Adams has brought a folder from his desk. He opens it and glances down at the papers. ‘As you know, Professor Cochella in Buenos Aires has referred your daughter to me because, while it is clear that she is suffering from a blood disorder, he has been unable to identify the precise type. The normal process of blood cell growth breaks down – we call this haematopoiesis. Sometimes there is an overproduction of a specific type of blood cell in the bone marrow or they produce abnormal cells that malfunction. There are also uncommon lymphoproliferative disorders, myeloproliferative disorders and other uncommon variations – some of them hereditary. If we can identify the type, then we can come up with a treatment but it isn’t straightforward. What I want to confirm with you is that, so far as you know, there is no history on either side of the family of blood disorders of this kind – no hereditary nonspherocytic haemolytic anaemia, or spherocyctic anaemia, no hereditary angioedema, hereditary haemorrhagic telangiectasia . . .’ He hands an A4 sheet of paper to Jomier and another to Tilly. ‘If there have been deaths in the family you may not have been told the cause, but it is worth just looking down the list to see if anything rings a bell.’

Jomier takes up the piece of paper – the haystack in which the needle is hidden – and runs his eye down the list. Aase syndrome, Blackfan Diamond anaemia, Fanconi’s anaemia, Frycht’s anaemia, haemolytic – warm antibody anaemia, hereditary nonspherocytic haemolytic anaemia, hereditary spherocytic haemolytic anaemia, megaloblastic anaemia, hereditary angioedema, antithrombin III deficiency, cor triatriatum, idiopathic oedema, endocardial fibroelastosis (EFE), factor XIII deficiency, congenital heart block, haemangioma thrombocytopenia syndrome, hereditary haemorrhagic telangiectasia, hypoplastic left heart syndrome, hereditary lymphoedema, Maffucci syndrome, perniosis, acquired pure red cell aplasia, pyruvate kinase deficiency, thalassaemia minor and Waldenstrom’s macroglobulinaemia.

‘What is Frycht’s anaemia?’ he asks Professor Adams.

‘We’ve excluded that,’ says Adams. ‘Your daughter has no Austrian blood. You only find Frycht’s anaemia in Austrians – in fact, in one Austrian family, the von Frychts.’

Jomier looks at Tilly. The skin of her cheeks is suddenly flushed. She does not raise her eyes from the piece of paper she holds in her hand.

‘Is this wrong?’ asks Adams. ‘Do either of you have Austrian blood?’

Tilly looks up and glances sideways at Jomier with an expression of terror. ‘No . . . no, I don’t think so . . . I’m sure I don’t.’

Jomier turns back to Adams. ‘My grandmother, Elise Jomier, had a long affair with a man called Ferdinand von Frycht. It is quite possible, even likely, that he was the natural father of my father.’

Adams is excited. ‘That is certainly something worth pursuing. There have been only two or three cases of Frycht’s anaemia this century, but it does crop up every now and sometimes skips several generations.’