Medical Importance of Mumps


Morphology and Biochemical properties
The mumps virus particle has the typical paramyxovirus morphology. Typical also are the biologic properties of hemmagglutination, neuraminidase, and hemolysin. Hemmaglutination can be inhibited by specific antisera to mumps virus, and this inhibition can be used to measure antibody responses. Similarly, the neucleocapsid of the virus particle forms the major component of the "S" (soluble) complement-fixing antigen.

Animal susceptibility and Growth of Virus
The hemagglutinin, the hemolysin and the infectivity of the virus are destroyed by heating at 56 degrees Celsius for 20 minutes. The skin test antigen and the complement -fixing antigen are more heat-stable.

Reactions to physical and chemical growth of virus
The hemagglutinin, the hemolysin and the infectivity of the virus are destroyed by heating at 56 degrees Celsius for 20 minutes. The skin test antigen and the complement-fixing antigen ate more heat-stable.

Pathogenesis and Pathology
Two theories exist regarding the pathogenesis of mumps.

  • The virus travels from the mouth by way of stensen's duct to the parotid gland, where it undergoes primary multiplication. This is followed by a generalized viremia and localization in testes, ovaries, pancreas, thyroid, or brain.
  • Primary replication occurs in the privileged epithelium of the respiratory tract. This is followed by a generalized viremia and simultaneous localization in the salivary glands and other organs.

Little tissue damage is associated with uncomplicated mumps. The ducts of the parotid glands show desquamation of the epithelium, and polymorphonuclear cells are present in the lumens. There are interstitial edema and lymphocytic infiltration. With severe orchitis, the testis is congested. The punctuate hemorrhage as well as degeneration of the epithelium of the seminiferous tubules is observed. Central nervous system pathology may vary from perivascular edema to inflammatory reaction, glial reaction, hemorrhage, or demyelination.

Clinical features
The incubation period is commonly 18-21 days. A prodromal period of malaise and anorexia is followed by rapid enlargement of parotid glands as well as other salivary glands. Swelling may be confirmed to one Parotid gland, or one gland may enlarge several days before the other. The gland enlargement is associated with pain, especially when tasting acid substance. The salivary adenitis is commonly accompanied by low-grade fever and lasts for approximately a week.

Testes and ovaries may be affected, especially puberty. 20% of males over 13 years of age who are infected with mumps virus develop orchitis, which is often unilaterally and does not usually lead to sterility. Due to the lack of elasticity of the tunica albuginea, which does not allow the inflamed testis to swell, atrophy of the testis may follow secondary to pressure necrosis. Secondary sterility does not occur in women because the ovary, which has no such limiting membrane, can swell when inflamed.

Mumps accounts for 10-15% of aseptic meningitis, observed in the USA and is more common among males than females. Meningoencephalitis usually occurs 5-7 days after the inflammation of the salivary glands, but it may occur simultanously or in the absence of parotitis and is usually self-lining. The cerebrospinal fluid shows pleocystosis (10-2000 / nL, mostly lymphocytes) that may persist after clinical recovery.

Rare complications of mumps include:

  • A self-limiting polyarthritis that resolves without residual deformity;
  • Pancreatitis associated with Transient by-perglycemia, glycosuria, and steatorrhea (it has been suggested that diabetes mellitus may occasionally follow);
  • Nephritis
  • Thyroiditis; and
  • Unilateral nerve deafness (hearing loss is complete and permanent)
  • Mumps may be a possible causative agent in the production of aquaductal stenosis and hydrocephalus in children. Injection of mumps virus into suckling hamsters has produced similar lesions.


Source by Funom Makama

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