The problem of community-acquired pneumonia in children remains relevant at the present time. Complicated forms, which include pleural empyema, abscess, necrotizing pneumonia, bronchopleural fistulas and acute respiratory distress syndrome do not decrease, despite modern antibacterial therapy and the availability of vaccination against pneumococcus. The main pathogens associated with lung destruction in children are S. pneumoniae and S. aureus, often MRSA. The role of other pathogens in necrotizing pneumonia is much less frequently reported: Streptococcus pyogenes, Haemophilus influenzae, Pseudomonas aeruginosa, Fusobacterium nucleatum, Legionella pneumophila, Klebsiella pneumoniae, anaerobes. However not only pathogenic factors of the pathogen are important for necrotizing pneumonia development. Often, a viral prodrome, often associated with the influenza A (H1N1) virus, precedes complicated pneumonia. During the epidemic of COVID-19, endothelial damage with a high degree of probability was a predisposing factor for the development of a secondary bacterial infection with lung tissue necrosis. Significant destruction and liquefaction of the lung tissue may develop despite adequate antibiotic therapy. Great importance in the development of necrosis is attached to the activation of hemostasis and thrombus formation in the vessels of the lungs. Timely diagnosis often is difficult due to the predominance of general symptoms over local ones, especially in young children. Chest x-ray is the standard for diagnosing. However, the diagnostic capabilities of this method in necrotizing pneumonia are limited. To assess a number of parameters of the state of the pleural cavity and lung tissue, ultrasound is preferred. It is necessary to analyze the current features of the course of necrotizing pneumonia in children and develop clinical guidelines for the management of patients in the acute period and rehabilitation.
The article presents clinical case of Job syndrome, variant of primary immune deficiency disease confirmed genetically. This case is interesting for its early diagnosis due to comprehensive assessment of anamnestic, clinical, and laboratory data. Such typical phenotypic features as facial dysmorphisms, recurrent localized purulent infections, and laboratory parameters (absolute neutropenia and eosinophilia) were the major signs of autosomal dominant hyper IgE syndrome in a child with normal IgE levels. The combination of 2 heterozygous mutations in STAT3 gene inherited from his father and his mother has played its role in disease clinical features in the child.
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