Genetic variation of Ascosphaera apis and colony attributes do not explain chalkbrood disease outbreaks in Australian honey bees

Gerdts, Jody; Roberts, John M. K.; Simone-Finstrom, Michael; Ogbourne, Steven M.; Tucci, Joseph

doi:10.1016/j.jip.2021.107540

Cited by 7 publications

(6 citation statements)

References 42 publications

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“…Chalkbrood is a honey bee brood disease caused by the fungus Ascosphaera apis (Ascomycota: Eurotiomycetes: Ascosphaerales). The disease is widespread worldwide, and there is evidence that the incidence of chalkbrood may be increasing [18][19][20][21]. The typical symptoms are irregular wax capping over the brood and uncapped cells scattered over the brood frames.…”

Section: Introductionmentioning

confidence: 99%

Micronutrient Deficiency May Be Associated with the Onset of Chalkbrood Disease in Honey Bees

Pavlović,

Brodschneider,

Goessler

et al. 2024

Insects

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Chalkbrood is a disease of honey bee brood caused by the fungal parasite Ascosphaera apis. Many factors such as genetics, temperature, humidity and nutrition influence the appearance of clinical symptoms. Poor nutrition impairs the immune system, which favors the manifestation of symptoms of many honey bee diseases. However, a direct link between dietary ingredients and the symptoms of chalkbrood disease has not yet been established. We show here that the elemental composition of chalkbrood mummies and healthy larvae from the same infected hives differ, as well as that mummies differ from larvae from healthy hives. Chalkbrood mummies had the highest concentration of macroelements such as Na, Mg, P, S, K and Ca and some microelements such as Rb and Sn, and at the same time the lowest concentration of B, As, Sr, Ag, Cd, Sb, Ba and Pb. Larvae from infected hives contained less Pb, Ba, Cs, Sb, Cd, Sr, As, Zn, Cu, Ni, Co, Mn, Cr, V and Al in contrast to healthy larvae from a disease-free apiary. This is the first study to demonstrate such differences, suggesting that an infection alters the larval nutrition or that nutrition is a predisposition for the outbreak of a chalkbrood infection. Though, based on results obtained from a case study, rather than from a controlled experiment, our findings stress the differences in elements of healthy versus diseased honey bee larvae.

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Section: Introductionmentioning

confidence: 99%

Micronutrient Deficiency May Be Associated with the Onset of Chalkbrood Disease in Honey Bees

Pavlović,

Brodschneider,

Goessler

et al. 2024

Insects

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show abstract

“…Recent studies suggest several factors involved in colony decline, such as parasite and pathogen invasion, pesticide use, and environmental stressors. Honeybees are susceptible to various pathogens and pests, including bacteria 1 , fungi 2 , viruses 3 , Varroa destructor 4 , and microsporidian parasites 5 .…”

Section: Introductionmentioning

confidence: 99%

Engineered symbiotic bacteria interfering Nosema redox system inhibit microsporidia parasitism in honeybees

Lang

Wang

et al. 2023

Nat Commun

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Nosema ceranae is an intracellular parasite invading the midgut of honeybees, which causes serious nosemosis implicated in honeybee colony losses worldwide. The core gut microbiota is involved in protecting against parasitism, and the genetically engineering of the native gut symbionts provides a novel and efficient way to fight pathogens. Here, using laboratory-generated bees mono-associated with gut members, we find that Snodgrassella alvi inhibit microsporidia proliferation, potentially via the stimulation of host oxidant-mediated immune response. Accordingly, N. ceranae employs the thioredoxin and glutathione systems to defend against oxidative stress and maintain a balanced redox equilibrium, which is essential for the infection process. We knock down the gene expression using nanoparticle-mediated RNA interference, which targets the γ-glutamyl-cysteine synthetase and thioredoxin reductase genes of microsporidia. It significantly reduces the spore load, confirming the importance of the antioxidant mechanism for the intracellular invasion of the N. ceranae parasite. Finally, we genetically modify the symbiotic S. alvi to deliver dsRNA corresponding to the genes involved in the redox system of the microsporidia. The engineered S. alvi induces RNA interference and represses parasite gene expression, thereby inhibits the parasitism significantly. Specifically, N. ceranae is most suppressed by the recombinant strain corresponding to the glutathione synthetase or by a mixture of bacteria expressing variable dsRNA. Our findings extend our previous understanding of the protection of gut symbionts against N. ceranae and provide a symbiont-mediated RNAi system for inhibiting microsporidia infection in honeybees.

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“…Recent studies suggest several factors involved in colony decline, such as parasite and pathogen invasion, pesticide use, and environmental stressors. Honeybees are susceptible to a variety of pathogens and pests, including bacteria 1 , fungi 2 , viruses 3 , Varroa destructors 4 , and microsporidian parasites 5 .…”

Section: Introductionmentioning

confidence: 99%

“…Honeybees are susceptible to a variety of pathogens and pests, including bacteria 1 , fungi 2 , viruses 3 , Varroa destructors 4 , and microsporidian parasites 5 .…”

Section: Introductionmentioning

confidence: 99%

Engineered symbiotic bacteria interferingNosemaredox system inhibit microsporidia parasitism in honeybees

Lang¹,

Wang²,

Wang³

et al. 2023

Preprint

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Nosema ceranae is an emergent microsporidia parasite of the European honey bee (Apis mellifera), which causes serious nosemosis implicated in honeybee colony losses worldwide. N. ceranae is an obligate intracellular eukaryotic parasite that mainly invades the midgut of honeybees. Recent studies find that bee gut microbiota is potentially involved in protecting against parasitism. Here, using laboratory-generated bees mono-associated with gut members, we find that Snodgrassella alvi inhibited microsporidia proliferation, potentially via the stimulation of host oxidant-mediated immune response. Accordingly, N. ceranae employs the thioredoxin and glutathione systems to defend against oxidative stress and maintain a balanced redox equilibrium, which is essential for the infection process. We knocked down the gene expression using nanoparticle-mediated RNA interference, which targets the γ-glutamyl-cysteine synthetase and thioredoxin reductase genes of microsporidia. It significantly reduces the spore load, confirming the importance of the antioxidant mechanism for the intracellular invasion of the N. ceranae parasite. Finally, we genetically modified the symbiotic S. alvi to deliver dsRNA corresponding to the genes involved in the redox system of the microsporidia. The engineered S. alvi induces RNA interference and represses parasite gene expression, thereby inhibits the parasitism by up to 99.8%. Specifically, N. ceranae was most suppressed by the recombinant strain corresponding to the glutathione synthetase or by a mixture of bacteria expressing variable dsRNA. Our findings extend our previous understanding of the protection of gut symbionts against N. ceranae and provide a symbiont-mediated RNAi system for inhibiting microsporidia infection in honeybees.

show abstract

Genetic variation of Ascosphaera apis and colony attributes do not explain chalkbrood disease outbreaks in Australian honey bees

Cited by 7 publications

References 42 publications

Micronutrient Deficiency May Be Associated with the Onset of Chalkbrood Disease in Honey Bees

Micronutrient Deficiency May Be Associated with the Onset of Chalkbrood Disease in Honey Bees

Engineered symbiotic bacteria interfering Nosema redox system inhibit microsporidia parasitism in honeybees

Engineered symbiotic bacteria interferingNosemaredox system inhibit microsporidia parasitism in honeybees

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