Heat shock proteins (HSPs), also known as stress proteins and extrinsic chaperones, are a suite of highly conserved proteins of varying molecular weight (c. 16-100 kDa) produced in all cellular organisms when they are exposed to stress. They develop following up-regulation of specific genes, whose transcription is mediated by the interaction of heat shock factors with heat shock elements in gene promoter regions. HSPs function as helper molecules or chaperones for all protein and lipid metabolic activities of the cell, and it is now recognized that the up-regulation in response to stress is universal to all cells and not restricted to heat stress. Thus, other stressors such as anoxia, ischaemia, toxins, protein degradation, hypoxia, acidosis and microbial damage will also lead to their up-regulation. They play a fundamental role in the regulation of normal protein synthesis within the cell. HSP families, such as HSP90 and HSP70, are critical to the folding and assembly of other cellular proteins and are also involved in regulation of kinetic partitioning between folding, translocation and aggregation within the cell. HSPs also have a wider role in relation to the function of the immune system, apoptosis and various facets of the inflammatory process. In aquatic animals, they have been shown to play an important role in health, in relation to the host response to environmental pollutants, to food toxins and in particular in the development of inflammation and the specific and non-specific immune responses to bacterial and viral infections in both finfish and shrimp. With the recent development of non-traumatic methods for enhancing HSP levels in fish and shrimp populations via heat, via provision of exogenous HSPs or by oral or water administration of HSP stimulants, they have also, in addition to the health effects, been demonstrated to be valuable in contributing to reducing trauma and physical stress in relation to husbandry events such as transportation and vaccination.

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A survey ot fish affected with epizoolic ulccralive syndrome taken from outbreaks in countries throughout South and South-East Asia showed that a morphologically typical fungus was consistently present within lesions. Although the majority of the fungal mycelium was dead in most lesions it proved possible to isolate a very delicate and culturally demanding Aphanomyces from such lesions in a few cases. It also proved relatively easy to isolate other members of the Saprolegniaeeae including Aphanomyces from the surface of lesions, but these were considered saprophytes derived from background spore burdens in the water. Sporangium morphology of the putatively pathogenic isolates oi Aphanomyces was different from that of saprophytie Aphanomyces strains and they also had a lower thermal tolerance. When a mycelium from these strains was placed below the dermis of healthy fish, it caused an inflammator)' response and proceeded to migrate down into the tissues of the fish, inducing severe myonecrosis with chronic epithelial reaction. The saprophytie isolates induced a local host response followed by healing of the induced lesion, and destruction or expulsion of the mycelium. It is considered that the speeific slow-growing, thermo-labilc Aphanomyces is the pathogenic fungus which causes so much tissue damage in this disease, although it may not be a primary pathogen in its own right.

Pathogenicity and cultural experiments described here provide futher evidence that a distinct species of Aphanomyces is responsible for much of the characteristic pathology of epizootic ulceration syndrome (EUS). Zoospores from 58 fungal isolates were injected intramuscularly in snakehead fish, Channa striata (Bloch). These fungi comprised: Aphanomyces strains isolated from EUS‐affected fish; saprophytic Aphanomyces, Achlya and Saprolegnia spp. from infected waters; and further saprolegniaceous fungi involved in other diseases of aquatic animals. Only the Aphanomyces strains isolated from fish affected by EUS, Australian red spot disease (already considered synonymous with EUS) or mycotic granulomatosis described from Japan were able to grow invasively through the fish muscle and produce the distinctive EUS lesions. In contrast to Aphanomyces astaci Schikora, the EUS‐Aphanomyces was shown to be unable to infect noble crayfish, Astacus astacus L. The snakehead‐pathogenic strains were further distinguished from all the other fungi under comparison by their characteristic temperature‐growth profile and inability to grow on certain selective fungal media.