Hoferellus Carassii (Kidney Bloater)
By: Dr. Al Camus
Read By: Pet Lovers
Hoferellosis carassii, or kidney bloater disease, is a disease of goldfish and other members of the genus Carassius. It is also known in the pet trade by several common names, including kidney enlargement disease (KED), or polycystic kidney disease of goldfish. Recognized in Japan and Europe for many years, the disease was not reported in the United States until 1984, but is now common throughout the goldfish industry, particularly in pond-raised fish. The causative agent is a small protozoan parasite named Hoferellus carassii (formerly Mitraspora cyprini).
The parasite invades the fish and develops within epithelial (surface) cells lining tubules that make up much of the kidneys. Infection causes these epithelial cells to enlarge and proliferate, interfering with the passage of urine to the bladder before it can be eliminated from the body. Retention of urine causes the tubules to dilate (expand) and over time they are transformed into the large fluid-filled cysts characteristic of the disease. The end result is massive enlargement of the kidneys, recognized externally as swelling of one or both sides of the abdomen. The abdomen may become so enlarged that the fish can no longer swim or feed effectively, and although it may take several months, death at this stage is inevitable.
The life cycle of the parasite is complex, involving stages that develop within the kidney and urinary bladder of the primary goldfish host and others that develop within the gut of an intermediate or secondary host called an oligochaete (segmented worm). Oligochaetes are small bottom dwelling aquatic cousins of the earthworm.
Mature spores (myxosporean) of H. carassii are passed in the urine of infected fish into pond or aquarium water and settle to the bottom. If the appropriate oligochaete host is present, it is believed that spores are ingested as the worms feed on the organic waste matter found in the sediments in which they live. Following a period of development and maturation, another type of spore (aurantiactinomyxon) is released from the oligochaete that infects the kidney of the fish and the life cycle begins again.
It has been noted that the parasite has a tendency to follow a seasonal pattern of infection and mortality in the goldfish. Initial infection occurs in the spring and progresses in the kidney throughout the summer. Spores mature during the winter and are released the following spring to infect the secondary oligochaete host and begin the process again. New infections acquired in the spring usually become visible by summer's end and most mortalities occur the following spring, particularly in young fish spawned the previous year.
There are no effective treatments that will eliminate the parasite from an infected fish, and once significant damage to the kidney has occurred, the disease is invariably fatal. A diagnosis of hoferellosis is suggested in any goldfish with prominent abdominal swelling, however, other conditions such as swim bladder abnormalities, gonadal tumors, and certain bacterial infections (Aeromonas septicemia) can produce similar signs.
Although spores can sometimes be identified in the urine of live fish, a definitive diagnosis is usually based on a post mortem examination and microscopic evaluation of affected kidney tissue.
Since there are no effective treatments against the parasite, only palliative measures can be performed at home. Provide an environment that is as low stress as possible by maintaining good water quality and assure the fish is eating. If an affected fish can no longer swim, feed, or is being traumatized by tank mates, it is usually best to have the animal euthanized by your veterinarian.
The key to prevention is to understand the life cycle of the parasite and the essential role of the oligochaete secondary host. If the intermediate host is eliminated from the environment, the life cycle will be broken and additional fish will not become infected.
The parasite does not spread directly from fish to fish, only through the release of aurantiactinomyxon spores from infected oligochaetes. Since oligochaetes require organic matter in which to live, they can be controlled by not allowing debris like uneaten food, feces and leaf litter to accumulate in ponds or tanks. This may be impossible in mud bottom ponds.
Infected ponds or tanks should be thoroughly cleaned, disinfected, and dried before replacing fish with disease-free stocks. If possible, avoid purchasing fish raised in mud bottom ponds. Remember, the disease progresses slowly, and apparently healthy fish may develop signs months after purchase or introduction to a pond or aquarium.