Mumps

Pathogen and epidemiological features

The causative agent of the disease is an RNA-containing virus from the Paramyxoviridae family (Paramyxoviridae). It is pathogenic for humans and monkeys. The virus exhibits low stability in the external environment: it is rapidly destroyed by high temperatures, ultraviolet light, drying, and standard disinfectants, but can remain viable at low temperatures for up to one year.

The infection is an anthroponosis — the source of infection is exclusively an infected human (including patients with mild and subclinical forms). The pathogen is excreted with saliva and urine, transmitting primarily via airborne droplets. A patient is contagious 1–2 days before the onset of the first symptoms and during the first 5–7 days of the acute phase.

The disease has a pronounced winter-spring seasonality and a cyclical rise every 7–8 years. The contagiousness index is moderate — approximately 50%. A persistent, lifelong immunity is formed after the infection.

Pathogenesis and dissemination

The entry gates of the infection are the mucous membranes of the upper respiratory tract and conjunctiva. Primary replication of the virus occurs in the epithelial cells of the respiratory tract, after which it enters the systemic bloodstream. The primary viremia phase develops, lasting no more than 5 days.

Carried by the bloodstream, the virus spreads throughout the body. It exhibits strict tropism for the interstitial tissue of glandular organs (salivary glands, gonads, pancreas) and structures of the central nervous system.

Following active replication in target tissues, the virus can re-enter the bloodstream (secondary viremia). This explains the asynchronous involvement of various organs and the appearance of new symptoms at different times. The body is cleared thanks to the production of specific virucidal antibodies that block the pathogen's entry into cells.

Clinical presentation

The disease begins acutely. The initial period is characterized by pronounced intoxication syndrome (fever, malaise) and local pain in the parotid region, which intensifies during chewing and mouth opening.

The main clinical sign is parotitis. A dough-like swelling forms behind the auricle and the angle of the mandible, leading to a characteristic deformation of the facial and neck contours. A specific sign — Mouratow's sign (edema and hyperemia of Stensen's duct opening) — is identified on the buccal mucosa. Patients experience decreased salivation and dry mouth.

Edema and tenderness of the salivary glands persist for 2–5 days and subside by the end of the first week. Within the first 1–2 days, the inflammatory process may involve the second parotid gland and submandibular glands (submaxillitis).

It is important to understand that lesions of the pancreas (pancreatitis), sex glands (orchitis, oophoritis), and the central nervous system (serous meningitis) are not complications, but typical symptoms of the systemic course of the disease. True complications, such as otitis media, pneumonia, or bartholinitis, are rare.

Diagnostics and differential search

Typical forms of the infection are diagnosed clinically, taking into account the epidemiological history. Atypical forms (mild, subclinical, or isolated CNS/pancreatic involvement) require laboratory confirmation:

• Molecular genetic methods: PCR to detect viral RNA in blood, CSF, or saliva.
• Serology: ELISA, CFT, and HI are used for retrospective diagnosis. When using CFT and HI, one should keep in mind possible cross-reacting false-positive reactions with the parainfluenza virus.

The differential diagnosis is structured according to the leading syndrome. Parotitis is distinguished from sialolithiasis, bacterial sialadenitis, and sarcoidosis; abdominal syndrome from surgical "acute abdomen"; testicular involvement from orchitis of tuberculous, gonococcal, or traumatic etiology.

Treatment and Prevention

There is no specific antiviral treatment; pathogenetic and symptomatic therapy is used. Most patients are treated at home; hospitalization is necessary for severe forms (meningitis, meningoencephalitis, orchitis) or when isolation is impossible.

Basic therapy:

• Bed rest and thorough oral hygiene.
• Dry heat to the affected gland area.
• Gentle dairy-vegetable diet. Raw fruits/vegetables and fresh bread are excluded so as not to stimulate secretion.
• Antipyretic medications.

For meningitis, dehydration and dexamethasone are prescribed; for orchitis, glucocorticosteroids and mandatory wearing of a scrotal support (suspensory) for at least 2–3 weeks. Antibacterial therapy is not indicated.

Prevention includes two-dose vaccination with a live cultured vaccine (at 12 months and 6 years of age). In an epidemic focus, contacts are quarantined for 21 days. The prognosis is generally favorable, but severe systemic lesions in patients over 15 years of age can lead to male infertility and diabetes mellitus in the long term.

Class and exam questions

What else to study on this topic

• Immunological aspects of pathogenesis: the role of T-lymphocyte deficiency and secretory IgA
• Features of the clinical course and treatment of mumps orchitis
• Differential diagnosis of mumps serous meningitis from enteroviral and tuberculous meningitis
• Long-term consequences of the infection: mechanisms of the development of diabetes mellitus and male infertility

Other topics from the section «Chapter 12. Infectious and parasitic diseases»

Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.