Review of the sequential development of Loma salmonae (Microsporidia) based on experimental infections of rainbow trout (Oncorhynchus mykiss) and Chinook salmon (O. tshawytscha).
Loma salmonae is a common gill parasite of salmonids, and essentially all species in the genus Oncorhynchus are susceptible. Infections occur in both fresh and salt water. Loma salmonae is directly transmissible by ingestion of spores or infected tissue. The parasite infects the wall of blood vessels of various organs, but the gill is the primary site of infection. Initial infection occurs in the intestine, and xenomas are easily detected in the gills by standard histology at 4-6 wk post-exposure. A few presporogonic stages of the parasite are found in the heart endothelium prior to xenoma formation in the gills. Ultrastructure studies of early infections demonstrated that wandering blood cells transport the meronts to the gills, and that merogony occurs in pillar cells and other cells underlying the gill endothelium. Xenomas develop in these cells, resulting in hypertrophied host cells filled with spores. Xenomas ultimately rupture, and are associated with severe inflammation in which free spores are found in macrophages. The parasites are most pathogenic during this phase of the infection, resulting in severe vasculitis and clinical disease. Both rainbow trout (Oncorhynchus mykiss) and Chinook salmon (Oncorhynchus ishawytscha) recover from infections, but free spores persist in kidney and spleen phagocytes for many months after xenomas are absent in Chinook salmon. Fish that have recovered from the infection show strong immunity against the parasite, lasting up to 1 year. Fish are susceptible to infection by other routes of exposure by spores; co-habitation, anal gavage, and intramuscular, intraperitoneal and intravascular injection. Autoinfection probably occurs following release of spores in blood vessels after xenomas rupture. The optimal temperature for L. salmonae infections is 15-17 degrees C, with a permissive range of 11-20 degrees C.
Kent
Michael L
ML
Center for Fish Disease Research, Department of Microbiology, 220 Nash Hall, Oregon State University, Corvallis, Oregon 97331-3404, USA. Michael.Kent@oregonstate.edu
Speare
David J
DJ
D000818:Animals; D001808:Blood Vessels / Q000382:microbiology; D005393:Fish Diseases / Q000276:immunology / Q000382:microbiology*; D015726:Giant Cells / Q000382:microbiology; D005880:Gills / Q000382:microbiology; D007422:Intestines / Q000382:microbiology; D008018:Life Cycle Stages / Q000502:physiology*; D046529:Microscopy, Electron, Transmission; D016816:Microsporida / Q000254:growth & development* / Q000472:pathogenicity / Q000648:ultrastructure; D016881:Microsporidiosis / Q000276:immunology / Q000635:transmission / Q000662:veterinary*; D017686:Oncorhynchus mykiss; D012474:Salmon; D013172:Spores, Fungal / Q000502:physiology*