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The likely source of streptococcal septicaemia in an African couple was an intrauterine contraceptive device (IUCD).
A woman of 36 sought advice after 5 days of general malaise and 3 days of watery diarrhoea, vomiting and abdominal pain. She had arrived from West Africa 2 weeks before admission. Her only medical history of note was recurrent falciparum malaria, but 4 weeks before admission she had had an IUCD inserted (Mirena) and subsequently experienced deep dyspareunia and an episode of clear vaginal discharge. She had not had extramarital intercourse and had not used intravenous drugs. On examination she was pyrexial (388C), tachycardic and tachypnoeic, with oxygen saturation 92% on air. Blood investigations showed renal failure and a neutrophil leucocytosis. There was right basal shadowing on the chest X-ray (Figure 1).
The provisional diagnosis was sepsis secondary either to community-acquired pneumonia or to infection of her IUCD, and initial treatment was with cefotaxime and clarithromycin. After gynaecological review her IUCD was removed. Respiratory function worsened and she required a period of ventilation. Blood cultures grew a Lancefield group A β-haemolytic streptococcus (Streptococcus pyogenes). No organisms were grown from a high vaginal swab or the IUCD. On the advice of the microbiologist the antibiotics were changed to cefotaxime and clindamycin. She tested positive for HIV. Her condition improved over the following week and she was discharged home after 2 weeks with good respiratory and renal function. She was well several months later, with CD4 count 0.71×109/L (normal range=0.4–1), not requiring retroviral therapy.
The patient's husband was admitted on the same day—a man of 34, likewise from West Africa. He had experienced 6 days of fevers and shivers associated with sharp left-sided chest pain. He was breathless with a cough and brown sputum. Recently he had been treated for genital warts and 2 years previously pneumonia. He had had sexual partners other than his wife but not since entering the UK 4 months earlier. He too denied intravenous drug abuse. On examination he was apyrexial but tachycardic and hypotensive, with a left pleural rub and oxygen saturation 80% while talking. Initial investigations showed a mild anaemia, a neutrophil leucocytosis, renal failure, and a raised creatine kinase. On the electrocardiogram there was widespread ST elevation (Figure 2) and a chest X-ray showed cardiomegaly. The initial diagnosis was of septic shock secondary to left basal pneumonia with pericarditis. He was treated with intravenous fluids and the same broad-spectrum antibiotics as patient 1. Over the next 24 hours he became progressively more hypoxic with worsening renal function; he was transferred to the intensive therapy unit where he was ventilated and supported with inotropes. Blood cultures collected on admission grew S. pyogenes and again the microbiologist advised a change to cefotaxime and clindamycin. Polyspecific immunoglobulin G was added to the management. Complications included purulent pericardial effusion causing tamponade, and worsening renal failure requiring haemofiltration. He developed pseudomonas pneumonia and died ten days after admission. The strain of streptococcus obtained from blood cultures and pericardial fluid was identical, on epidemiological typing, to that from patient 1. He too was HIV-positive.
The source of the streptococcus is not clear. One possibility is asymptomatic carriage by the couple's two children (5–15% of schoolchildren are symptomless carriers of group A streptococcus).3 A more likely source in our opinion is the IUCD, with transmission to the man by the sexual route. Group A streptococcus infection of an IUCD has been associated with transmission via oral sex.2 The negative microbiological results from the IUCD might have been due to previous antibiotic therapy. A risk factor in these cases was HIV infection: in one review, HIV-positive individuals had a 39 times excess risk of group A streptococcal infection.1