Fishers have been complaining about the effects of bottom trawl gear on the marine environment since at least the 14th century. Trawl gear affects the environment in both direct and indirect ways. Direct effects include scraping and ploughing of the substrate, sediment resuspension, destruction of benthos, and dumping of processing waste. Indirect effects include post-fishing mortality and long-term trawl-induced changes to the benthos. There are few conclusive studies linking trawling to observed environmental changes since it is difficult to isolate the cause. However, permanent faunal changes brought about by trawling have been recorded. Research has established that the degree of environmental perturbation from bottom trawling activities is related to the weight of the gear on the seabed, the towing speed, the nature of the bottom sediments, and the strength of the tides and currents. The greater the frequency of gear impact on an area, the greater the likelihood of permanent change. In deeper water where the fauna is less adapted to changes in sediment regimes and disturbance from storm events, the effects of gear take longer to disappear. Studies indicate that in deep water (>1000 m), the recovery time is probably measured in decades.

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A large-scale eplzootic occurred In the Austialas~an pllchard S a r d~n o p s sagax neop~l c h a r d u s between March and September 1995 ovei more than 5000 km of the Australian coastline and 500 km of the New Zealand coastline Affected fish died wlthln a tew mlnutes of cl~nical slgns of respiratory distress and death was associated wlth hypoxaemla a n d hypercapnea Significant leslons were confined to the gllls and comprised acute to subacute inflammation followed by blzal re epithelia1 hypertrophy and hyperplasia The lesions were initially focal but progressed to become generalised over about 4 d Pathological changes in atfeded fish from xvestern Australia eastern Australia a n d New Zealand were simila~, suggesting a common aetiology The lesions were unllke those associated w~t h ichthyotoxic algae, s~l~c e o u s algae, phys~cochemical factors fungi, bacterla dinoflagellates, amoebde, other protozoa and inetazoa A herpesvlrus was consistently present In gills of affected flsh and absent from unaffected pilchards and IS proposed as the aetiological agent T h e late of spread of the mortal~ty front (approulmately 30 km d ' ) In relation to the migration late of pilchaids a n d plevaillng currents suggests that a vector was involved The dlsease may have been newly introduced lnto Australian wateis KEY WORDS Clupeoldel . Pllchard . Sardinops sagax neopilchardus . Gill dlseases . Pathology .

Epitheliocystis in leafy seadragon (Phycodurus eques), silver perch (Bidyanus bidyanus), and barramundi (Lates calcarifer), previously associated with chlamydial bacterial infection using ultrastructural analysis, was further investigated by using molecular and immunocytochemical methods. Morphologically, all three species showed epitheliocystis cysts in the gills, and barramundi also showed lymphocystis cysts in the skin. From gill cysts of all three species and from skin cysts of barramundi 16S rRNA gene fragments were amplified by PCR and sequenced, which clustered by phylogenetic analysis together with other chlamydia-like organisms in the order Chlamydiales in a lineage separate from the family Chlamydiaceae. By using in situ RNA hybridization, 16S rRNA Chlamydiales-specific sequences were detected in gill cysts of silver perch and in gill and skin cysts of barramundi. By applying immunocytochemistry, chlamydial antigens (lipopolysaccharide and/or membrane protein) were detected in gill cysts of leafy seadragon and in gill and skin cysts of barramundi, but not in gill cysts of silver perch. In conclusion, this is the first time epitheliocystis agents of leafy seadragon, silver perch and barramundi have been undoubtedly identified as belonging to bacteria of the order Chlamydiales by molecular methods. In addition, the results suggested that lymphocystis cysts, known to be caused by iridovirus infection, could be coinfected with the epitheliocystis agent.

One of 14 goldfish (Carassius auratus) died 4 weeks after purchase and was investigated by necropsy and histological examination. Routine formalin fixation of the goldfish was followed by histopathology. Formalin fixed spleen and kidney from the fish was further processed by embedding in epoxy resin and examined by transmission electron microscopy (EM). Severe, diffuse necrosis of haematopoietic tissue in the spleen, thymus and kidney and severe, diffuse hyperplasia in the gill epithelial cells were seen. In the spleen there was severe, diffuse necrosis of lymphocytes and many nuclei with marginated chromatin and intranuclear inclusions were scattered throughout the necrotic tissue. EM of affected tissues demonstrated intranuclear particles morphologically similar to herpesvirus. The presence of an agent similar to a herpesvirus in a goldfish with severe haematopoietic necrosis suggests that the herpesvirus responsible for haematopoietic necrosis in cyprinid species throughout the world has entered the goldfish population in Australia.