Abstract
Nosema ceranae infections in honey bees (Apis mellifera) pose a severe threat to colony health. Beekeepers have used dicyclohexylammonium fumagillin to control Nosema apis, although it may be ineffective against N. ceranae. We investigated the ability of various propolis extracts collected from Upstate New York (United States) to decrease in vivo N. ceranae infection levels when fed ad libitum to N. ceranae-infected honey bees. Propolis extracts, most notably a dichloromethane extract, significantly lowered spore levels in a dose-dependent fashion 4 days post inoculation. When testing the in vitro anti-Nosema activity of propolis extracts, we report for the first time that spore viability was unaffected after a 24 h exposure to propolis extracts. These results present evidence that propolis extracts may effectively lower Microsporidia infections in honey bees, and that direct exposure of environmental spores to propolis alone does not kill N. ceranae.
Highlights
Nosemosis is a prevalent bee disease caused by fungal microsporidian parasites, Nosema apis and Nosema ceranae (Chen and Huang, 2010)
We demonstrated for the first time that oral treatments of North American propolis (UNYP) extracts, most notably a DCM extract, significantly lowered N. ceranae spore levels in European honey bees
We further report that DCM Upstate New York propolis (UNYP) extracts have dose-dependent activity and significantly higher potency than ethanol and methanol extracts on N. ceranae infections
Summary
Nosemosis is a prevalent bee disease caused by fungal microsporidian parasites, Nosema apis and Nosema ceranae (Chen and Huang, 2010). Nosema ceranae is a spore-forming obligate intracellular parasite whose reproductive cycle initiates in the honey bee midgut lumen after being orally ingested by an adult bee (Higes et al, 2007; Texier et al, 2010; Smith, 2012). Secondary meronts are formed and may be released back into the lumen by cell lysis as environmental spores or excreted in host feces and infect other animals (Fries and Granados, 1992; Franzen, 2004; Gisder et al, 2011; Smith, 2012; Han and Weiss, 2017). The vegetative cycle is complete 4 days post infection, and high numbers of primary and environmental spores are found in the host within this time period (Gisder et al, 2011)
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