No abstract

ABSTRACT-Chaetoceros concavicornis and C. convolutus are harmful diatom species which commonly occur in many temperate coastal marine waters and which can cause finfish mortalities when present at concentrations as low as 5 cells ml-' of seawater. Death of finfish, including salmonids, by these harmful Chaetocerosspp. has been suggested to be caused by: (1) microbial infections of damaged gill tissue; (2) hemorrhage of gill capillaries; or (3) suffocation from excess mucus production at the sites of penetration of the gills by the spines. Our data indicate that the barbed spines of these diatoms damage the physical integrity of the respiratory epithelium of rainbow trout Oncorhynchus mykiss. The trout responds to this physical impairment of gill tissue by producing excessive amounts of mucus. The accumulation of this mucus on and between the secondary lamellae inhibits the gill function of O2 uptake (and likely metabolic waste products release). The hypoxic conditions which result within the fish then cause a cascade of events, including anaerobic metabolism. Trout mortalities occur coincident with severe decreases in O2 concentration and pH as well as increases in lactate and glucose concentrations of the arterial blood.

The harmful diatoms Chaetoceros concavicornis and C. convolutus will kill salmonids such as rainbow trout Oncorhynchus rnykiss and coho salmon 0. kisutch if present at as few as 5 cells ml-' seawater. Our previous research has shown that the barbed spines of these diatoms become wedged between the secondary lamellae of salmonids, where they cause excessive production of mucus by goblet cells. This mucus and the diatoms accumulate on and between the secondary lamellae to such a n extent that the fish suffocate. A class of pharmacolog~cally active compounds (mucolytic agents, e.g. L-cysteine ethyl ester) exists which decrease mucus production in mammals and humans when ingested. When coho salmon Ingest this agent at up to 12 mg kg-' biomass d-l, mucus synthes~s is reduced to such an extent that an accumulation of this mater~al does not occur on and between the secondary lamellae; the fish remain viable in what would otherwise be a lethal exposure to C concavicornis cells. KEY WORDS: Anti-phytoplankton therapy. Mucolytic agent. Mucus. L-cysteine ethyl ester. Harmful phytoplankton. Salmon. Chaetoceros concavicorn~s

Chaetoceros concavicornis is a harmful phytoplankter that occurs in many temperate coastal seawaters and can cause fin fish mortalities when present at concentrations as low as 5 cells∙mL−1. At even lower concentrations, this diatom can stress salmonids to such an extent that they may express a disease to which they are most prone at the time of C. concavicornis exposure. We report mortality rates of coho salmon (Oncorhynchus kisutch) and chinook salmon (O. tshawytscha) exposed to different concentrations of C. concavicornis. Our data indicate that in the presence of harmful concentrations of C. concavicornis, blood hematocrit and erythrocyte, glucose, and lactate concentrations of yearling chinook salmon (O. tshawytscha) increase. The microridges of the primary lamellae decreased in prominence in the presence of harmful concentrations of this phytoplankter, while the goblet cells became more prominent and more numerous. Neutrophil, lymphocyte, and thrombocyte concentrations in the blood became depleted. These data suggest that suppression of a portion of the Chinook's immune system is occurring which may partially explain the earlier observation that salmonids cultured in the presence of harmful C. concavicornis phytoplankton became more susceptible to disease, including Vibrio infections.

Changes in plasma eortisol concentrations and inter-renal and chromaffin tissues of rainbow trout, Oncorhynehus mykiss (Walbaum), exposed to harmful concentrations of the diatom Chaetoceros eoncavicornis were investigated. The plasma cortisol level of trout exposed to C. eoncavicornis was over 10-fold greater than that of untreated trout. Computerassisted feulgen-microspectrophotometry was employed in order to assess the activity of inter-renal and chromaffin cells. The total areas of inter-renal and chromaffin nuclei in trout treated with C coneavicornis significantly inereased compared to those of untreated fish. In contrast, the chromatin density of inter-renal and chromaffin nuclei in treated trout decreased significantly. This decrease of chromatin density in treated fish was caused by an increase in the low-density components, and a decrease in the middle-density and high-density components. Although the hypertrophic changes to the inter-renal and chromaffin nuclei of treated fish exhibited the same general trend, the extents to which the changes took plaee were different, oecurring more rapidly within inter-renal tissues. The rainbow trout exposed to harmful concentrations of C. eoneavicornis were experieneing a severe physiological disturbance to which they tried to adapt.