– non suppurative enlargement of one or both salivary glands.
– Causes a mild childhood disease; in adults complications including meningitis and orchitis are common.
– >1/3rd of all mumps infection are asymptomatic.
– A berring- bone or zipper- like RNP is frequently seen to leak from the virions in preparation examined by electron microscope (common to all paramyxoviruses).
PATHOGENESIS– human are the only natural hosts.
– 10– replication occurs in nasal or upper respiratory tract epithelial cells; viremia disseminates virus to salivary glands (involvement of parotid glands not obligatory).
– Incubation period ranges from 2 weeks- 4 weeks (typically 16-18 days); virus shed in saliva from about 2 days before to 9 days after onset of swelling.
– Mumps is a systemic viral disease.
– Frequently infects the kidneys; viruria persists for upto 14 days after onset of symptoms.
– CNS is also commonly infected.
– mumps is an iceberg disease, which although common as childhood infection is often subclinical( at least one- third of all infection).
– After an incubation period of 14-18 days; prodromal period of ‘ flu-like’ illness ( fever, malaise, anorexia) is seen which is followed by developing pain in parotids, which then swell rapidly ( due to blockage of efferent duct), sucking of a lemon infront of a sufferer is a refined form of torture! Paratitis resolves in 1 week.
– CNS involvement is common ( about 50 % of infection), majority are clinically inapparent ; meningitis in 15% of cases and encephalitis in 0.3%.
– 20-50% of men develop architis ( often unilateral); complication is painful and atrophy of testis may occur, but only rarely does sterility result.
– Oophoritis in about 5% girls, develops after parotitis resolves.
– immunity is permanent after a single infection; even subclinical infection generate life long immunity.
– there is only one antigenic type and it doesn’t exhibit significant Ag- variation.
– Ab to HN gp (V-Ag), the F-gp and internal nucleocapsid protein (S-Ag) develop in serum following natural infection; CMI response also develops.
– Passive immunity from mother confers immunity in infants for 6 months.
– Ab to S-Ag appear earlier (3-7 days after onset of symptoms) but disappear within 6 months; Ab to V-Ag develop after 4 weeks of onset, but persists for years.
Lab studies not required to establish diagnosis of typical cases, however may sometimes be confused with enlargement of parotids due to suppuration, drug sensitivity, tumors etc.
Isolation and identification of virus
– saliva, CSF, urine collected with in few days after onset of illness
– monkey kidney cells preferred for viral isolation; samples should be inoculated shortly after collection.
– For rapid diagnosis, IFT to detect viral Ag in 2-3 day cell culture.
– Virus produces little CPE (cell rounding, giant cell formation)
– Haemadsorption test to demonstrate presence of haemadsorbing agent.
Ab- rise detected using paired sera; ELISA or HI test commonly used.
– Mumps IgM present, early in illness and lasts for 60 days; the heterotypic Ab induced by parainfluenza virus infection don’t cross- react in mumps IgM, ELISA.
– CFT using S- and V- Ag is also performed.
– endemic worldwide; disease incidence highest in children aged 5-9 yrs.
– Humans are the only natural hosts; transmission by direct contact, air- borne droplets or contaminated fomites.
– Subclinical cases can transmit the virus.
– Mortality rate is low (0.01%), mostly due to encephalitis.
Treatment / Prevention / control:
– no specific therapy
– immunization with attenuated live mumps vaccine ( made in chick embryo culture) produces a subclinical , non communicable infection; it is available in monovalent form ( mumps only) or in combination with measles and rubella (MMR vaccine) and given as single subcutaneous injection ; provides protection for at least 10 yrs.
– Vaccine contains the Jeryl Lynn or Urabe strains.
– Contraindications are pregnancy, immunodeficiency and hypersensitivity to neomycin and egg protein.
Passive immunization not very reliable.