This review surveys the available literature on the effieaey and eeotoxieology of chemotherapeutic agents for the control of sea lice (Copepoda: Caligidae) infestations in marine aquaculture. To date, treatment for the disease has relied almost exclusively on the use of the organophosphorus pesticides, trichlorfon and dichlorvos. While use of dichlorvos and trichlorfon appears to have little, if any, environmental impact, protracted use in some areas has led to reduced efficacy. Compounds proposed for sea lice control currently under field evaluation include azamethiphos (organophosphate), ivermectin (avermectin), pyrethrum (pyrethrin) and hydrogen peroxide. Although all of these eompounds are effi cacious, at present published information on marine environmental toxicology is scarce and is limited to in vitro toxieity testing. Other compounds that have been considered for sea lice control include formalin, malathion (organophosphate), earbaryl (earbamate), diflubenzuron (insect growth regulator) and natural remedies (i.e. onions and garlic). In general, formaldehyde (aldehyde), malathion and natural compounds show either poor efficacy or unsuitable therapeutic margins. Although earbaryl and diflubenzuron are both efficacious and exhibit suitable therapeutic margins, available data suggests that the compounds, due to undesirable environmental toxieologieal characteristics, would be unsuitable for sea lice control.

A histopathological study was carried out on rainbow trout suffering from acute and chronic diplostomiasis. Clinical signs were few in acutely infected fish but in chronic cases fish were blind, exophthalmic and emaciated. Acute infections resulted in subcapsular cataract formation with varying capsular change. Chronically infected fish frequently showed lens dislocation, capsular rupture or duplication and the formation of Elschnig's pearls and Wedl cells. Phacogenic uveitis was seen in many fish with capsular rupture and retinal detachment frequently occurred as a sequal to vitreous detachment.

. A histological study of 0+ rainbow trout, exposed to proliferative kidney disease (PKD) on an infected farm, showed evidence of infection from the beginning of June, gross pathological changes from the beginning of July, and clinical signs from mid‐July. Evidence of healing was present in some samples from the second week of August. Kidney samples were divided into five grades (0–4) representing increasing severity of pathology. A sixth grade (H) was applied to kidneys showing signs of healing. The most frequent clinical signs were abdominal distension and exophthalmos. Melanosis, corneal cloudiness and ecchymoses were observed occasionally. Apart from renal enlargement, other internal gross pathological changes included ascites, gill and liver pallor, oedema, petechiation, and splenic enlargement. The majority of clinical signs and internal changes were only seen in fish with advanced renal swelling (grades 3 and 4). Histopathology was most marked in the kidney and was of three types: haemopoietic hyperplasia, vascular pathology and diffuse inflammatory change. Vascular changes, including occlusion of blood vessels in several organs and apparent haemoglobin crystallization, and destruction of renal excretory structures within areas of chronic diffuse inflammation were marked features of the histopathology in fish with clinical signs. The pathogenesis of PKD is discussed with reference to the histopathological changes.

. Fungal infection of sexually mature brown trout and char was associated with a particular type of Saprolegnia exhibiting a low degree of homothallic sexuality. Hatchery‐reared brown trout were more severely infected (in terms of the % area of the body covered with the fungus) than were wild fish. The fins of hatchery‐reared fish were particularly prone to Saprolegnia infection regardless of sex. In wild brown trout, a sexual difference in the pattern of infection was demonstrated. The flanks of the male fish appeared to be more prone to infection when compared with the female and there was a greater susceptibility of the caudal and ventral fin of the female when compared with the male. Evidence is presented which suggests that the incidence of infection in mature male salmonid fish prior to spawning is significantly greater than in the females. This difference may not be apparent in spent fish after spawning. These findings are discussed in relation to the background concentration of fungal spores in the water, the behavioural characteristics of spawning fish and differences in epidermal structure.

The duration of efficacy of emamectin benzoate in the oral treatment of sea lice, Lepeophtheirus salmonis, infesting Atlantic salmon, Salmo salar L., was evaluated in a tank study. One group of salmon was treated at a nominal dose of 50 μg kg−1 biomass day−1 for 7 consecutive days and a second group was untreated. Fish were then redistributed to 16 tanks, each holding 17 control and 17 treated fish. On days 34, 41, 48, 55, 62, 69, 76 and 83, two tanks were challenged with L. salmonis copepodites. Eight to 14 days after each challenge, fish were anaesthetized and numbers of lice recorded. Treatment with emamectin benzoate prevented development of copepodites for up to 62 days from the start of treatment, and chalimus numbers remained low for 69 days. Treated fish, challenged from days 34 to 69, had significantly (P<0.01) fewer lice than control fish. Treated fish challenged at days 76 and 83 still had fewer lice than control groups, although differences were not statistically significant for both replicates. When chalimus appeared on treated fish challenged at days 69–83, survival of chalimus to adult stages was lower than on control fish. Louse egg production on treated fish challenged at days 62–83 was not reduced compared to control groups.

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The gross, histological and scanning electron microscopic appearance of dorsal fin rot in farmed Atlantic salmon parr, Salmo salar L. is described. The lesions were grouped into seven categories: (1) peripheral erosion and ray splitting; (2) peripheral erosion with some nodularity; (3) severe nodularity with differing degrees of tissue loss; (4) extensive to total loss of the dorsal fin; (5) smooth thickening of the dorsal fin; (6) haemorrhagic dorsal fin lesions; and (7) healed dorsal fin rot lesions. The main sign of injury was clefts extending through the epithelium. These injuries were consistent with bites from other parr. During healing from such wounds, damaged cells sloughed from the surface, and there was swelling and hyperplasia in the remaining cells. The majority of the thickening in the fins was the result of epithelial hyperplasia with a variable cellular inflammatory response. The distal epithelium of fins with severe fin rot (i.e. nodular and eroded) was rough, irregular and swollen with superficial nodular extensions. Wounds in all stages of repair were more numerous in such areas. Fin rays were frequently observed protruding from the abnormal epithelium at the distal edge of the fin. With the exception of the isolation of Aeromonas salmonicida from a small number of cases, no significant bacterial involvement was detected. Under scanning electron microscopy, bacteria were only detected on the exposed fin rays and not in association with the abnormal epithelium. In the majority of cases, the dorsal fin was either the only fin damaged or the most severely damaged. It is suggested that the hyperplastic response to numerous bite wounds is responsible for the accumulation of abnormal epithelium typical of dorsal fin rot in farmed Atlantic salmon parr.

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