A 22-month-old African boy, born at full-term after normal pregnancy in Belgium, with no relevant medical history nor recent travel history and fully vaccinated according to the Belgian schedule, presented with dry cough and high fever for 3 days and respiratory distress for 24 h.
At admission, the child appeared grumpy, had tachycardia, and had a high fever (40 C). The first blood test showed mild inflammatory syndrome.
Pneumonia with pleural effusion was diagnosed clinically and on a chest X-ray. Intravenous (IV) penicillin (500,000 units/kg/day) was the first chosen antibiotic. Respiratory conditions worsened quickly, requiring a transfer to our pediatric intensive care unit (PICU) 6 h after admission.
Then, another chest X-ray showed a massive pleural effusion with tracheal deviation and a partial collapse of the left lung. At that time, the inflammatory syndrome had increased showing a discrepancy between leukocytes count (4160/mul) and C-reactive protein (CRP; 265 mg/L). IV flucloxacillin (200 mg/kg/day) and clindamycin (30 mg/kg/day) immediately replaced penicillin. The pleural effusion required a surgical drain placed by video-thoracoscopy.
Two days after thoracoscopy, the patient's general status deteriorated and he developed a septic shock requiring invasive ventilation, fluid resuscitation, and vasoactive amines. The shock remained refractory despite the adjunction of hydrocortisone, and an acute respiratory distress syndrome (ARDS) arose. Impaired cardiac function and ARDS led to venoarterial extracorporeal membrane oxygenation (ECMO) support for 9 days whereas invasive ventilation was required for 6 weeks. Acute renal insufficiency (KDIGO stage 3) was treated by continuous hemodiafiltration for 5 weeks with complete resolution of the renal insufficiency before discharge.
Because of the brutal degradation, the antibiotic therapy was transiently extended to IV ceftriaxone (100 mg/kg/day) and IV vancomycin (40 mg/kg/day continuously after a charge IV dose of 10 mg/kg) for 2 days, until obtaining the isolation of an MSSA from the pleural sample. Blood cultures remained negative. Flucloxacillin was finally administrated for 6 weeks and clindamycin for 10 days. IV human immunoglobulins (2 g/kg) were administered due to the initial suspicion of toxic shock syndrome.
Gradually, pulmonary lesions turned into bilateral pneumatoceles and necrotizing pneumonia (Figure 1). The pleural drain was left in place for several days because of persistent pneumothorax secondary to bronchopleural fistulas.
Based on the severe presentation and the unusual aggressive clinical course, we requested both spa-typing and the detection of a PVL toxin by polymerase chain reaction (PCR) on the SA recovered from the pleural sample and results came positive 13 days after admission (spa-type t021). Other exotoxins (toxic shock syndrome toxin-1 - TSST-1, exfoliatin A - eta, and exfoliatin B - etb) were negative. Enterotoxins had not been tested. The presence of PVL, TSST-1, eta, and etb genes was tested by end-point PCR using primers previously described. No contact with people having skin or soft tissue infections have been reported.
The patient showed mild short-term neurological disability (mild encephalopathy on the electroencephalogram) but gradually improved. One month after his admission, a cerebral magnetic resonance imaging (MRI) showed intraventricular, right lateral ventricle occipital horn, and right frontal white matter hemosiderin deposits, as well as ventricular dilatation. On a control 5 months later, the hemosiderin deposits remained with a significant decrease of ventricular dilatation.
At the 2-month follow-up, he presented unsteady walking, poor language for his age, and also sleep disorders. He recovered stable walking and good sleep quality at the 9-month follow-up even if his language remained underdeveloped for age.
The pneumatoceles were still seen on chest X-ray at the 2-month follow-up but without clinical impact. Chest X-ray significantly improved 1 year later.