Adenoviral infection

Pathogenesis and clinical presentation

The development of the disease is based on the direct cytopathic effect of the pathogen. Penetrating epithelial cells, the virus initiates the formation of intranuclear inclusions consisting of viral particles. This process inevitably leads to severe dystrophic changes and subsequent necrosis of the affected tissues. The destruction of cells is accompanied by the release of new virions into the bloodstream, developing viremia. As a rule, this stage is short-lived; however, in cases of latent infection, viral circulation in the blood can persist for up to three weeks.

The clinical presentation consists of two main syndromes:

• Intoxication syndrome: manifests as general weakness, malaise, headache, low-grade fever, as well as nausea, vomiting, and diarrhea.
• Specific symptoms: include signs of respiratory tract involvement (rhinitis, pharyngitis, sore throat, cough, and rales in the lungs).

Pathological anatomy of the mild form

Morphological changes directly depend 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 mucous membrane of the respiratory tract appears edematous and hyperemic, with multiple punctate diapedetic hemorrhages visible on its surface.

Microscopic examination reveals lymphohistiocytic infiltration of the mucous membranes and pronounced desquamation of the epithelial layer. A key specific sign is the detection of "adenoviral cells". These are altered cells of the affected epithelium containing fuchsinophilic inclusions in the cytoplasm and viral inclusions directly within the nuclei.

Particular attention should be paid to the course of the infection in infants under 1 year of age. In these patients, the mild form may be accompanied by the development of serous bronchopneumonia:

1. Exudate (macrophages, lymphocytes, isolated neutrophils, and desquamated epithelium) accumulates in the alveolar lumens, adenoviral cells are detected, and hyaline membranes are rarely present.
2. Proliferation of the epithelium and lymphohistiocytic infiltration are observed in the interstitial tissue.
3. The inflammatory process concludes with blocky disintegration of epithelial cells and exudate elements, forming characteristic basophilic rounded bodies.

Severe form and potential complications

The severe form of the disease occurs predominantly in young children. Its pathogenesis is driven by the generalization of the infection and secondary replication of the virus in internal organs. The pathological process extends beyond the respiratory system: the epithelial lining of the intestine, liver, kidneys, urinary tract, and pancreas is affected. Additionally, ganglion cells of the brain may be involved. Morphologically, these organs exhibit typical adenoviral cells, interstitial inflammation, and pronounced microcirculatory disorders.

Complications most frequently arise in the severe form against the background of secondary bacterial infection, leading to suppuration, necrosis, and worsening of general symptoms:

• Pulmonary complications: development of secondary bronchopneumonia, atelectasis, obliterative bronchiolitis, and perifocal pulmonary emphysema.
• Chronic progression: in children, inflammation can become chronic with the formation of bronchiectasis as an outcome of prior pneumonia.
• Extrapulmonary infections: otitis media, sinusitis, and tonsillitis.

In most cases, the prognosis remains favorable, and the infection resolves spontaneously. However, immunocompromised patients and infants in their first year of life constitute a high-risk group, in whom an extremely severe and potentially fatal course may occur.

Briefly: answers to topical questions

Class and exam questions

What else to study on this topic

• Mechanisms of hyaline membrane formation in serous bronchopneumonia in children.
• Pathogenesis of microcirculatory disorders during the generalization of viral infection.
• Morphological differences between adenoviral pneumonia and bacterial lung lesions.
• The process of bronchiectasis formation as an outcome of chronic pulmonary disease.
• The effect of secondary bacterial flora on the nature of necrotic tissue changes.

Other topics in "Chapter 16. Infectious and Parasitic Diseases"

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