Dr. Ramsey Fundamentally Changes Our Understanding of Varroa destructor Mites

Dr. Samuel Ramsey,
University of Maryland

Varroa destructor mites are responsible for the transmission of over a dozen viruses associated with the decline in honey bee health, contributing to annual colony loss rates exceeding 30%. The assumption that Varroa feed on bee blood (hemolymph) has not been questioned until University of Maryland Ph.D graduate Dr. Samuel Ramsey doubted the ability for mites to sustain themselves on hemolymph so he dug deeper to discover Varroa destructor feeds primarily on honey bee fat body tissue and not hemolymph. This publication fundamentally changes our understanding of Varroa mites and will likely lead to better treatment options to control them.

Dr. Samuel Ramsey Webinar: Varroa Does Not Feed on Hemolymph.

Past Assumptions

Much of the knowledge about Varroa was derived from closely related parasitic and predatory mites. Assumption that Varroa mites were blood-sucking was propagated by “chain citing” an English-language study referring to rudimentary Russian-language Varroa publications. However, there are some important differences that prompted Dr. Ramsey to investigate whether this assumption was false. First, hemolymph feeding insects have physiological adaptations to process large quantities of nutrient poor blood, which are not found in Varroa. Moreover, hemolymph feeders’ excrement is liquid, and Varroa excrement is not.

Honey bee fat bodies appeared to be another plausible food source for Varroa mites. Fat bodies in honey bees are responsible for many essential functions including: growth regulation, nutrient storage, pesticide detoxification, immune response, thermoregulation, protein and fat synthesis. Impact of Varroa parasitism on these essential functions is consistent with high honey bee disease and colony loss rates.

Varroa spend two weeks on average in a “phoretic stage”, latched onto the abdomen of adult workers before entering brood cells for reproduction. This stage of transportation into the hive was previously thought to be commensal, meaning the mite gains the advantage of transportation at no cost to the honey bee host. Dr. Ramsey’s recent publication revealed that commensalism is not the case. Tissue damage due to parasitism is occurring during this stage.

Ramsey et al. catalogued hundreds of bees to determine where Varroa were found parasitizing adult honey bees. They used fat and water soluble fluorescent dyes to stain different honeybee tissues and Varroa gut contents. This work was further validated through feeding Varroa artificial diets using different blood to fat ratios to determine which diet supports its survival. 

Figure 1. Feeding site preference located near fat body of honey bee.

Worker bees were randomly selected from mite-infested colonies and examined to determine where the Varroa mites were found. Most mites were found near the fat body, concealed between the left ventral abdominal plates (Figure 1).

Ramsey et al. rapidly froze honeybees with Varroa mites in liquid nitrogen and then used electron microscopy to visualize feeding behavior. This revealed damaged fat body tissue in the wounds of parasitized bees.

Figure 2. Comparison Uranine (water-soluble hemolymph biostain) and Nile Red (fat-soluble fat body biostain) in Varroa  mite 24 hours after feeding on adult honey bee.

To test whether Varroa were feeding on the fat bodies or hemolymph, emerging bees from capped brood frames were fed fluorescent biostains for five days: Nile red and Uranine yellow in sugar syrup and pollen substitute. Nile red stained honey bee fat body. Uranine yellow stained honey bee hemolymph. Female Varroa mites were placed on the body of each adult bee and imaged 24 hours later to determine which biostain was ingested. Figure 2 shows that more than twice Nile red as Uranine was detected in Varroa.  This confirms fat body consumption by Varroa.

Figure 3. Results following 7-day in vitro Varroa feeding of different hemolymph and fat body diets.

Further tests were conducted with Varroa mites in the lab. Reproductive mites were removed from capped brood cells and transferred to artificial enclosures. Varroa were fed artificial diets with different blood to fat ratios: 100% hemolymph, 75% hemolymph/25% fat body, 50% hemolymph/50% fat body, 25% hemolymph/75% fat body, 100% fat body. Live mites were counted every day for 7 days. Varroa mites fed a diet high in hemolymph had decreased survivorship and reproduction than did mites fed a diet high in fat (Figure 3). These results indicate inability of hemolymph to support Varroa mites’ survival.

These findings reveal honey bee fat bodies are the primary food source for Varroa mites, contrary to previous studies. Ramsey et al. have shown that the mites are not just hitching a ride on adult honey bees but are damaging and consuming their fat bodies, leading to decreased honey bee health and longevity. Complete understanding of the Varroa mite lifecycle is essential to overcome these parasites. Future studies should focus on alternative techniques to rear Varroa in vitro for entire lifecycles. The work of Ramsey et al. comes at a crucial time when beekeepers are begging for new Varroa treatment options. Results from this publication offer a significant window of opportunity for researchers to develop fat-soluble anti-Varroa treatments to control and counter the impact of Varroa mites in honey bee hives.

Mite master, Dr. Ramsey, is currently raising funds to continue research on another parasitic honey bee mite, Tropilaelaps, a serious future threat to the U.S. beekeeping industry more serious than Varroa.

Author: Jennifer Gordon

Honeybee Research Scientist, Farmer

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