| Abstrakt: |
Simple Summary: Chalkbrood is a mycological brood disease of the Western honey bee (Apis mellifera), caused by the fungus Ascosphaera apis. To date, the course of this disease (pathogenesis) has not been investigated in depth. In this study, the pathogenesis will be described in detail using macroscopy and histology under controlled experimental conditions. For this purpose, Apis mellifera larvae were artificially reared and experimentally infected with Ascosphaera apis spores. The infected larvae were then evaluated macroscopically and histologically, and the findings were compared to non-infected control larvae. Histological signs of infection were observed in 26 out of 64 infected larvae, first on day 3 p.i. Of these 26 larvae, 23 were already dead at the time of collection and showed macroscopic changes. The histological findings indicate a fulminant infection process from the germination of the spores in the intestinal lumen to the death of the larva. This study's results are crucial for an improved understanding of the pathogenesis of chalkbrood disease. Chalkbrood is a mycological brood disease of the Western honey bee (Apis mellifera), caused by the fungus Ascosphaera apis. The aim of this study was the investigation of the pathology of artificially reared Apis mellifera larvae, experimentally infected with A. apis spores (1.0 × 103 spores/larva). Non-infected larvae served as control. Five living larvae and every dead larva were collected daily (day 1–7 p.i.). All larvae were macroscopically measured, photographed, formalin-fixed, and histologically processed (hematoxylin-eosin stain, Grocott silvering). Histological sections were digitized, and the size of the larvae was measured (mouth-after length, area) and statistically analyzed. Twenty-six larvae from the collected larvae (n = 64; 23 dead, 3 alive) showed histological signs of infection from 3 d p.i. onwards. The dead larvae showed macroscopically white/brown deposits, indistinct segmentation, and a lack of body elongation. Infected larvae were significantly smaller than the controls on days 3 p.i. (p < 0.05), 4 p.i. (p < 0.001), and 6 p.i. (p < 0.05). The early time of death, the low number of transitional stages, and the strong penetration of the larval carcass with fungal mycelium indicate a rapid and fulminant infection process, which is probably relevant for spreading the disease within the colony. [ABSTRACT FROM AUTHOR] |
