Cold Water Disease

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Also Known As: Fin Rot — Tail Rot — Peduncle Disease — CWD — Rainbow Trout Fry Mortality Syndrome

Caused by: Flavobacterium psychrophilum previously known as: Cytophaga psychrophila — Flexibacter psychrophilus

Introduction

Cold water Disease in an ayu (Plecoglossus altivelis altivelis). Wikimedia Commons

Flavobacterium psychrophilum is a gram negative rod shaped bacterial pathogen, known for causing Cold Water Disease (CWD) in salmonid fish. The disease typically occurs at temperatures below 13⁰C, and is most serious and prevalent below 10⁰C.

This disease is not zoonotic and poses no public health risk.

Distribution

CWD is common in any area where water temperatures are consistently below 15⁰C. This includes North America, the UK, Europe and parts of Oceania.

Asymptomatic carrier fish and contaminated water provide reservoirs for disease. Transmission is mainly horizontal from these sources. Vertical transmission is also possible, via ovarian fluid, milt, egg surfaces and mucus. Eggs can also be experimentally contaminated and infected.

Signalment

Most fishes worldwide are susceptible and the organism is ubiquitous.

Cultured salmon species are the most frequently affected. Susceptible fish include: brook trout, rainbow trout, brown trout, lake trout, walleye, whitefish, carp, dace and suckers.

Clinical Signs

Fish infected with typical CWD have external skin lesions, often on the dorsum, lose their fins and may also have severe erosion of the caudal fin. Fins may appear dark, torn, split, ragged, frayed or have haemorrhagic red patches/spots visible. Affected fish are often lethargic and stop feeding.

Internal, systemic infection can also be a sequel of CWD.

In Rainbow Trout Fry Syndrome, acute disease is usual and mortality can approach 60% which is devastating in the commonly affected populations of tens of thousands of young fish. Shortly before death, fish are lethargic, have darkened skin, inappetance and demonstrate exopthalmos.

Salmonid fish can also acquire a chronic form of CWD characterised by erratic “corkscrew” swimming, blackened tails and spinal deformities. This may follow recovery from typical CWD.

Diagnosis

Diagnosis is often presumed from history, clinical signs, pattern of mortality and water temperature etc, especially if the location has previously encountered CWD.

Cultures can be made from smears or samples of lesions and the organism cultured on reduced nutrient agar, e.g. cytophaga agar, forming yellow creamy non-adhered colonies in 2-4days.

Histologically, periostitis, osteitis, meningitis and ganglioneuritis may be observed. In chronic disease cases, bacterial cells can accumulate in the cranial and vertebral areas causing inflammation and cartilage necrosis which leads to the spinal deformities noted.

Treatment

Quaternary ammonium compounds can be delivered in a static bath or flow through system for infected adult fish and fry. Potassium permanganate, copper sulphate and hydrogen peroxide can be applied externally but they can be toxic at high concentrations.

Terramycin can be added to feed as an alternative for adults, fry and broodstock. This can also be used preventively. Some resistance is emerging however.

Control

Ensuring water is pathogen-free and that water hardening is completed effectively for eggs is imperative.

Prophylactic antibiotic use should be carefully considered before implementation due to emerging resistance.

Cold Water Disease Learning Resources
Flashcards Test your knowledge using flashcard type questions	Cold Water Disease Flashcards Ornamental Fish Q&A 12

References

Starliper, C.E. and Schill, W.B. 2011. Flavobacterial Diseases: Coldwater Disease, Columnaris Disease, and Bacterial Gill Diseases. In: Fish Diseases and Disorders Volume 3: Viral, Bacterial and Fungal Infections, 2nd. Edition (eds. P.T.K. Woo and D.W. Bruno), CABI, Wallingford, UK, pp. 606-631

This article was originally sourced from The Animal Health & Production Compendium (AHPC) published online by CABI during the OVAL Project. The datasheet was accessed on 10 July 2011.