Whirling disease caused by Myxobolus cerebralis has become the most widely known disease of salmonids in the 1990s. In the last 5 years we have studied many aspects regarding the host-pathogen relationship of this parasite. The parasite's histozoic development causes significant damage to cartilage and induces CNS symptoms by pressure on the brain and spinal cord. Myxobolus cerebralis has a two-host life-cycle involving a salmonid fish and a tubificid oligochaete. Two different stages of sporogony occur, one in each host. Early developmental stages in the fish can be found multiplying in the epidermis and peripheral and central nervous systems. The presporogenic stages then migrate to vertebral and cranial cartilages, where the first sporogonic phase occurs. Mature M. cerebralis spores found in fish cartilage are infectious for T. tubifex when ingested by the oligochaete after destruction of the infected fish. In the gut lumen of the tubificid, the spores extrude their polar capsules and attach to the gut epithelium by polar filaments. The shell valves then open along the suture line and the sporoplasm penetrates between the gut epithelial cells. The binucleate sporoplasm multiplies by schizogony, producing many one-cell stages which begin gamogonic development. As a result of the multiplication process, the intercellular space of the epithelial cells in more than 10 neighbouring worm segments may become infected. At this time (60-90 days p.i.), pansporocysts with eight zygotes start the sporogonic phase. The final stage of this development is a pansporocyst containing eight folded triactinomyxon spores. Shortly afterwards, the spores are liberated into the gut lumen. The spores reach the water either by egestion or following the death of the infected tubificids. Infected tubificids can release triactinomyxons for at least 1 year. The ultrastructure of all four phases, schizogony, gametogony, gametogamy and sporogony, is demonstrated and discussed.