Initial period and pharyngeal involvement
The initial stage of the disease lasts up to 4–5 days. The disease can debut both acutely and gradually, accompanied by febrile fever, weakness, decreased appetite, and headache.
One of the first manifestations is nasopharyngeal involvement. Due to hyperplasia of the pharyngeal tonsil, adenoiditis develops: lymphatic drainage is disrupted, the nose becomes stuffy, the voice acquires a nasal tone, and nocturnal snoring appears. Externally, this manifests as pastosity of the upper half of the face and eyelid edema. In severe cases, a puffy "adenoid face" forms due to the complete absence of nasal breathing.
Moderate pain and catarrhal symptoms are noted in the oropharynx. An important diagnostic marker: at this stage, the severity of intoxication significantly outweighs local catarrhal changes.
Regional lymphadenopathy forms early. The cervical, occipital, and submandibular nodes enlarge significantly, changing the contours of the neck. They are clearly contoured, not fused to surrounding tissues, moderately painful, while subcutaneous tissue edema is completely absent.
Peak period: generalization of the process
The peak of the disease takes from one to three weeks. The temperature can reach 40°C, and the intoxication syndrome progresses.
Acute tonsillopharyngitis develops with severe pain upon swallowing. Against the background of grade II–III tonsillar hypertrophy, loose whitish patches appear in the form of islands or "columns" (lacunar tonsillitis picture). Unlike diphtheritic patches, these have a different structure, although they may visually resemble them. Multiple petechiae are possible on the soft and hard palate, and the posterior pharyngeal wall becomes hyperemic, loose, and granular due to hyperplastic follicles.
Lymphadenopathy becomes generalized. Nodes are palpated symmetrically in all accessible areas, reaching sizes from 0.5 to 3 cm. They are dense, mobile, and practically painless. Enlargement of mesenteric lymph nodes (mesadenitis) can provoke abdominal pain.
Liver, spleen involvement and exanthema
From the 6th day of the disease, hepatosplenomegaly joins, with the spleen enlarging more intensively than the liver.
Liver damage proceeds without jaundice in 70% of cases. ALT and AST moderately increase in the blood, and bilirubin levels rise. The icteric syndrome occurs in only 5% of patients and is accompanied by dark urine, dyspepsia, and scleral icterus.
On the 8th–11th day of the disease, a maculopapular rash (exanthema) may appear. It has no favored localization, and itching is usually absent. The rash disappears quickly and without a trace. Special attention should be paid to the "ampicillin rash" — if ampicillin is mistakenly prescribed at the peak of the disease, immune complexes form due to polyclonal B-lymphocyte activation, and the rash acquires a vivid hemorrhagic character. This sensitization to penicillins disappears after recovery.
Convalescence, severity of the course and complications
The recovery period takes from 1 to 3–4 months. Tonsillitis and fever disappear first, but lymphadenopathy can persist for more than 1.5 months, and hepatosplenomegaly for up to six months. A pronounced asthenic syndrome also bothers the patient for several months.
The severity of the disease correlates with the number of atypical mononuclear cells in the peripheral blood. In the severe form, high fever (above 39.5°C), marked adynamia, vomiting, severe purulent-necrotic inflammation of the tonsils, and slow regression of symptoms are observed.
Complications can occur at any stage:
- Specific: asphyxia (due to supraglottic stenosis caused by hyperplastic lymphoid tissue), spontaneous splenic rupture (including during rough palpation), central nervous system lesions (encephalitis, Guillain-Barré syndrome), hemolytic anemia, and thrombocytopenia.
- Nonspecific: secondary staphylococcal or streptococcal infection (otitis media, pneumonia).
Most patients achieve clinical recovery. At the same time, viral DNA persists for life in the nuclei of isolated B-lymphocytes and epithelial cells as a circular structure — an episome.
Briefly: answers to topical questions
How do tonsillar patches in infectious mononucleosis visually and structurally differ from patches in diphtheria?
Differences should be formulated with a caveat: in infectious mononucleosis, a lacunar picture is more often described, but patches may resemble diphtheritic ones.
| Sign | Infectious mononucleosis | Diphtheria |
|---|---|---|
| General appearance | More commonly a picture of lacunar tonsillitis: grade II–III tonsillar hypertrophy, loose whitish patches in the form of islands or "columns". | Dense patches on the tonsils, arches, uvula, soft palate; in the toxic form, a fibrinous film extending beyond the tonsils. |
| Separability | In the clinical description of IM, patchy white plaques are easily separated with a spatula; at the same time, the patches may resemble diphtheritic ones — being difficult to remove and tightly bound to the tissue. | The patches are dense and difficult to separate. |
| Structure | For lacunar tonsillitis: seropurulent or mucopurulent exudate in the lacunae, neutrophilic infiltration of the epithelium, erosions, admixture of fibrin. | Diphtheritic inflammation with deep precipitation of fibrin into the necrotic mucosa, dense fibrin film. |
Which biochemical markers indicate liver damage in infectious mononucleosis?
Biochemical markers of liver damage in infectious mononucleosis are elevated levels of bilirubin, aminotransferases, and lactate dehydrogenase.
- Bilirubin — its content in blood serum increases, and hyperbilirubinemia develops.
- Aminotransferases — a moderate increase in ALT and AST activity is observed (cytolytic syndrome).
- Lactate dehydrogenase — an increase in LDH activity is a specific marker of liver damage in this disease.
Class and exam questions
Why does an "adenoid face" develop in mononucleosis?
This is a consequence of lymphoid tissue hyperplasia of the nasopharyngeal vault, which leads to impaired lymphatic drainage, facial pastosity, eyelid edema, and the complete absence of nasal breathing.
What happens to the virus after recovery?
The Epstein-Barr virus transforms into an episome (closed circular DNA) and persists for life in a small number of B-lymphocytes and epithelial cells.
What else to study on this topic
- Mechanism of Epstein-Barr virus replication (from adsorption to exocytosis)
- Epidemiology and transmission routes (aerosol, contact, transfusion)
- Pathogenesis of cellular reactions and immune-mediated cytolysis
- Histological picture of organ damage (periportal infiltration, necrosis)
- Features of asymptomatic and mild forms of the disease
Master the complete topic in the «Infectious Diseases» course
This is a summary. The course covers everything tested in classes and exams.
- Full study guide on "Clinical Manifestations of Infectious Mononucleosis" and 3,312 more pages of the subject
- Assignments and quizzes after every topic — just like in a colloquium
- AI tutor answers questions on the topic anytime
- 41 video lessons on the subject
Other topics in the "Respiratory Infections" section
Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.