| Abstract: | Pathological alterations being similar to those that can be seen while hormonal dysbalance, particularly the increase of juvenile hormone (JH) titre, is one of the consequences of microsporidian infections. Though the increase of JH in insects infected with microsporidia has not been shown directly, there are many indirect proofs of this. It has been believed that JH is produced by microsporidia. But this has not been shown for microsporidia or for other endoparasites. In this article we want to propose another hypothesis. We suppose that during microsporidiosis the following events develop: exhaustion of host nutrition stores and other destructive consequences of microsporidian dwelling in host cells lead to the decrease of host biosynthetical and reparation activity in the infected cells and then to destructive alterations that can be seen by electro-microscopic methods. The infected cells are stressed and then the typical answer for many physiological stresses follows. Secretion of prothoracicotropic hormone by brain neurosecretory cells is inhibited and as a result the production and release of ecdysone is also inhibited and ecdysteroid titre decreases. The activity of JH-esterases is decreased and as a result the JH titre is increased. If microsporidian infection causes the stress in the host cells, the endocrine system will undoubtedly answer to this stress and this answer will definitely be the same as for all other stresses. Thus, in any case JH titre will be increased in infected insects independently of whether microsporidia produce JH or not. So, hormonal alterations in infected insects should be the consequence not of the microsporidian JH production but of the host response reaction to infection. We suppose that microsporidia do not differ from other parasites of insects and that they can not produce JH. |
