Myxosoma cerebralis, an important pathogen of young salmonids, is responsible for whirling disease, also known as “blacktail.” Typically, infected fingerlings show rapid tail-chasing behavior when startled, and the peduncle and tail may darken significantly. As infected fish age, skeletal deformity may result from damage to the cartilaginous structures, particularly the skull and vertebral column. Recovered fish remain carriers, and adults do not show signs, although skeletal deformities do not resolve. The disease can be prevented by purchasing uninfected breeding stock and maintaining them in an environment free of the intermediate hosts. A presumptive diagnosis of whirling disease is made by detection of spores from skulls of infected fish. Samples can be submitted to a fish disease laboratory, or procedures described by the American Fisheries Society can be followed. Diagnosis may be confirmed histologically or serologically. Whirling disease is of regulatory concern in some states.
Salmonid ceratomyxosis is caused by Ceratomyxa shasta , a myxosporidian endemic to specific watersheds in the Pacific northwest. The disease occurs in wild fish as well as in fish from hatcheries that use contaminated water. The most typical presentation includes hemorrhage and fibrinous inflammation in the posterior intestine, but other visceral organs and musculature can also be infected. Grossly, fish may appear emaciated, with a distended abdomen and hemorrhagic vent. A presumptive diagnosis can be made by examination of a wet mount of the posterior intestine and visualization of the kidney-bean-shaped trophozoites. The presence of the organism can be confirmed histologically. Some states consider C shasta a reportable disease. Proliferative gill disease of catfish is caused by the myxosporidian Aurantiactinomyxon ictaluri . The organism has a complex life cycle, with the oligochete worm Dero digitata serving as the intermediate host. Channel catfish may be an aberrant host for A ictaluri , and the disease is usually associated with new ponds or previously infected ponds that have been drained and refilled. Although proliferative gill disease can cause catastrophic mortality approaching 100%, losses may be as low as 1%. Disease occurs at water temperatures of 16-26°C, and mortality is exacerbated by poor water quality, particularly low dissolved oxygen or high levels of un-ionized ammonia. Gills of affected fish are severely swollen and bloody, resulting in the colloquial name “hamburger gill disease.” A presumptive diagnosis can be made from a wet mount of infected gill tissue, in which filaments appear swollen, clubbed, and broken. Cartilaginous necrosis is strongly supportive of a diagnosis of proliferative gill disease; however, histology is required for confirmation. Many species of myxosporidians produce nodular or cystic lesions in the skin, gills, muscle, or visceral organs of fish, depending on their host species and tissue preference. Henneguya is commonly found in white, cystic skin lesions of cultured channel catfish and aquarium fish; it is easily identified by the forked-tail appendage of the spore seen microscopically. If ponds are dried and limed heavily, infection can be eliminated, apparently by reduction of the intermediate hosts. Aquarium infection can be self-limiting in the absence of intermediate hosts. Henneguya may also be seen in wet mounts of gill tissue. Although an occasional cyst may be considered an incidental finding, severe damage has been associated with diffuse distribution of interlamellar cysts. Renal dropsy in pond-reared goldfish is caused by the myxosporidian Sphaerospora auratus . The disease is characterized by renal degeneration and ascites and is usually diagnosed by identification of spores in histologic sections of the kidney. Newly purchased pond-reared goldfish placed in aquaria may show signs of the disease, including death. No practical treatment is available. The carp-dropsy complex is a disease of carp and goldfish characterized by dropsy and exophthalmos. It is associated with S angulata infection and may be complicated by viral infections (such as spring viremia of carp), carp swim-bladder disease, or bacterial septicemias. Deaths may be acute or occur over a 6-mo period. The response to drug treatment is generally poor. Proliferative kidney disease (PKD) is one of the most economically important diseases affecting salmonid industries of North America and Europe. Rainbow trout are particularly sensitive to the disease, although all salmonids seem susceptible. PKD is caused by an unnamed myxosporidian parasite, sometimes referred to as the PKD parasite. PKD has been reported in both captive and free-ranging salmonid populations. It occurs most commonly in the summer when water temperatures are >12°C, and the parasite primarily infects yearling and younger fish. Clinical signs include lethargy, darkening, and fluid accumulation indicated by exophthalmos, ascites, and lateral body swelling. Infected fish are frequently anemic, resulting in gill pallor. Grossly, the posterior kidney appears gray, mottled, and significantly enlarged. Presumptive diagnosis can be based on observation of suspect organisms, 10-20 µm in diameter, in Giemsa-stained wet mounts of kidney tissue. Histologic examination of infected tissue, stained with H&E, is required for confirmation. Avoidance is the best preventive measure, although losses may be minimized by improved husbandry. Bacterial infections, particularly Aeromonas salmonicida , are common sequelae of PKD epizootics and, if uncontrolled, can result in substantially increased mortality. There is no treatment; however, fish that recover from the infection are resistant to subsequent outbreaks. Infected stocks in nonendemic areas should be depopulated, the premises sanitized, and disease-free stock obtained for replacement.