The pathology of Flexibacter maritimus in aquaculture species in Tasmania, Australia

Abstract

Macroscopic and microscopic features of natural and experimental Flexibacter maritimus infection, and epidemiological aspects of the disease, have been reported in a number of species of fish in Tasmanian aquaculture including Atlantic salmon, Salmo salar L., rainbow trout, Oncorhynchus mykiss (Walbaum), greenback flounder, Rhombosolea tapirina Günther, and striped trumpeter, Latris lineata (Bloch & Schneider). There is a great deal of consistency in the pathology in salmonids and non‐salmonid species, with erosive lesions of external surfaces being the most prominent clinical sign. Experimentally induced disease of salmonids and flounder is similar to natural infection. Mature lesions show dermal and gill erosion, with dermal bacterial invasion into the dense connective tissue and occasionally underlying musculature, but a remarkable lack of inflammatory response. The earliest lesions show consistent fragmentation and degeneration of the epithelium, with infiltration of amorphous protein‐like materials and occasionally intra‐epithelial cellular inflammatory cells, plus congestion and haemorrhage of the superficial dermis, but without visible bacteria in standard sections. Variable scale loss, oedema and a low level of inflammation in scale pockets, plus variable small adherent bacterial mats, are evident before full epithelial erosion.

Experimentally induced marine flexibacteriosis in Atlantic salmon smolts Salmo salar. I. Pathogenicity

“…Anecdotal evidence from the present study suggests that attenuation occurs quickly in Tenacibaculum maritimum isolates (R. van Gelderen unpubl.). The cause of the non-pathogenic results of strain 89/4747 in the present study may be attenuation, but this requires further investigation as there are many other factors to consider, such as preservation techniques, age of isolate, culture media and storage over time (Michel & Garcia 2003, O'Keefe et al 2006.In contrast, strains 00/3280 and 89/4762 were highly virulent, resulting in 100% mortalities in 3 d. Both strains have previously been demonstrated as highly pathogenic (Carson et al 1992, Handlinger et al 1997, Powell et al 2004. Experimental application of Tenacibaculum maritimum to the gills of Atlantic salmon using strain 00/3280 caused high levels of mortalities within 48 h (Powell et al 2004).…”

“…Salmonids are competitive and will bite and harass each other when held in captivity (Mork et al 1999, MacLean et al 2000. The observed size difference of fish in each experiment would have contributed to this behaviour, which is likely to facilitate bacterial invasiveness, as damage to the epithelium would create a portal of entry for the bacteria to colonise and proliferate (Handlinger et al 1997).…”

“…Marine Shieh's and marine Ordal's media were the 2 growth media used previously (Carson et al 1992, Soltani 1995, Handlinger et al 1997) to investigate Tenacibaculum maritimum in Tasmania. Bacteria cultured from both media were able to cause infection and mortalities in Atlantic salmon Salmo salar within the 10 d experimental period.…”

“…In Tasmania, Australia, the disease has affected Atlantic salmon Salmo salar, rainbow trout Oncorhynchus mykiss, greenback flounder Rhombosolea tapirina and striped trumpeter Latris lineata (Handlinger et al 1997). Previous work has investigated similarities and differences in characteristics amongst bacterial isolates of T. maritimum (van Gelderen 2007).…”

“…Salmonids are competitive and will bite and harass each other when held in captivity (Mork et al 1999, MacLean et al 2000. The observed size difference of fish in each experiment would have contributed to this behaviour, which is likely to facilitate bacterial invasiveness, as damage to the epithelium would create a portal of entry for the bacteria to colonise and proliferate (Handlinger et al 1997).Other successful methods of inducing marine flexibacteriosis are usually associated with direct application to various areas of the body and scarification by different means (Masumura & Wakabayashi 1977, Wakabayashi et al 1984, Baxa et al 1987, Carson et al 1992, Bernardet et al 1994, Powell et al 2004. While intraperitoneal and intramuscular injections are ineffective (Campbell & Buswell 1982, Baxa et al 1987, Carson et al 1992, subcutaneous injection has worked on occasion, which is probably a result of injecting into the dermal layer, where bacteria are found in natural outbreaks (Masumura & Wakabayashi 1977, Wakabayashi et al 1984, Alsina & Blanch 1993, Bernardet et al 1994, Soltani 1995, Avendaño-Herrera et al 2006.…”