Dr. Murai Éva - Gubányi András szerk.: Parasitologia Hungarica 27. (Budapest, 1994)

Thesporogonicstageof Sphaerospora species forming spores in the kidney invariably takes place in coelozoic manner, although Lorn and Dyková (1985) assumed that certain Sphaerospora stages undergo abortive intracellular development in the tubular epithelium. However, these forms are undoubtedly identical with the developmental stages of Hoferellus cyprini and are unrelated to the concurrent Sphaerospora infection. Similarly, we can rule out that the forms occasionally seen in the wall of renal tubules by Odening et al. (1989) and probably representing macrophages would be identical with sphaerospores. According to Odening et al. (1988), the population dynamics of Sphaerospora renicola shows a distinct seasonality. In my experience, that seasonality is shared by all Sphaerospora species and manifests itself in the phenomenon that spore formation and dejection take place during spawning in older fish (primarily broodstock) and at the age of 2-3 months in fry. Although occasionally large masses of spores are produced in fry, not these fish but the egg-producing breeders act as the source of the subsequent year's infection. Probably a similar process takes place in the case of proliferative kidney disease which is now unambiguously considered a sphaerosporosis. During that disease, the so-called PKX organism (a developmental stage occurring in all organs but mainly in the renal parenchyma) is detectable along with Sphaerospora developmental stages present in the renal tubules (Kent and Hedrick 1985). As the sporogonic forms found in affected salmonid fry never reach complete sporogony in the renal tubules, Kent and Hedrick (1986) suggested that this infection is caused by a Sphaerospora species for which the salmonids are not suitable hosts. In my opinion, this "blind alley" hypothesis is also built upon an error. Blind alleys are rare in nature, while unsolved problems are much more common. My supposition, supported by the observation of Kent et al. (1993), is that proliferative kidney disease is caused by spores excreted by older fish after the appropriate Actinosporea stage, in the same way as is the swimbladder inflammation of common carp fry. Naturally, the existence of developmental models other than the three basic types outlined above {Myxobolus, Hoferellus and Sphaerospora) cannot be ruled out either. It seems probable that after acquiring a more in-depth knowledge of the intrapiscine development of different parasites numerous other types of development will be identified. The development of different myxosporean species in alternative hosts also poses numerous problems to be solved. From the work of Janiszewska (1957) it is known that Actinosporea also include species developing in the gut epithelium or in the body cavities. At the same time, the specificity of myxosporeans (actinosporeans) for alternative Oligochaeta hosts is unknown. Should it prove true that myxosporeans show a strict specificity also for oligochaetes, monitoring of the entire developmental cycle could become extremely difficult.