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

ner organs, those of parasitic SBI of fry are for the most part restricted to the swim bladder, indicating a distinct disease entity. Of the authors suggesting bacterial aetiology, JAHNEL (1938), SZAKOLCZAI (1967), KOKURITSEVA (1969), ANTYCHOWICZ and ROSZKOWSKI (1971) and PANDEY (1974) observed the most severe changes in the loose connective tissue. These lesions were characteristic not only for the anterior but also for the posterior sac. In the order of severity of changes, BRAUN (1969) mentioned the epithelium of the swim bladder after the peritoneum. Also according to the above authors, the process starts from the epithelium, and bacteria can be demonstrated from the swim bladder already in the acute stage. In SBI of parasitic origin, microorganisms were not demonstrable in the acute cases. Although presuming bacterial aetiology, in his description PANDEY (1974) emphasized also the changes of other organs. The observations of GRISHCHENKO (1967) and PANDEY (1974) are in agreement with my own observations. These authors found protozoon-like forms in the lumina of convoluted tubuli of the kidney, but failed to establish a causal relationship between these and SBI. These parasites can be found in the renal tubuli, mistakenly referred to as swim bladder wall, mentioned in the description of swim bladder inflammation in the manual of SCHAPERCLAUS (1979). The statement that the acute and chronic inflammatory processes are well-distinguishable by histopathological examination is in good agreement with the results of KOKURITSEVA (1969) and PANDEY (1974), and also with my own observations. Also a common feature of authors suggesting bacterial aetiology is that they focused their attention on describing the chronig inflammatory processes, and neglected the acute stages. The studies of CSABA et al. (1983), performed with impression smears, confirmed the results of histopathological examinations. They established that the swim bladder and the kidney contained ontogenetically closely related protozoa belonging to Myxozoa. KÖRTING (1982) confirmed the protozoan aetiology of SBI of fry also in the case of tench affected with SBI. He also confirmed the correlation existing between SBI and renal sphaerosporosis first demonstrated by MOLNÁR in 1980, and occasionally observed similar protozoa and developmental stages also in tissues of the head and liver. The greatest similarity was found to exist with the description of SZAKOLCZAI (1967). This correlation was apparent primarily in the pathogenesis of inflammation. However, the parasite forms demonstrated by SZAKOLCZAI were larger than those observed in parasitic SBI of fry. These parasite cysts contained more than 20 spores, did not stain with GIEMSA, and did not divide to smaller formations. It is hard to find any correlation with the results of WALUGA and BUDZYNSKA (1980),.. It can only be supposed that the sphaerospora forms found by them correspond to the blood protozoan described by CSABA (197 6) and demonstrable in most organs. Differences between authors in the description of swim bladder inflammation of the common carp may be due to the fact that the methods used in studying SBI were not uniform, the fish studied were of different age, and the nomenclature used lacked uniformity. There are significant differences between SBI of fry and that of several summers old carp, obviously due to the different aetiology. Therefore, in discussing the pathology and histopathology of SBI, it is indispensable to indicate the age of fish and the causative agent. By regular histopathological examination, SBI of fry can be demonstrated already in its early stage, before the appearance of clinical symptoms, and the acute and chronic inflammatory processes are also easily distinguishable. Protozoa can be demonstrated in the swim bladder wall for approximately 10 days, and the aggravation of lesions can be attributed to bacteria joining the process as secondary invaders.