Measles

Etiology and pathogenesis

The causative agent of measles is an RNA virus of the genus Morbillivirus. It is extremely unstable in the external environment: it is destroyed by sunlight and disinfectants within 30 minutes, but withstands low temperatures well. Despite its rapid destruction, the virus has immense airborne longevity.

The entry gates are the mucous membranes of the respiratory tract and the conjunctiva. Following primary viremia, the virus settles in lymphoid tissue (tonsils, lymph nodes), where it forms specific giant multinucleated cells. Massive secondary viremia then occurs, coinciding with the onset of clinical manifestations. The virus is characterized by pronounced epitheliotropism. An important link in the pathogenesis is the development of post-infectious immunosuppression (T- and B-lymphopenia), which paves the way for secondary infections.

Epidemiology

Measles is a strict anthroponosis (only humans are affected). Susceptibility is universal, though infants in their first 3–6 months are protected by maternal antibodies (immunity completely wanes by 1 year of age). There is currently an alarming trend toward increased incidence among older children and adults.

A patient is contagious from the last two days of the incubation period until the 4th day after the appearance of the rash. A winter-spring seasonality is typical, with incidence peaks every 5–7 years.

Clinical presentation of typical form

The incubation period lasts from 9 to 17 days. The course of the disease is strictly cyclic:

1. Catarrhal period (3–6 days). Begins with acute fever, rhinitis, harsh cough, and photophobia. A key early marker is Koplik's spots (whitish specks with a hyperemic halo on the buccal mucosa). The fever is biphasic.
2. Eruption period (3–5 days). Temperature spikes again to 38–40 °C, cough and intoxication worsen. A maculopapular rash appears, tending to coalesce. The main diagnostic sign is strict craniocaudal progression: day 1 — face and neck; day 2 — trunk; days 3–4 — extremities. Meanwhile, Koplik's spots disappear.
3. Pigmentation period (5–8 days). Temperature drops, the rash darkens (acquires a brownish hue) in the same order as it appeared. Branny desquamation begins.

Diagnostics and treatment

Clinical triad for an undisputed diagnosis: hyperthermia (up to 40 °C), rash progression, and regular transition of the rash to pigmentation. Laboratory confirmation is performed using PCR (blood, urine, swabs in the first 3–7 days from rash onset) or ELISA (detection of specific IgM).

Treatment is mainly outpatient, aimed at symptom management. Dimmed lighting must be provided in the room (due to photophobia) and an optimal microclimate maintained. It is strictly contraindicated to use acetylsalicylic acid to reduce fever.

Specific prophylaxis and quarantine

To control epidemics, a vaccination coverage of over 95% of the population is required. According to the immunization schedule, live measles vaccine is administered at 12–14 months, with revaccination before school. The normal vaccination process does not make a child contagious.

Focus measures:

• Isolation of the patient up to the 5th day of the rash inclusive.
• Quarantine for non-immune contacts: from the 7th to the 17th day (up to the 21st day if immunoglobulin was administered).
• Emergency prophylaxis: vaccination of contacts older than 1 year within the first 72 hours, or administration of normal human immunoglobulin (indicated for children under one year and pregnant women).

Class and exam questions

What else to study on this topic

• Early and late complications of measles (measles croup, pneumonia, encephalitis)
• Pathogenesis of subacute sclerosing panencephalitis
• Differential diagnosis of measles with rubella and enteroviral exanthems
• Management tactics for severe forms of measles in a hospital setting
• Impact of measles-induced immunosuppression on the activation of chronic foci of infection

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

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