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Summary Following the successful treatment of infectious fish diseases using dimerized lysozyme (KLP‐602), its influence on the nonspecific cellular and humoral defence mechanisms and protection against viral diseases in rainbow trout (Oncorhynchus mykiss) was evaluated. KLP‐602 was applied in diets, at a dose of 10 μg kg‐1 body weight, for a period of 7 days. One week after feeding with the diets containing KLP‐602, the immunomodulatory effects on the suppressed cellular and humoral defence mechanisms were observed in fish naturally infected by infectious pancreatic necrosis virus (IPNV). All immunological parameters were significantly increased in comparison with untreated fish. Cumulative mortality was lower in fish fed the dietary treatment containing dimerized lysozyme (30%), compared with untreated fish (65%). The results showed that the lysozyme dimer (KLP‐602) modulated the cellular and humoral defence mechanisms after suppression induced by IPNV.

Siwicki, A. K., M. Morand, P. Klein, M. Studnicka. E. Terech-~!ajewska: Modulation of Non-specific Defence Mechanisms and Protection against Diseases ill Fish. Acta vet. Emo, 1998,67: 323-328.The use of immunomodulators in fish culture offers a wide range of attractive methods for inducing or modulating protection against diseases. Several promising synthetic drugs and biological response modifiers stimulate or modulate the nonspecific defence mechanisms and specific cellular and humoral immune responses in fish. This article reviews the literature on the influence of biostimulants on the cellular and humoral defence mechanisms in fish, and present the possibility to application of immunostimulants for control of infectious diseases in aquaculture. Fish, immllflostimuiallts, defence mechanismsProtection of fish against bacterial diseases by specific vaccines has been an important method for many years in aquaculture. However, defence mechanisms in the lower vertebrates are somewhat different from those in mammals, and some immunization techniques when actually applied to hatchery conditions are not as effective as they should be. Therefore, research is concentrating on how to improve the potency and efficacy of the antigens and how to optimally activate the nonspecific defence mechanisms and specific cellular and humoral immune responses. When a fish initially encounters a pathogen, the nonspecific defence mechanisms are more important than the specific immune response, as the latter requires a long time for antibody build-up and specific cellular activation. In general, fish have short life spans and most live in cool water environments which slows development of the specific immune response. Nonspecific defence barriers and mechanismsThe nonspecific defence barriers already in place include physical epithelial shield of the scales, skin and the mucus. If an infectious agent is entrapped by the mucopolysaccharide complexes of the mucus, it may be scuffed from the fish or held to be digested by the mucus lytic enzymes. In most cases, the pathogenic microorganisms are destroyed by digestive and lytic enzymes. Inflammation may result at a tissue-damaged site, resulting in the migration of leukocytes to wound areas and the elevation of serum component concentrations, including C-reactive protein, transferrin, lysozyme, ceruloplasmine and complement components.

A mathematical model of B lymphocyte differentiation, based on experimental results, has been developed. The model focuses on the role of antigen in initiating and regulating B cell differentiation while other mechanisms, acting in concert with antigen but the functioning of which can be circumvented under appropriate conditions, are not considered. The importance of presence of antigen at individual stages of B cell differentiation was studied in experiments with an easily metabolizable antigen. Immunocompetent cells (ICC), arising by antigen-independent differentiation of stem cells, are activated by antigen (they become immunologically activated cells--IAC). Excess of antigen drives IAC into the terminal stage (antibody-forming cells--AFC) thereby restricting proliferation. Exhaustive terminal differentiation results in tolerance. A low primary dose permits IAC to escape antigen; IAC proliferate and later give rise to resting memory cells (MC) which are amenable to reactivation. MC have higher avidity for antigen (due to higher affinity, number and density of receptors) and the effect of different doses of antigen on MC is diverse. A very low secondary dose induces tolerance, a medium dose secondary response, and the administration of a high dose of antigen also brings about tolerance. The model suggests that the fate of memory cells is controlled by the ratio R:Ag, of the number of immunoglobulin receptors on B cells (R) to the number of available antigenic molecules (Ag), low values R:Ag favouring stimulation to differentiation while high values of R:Ag favouring inactivation. A nonlinear system of ordinary differential equations, describing the development of the populations involved in antigen-driven B cell differentiation, was used to simulate experiments and good qualitative agreement was achieved.

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