Infectious mononucleosis

Pathogenesis and pathogen specifics

Primary replication of the Epstein–Barr virus occurs in the mucous membrane of the upper respiratory tract and structures of the lymphoid pharyngeal ring. Following the initial local inflammatory response, the pathogen spreads hematogenously to the organs of the reticuloendothelial system — peripheral lymph nodes, liver, and spleen.

A key feature of the virus is its strict B-lymphotropism. Unlike most intracellular pathogens, EBV does not provoke cytolysis (destruction) of infected cells. Infection of macrophages and lymphoid elements stimulates their active proliferation, which morphologically manifests as the appearance of altered cells in the blood — atypical mononuclear cells. Latent infection of B-lymphocytes leads to their polyclonal activation followed by the synthesis of low-specificity heterophile antibodies.

Clinical presentation

The disease begins gradually, reaching the peak of clinical manifestations by the end of the first week. In young children, the infection is often asymptomatic, whereas in adolescents and adults it manifests as classic mononucleosis. Several leading syndromes are distinguished:

• Lymphadenopathy. The posterior cervical lymph nodes are predominantly affected (along the posterior border of the sternocleidomastoid muscle). The nodes enlarge up to 1–3 cm, group into clusters or chains, and upon palpation remain mobile, not fused to tissues, and slightly tender.
• Oropharyngeal and nasopharyngeal involvement. Nasopharyngitis develops with pronounced nasal breathing obstruction and a characteristic nasal voice quality. Lacunar-follicular tonsillitis is observed in almost all patients. The deposits on the tonsils are friable, easily removed with a spatula, and do not spread to the faucial pillars and soft palate.
• Hepatosplenic syndrome. Splenomegaly is usually more pronounced than liver enlargement. A cytolysis syndrome with elevated ALT frequently occurs, and mild jaundice is noted in rare cases.

The febrile period varies greatly — from several days to three weeks, and the temperature can reach febrile values (38–39.5 °C).

Peripheral blood changes

The hematological profile is a critical criterion for establishing a diagnosis. Mononuclear leukocytosis is recorded in the blood test. Pronounced lymphocytosis (from 35–50%) and monocytosis (more than 10–15%) are typical for the leukogram.

A diagnostic marker is the detection of atypical mononuclear cells at a concentration exceeding 10% (often around 12%). Morphologically, they are large cells with wide cytoplasm. These shifts, along with hepatosplenomegaly, can persist as residual phenomena for a long time — up to 2 months or more after clinical recovery.

Diagnostics and differential search

Priority in laboratory confirmation is given to serological methods and PCR diagnostics (detection of viral DNA).

• Acute phase markers: detection of IgM class antibodies to the viral capsid antigen (VCA). They are produced as early as the incubation period and are eliminated after 2–3 months.
• Markers of past infection: IgG antibodies to the capsid antigen, which persist in the body for life.
• Nonspecific tests: the Paul–Bunnell reaction (heterohemagglutination) is rarely used in modern practice and is considered merely orientational.

In differential diagnosis, the infection must be distinguished from adenovirus infection, pharyngeal diphtheria, and rubella. With profound shifts in the hemogram and the presence of "red flags" (persistent fever, anemia, sharp acceleration of ESR), it is critically important to rule out acute leukemia. To verify it, a bone marrow examination (sternal puncture) is performed.

Treatment Management

There is no specific vaccine against EBV. The infection has low contagiousness: quarantine in groups is not imposed, and focal disinfection is not required. Hospitalization is carried out exclusively based on the severity of the clinical condition.

In the acute phase, strict bed rest is indicated for the patient. Etiopathogenetic therapy includes antiviral drugs and immunomodulators (interferon alfa-2b, meglumine acridoneacetate). Nonsteroidal anti-inflammatory drugs (ibuprofen, paracetamol) are used to relieve fever.

Antibacterial therapy is prescribed only when secondary bacterial flora joins. When a life-threatening complication develops — the risk of asphyxia due to edema of the airway lymphoid tissue — systemic glucocorticosteroids are used (e.g., prednisolone 2 mg/kg per day in a 5–7 day course with gradual tapering).

Class and exam questions

What else to study on this topic

• Mechanisms of mononucleosis-like syndrome formation in CMV, HIV, and human herpesvirus 6 infection
• Progressive lymphoproliferative disorders and CNS lymphomas in immunocompromised patients
• Features of the clinical and laboratory profile of EBV infection with severe hepatitis syndrome (cholestasis and cytolysis)
• Interpretation of serological markers: dynamics of antibodies to viral capsid antigen (VCA)
• Criteria for assessing the severity of typical forms of infectious mononucleosis

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

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