R. salmonina, Corynebacterium salmoninus, corynebacterial kidney disease, salmonid kidney disease

Renibacterium salmoninarum occurs primarily in salmon, trout, and char. It is an obligate fish pathogen and survives intracellularly. It has been recorded from around 13 salmonid species in Europe, North America, and Asia.

The following host species are only somewhat susceptible to BKD and may not necessarily experience mortality upon contracting the disease: Lake Trout (Salvelinus namaycush), Rainbow Trout or steelhead (Oncorhynchus mykiss), Brook Trout (Salvelinus fontinalis), Lake Whitefish (Coregonus clupeaformis), and Bloater (C. hoyi). Other host species are relatively more susceptible to BKD and more prone to experiencing mortality due to the disease: Coho Salmon (O. kisutch), domestic Atlantic Salmon (Salmo salar), and Chinook Salmon (O. tshawytscha) (Starliper et al. 1997; Jonas et al. 2002; Hay 2003; Nuhfer et al. 2005). Occurrences as far north as the Northwest Territories have been recorded in wild Arctic Char (Salvelinus alpinus) and Lake Trout (S. namaycush) (Souter et al. 1987).         

Species other than salmonids are capable of acting as reservoirs that harbor this bacterium, although their potential role in contributing to transmissions is unknown. R. salmoninarum has recently been isolated from Sea Lamprey (Petromyzon marinus) kidneys in the Lake Ontario watershed (Eissa et al. 2006). Pacific Hake (Merluccius productus) has been recorded carrying this bacterium in the wild in coastal areas of British Columbia (Kent et al. 1998), and Pacific Herring (Clupea harengus pallasi) in B.C. fish hatcheries is also capable of harboring it (Paclibare et al. 1988).

Life history: Genetic diversity amongst isolates within North America is considered relatively low. However, strains isolated from Lake Michigan are found to be more virulent than those from the Pacific Northwest. R. salmoninarum can occur and survive in freshwater and marine environments (Austin and Austin 1987; Starliper et al. 1997; Grayson et al. 1999; Thomas et al. 1999; Jonas et al. 2002).           

Transmission can occur vertically from adult fish to eggs or horizontally from one fish to another (Dar et al. 2020). Both symptomatic and asymptomatic fish shed bacteria, which can be ingested by other fish as a common transmission vector (Rhodes and Mimeault 2019).  Shedding rates can be extremely high, in some cases exceeding 6,500,000 bacteria per fish per hour (Purcell et al. 2016 in Rhodes and Mimeault 2019). R. salmoninarum has survived in sterile water up to 28 days, though survival in natural water is significantly shorter (typically <1 week). It is probably capable of forming an inactive or dormant stage in host fish, after which it can either lyse or reactivate depending on changes in abiotic conditions or fish stress. It probably resides in the kidneys or the digestive tracts of fish hosts for long periods of time. When hosts undergo stress, contracting other infections, sustaining digestive tract or kidney damage, experiencing starvation or undernourishment, undergoing temperature shock, or experiencing crowding, R. salmoninarum may multiply in the kidneys of the host and lead to BKD (Goodfellow et al. 1985; Austin and Austin 1987; Brown et al. 1994; Holey et al. 1998; Thomas et al. 1999; Hirvela-Koski et al. 2006).

Summary of species impacts derived from literature review. Click on an icon to find out more...

Environmental	Socioeconomic	Beneficial

While R. salmoninarum affects multiple Great Lakes native species, prevalence and mortality in infected fish have been relatively low (GLFHC 2006). Great Lakes native salmonid species that have tested positive for the bacterium include Atlantic Salmon (Salmo salar), Lake Trout (Salvelinus namaycush), Brook Trout (S. fontinalis), and Splake (S. fontinalis x S. namaycush) (GLFHC 2006, GLFHC 2012, Hay 2003, Jonas et al. 2002, Nuhfer et al. 2005, Starliper et al. 1997). Atlantic Salmon are most susceptible and prone to mortality (Hay 2003, Jonas et al. 2002, Nuhfer et al. 2005, Starliper et al. 1997). Other Great Lakes native species found harboring R. salmoninarum include Lake Whitefish (Coregonus clupeaformis), Bloater (C. hoyi), Lake Herring (C. artedi), Mottled Sculpin (Cottus bairdi), White Sucker (Catostomus commersonii), Muskellunge (Esox masquinongy), Channel Catfish (Ictalurus punctatus), Lake Sturgeon (Acipenser fulvescens), and Walleye (Sander vitreus) (COSEWIC 2005, GLFHC 2006, GLFHC 2012, Hay 2003, Jonas et al. 2002, Nuhfer et al. 2005, Starliper et al. 1997). Strains of the bacterium isolated from Lake Michigan have been found to be more virulent than those from the Pacific Northwest (Austin and Austin 1987, Grayson et al. 1999, Jonas et al. 2002, Starliper et al. 1997).

Renibacterium salmoninarum has a high socio-economic impact in the Great Lakes.
Lake Whitefish (C. clupeaformis) collected from Lake Michigan and Lake Huron between 2003 and 2006 tested positive for R. salmoninarum at 62.31% prevalence. Lake Whitefish has a high commercial value in the Great Lakes (Nalepa et al. 2005, Ebener et al. 2008), and if as a result of BKD infection, populations were to fluctuate significantly, there could be serious economic effects. Great Lakes non-native species sportfish that have tested positive for R. salmoninarum include Chinook Salmon (Oncorhynchus tshawytscha) (Holey et al. 1998), Coho Salmon (O. kisutch), and Rainbow Trout (O. mykiss) (Jonas et al. 2002). Prevalence rates of R. salmoninarum were up to 100% in some parts of the Lake Michigan drainage around 1986. This outbreak of BKD caused heavy mortality in Chinook Salmon in 1988 and persisted in the population until 1992. That year, boat fisheries observed at least a 40% decline in Chinook salmon catch per unit effort levels. By 1993, catch per unit effort was 15% of the peak observed in 1986 (Holey et al. 1998). In 1986, the Strawberry Creek spawning weirs in Wisconsin documented no presence of R. salmoninarum. In 1988, the bacterium was isolated in 67% of the returning Chinook Salmon and then persisted at moderate levels through 1992 (Holey et al. 1998). The 1980s’ mortality events are believed to have also been influenced by increased vulnerability due to food shortages, particularly alewives (Alosa pseudoharengus), high Chinook Salmon density, and high parasite loads (Holey et al. 1998). While significant for the fisheries at that time, given the magnitude of the stocks present in Lake Michigan, it is improbable that the Chinook Salmon die-offs observed in the late 1980s and early 1990s caused a residual demographic bottleneck in those populations (Weeder et al. 2005).
As of 2006, the overall prevalence of R. salmoninarum in non-native Great Lakes species was thought to be low and declining over time (GLFHC 2006, Jonas et al. 2002). However in 2011, R. salmoninarum was widely distributed with varying prevalence throughout Michigan state hatcheries and wild populations. The bacterium was detected in Brown Trout (Salmo trutta) at 1.7% to 54% prevalence, rainbow trout at 1.7% to 40%, coho salmon at 1.7% to 10%, and Chinook salmon at 1.7% to 5% prevalence (GFLHC 2012).

There is little or no evidence to support that Renibacterium salmoninarum has significant beneficial effects in the Great Lakes.
 

Regulations: (pertaining to the Great Lakes)
 

New York, Pennsylvania, Ohio, Michigan, Indiana, Illinois, Wisconsin, and Minnesota have instated similar baitfish regulations to control the spread of BKD and other fish pathogens. Those of New York include that bait harvested from inland waters for personal use is only permitted to be used within the same body of water from which it was taken and cannot be transported overland (with the exception of smelt, suckers, alewives, and blueback herring). Once transported, baitfish cannot be replaced to its original body of water (NYSDEC 2012). Live or frozen bait harvested from inland New York waters for commercial purposes is only permitted to be sold or possessed on the same body of water from which it was taken and cannot be transported over land unless under a permit and or accompanied by a fish health certification report. Bait that is preserved and packaged by any method other than freezing, such as salting, can be sold and used wherever the use of bait fish is legal as long as the package is labeled with the name of the packager-processor, the name of the fish species, the quantity of fish packaged, and the means of preservation (NYSDEC 2012). Certified bait may be sold for retail and transported overland as long as the consumer maintains a copy of a sales receipt that contains the name of the selling vendor, date sold, species of fish sold, and quantity of fish sold. Bait that has not been certified may still be sold but the consumer must maintain a sales receipt containing the body of water where the bait fish was collected and a warning that the bait cannot be transported by motor vehicle. Bait sold for resale require a fish health certification along with a receipt that contains the name of the selling vendor, date sold, species of fish sold, and quantity of fish sold, which must be kept for 30 days or until all bait is sold (NYSDEC 2012).

Note: Check federal, state/provincial, and local regulations for the most up-to-date information.

Control
Most control methods are developed for use in aquaculture and not suitable for open-water applications.

Physical
Culling infected stock has reduced the prevalence of R. salmoninarum in aquaculture (Gudmundsdóttir et al. 2000, Maule et al. 1996, Pascho et al. 1991).

Chemical
Antimicrobial agents used to treat R. salmoninarum include nitrofurans (now banned in the US), bacitracin, chlortetracycline, oxytetracycline, novobiocin (Wolf and Dunbar 1959), cephalosporins, gentamicin, clindamycin, lincomycin, oleandomycin, kitasamycin, spiramycin, penicillin (Austin 1985), cefazolin, tiamulin (Bandín et al. 1991), cephradine, rifampicin, (Brown et al. 1990), tetracycline (Austin 1985, Bandín et al. 1991), chloramphenicol (Austin 1985, Wolf and Dunbar 1959), and erythromycin (Austin 1985, Bandín et al. 1991, Lee and Evelyn 1994, Wolf and Dunbar 1959).  Trimethoprim show significant potential for inhibition of R. salmoninarum’s dihydrofolate reductase protein (Kumar et al. 2021)

Erythromycin-enhanced feed administered at 100 mg/kg/day for 21 days (Wolf & Dunbar 1959) or for 10 days (Austin 1985) is believed to be the most effective treatment for bacterial kidney disease (Hirvela-koski 2005).  Erythromycin phosphate is an effective chemoprophylaxis in pre-spawning adult brood fish. Subcutaneous injections of 11 mg/kg (Hirvela-koski 2005) or 20 mg/kg (Gudmundsdóttir et al. 2000, Pascho et al. 1991) administered to fish entering trapping facilities and at 21-30 day intervals thereafter (Hirvela-Koski 2005) has reduced mortality in re-spawning Pacific salmon by 10-50% (Groman and Klonz 1983). However, this treatment does not effectively destroy the pathogen from all eggs (Brown et al. 1990). A study by Lee and Evelyn (1994) showed female coho salmon treated with 20 mg/kg erythromycin prior to spawning yielded no vertical transmission of BKD. Treatment success relies on careful timing of the injections in adult salmonids before spawning (Elliott et al. 1989).

Disinfecting eggs with 100 mg/L of iodine for 15 minutes may not eliminate vertical transmission, but can reduce the severity of the disease (Bullock et al. 1978). Treating eggs with iodine at 250 or 500 mg/L for 15-120 minutes is effective at eliminating R. salmoninarum. However, after treatment, variable numbers of R. salmoninarum cells have survived. This is due to cells within the cell aggregates never coming in contact with the iodine (Evelyn et al. 1984, 1986). Renibacterium salmoninarum is inactivated by free chlorine (≤0.05 mg/L), which can be used as a disinfectant and to treat intake and effluent (Pascho et al. 1995).

Other
Prevention is the preferred control method of BKD in cultured stocks (OIE 2003).

Note: Check state/provincial and local regulations for the most up-to-date information regarding permits for control methods. Follow all label instructions.