Bacterial Coldwater Disease: Review And Current Status

Bacterial coldwater disease (BCWD) was first noted in the United States in 1941. The bacterium Flavobacterium psychrophilum was identified and proven to be the cause of outbreaks. Outbreaks occurred in salmonids at low water temperatures (43-50°F) and the disease gained the common name of bacterial coldwater disease or low-temperature disease. It was also called peduncle disease due to characteristic fraying and erosion of the caudal fin and caudal peduncle.

The disease was only found in North American salmonids until the 1980s, when it was found in Germany, France and other European countries, and is now found worldwide. In Europe, the disease is called rainbow trout fry syndrome or fry mortality syndrome. The disease has subsequently been found in non-salmonid hosts, including ayu, common and Crucian carp, European eels, forktongue and lake gobies, Japanese dace, pale chubs, perch, roach and tench. The bacteria are ubiquitous in freshwater systems and may be part of the normal flora of gills and skin of fish.

The bacteria has not only spread globally and increased its host range, but in more recent years is capable of causing disease at warmer water temperatures, ranging up to 64°F. The most severe disease occurs in sac fry, where mortalities up to 50 per cent occur. As the fry grow into fingerlings, the classic external erosive lesions of the caudal peduncle, sides and back of the fish with ulcers extending into the muscle and invasion of internal organs occurs, with mortality ranging from 5-20 per cent.

Outbreaks can be related to stress, and it also occurs concurrently with other bacterial or viral diseases. Infestations of certain external parasites such as Costia and Gyrodactylus may precede an outbreak of BCWD, probably due to stress and damage of the epithelial barrier of the fish. In fry that survive an outbreak, bacteria can become sequestered in the cranial cavity and spinal column and can interfere with normal growth. The vertebrae become short and fused, causing curvature of the spine of the fish and overall decrease in the length of the fish; such fish are often called “pumpkinseeds” or “stumpies” (see photo).

If the disease becomes generalised throughout the body of the fish, bacteria can be found in the spleen, heart, kidneys and other tissues, causing osmotic imbalances, organ failure and death. The fish become darkened, lethargic, anorectic, may have abnormal swimming behavior and loss of equilibrium, exophthalmia (“pop-eye”), hemorrhages within the eye, and a bloated appearance due to fluid accumulation in the visceral cavity. Internal examination reveals an enlarged and soft spleen, a swollen hind kidney, clear to bloody fluid in the visceral cavity, hemorrhages in the heart muscle, and anemia.

Although it has not been proven that the bacteria produce toxins, they do produce enzymes responsible for breakdown of protein which contributes to tissue damage. The disease is probably more severe in young fish due to their immature immune systems and inability to mount an effective response to the bacteria.

The disease is passed from fish to fish via contaminated water or direct contact and is often associated with sub-optimal environmental conditions and the stress of handling or crowding. Fish that die of the disease are significant reservoirs and shedders of the bacteria, so frequent removal of mortalities helps decrease numbers of bacteria in the water. The bacteria are also found in milt, ovarian fluid and on the surface of eggs, and via DNA studies found to reside within the egg, an example of true vertical transmission.

Despite the great negative economic impact of this disease in salmonid culture, especially in the western US, little progress has been made in the field of vaccine development. This leaves antibiotic treatment as the mainstay of disease control, but with continued evolution of antibiotic resistance in this and other bacteria, antibiotics as a method of control is not sustainable.

Experimental injectable vaccines using formalin- killed or heat-inactivated bacteria have shown some promise, but are not useful for large-scale vaccination of fry. It is not clear if the killed bacteria or the vehicle used in the injectable vaccine (adjuvant) is the source of any developing resistance.

It may be related to a non- specific stimulation of the immune system rather than a specific immunity to F. psychrophilum. Various strains or serotypes of the bacteria exist, further complicating vaccine development. Vaccines made from the capsule of the bacteria (rather than the whole bacteria) or other specific portions of the bacteria have shown some promise.

Although some success was found with injectable vaccines, delivery of vaccine via immersion has been more problematic, immunity being dependent on age and size of fry and usually resulting in less effective levels of immunity than injection.

In 2010, a promising vaccine candidate was patented by researchers at the University of Idaho, and field trials are currently being conducted. Although the vaccine contains live organisms, they have been attenuated, or weakened, so they don’t cause disease but do stimulate development of immunity.

It does not contain an adjuvant. Details about the vaccine, such as duration of immunity, need to revaccinate or “boost” vaccinations, and costs will not be known until completion and evaluation of the field trials. If the field trials prove successful, the vaccine may become available commercially for sale to both public and private aquaculture operations in the next several years.

Until development of a vaccine, effective treatment of outbreaks depends on use of approved antibiotics to which the bacteria is sensitive. The bacteria are capable of becoming resistant to antibiotics used in an injudicious manner and various strains of the bacteria show different degrees of disease-causing capabilities and response to antibiotics. If disease has become well- established, a therapeutic dosage of antibiotic will not be ingested by fish with a decreased appetite or that refuse to feed.

Since the bacteria is contained in milt, ovarian fluids and eggs, povidone iodine treatments during water-hardening of eggs at 100mg/L for 10 minutes or 50mg/L for 30 minutes can be used. Although this does not kill all surface bacteria, and some bacteria may be sequestered within the egg, such treatment substantially reduces numbers of bacteria and has been shown to be beneficial. If an injectable vaccine is licensed, use in broodstock may substantially decrease transmission of the bacteria to offspring.

Until safe and efficacious vaccines have been licensed and made commercially available, other management practices must be employed to try to avoid disease outbreaks. Careful attention to stress mitigation, elimination of external parasites, ensuring good water quality, and providing good nutrition are all important management elements. Once an outbreak is suspected, early and accurate diagnosis and proper treatment regimens can prevent high losses.