Figure 1. Intensively-reared goldfish with sub-acute/chronic BGD. Note the pale areas of hyperplasia and fusion within the gills (arrow). Although salmonids are most commonly affected, other species are also susceptible.

Bacterial gill disease – Gross Pathology

Bacterial gill disease (BGD) occurs in several species, but it is an especially serious problem of intensive salmonid culture, and in some parts of the world it is the most common disease, especially in fry and fingerlings. BGD is characterized by explosive morbidity and mortality rates, attributable to bacterial colonization of gill surfaces.

Figure 1. Intensively-reared goldfish with sub-acute/chronic BGD. Note the pale areas of hyperplasia and fusion within the gills (arrow). Although salmonids are most commonly affected, other species are also susceptible.
Figure 1. Intensively-reared goldfish with sub-acute/chronic BGD. Note the pale areas of hyperplasia and fusion within the gills (arrow). Although salmonids are most commonly affected, other species are also susceptible.

Despite such pronounced clinical signs and high mortality, pathological changes are surprisingly few and hard to find in the acute disease. It is only when (if) the fish survive for a few days, more commonly seen in older fish, that changes such as lamellar fusion and hyperplasia can be seen.

Figure 2.  Biopsy from rainbow trout fry with acute BGD, as seen in phase contrast. Although they are hard to spot, and at least x25 objective is needed, long filamentous bacteria can be seen attached to the gill surface (arrow). Note that these bacteria do not invade the gill tissue.
Figure 2. Biopsy from rainbow trout fry with acute BGD, as seen in phase contrast. Although they are hard to spot, and at least x25 objective is needed, long filamentous bacteria can be seen attached to the gill surface (arrow). Note that these bacteria do not invade the gill tissue.











Affected fish can be seen gasping at the surface of the water. Fish show a greatly reduced fright response and they have no interest in feed. When they die, they usually have flared opercula, probably due to lactic acid build-up in the head muscles. Mortality can reach 50% or higher within 48 hours.

Figure 3. Rainbow trout fingerling with flared opercula that died from respiratory distress. Causes of this would include BGD.
Figure 3. Rainbow trout fingerling with flared opercula that died from respiratory distress. Causes of this would include BGD.

The causative agent of BGD, Flavobacterium branchiophilum, is a yellow-pigmented, filamentous, Gram-negative bacterium, which is considered ubiquitous in the freshwater environment; it is horizontally transmitted between fish.

Figure 4. This rainbow trout fingerling with BGD shows the typical flared opercula of respiratory distress. Note that the edge of the flared operculum is eroded. This erosion is typical of intensively-reared fish; its cause is unknown, but might be the result of higher-than-optimal bacterial enzymes in and around the branchial cavity. Whatever the cause, the consequence is a huge reduction in the ability of the animal to pump water due to elimination of the water-tight seal between the trailing edge of the operculum and the body of the fish (the cleithrum). Thus the negative pressure of the opercular pump is greatly reduced. And this in an animal that is trying to pump larger-then-normal volumes of water over its gills due to the hypoxaemia of BGD!
Figure 4. This rainbow trout fingerling with BGD shows the typical flared opercula of respiratory distress. Note that the edge of the flared operculum is eroded. This erosion is typical of intensively-reared fish; its cause is unknown, but might be the result of higher-than-optimal bacterial enzymes in and around the branchial cavity. Whatever the cause, the consequence is a huge reduction in the ability of the animal to pump water due to elimination of the water-tight seal between the trailing edge of the operculum and the body of the fish (the cleithrum). Thus the negative pressure of the opercular pump is greatly reduced. And this in an animal that is trying to pump larger-than-normal volumes of water over its gills due to the hypoxaemia of BGD!











It attaches exclusively to respiratory surfaces, including the epithelium lining the branchial cavity, but not to skin. And it does not invade the tissue. Attachment of the bacteria leads to a toxin-induced reduction in blood oxygen levels, down to roughly 30% of normal under experimental conditions. This is caused by a prostaglandin-mediated vasoconstriction of the blood vessels in the gills.

Treatment of acutely-affected fish with chemicals such as formalin, chloramine-T or hydrogen peroxide, leads to an almost instantaneous recovery in clinical signs, due no doubt to a reversal of the vasoconstriction and resulting hypoxaemia.




REFERENCES

  • Ferguson, H.W., 2006, Systemic Pathology of Fish, London, UK, Scotian Press.
  • Ferguson, H.W., Ostland, V.E., Byrne, P., & Lumsden, J.S. 1991.  Experimental production of bacterial gill disease in trout by horizontal transmission and by bath challenge.  J. Aquat. An. Health 3:118-123.
  • Speare, D. J., Markham, R. J. F., Despres, B., Whitman, K., & MacNair, N. (1995). Examination of Gills from Salmonids with Bacterial Gill Disease using Monoclonal Antibody Probes for Flavobacterium Branchiophilum and Cytophaga Columnaris. Journal of Veterinary Diagnostic Investigation, 7(4), 500–505.doi:10.1177/104063879500700413 
  • Speare, D.J., & Ferguson, H. W. & Beamish, F. & YAGER, J. & Yamashiro, S. (2006). Pathology of bacterial gill disease: Sequential development of lesions during natural outbreaks of disease. Journal of Fish Diseases. 14. 21 – 32. 10.1111/j.1365-2761.1991.tb00573.x.

By: Hugh Ferguson

Dr Ferguson earned his veterinary degree from the Royal (Dick) School of Veterinary Studies, Edinburgh, Scotland and held a Wellcome Research Fellowship at the Institute of Aquaculture, Stirling University where he obtained his PhD. He subsequently worked for 4 years as a diagnostic pathologist at the Veterinary Research Laboratories, Belfast, Northern Ireland, prior to moving to Canada. He is board-certified in the American college of veterinary pathology (ACVP), and is a Fellow of the Royal College of Pathologists (FRCPath, London). Dr Ferguson is currently professor of veterinary pathology, and Senior Research Fellow in Windward Islands Research and Education Foundation (WINDREF), St George’s University (SGU), Grenada, West Indies.

2 Comments

  1. Prof. David A. Conroy

    Congratulations are in order to Prof. Ferguson for having written such an interesting, informative and fact-filled article on bacterial gill disease. Fortunately, the condition is fairly easy to diagnose based on the clubbed appearance of the gill lamellae, the obvious hyperplasia, and the presence of numerous myxobacteria which are recognisable by their characteristic cell movements in wet preparations.

totop