Necrotizing pneumonia in a three-year-old child: a case report

Community-acquired pneumonia remains a leading cause of morbidity and mortality among children. One of the most serious complications of community-acquired pneumonia is pulmonary tissue destruction which may result in lung abscess, pleural empyema, and other pathological conditions. The key etiologic agents of necrotizing pneumonia are Streptococcus pneumoniae (serotypes 3 and 19A) and Staphylococcus aureus. Other potential pathogens include Haemophilus influenzae, Aspergillus spp., Mycobacterium tuberculosis, Legionella pneumophila, Klebsiella pneumoniae. Necrotizing pneumonia should be suspected in patients with persistent fever and inflammatory changes in laboratory blood tests despite ongoing antibacterial therapy.

This article describes a case of necrotizing pneumonia in a 3-year-old child caused by mixed infection with S. pneumoniae, Mycoplasma pneumoniae and K. pneumoniae. The patient experienced fever for 15 days without signs of respiratory failure. Blood tests revealed pronounced inflammatory changes, including leukocytosis up to 21.9 × 10⁹/L, neutrophilia up to 82.9%, and elevated C-reactive protein up to 189.9 mg/L. Combined therapy with cephalosporins and macrolides was ineffective. Contrast-enhanced chest computed tomography performed on day 13 of disease demonstrated a large area of pulmonary tissue destruction with irregularly thickened walls in segments S VI–S IX of the right lower lobe. K. pneumoniae was isolated from sputum, S. pneumoniae antigen was detected in urine, and IgM antibodies to M. pneumoniae were identified in serum. Antibacterial therapy with linezolid, aminoglycosides, and β-lactam/β-lactamase inhibitor combinations (“protected aminopenicillins”) resulted in clinical improvement, and the patient was discharged on day 24 of disease.

This case demonstrates the potential for necrotizing pneumonia to develop due to co-infection with S. pneumoniae, M. pneumoniae and K. pneumoniae. These findings should be considered when adjusting ineffective antibacterial therapy in this condition.