John was healthy until he was 7 years old, when his mother noticed that he had become very pale. She also noticed small hemorrhages (petechiae) on the skin of his arms and legs and took John to the pediatrician. Apart from the pallor and skin petechiae, a physical examination showe d nothing unusual. The pediatrician ordered blood tests, which revealed that John was indeed very anemic. His hemo- globin was 7 g dl–1 (normal 10–15 g dl–1) and platelet count was 20,000 ?l–1 (normal 150,000–300,000 ?l–1). His white blood cell count was also lower than normal. The pediatrician sent John to a hematology consultant for a bone marrow biopsy. The biopsy showed that John’s bone marrow had very few cells and that red cell, platelet, and white cell precursors were almost completely absent. Aplastic ane- mia (bone marrow failure) of unknown cause was diagnosed. Aplastic anemia is ultimately fatal but can be cured by a successful bone marrow transplant. Fortu- nately, John had an HLA-identical 11-year-old brother who could be the bone mar- row donor. John was admitted to the Children’s Hospital and given a course of horse anti-thymocyte globulin (ATG), fludarabine, and cyclophosphamide to eradicate his own lymphocytes. He was then given 2 × 108 nucleated bone marrow cells per kg body weight obtained from his brother’s iliac crests. He was also started on cyclo- sporin A (CsA) to prevent GVHD. John did well for 3 weeks after the bone marrow transplant. However, on the 24th day after the transplant he developed a skin rash and watery diarrhea. He had a patchy red rash on palms and soles, scalp, and neck. He had no fever and was not jaundiced. His lungs were clear and the heartbeat normal. The liver and spleen were not enlarged. John was treated with corticosteroids. His skin rash faded, but the intestinal symptoms did not abate, and the diarrhea became more profuse. He was given rabbit ATG for two consecutive days. This brought about a 90% decrease in the volume of his stool and the intestinal bleeding stopped. Two weeks later, John was sent home, with continuing treatment with low doses of corticosteroid. Questions: 1. What is John’s disorder? 2. How do you know? 3. Could this have been prevented? Why are the skin and intestinal tracts t