Differential diagnosis of ulcerative lesions in fish.

Abstract

Tissues such as skin and muscle have a limited repertoire of morphological response to injury. The two most important phenomena that determine the outcome of cell injury appear to be a) critical cell membrane damage, with associated fluid and ionic imbalances; and b) inability of mitochondria, the powerhouse of the cell, to restart ATP synthesis. In fish, skin ulcers can have many different etiologies, including infectious agents, toxins, physical causes, immunologic causes, and nutritional and metabolic perturbations. This article is concerned primarily with the possible pathways of disease involved in ulcerative lesions of fish. In particular, the high prevalence of ulcerative lesions in Atlantic menhaden found along the mid-Atlantic coast, especially in North Carolina estuarine waters, has received much recent attention. These ulcerative lesions are likely to be initiated by a series of factors that lead ultimately to a breach of the normal barrier function of the skin. Bioassays that attempt to define the role of individual etiologic agents such as fungi (oomycetes) or putative Pfiesteria toxin(s) should recognize this multiplicity of factors and should include appropriate quality control measures for water quality parameters (temperature, dissolved oxygen, nitrogenous wastes, etc.) as well as bacterial and other contaminants that may confound bioassay results and their interpretation. Consideration of these factors along with the whole animal in the context of its environment can only advance the science, perhaps provide clues to the causative pathways of skin ulcers in fish, and give us keener insight into the health of the aquatic environment.