Pathogenesis and clinical presentation of influenza

Initial stages of pathogenesis

The upper respiratory tract most commonly serves as the port of entry for the infection. In complicated cases, the pathogen can immediately penetrate the lower parts of the respiratory tract and affect the alveoli. This leads to the development of primary acute pneumonia, which is one of the main causes of death in risk group patients.

At the cellular level, the pathological process unfolds in several stages:

1. Reproduction: the virus actively multiplies inside the epithelial cells of the respiratory tract.
2. Macrorganism response: as a non-specific antiviral defense, infected cells begin to synthesize interferon.
3. Morphological changes: inflammation and edema rapidly increase in the tissues. The basement membrane swells, and the superficial layer of the epithelium undergoes desquamation (shedding).
4. Consequence: the epithelial barrier is destroyed, which opens the way for the virus to spread further through the body.

Pathogenetic mechanisms of damage

After overcoming local defense barriers, systemic mechanisms of body damage are triggered, which determine the severity of the disease course:

• Toxic and sensitizing effect. The main cause of intoxication is not only the pathogen itself, but also the breakdown products of the patient's own destroyed cells, which are actively absorbed into the systemic bloodstream.
• Vascular bed involvement. The pathogen is capable of activating the proteolytic system. This leads to direct damage to the capillary endothelium and a sharp increase in the permeability of vascular walls and serous membranes. In clinical practice, this mechanism manifests as hemorrhages, severe hemodynamic disorders, and microcirculation failures.
• Effect on the immune system. Against the background of infection, the patient develops transient secondary immunodeficiency. Temporary suppression of defenses creates ideal conditions for secondary bacterial flora to join.

Clinical presentation and periodization

The course of the disease can be divided into three key periods: incubation (lasting 1–2 days), period of clinical manifestations (from 3 to 7 days), and convalescence (recovery takes 7–10 days).

Influenza A has the most severe course, characterized by the following syndromes:

• Intoxication syndrome: onset is always acute, accompanied by severe chills, high fever, cephalgia, as well as muscle pain (myalgia) and joint pain (arthralgia).
• Respiratory syndrome: pronounced catarrh of the upper respiratory tract develops. Patients are bothered by rhinitis, dysphonia, retrosternal pain, and a characteristic dry, "scratchy" cough.
• Neurotropism: type A virus is capable of affecting the nervous system. There is a high risk of developing neurotoxicosis, which is especially dangerous in pediatric practice, even resulting in death.
• Hemorrhagic syndrome: due to vascular damage, increased bleeding is observed, with possible hemorrhages in the skin, mucous membranes, and parenchymatous organs.
• Abdominal syndrome: occurs relatively rarely, predominantly in children. It manifests as abdominal pain and dyspeptic disorders.

Complications and features of other virus types

Infections complications pose a direct threat to the patient's life and are divided into three main groups:

1. Specific: caused by the virus itself (e.g., hemorrhagic pneumonia or pulmonary edema).
2. Bacterial: superinfection against the background of immunodeficiency. Most often, the pathogens are S. pneumoniae or S. aureus.
3. Organic: severe systemic impairments of central nervous system, liver, kidney, and cardiovascular functions.

Unlike type A, influenza B is tolerated much more easily. It is completely devoid of neurotropism, but has a specific clinical feature — a tendency to eye involvement (conjunctivitis and photophobia develop). Influenza C is characterized by the mildest course among all variants.

Immune response

The body's fight against infection proceeds in stages, involving various components of immunity:

• Early phase (during illness): innate immunity factors react first. Massive production of $\alpha$-interferon is triggered. Local immunity is formed at the respiratory tract level through secretory IgA.
• Humoral response: the synthesis of strain-specific virus-neutralizing antibodies begins. Their concentration in the blood reaches its peak 2–3 weeks after the onset of the disease.
• Cellular response (during convalescence): for the final clearance of the pathogen from the body, NK cells (natural killers) and specific cytotoxic T lymphocytes are activated.

The formed post-infection immunity is long-lasting and robust, but it is highly specific — protection works only against that specific variant of the virus that caused the disease.

Class and exam questions

What else to study on this topic

• Mechanisms of transient secondary immunodeficiency formation
• Pathogenesis of primary viral pneumonia development
• Proteolytic system and mechanisms of vascular bed damage
• Features of neurotoxicosis in pediatric practice
• Formation of local specific immunity in the respiratory tract

Other topics in the section "Orthomyxoviruses (Influenza)"

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