Pathogenesis and Clinical Presentation
The pathogenesis is driven by the direct cytopathic effect of the pathogen. Upon entering epithelial cells, the virus triggers the formation of intranuclear inclusions consisting of viral particles. This process inevitably leads to severe dystrophic changes followed by necrosis of the affected tissues. Cell destruction is accompanied by the release of new virions into the bloodstream, resulting in viremia. Typically, this phase is brief; however, in latent forms of the infection, viral circulation in the blood can persist for up to three weeks.
The clinical presentation consists of two main syndromes:
- Intoxication syndrome: manifested by general weakness, malaise, headache, low-grade fever, nausea, vomiting, and diarrhea.
- Specific symptoms: include signs of respiratory tract involvement (rhinitis, pharyngitis, sore throat, cough, and pulmonary rales).
Pathology of Mild Form
Morphological changes depend directly on the severity of the disease. In the mild form, macroscopic findings reveal acute catarrhal rhinolaryngotracheobronchitis, pharyngitis, and acute conjunctivitis, accompanied by regional lymphadenopathy and moderate splenomegaly. The respiratory mucosa appears edematous and hyperemic, with multiple punctate diapedetic hemorrhages visible.
Microscopic examination reveals lymphohistiocytic infiltration of the mucous membranes and prominent desquamation of the epithelial layer. A key diagnostic feature is the presence of "adenovirus cells." These are altered epithelial cells containing fuchsinophilic inclusions in the cytoplasm and viral inclusions directly within the nuclei.
Of particular note is the infection in infants under 1 year of age. In this group, the mild form can be accompanied by serous bronchopneumonia:
- The alveolar lumen accumulates exudate (macrophages, lymphocytes, occasional neutrophils, and desquamated epithelium), adenovirus cells are found, and hyaline membranes are rarely present.
- The interstitial tissue shows epithelial proliferation and lymphohistiocytic infiltration.
- The inflammatory process culminates in granular disintegration of epithelial cells and exudate components, forming characteristic basophilic rounded bodies.
Severe Form and Potential Complications
The severe form of the disease occurs primarily in young children. Its pathogenesis is driven by the generalization of the infection and secondary viral replication in internal organs. The pathological process extends beyond the respiratory system, affecting the epithelial lining of the intestines, liver, kidneys, urinary tract, and pancreas. In addition, ganglion cells of the brain may be involved. Morphologically, these organs reveal typical adenovirus cells, interstitial inflammation, and pronounced microcirculatory disturbances.
Complications typically arise in the severe form due to superimposed secondary bacterial infection, leading to suppuration, necrosis, and worsening of systemic symptoms:
- Pulmonary complications: development of secondary bronchopneumonia, atelectasis, obliterating bronchiolitis, and perifocal pulmonary emphysema.
- Chronic progression: in children, inflammation may become chronic, leading to bronchiectasis as a sequela of resolved pneumonia.
- Extrapulmonary infections: otitis media, sinusitis, and tonsillitis.
In most cases, the prognosis remains favorable, and the infection is self-limiting. However, immunocompromised patients and infants under one year of age constitute a high-risk group, potentially experiencing a severe, fatal clinical course.