Dr. Murai Éva szerk.: Parasitologia Hungarica 16. (Budapest, 1983)

observed also infiltration by eosinophil cells and parasite-like forms of approximately 1530 urn in size. The majority of authors demonstrated bacteria in the swim bladder wall already in the initial stage of inflammation, and in the stage of chronic inflammation also in other inner organs. In PANDEY's (1974) opinion, the dorsoventral thickening of the adventitia of the posterior sac was also characteristic of the chronic process. This resulted in cyst formation between the anterior and posterior sacs. The cyst was made up of loose connective tissue and contained serous-fibrinous exudation. According to PANDEY (1974), acute SBI was characterized histopathologically by alterative and exudative processes, while chronic SBI by exudative ones. In addition to SBI of older fish, PANDEY (1974) also examined fry. However, in his histopathological description he did not mention any difference between age groups. According to GRISHCHENKO (1967), SBI of fry frequently occurs also as a subacute process, when the disease takes a symptomless course. The latter author observed the presence of sporelike forms in the kidney, in addition to the swim bladder lesions. So far, several publications have dealt with the aetiology of the disease. However, no uniform attitude has been assumed as yet. Part of the investigators, e.g. AHNE (1973) and BACHMAN and AHNE (1973) considered SBI a viral disease, whereas others (NECIPORENKO et al., 1963; KANAEV et al. , 1967; MARKIEWICZ, 1966; SZAKOLCZAI (1967), MATHEIS and KULOW, 1967; KOCYLOVSKI et al. , 1970; ANTYCHOWICZ and ROSZKOWSKI, 1971) isolated various species of bacteria from fish affected by swim bladder inflammation. Considerably fewer investigators supposed parasitic aetiology. SZAKOLCZAI (1967) demonstrated forms resembling coccidia and Plistophora in the wall of the affected swim bladder of common carp. KANAEV and KUZMIN (1970) reported that it was possible to reproduce SBI by feeding Myxobolus spores to common carp. OTTE (1966) also thought possible parasitic aetiology of SBI, and supposed a causative role of blood flagellates. On the basis of statistical data, MOLNÁR (1980) demonstrated high correlation between SBI and renal sphaerosporosis. KOVÁCS-GAYER (cited by MOLNÁR, 1980) found in the swim bladder wall protozoa of unelucidated taxonomical position. KOVÁCS-GAYER et al. (1982) could establish a causal relationship between these protozoa and the swim bladder inflammation of common carp fry. Namely, the latter authors presumed that the swim bladder parasite was a developmental stage of Sphaerospora angulata responsible for renal sphaerosporosis. The presumed identity and developmental cycle of the swim bladder and renal protozoa and the parasite occurring in the blood described by CSABA (1976) were discussed in detail by CSABA et al. (1983). KÖRTING (1982) confirmed the above results by reporting the simultaneous occurrence of protozoa in the swim bladder wall and the kidney of common carp and tench fry. Legends to the figures: Fig. 1 Swim bladder of healthy common carp fry (Photo: Dr. G. Csaba) Fig. 2 Tissue structure of the anterior sac of swim bladder of healthy common carp fry: tunica externa (E), tunica interna (I). H-E. x 100 Fig. 3 Initial, acute swim bladder inflammation (Photo: Dr. G. Csaba). Dilated blood vessels and haemorrhages in the t. interna of the anterior sac of the swim bladder Fig. 4 Initial, acute swim bladder inflammation. Frozen section, H-E. x 100 Fig. 5 Protozoa of perivascular localization (P)

. H-E. x 1100, magnified detail of Fig. 4 Fig. 6 Degeneration of the tunica interna, with protozoa. Giemsa x 100 Fig. 7 Masses of protozoa. Mother cell (M) with daughter cells, tertiary cells (T). Giemsa x 1100 Fig. 8 Degeneration in the loose connective tissue. H-E. x 100 Fig. 9 Subacute SBI with infiltration by eosinophil cells (Eo)

. H-E. x 400 Fig, 10 Chronic SBI. Diffuse haemorrhages in the anterior sac of the swim bladder, degenerated erythrocytes and connective tissue fibres. H-E. x 100 Fig. 11 Chronic SBI. Adhesion of the tunica interna and t. externa, peritonitis (Pt). H-E. x 100