Proliferative gill disease (PGD) is a serious and potentially devastating condition found in channel catfish culture. Epizootics of PGD have been observed in increasing numbers in recent years. PGD can cause mortalities ranging from less than 1 percent up to 100 percent of the pond's population. All life stages from fry to food fish are susceptible to PGD.

Fish affected with PGD will drop off feeding initially. As the disease condition intensifies, catfish swim lethargically along the pond's surface with some fish piping for oxygen. Affected fish may lie quietly in shallow water near the bank or congregate around aeration equipment. All affected catfish exhibit signs of severe oxygen shortage.

When PGD-infected fish are examined, serious gill damage can be detected by lifting the operculum (gill cover). The gills of these fish are swollen and mottled in color with bloody red and pale streaks (Figure 1). The appearance of the affected gills gave rise to the term "hamburger gill disease." The affected gills bleed easily when touched. When affected fish are removed from the pond, a bloody ooze can often be seen coming from under the operculum.

A tentative diagnosis of PGD can be made on the basis of behavioral signs and observation of gill condition. However, only a microscopic examination of the gill filaments can provide positive proof of PGD and exclude other diseases with similar clinical signs. Under the microscope, thickening of gill epithelium (hypertrophy and hyperplasia) and fusion of gill lamellae are observed. The presence of clear areas in the gill filament cartilage and even complete breaks in the cartilage are confirming signs of PGD (Figure 2).

PGD cases have been reported throughout the year, but the disease has a definite bimodal distribution. PGD is most common in the late winter/early spring and in the fall when the water temperature is between 60 and 70 degrees F. The number of reported cases is greater in the late winter/early spring period. PGD epizootics, however, have been seen throughout the year. Cases occurring during the late winter/early spring period appear to be the most devastating to catfish producers.

The search for the cause of PGD has been relatively long. Toxic algae, toxic ammonia or various types of protozoan parasites were thought to be responsible for PGD. Recently, however, researchers at the University of Georgia have identified the causative agent of this mysterious syndrome. It is a myxozoan protozoan called Aurantiactinomyxon ictaluri. The parasite has a complex life cycle which delayed its discovery and made its identification extremely difficult (Figure 3). This myxozoan parasite requires an oligochaete worm, Dero digitata, to serve as an intermediate host in its development.

The worm D. digitata is up to ½ inch in length, very thin (hairlike) and brownish gray in color (Figure 4). They can be seen actively flexing when alive. These oligochaete worms require good water quality and an aerobic bottom mud environment to live and reproduce. The worms reproduce asexually.

The intermediate host, D. digitata, becomes infested with spores from the myxozoan A. ictaluri. The source of the initial infestation of the oligochaete worms is unknown at present. After the worm D. digitata is infested, this myxozoan can be found in the worm's intestinal lining where it develops into spores (Figure 5). The catfish infesting spores are passed from the intestinal lumen out into the bottom mud and pond water column where they can come in contact with catfish gill tissue.

The microscopic spores released from the worm have a round center with three attached float-like structures (Figure 6). The spore structure is used in identification. Once the spore contacts the gills of catfish, it "germinates," migrates into the gill filament and begins to cause damage.

The environmental requirements of the intermediate host D. digitata determine which ponds may develop PGD.  D. digitata are classified as pioneering organisms. This means that when a new environment is created they are one of the first types of organisms to gain a foothold. However, as the watery environment ages, other species out-compete D. digitata, and D. digitata numbers decline. As a result of the worm's requirements, most PGD outbreaks occur in new ponds (one to two years) and older ponds that have been drained and reworked.

Research at the University of Georgia has shown that the higher the density of D. digitata, the more PGD-infested fish are found in the pond. Intense infections of PGD can be seen with densities of about 1,000 worms per cup of bottom mud. Infestations of catfish are milder when worm populations do not exceed around 100 per cup of bottom mud.

The water exchange method has been shown to reduce or stop PGD epizootics in some cases. Why does this work? It may have a twofold mechanism for activity. First, it may increase dissolved oxygen, and second, it may create an area in the PGD pond where A. ictaluri spore concentrations are low and the catfish have time to combat the infestation and recover. The bottom line is that it is not known why pumping pond water from an adjacent unaffected pond reduces or stops losses.

(Acknowledgment: Dr. Eloise L. Styer and Dr. Gary Burtle, Univerity of Georgia, for providing up-to-date PGD research information.)

FSA9073-5M-5-94-S525