Rare Severe Complications of a Group A Streptococcal Infection in a Young Child: A Case Report

To the Editors: Group A streptococcus (GAS), also known as Streptococcus pyogenes, is an anaerobic, gram-positive beta-hemolytic bacterium that commonly colonizes the nasopharynx and skin.1 M proteins facilitate adhesion to the mucosal membrane, particularly the tonsils, facilitating epithelial invasion. GAS produces toxins, resulting in tissue damage and deeper infections due to immune complex formation.1 Clinical manifestations range from localized infections of the ear, nose, throat and lungs to disseminated infections, cytokine-induced shock, immune complex-mediated diseases and diseases associated with molecular mimicry. We present a case of a 3-year-old girl with a severely complicated invasive GAS (iGAS) infection, highlighting the importance of early recognition, prompt initiation of appropriate treatment and awareness of potential severe complications. A previously healthy 3-year-old girl presented with a 5-day history of high fever, ear pain, poor oral intake, oliguria and vomiting. One day before admission, she was diagnosed with bilateral acute otitis media and treated with oral amoxicillin. On examination, she appeared ill with tachypnea (36 per minute), tachycardia (163 per minute), high blood pressure (103/70 mm Hg), cold extremities and delayed capillary refill, with normal oxygen saturation. Breath sounds were reduced on the right. Laboratory tests showed elevated C-reactive protein (429 mg/L), leukocytosis (18.3 × 109/L) and mild thrombocytopenia (113 × 109/L). Chest radiograph revealed bronchial wall thickening and left-sided multifocal consolidations suspicious for pneumonia, and intravenous amoxicillin–clavulanic acid was initiated. One day after admission, an adenovirus was detected in the nasopharynx, and blood cultures grew GAS. She rapidly developed sepsis, requiring fluid resuscitation and the addition of clindamycin for suspected toxic shock. The following days, her condition deteriorated with edema, strawberry tongue, coagulopathy and the need for oxygen therapy. Also, the patient developed an isolated horizontal and vertical nystagmus, which raised suspicion for intracranial spread, whereafter amoxicillin–clavulanic acid was switched to ceftriaxone. Magnetic resonance imaging showed acute otomastoiditis, suspected labyrinthitis, and transverse and sigmoid sinus thrombosis with internal jugular vein thrombophlebitis (Fig. 1). Subsequently, she developed meningitis, culture-positive mastoiditis requiring mastoidectomy and bilateral hip arthritis. After more than 4 weeks of hospitalization, intravenous antibiotics and anticoagulation, she was discharged home for further recovery.FIGURE 1.: Axial slices T2 (A), B1000 diffusion weighted image (B) and fat saturated T1 after contrast (C). A: Mastoid and middle ear are bilaterally completely filled with fluid (arrows). Additionally, no flow void in the right dural sinus whereas left dural sinus does show normal flow void (dotted arrows). B: Restricted diffusion in the right mastoid and middle ear indicating pus and therefore otomastoiditis. In contrast, the left mastoid and middle ear show no restricted diffusion indicating uncomplicated fluid. C: Filling defect in the right dural sinus (arrow) confirming the thrombosis already suspected on the T2 image. Of note: not shown are the labyrinthitis and the extracranial thrombophlebitis.Although initial treatment with amoxicillin–clavulanic acid was appropriate for community-acquired pneumonia, the rapid septic dissemination and multiorgan involvement highlight the need for early recognition of iGAS and escalation of antimicrobial therapy. Treatment of iGAS depends on clinical presentation and includes antibiotics targeting both toxin-mediated disease and metastatic spread.2 Clindamycin inhibits protein synthesis and toxin production and, when combined early with a broad-spectrum agent such as ceftriaxone, may reduce morbidity.3 Several theories could explain the recent increased incidence of iGAS.4 Reduced immune exposure during COVID-19 lockdowns may have increased susceptibility to both viral and bacterial infections, while circulating GAS strains may have led to more pathogenic and invasive bacteria. In addition, the post-pandemic rise in viral infections may predispose to secondary invasive bacterial disease.5 This case illustrates the severe and multifaceted course of iGAS infection in a young child, involving both toxic shock and bacterial dissemination. Early recognition of disease and possible complications, as well as adequate treatment, are essential to reduce adverse outcomes.