to hormonal
imbalances caused by virus infection.
Thyroiditis ;- there is evidence for a role of
mumps virus in the causation of subacute thyroditis.
However, the evidence is not strong.
E. Laboratory Diagnosis
During mumps infection, several non-specific findings may be
present in the blood. The WBC may be low with lymphocytes
predominating. ESR and CRP may be normal or slightly elevated.
Amylase levels may be elevated.
1. Serology ;- a serological diagnosis is usually made
by finding a significant increase in Ab titres in 2 serum samples
taken 10 - 14 days apart. In some cases, the detection of IgM may
be used to diagnosis acute infection. Although only 1 serotype of
mumps exist, cross-reactions between mumps virus and
paramyxovirus makes serological results difficult to interpret on
occasions. Several techniques are available :
CFT - the CFT is still the widely used
for the diagnosis of mumps. Two antigenic preparations
are commonly used, the V antigen (consists mainly of HN
glycoprotein), and the S antigen (consists mainly of the
NP). Antibodies against S appear early and are
short-lived, whilst antibodies to V antigens appear
slowly but persists longer. By comparing titres using the
two different antigens, it is often possible to make a
serological diagnosis early in the course of illness.
However, due to problems with cross-reactivity, a paired
serum sample is always needed for a reliable by CFT.
HAI - this test measures antibodies
similar to those reacting with the V antigen in the CF
test.
Neutralization test - virus
neutralization has long been regarded as the most
reliable serological marker for immunity but is very
tedious to carry out and thus rarely used.
SRH - this technique has been adapted
for use for the diagnosis of mumps.
Solid phase ELISA or RIA - various
assays are available for the determination of IgM and
IgG. However, capture IgM assays are liable to
interference from Rheumatoid Factor. Elisa tests are
useful in the measurement of mumps antibodies in CSF. The
greater sensitivity allows the determination of the exact
CSF/serum ratio and a ratio of greater than 100 signifies
intrathecal synthesis. However, the blood-brain barrier
should be intact and proper controls should be used. This
may be an unrelated antibody or albumin.
2. Virus Isolation ;- virus isolation may be carried
out by allantoic inoculation of 6 day old embryonated eggs or by
tissue culture methods. Virus can be isolated from the CSF during
the first 2 - 3 days after the onset of disease, and is present
in urine and saliva for 2 to 3 weeks. Monkey kidney cells are
generally used for virus isolation where a CPE is seen which
consists of the formation of syncytia and the focal rounding of
cells. Virus identification can be performed by neutralization or
inhibition of haemadsorption by specific sera.
Syncytial formation caused by mumps virus. Note the
presence of red blood cells on the surface of the cell sheet
(haemadsorption). Courtesy of Linda Stannard, University of
Cape Town, S.A.
F. Management and Prevention
No specific treatment is available for mumps. Uncomplicated
parotitis seldom require treatment except adequate. Some
authorities recommend a short course of corticosteriods in severe
cases. Mumps is the commonest cause of meningitis and
encephalitis in many countries such as USA and Scandinavia and
many countries have mumps vaccination as part of their
vaccination program. At one time, there was some argument as to
whether a vaccination program against mumps was necessary but the
combination of mumps with rubella and measles in the same vaccine
had swung the argument vastly in its favour. An inactivated
vaccine was first used in the 1940s successfully. This has now
been replaced by a live attenuated vaccine. The protection rate
is over 95% and no adverse reactions are associated with the
vaccine. In the USA, where more than 40 million doses of mumps
vaccine have been administered, a cost-benefit analysis has been
carried out. In a cohort of 1 million people, the vaccine would
prevent over 74,000 cases of mumps and 3 deaths and the
cost-benefit ratio is 7.4:1. Mumps vaccine is now routinely given
as part of the MMR regimen in many countries to all infants.
