Related Experiment Videos
Group A beta-haemolytic streptococcal acute chest event in a child with sickle cell anaemia
1Division of Paediatric Infectious Diseases, Department of Paediatrics, Vanderbilt University School of Medicine, D-7235 MCN, Nashville, TN 37232-2581, USA. rahaman.o.suara@vanderbilt.edu
Insights
Group A beta-haemolytic Streptococcus (GABHS) pneumonia is an uncommon but serious cause of acute chest syndrome in children with sickle cell anaemia. Early recognition and treatment are crucial for better outcomes.
Area of Science:
- Pediatrics
- Infectious Diseases
- Hematology
Background:
- Acute chest syndrome (ACS) is a leading cause of mortality and hospitalization in pediatric sickle cell anaemia (SCA).
- Infections, particularly pneumonia, are common triggers for ACS.
- Emerging microbial pathogens are increasingly implicated in ACS development.
Observation:
- A 15-year-old African-American female with SCA presented with symptoms of ACS, including fever, cough, chest pain, dyspnea, RUQ pain, jaundice, and otitis media.
- Chest radiography revealed multilobar pneumonia with a left pleural effusion.
- Group A beta-haemolytic Streptococcus (GABHS) was identified in pleural and middle ear fluid cultures.
Findings:
- GABHS was confirmed as the causative agent of pneumonia and subsequent ACS in this SCA patient.
- The patient demonstrated a positive response to a comprehensive treatment regimen including antibiotics, exchange transfusion, oxygen, and surgical intervention (thoracotomy with chest tube drainage and decortication).
Implications:
- GABHS should be considered as a potential pathogen in pediatric SCA patients presenting with fever and acute chest events.
- Prompt chest X-ray and empiric antibiotic therapy targeting community-acquired pneumonia agents are recommended.
- This case highlights the importance of recognizing less common etiologies of pneumonia in SCA to guide appropriate management and improve patient prognosis.
Abstract:
Acute chest syndrome is a major cause of death and hospitalisation in children with sickle cell anaemia. It is often initiated by an infection, particularly pneumonia. Microbial agents previously not associated with acute chest syndrome are becoming increasingly important. Group A beta-haemolytic Streptococcus (GABHS) is thought to be an uncommon cause of pneumonia in children with sickle cell anaemia. We report a 15-year-old African-American girl who presented with an acute chest event characterised by fever, cough, chest pain, shortness of breath, right upper abdominal quadrant pain, jaundice and otitis media. Chest radiograph showed multi-lobar pneumonia with left pleural effusion. Group A beta-haemolytic Streptococcus was isolated from culture of pleural and middle ear fluids. She responded to therapy that included antibiotics, exchange blood transfusion, oxygen, thoracotomy chest tube drainage and decortication. In a child with sickle cell anaemia presenting with fever and an acute chest event, pneumonia should be considered and GABHS recognised as a possible aetiological agent. In addition, a chest X-ray should be obtained and antibiotics against agents causing community-acquired pneumonia instituted.