Mumps
Mumps is one of the commonly acquired viral diseases of childhood and is the most common cause of aseptic meningitis. However, its incidence in developed countries has decline dramatically since the advent of vaccination.
A. Properties
A member of the paramyxovirus family, closely related to parainfluenza viruses
ss RNA, enveloped virus of helical symmetry.
Single RNA molecule of 16 - 18 kbp, in a helical nucleocapsid in association with the nucleoprotein (NP)
M protein forms the structure which underlies the viral envelope. The HN (haemagglutination and neuraminidase protein) and the F (fusion) protein form the spikes present on the lipid bilayer envelope
only one serotype of the virus exist
significant antigenic cross-reaction occurs with other members of the paramyxovirus genus.
Mumps is a disease of childhood, the highest incidence occurs
in children between 5 - 9 years of age. The disease is less
contagious than other childhood diseases such as measles and
varicella. According to a recent epidemiological survey in
America, 10% of the population had mumps during each of the first
5 years of life, 74% had it by age 10, and 95% by 20 years of
age. Mumps is endemic in most urban areas. In temperate zones, a
seasonal variation is evident, the highest incidence being around
January to May. No such seasonal variation exists in tropical
countries. Subclinical infections are common in very young
infants (2 - 3 years of age), and the proportion increases with
age in adulthood. Up to 90% of infections at the age of 10 - 14
age were associated with symptoms whilst almost all infections
are subclinical beyond 60 years of age.
Mumps is transmitted by droplet spread or by direct contact.
The primary site of viral replication of the epithelium of the
upper respiratory or the GI tract or eye. The virus quickly
spreads to the local lymphoid tissue and a primary viraemia
ensues, whereby the virus spreads to distant sites in the body.
The parotid gland is usually involved but so may the CNS, testis
or epididymis, pancreas and ovary. A few days after the onset of
illness, virus can again be isolated from the blood, indicating
that virus multiplication in target organs leads to a secondary
viraemia Parotitis is the most frequent presentation, occurring
in 95% of those with clinical symptoms. Occasionally, meningitis
may precede parotitis by a week. Virus is excreted in the urine
in infectious form during the 2 weeks following the onset of
clinical illness. It is not known whether virus actually
multiplies in renal tissues or whether the virus is of
haematogenous origin. Life-long immunity is the rule after
natural infection, but reinfections can occur and 1 - 2% of all
cases are thought to be reinfections.
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.
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. RT-PCR - can be performed on oral or buccal swabs for a rapid diagnosis. It may also be used on CSF for diagnosing mumps menigitis.
3. 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.
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.
