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Secondary bacterial pneumonia after influenza: characteristics of the pathogenesis, etiology and choice of antibacterial drugs for its treatment

Secondary bacterial pneumonia, which develops in influenza patients, is a serious complication resulting in high mortality rates. In the United States, for example, mortality due to secondary bacterial complications during seasonal influenza epidemics is in 7th place in the overall structure of mortality in adults and 5th in children.

The most common pathogens that cause pneumonia after the flu are Streptococcus pneumoniae, Staphylococcus aureus and Haemophilus influenzae. Pneumonia, developing as a result of the joint pathological effect of the influenza virus and the bacterial pathogen, is characterized by certain specific characteristics and requires a special approach in the choice of antibacterial treatment.

It is well known that post-influenza pneumonia, as a whole, is much more difficult than "ordinary" community-acquired pneumonia, and measures to prevent influenza (vaccination, prophylactic administration of specific antiviral drugs) contribute to a significant reduction the incidence of bacterial co-infections and their mortality in some countries. population groups (especially the elderly).

The influenza virus significantly reduces the anti-infective resistance of the patient's body and contributes to the development of secondary bacterial infections through a number of pathogenetic mechanisms. The most important factor is the loss of integrity of the airway epithelium under the influence of the influenza virus with cytolytic activity. In addition, the influenza virus increases the expression of adhesion molecules on the surface of affected epithelial cells to which bacteria can attach, and also induces apoptosis of the main immune defense cells (alveolar macrophages and neutrophils), leading to local immunosuppression. In addition to this, there is an increase in the production of the pro-inflammatory cytokine - interferon-α, which reduces the antibacterial properties of alveolar macrophages and also impairs the function of the immune defense cells of the respiratory tract, which can secrete antibacterial peptides. As a result of all of the above, there is a special condition of the respiratory tract with influenza which predisposes to the development and in particular to the severe course of secondary bacterial pneumonia.

In a retrospective analysis of the influenza pandemics of 1957 and 1968. it was noted that, despite the use of antibiotics, the mortality in the vast majority of cases was due to secondary bacterial infections. Thus, there is no doubt that it is important to choose the most effective and safest antibacterial drugs to improve the results of treatment for secondary influenza pneumonia.

Experimental animal studies have shown that administration of β-lactams (ampicillin), which have a bactericidal effect, causes the eradication of S. pneumoniae, however, the concentration of pro cytokines -inflammatory and mortality rates in laboratory animals are increased. Antibiotics that disrupt protein synthesis in a bacterial cell (clindamycin, azithromycin), on the contrary, to a lesser extent eliminate the bacteria, but lead to an improvement in survival rates.

Researchers have suggested that the animal body is able to cope with a number of bacteria that have survived when using clindamycin or azithromycin, while their lysis under the influence of β-lactams causes the release of many pro-inflammatory mediators, causing excessively pronounced inflammation, leading to the death of laboratory animals.

In order to improve the eradication of S. pneumoniae in one experiment, attempts were made to prescribe higher doses of clindamycin, but this caused pronounced toxic reactions. Promising results have been obtained in animals whose treatment started with small doses of clindamycin, which reduced the bacterial load, followed by the administration of ampicillin.

The best results were obtained with the use of azithromycin: for example, the survival of the animals in the experiment was 56% with treatment with ampicillin, 82% with treatment with clindamycin as monotherapy, 80% with a combined clindamycin + ampicillin treatment and 92% with azithromycin.

The improvement in survival was apparently due to a decrease in the severity of inflammatory reactions, because in groups of animals treated with clindamycin and azithromycin, fewer inflammatory cells and pro-inflammatory cytokines and Less pronounced histopathological changes in the lungs were noted.

Thus, experimental data indicate that β-lactam monotherapy may not be the optimal choice in the treatment of secondary bacterial pneumonia after influenza. Attention should be paid to the ability of antibiotics with a bacteriostatic mechanism of action to reduce an overly pronounced inflammatory reaction in the airways, which causes both viral and bacterial infection itself and cell lysis bacteria during treatment with β-lactams. The experimental results should undoubtedly be confirmed in clinical trials in patients with post-influenza pneumonia, but they are in good agreement with the data according to which in patients with severe community-acquired pneumonia, the best results are obtained with a combined therapy with β-lactam + macrolide.