In June, 2003, 10 days after an uncomplicated vaginal delivery at home, a 35-year-old woman presented to the obstetric department with a 16 h history of severe, burning right breast pain, and 2 h of diarrhoea and vomiting. She was taking ibuprofen for an upper-respiratory-tract infection and had been breastfeeding without problems. On examination, her temperature was 37·9°C, she was tachycardic (120/min), and her blood pressure was 100/70 mm Hg. Her chest was clear, with oxygen saturation 96–98% on air. The lower inner quadrant of her right breast was swollen and erythematous, with no evidence of a localised abscess or discharge. Blood tests showed a leucocytosis of 11·3×109/L and a high C-reactive protein (CRP) of 61 mg/L. The initial diagnosis was mastitis; microscopy of expressed breastmilk showed many white cells, but no organisms. Despite two intravenous doses of amoxicillin/clavulanic acid, her pain worsened and the erythema continued to extend. Over the next 8 h, pain prevented her from breastfeeding; she was hypotensive and had rigors and persisting pyrexia (38·0°C). Ominously, a prominent vein appeared on the right breast—indicative of incipient skin necrosis (fi gure, A). Blood tests showed leucocytosis (12·5×109/L) and high CRP (183 mg/L) and creatine kinase (150 IU/L). A diagnosis of necrotising fasciitis was considered, and a more detailed history of group A streptococcal (GAS) infection (impetigo, scarlet fever, and fl u-like illness) in family contacts was sought. The patient’s mother-in-law had a sore throat associated with a rash, and her husband had had a fl u-like illness. This search implicated GAS as the causative organism. Intravenous clindamycin (2·4 g four times daily) and imipenem (1·0 g four times daily) was started according to our hospital’s protocol; intravenous polyspecifi c immunoglobulin (20 g) was also given. 11 h after presentation, our patient was transferred for emergency surgical debridement. She was hypoxic and oliguric, and her breast was developing further dusky patches towards the midline. At operation, the classic dishwater pus associated with necrotising fasciitis and extensive liquefying necrosis of subcutaneous fat and fascia of the right breast were found. Microbiological examination of specimens showed chains of gram-positive cocci, later yielding GAS, sensitive to penicillin, imipenem, and clindamycin. Postoperatively, ventilatory and inotropic support was needed on the intensive-care unit and further debridement was done on day 3, yielding sterile tissue samples. Histopathology showed an acute infl ammatory infi ltrate dissecting along fascial planes consistent with necrotising fasciitis. Penicillin prophylaxis was given to family contacts and to the patient’s baby. On day 13, her breast wound was resurfaced with a split skin graft (fi gure, B). In December, 2003, her breast was reconstructed with a subpectoral tissue expander. When last seen in April, 2005, the patient was happy with her breast reconstruction. In the setting of what initially appeared to be simple mastitis, the history of gastroenteritis and family members having streptococcal-type illness was initially overlooked. Anaesthesia of the breast following severe pain suggested full-thickness necrosis. This case reminds us that GAS necrotising fasciitis can present with a fulminant sepsis syndrome despite limited skin changes. Sepsis and toxic shock syndrome justifi ed large doses of clindamycin to inhibit exotoxin protein synthesis, and immunoglobulin acted to neutralise exotoxins and superantigens. Nonsteroidal anti-infl ammatory drugs were avoided—they can adversely impair immune responses or mask symptoms and delay diagnosis. In the past 5 years mortality rates from GAS necrotising fasciitis in our hospital have fallen to 8%, coinciding with shorter door-to-theatre times and increased intensive-care admissions. Early clinical suspicion, aggressive antimicrobial therapy, and the early multidisciplinary involvement of senior team members facilitate optimum management.