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Steel composites for application as protective plates were produced via diffusion bonding. Cold work tool steels were combined with a precipitation hardening steel or a maraging steel using a deformation dilatometer and a vacuum furnace at 1150 °C for 8 h in total. Subsequently, a heat treatment was applied to achieve the final mechanical properties. The microstructure of the interface was investigated by optical microscopy, scanning electron microscopy, electron backscatter diffraction, energy dispersive X-ray spectroscopy and hardness measurements. The results are compared with a simulation of the diffusion of elements performed by MatCalc. Both composites achieve high hardness near the surface of the cold work tool steels, which can have a positive effect on the destruction of projectiles on impact. The influence of carbon diffusion can be observed up to a depth of 3 mm from the interface. As a result of carbon diffusion, soft zones are formed on both sides of the interface, which can be attributed to decarburization, phase transformation and carbide formation. The tough back layer is designed to absorb the remaining energy of the projectile. The combination of a hard front layer and a tough rear layer provides an optimal combination of materials against ballistic threats.

Honey bees use several strategies to protect themselves and the colony from parasites and pathogens. In addition to individual immunity, social immunity involves the cumulative effort of some individuals to limit the spread of parasites and pathogens to uninfected nestmates. Examples of social immunity in honey bees that have received attention include hygienic behavior, or the removal of diseased brood, and the collection and deposition of antimicrobial resins (propolis) on interior nest surfaces. Advances in our understanding of another form of social immunity, social fever, are lacking. Honey bees were shown to raise the temperature of the nest in response to temperature-sensitive brood pathogen, Ascosphaera apis. The increase in nest temperature (−0.6 °C) is thought to limit the spread of A. apis infection to uninfected immatures. We established observation hives and monitored the temperature of the brood nest for 40 days. This observation period was broken into five distinct segments, corresponding to sucrose solution feedings—Pre-Feed, Feed I, Challenge, Feed II, and Post-Feed. Ascosphaera apis was administered to colonies as a 1% solution of ground sporulating chalkbrood mummies in 50% v/v sucrose solution, during the Challenge period. Like previous reports, we observed a modest increase in brood nest temperature during the Challenge period. However, all hives presented signs of chalkbrood disease, suggesting that elevation of the nest temperature was not sufficient to stop the spread of infection among immatures. We also began to explore the molecular mechanisms of temperature increase by exposing adult bees in cages to A. apis, without the presence of immatures. Compared to adult workers who were given sucrose solution only, workers exposed to A. apis showed increased expression of the antimicrobial peptides abaecin (p = 0.07) and hymenoptaecin (p = 0.04), but expression of the heat shock response protein Hsp 70Ab-like (p = 0.76) and the nutritional marker vitellogenin (p = 0.72) were unaffected. These results indicate that adult honey bee workers exposed to a brood pathogen elevate the temperature of the brood nest and initiate an immune response, but the effect of this fever on preventing disease requires further study.

Throughout a honey bee queen’s lifetime, she is tended to by her worker daughters, who feed and groom her. Such interactions provide possible horizontal transmission routes for pathogens from the workers to the queen, and as such a queen’s pathogen profile may be representative of the workers within a colony. To explore this further, we investigated known honey bee pathogen co-occurrence, as well as pathogen transmission from workers to queens. Queens from 42 colonies were removed from their source hives and exchanged into a second, unrelated foster colony. Worker samples were taken from the source colony on the day of queen exchange and the queens were collected 24 days after introduction. All samples were screened for Nosema spp., Trypanosome spp., acute bee paralysis virus (ABPV), black queen cell virus (BQCV), chronic bee paralysis virus (CBPV), Israeli acute paralysis virus (IAPV), Lake Sinai virus (LSV), and deformed wing virus master variants (DWV-A, B, and C) using RT-qPCR. The data show that LSV, Nosema, and DWV-B were the most abundant pathogens in colonies. All workers (n = 42) were LSV-positive, 88% were Nosema-positive, whilst pathogen loads were low (6 genome equivalents per pooled worker sample). All queens (n = 39) were negative for both LSV and Nosema. We found no evidence of DWV transmission occurring from worker to queen when comparing queens to foster colonies, despite DWV being present in both queens and workers. Honey bee pathogen presence and diversity in queens cannot be revealed from screening workers, nor were pathogens successfully transmitted to the queen.

Failure of the queen is often identified as a leading cause of honey bee colony mortality. However, the factors that can contribute to “queen failure” are poorly defined and often misunderstood. We studied one specific sign attributed to queen failure: poor brood pattern. In 2016 and 2017, we identified pairs of colonies with “good” and “poor” brood patterns in commercial beekeeping operations and used standard metrics to assess queen and colony health. We found no queen quality measures reliably associated with poor-brood colonies. In the second year (2017), we exchanged queens between colony pairs (n = 21): a queen from a poor-brood colony was introduced into a good-brood colony and vice versa. We observed that brood patterns of queens originally from poor-brood colonies significantly improved after placement into a good-brood colony after 21 days, suggesting factors other than the queen contributed to brood pattern. Our study challenges the notion that brood pattern alone is sufficient to judge queen quality. Our results emphasize the challenges in determining the root source for problems related to the queen when assessing honey bee colony health.