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Before an effective vaccine against mumps was developed, the disease was a common childhood illness, commonly expressed as parotitis. It is also capable of causing aseptic meningitis, encephalitis, and (in adults) acute orchitis.
The highest frequency of mumps infection is observed in the 5- to 15-year age group. Infection is rarely seen in the first year of life. Although about 85% of susceptible house-hold contacts acquire infection, approximately 30 to 40% of these contacts do not de-velop clinical disease. The disease is communicable from approximately 7 days before until 9 days after onset of illness; however, virus has been recovered in urine for up to 14 days following onset. The highest incidence of infection is usually during the late win-ter and spring months, but it can occur during any season.
After initial entry into the respiratory tract, the virus replicates locally. Replication is fol-lowed by viremic dissemination to target tissues such as the salivary glands and central ner-vous system (CNS). It is also possible that before development of immune responses, a sec-ondary phase of viremia may result from virus replication in target tissues (eg, initial parotid involvement with later spread to other organs). Viruria is common, probably as a result of di-rect spread from the blood into the urine, as well as active viral replication in the kidney. The tissue response is that of cell necrosis and inflammation, with predominantly mononuclear cell infiltration. In the salivary glands, swelling and desquamation of necrotic epithelial lining cells, accompanied by interstitial inflammation and edema, may be seen within dilated ducts.
As in most viral infections, the early antibody response is predominantly with IgM, which is replaced gradually over several weeks by specific IgG antibody. The latter per-sists for a lifetime but can often be detected only by specific neutralization assays. Immu- nity is associated with the presence of neutralizing antibody. The role of cellular immuneresponses is not clear, but they may contribute both to the pathogenesis of the acute dis-ease and to recovery from infection. After primary infection, immunity to reinfection is virtually always permanent.
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