Microsporidia in Predator–Prey and Parasitoid–Host Systems: Evaluation of Evidence Levels for Non-Target Infection
16TH AZERBAIJAN CONGRESS ON LIFE, ENGINEERING,MATHEMATICAL, AND APPLIED SCIENCES, Baku, Azerbaycan, 20 Eylül - 22 Ekim 2026, ss.384-394, (Tam Metin Bildiri)
- Yayın Türü: Bildiri / Tam Metin Bildiri
- Doi Numarası: 10.30546/19023.978-9952-610-91-5.2026.100.1148.
- Basıldığı Şehir: Baku
- Basıldığı Ülke: Azerbaycan
- Sayfa Sayıları: ss.384-394
- Karadeniz Teknik Üniversitesi Adresli: Evet
Özet
Microsporidia may contribute to natural or applied biological control by reducing the development, reproduction, and longevity of insect pests; however, exposure of predators feeding on infected prey or parasitoids developing within infected hosts raises concerns about non-target effects. In this perspective study, experimental evidence from predator-prey and parasitoid-host systems, together with limited field data, was evaluated to determine whether trophic exposure progresses to true infection and what such progression means for biological control function. The assessment focused on three questions: can microsporidia reach a natural enemy, does exposure progress to an established and productive infection, and does this process cause a measurable loss in biological control function? The available evidence shows that detection of spores or microsporidial DNA alone does not demonstrate an established or productive infection. In some predators, spores can pass through the digestive tract while remaining viable and can subsequently be disseminated into the environment, whereas infection does not develop in predator tissues. In particular microsporidium-natural enemy combinations, however, passage into host tissues, intracellular developmental stages, mature spore formation, and either limited or substantial persistence across generations have been reported. Outcomes in parasitoids are similarly variable: development within an infected host may result only in carriage of spores in the digestive tract, but in other systems it can progress to extensive tissue infection. In addition, natural-enemy performance may decline even without infection because infection can alter the nutritional or physiological quality of prey or hosts, affecting development time, longevity, fecundity, parasitism success, or host-location behavior. Non-target risk should therefore be evaluated through four linked components: ecologically meaningful exposure, active development and mature spore formation in natural-enemy tissues, biologically meaningful impairment of control functions, and persistence through horizontal, vertical, or transstadial transmission. Current evidence indicates that risk is not a general property of Microsporidia but depends on the microsporidium species or isolate, natural-enemy species, life stage, exposure route, and dose. Accordingly, positive spore or DNA detection should not by itself be interpreted as high non-target risk, laboratory susceptibility should not be equated with ecological risk, and each pathogen-natural enemy system should be assessed according to its specific level of evidence. Distinguishing direct pathogenic effects from indirect performance losses caused by reduced prey or host quality is particularly important for interpreting biologically meaningful risk in biological control programs.