Varroa Destructor information




varroa paper.pdf (PDF — 1 MB)




This is the best paper we've encountered on this mite. A recommended reading for anyone who keeps bees.
Predictive Markers of Honey Bee Colony Collapse

Varroa, Virus and Winter Bees

Dainatn, B., J.D. Evansg, Y.P. Cheng, L. Gauthiern & P. Neumannn,o – DEAD OR ALIVE? PATHOGENS AND LIFE SPAN OF WINTER HONEY BEES -

Honey bees, Apis mellifera, suffer numerous biotic and abiotic stresses and have recently faced large repeated losses. Although the scientific community agrees that losses may result from several factors acting synergistically, it is not clear yet what causes this phenomenon. It has been proposed that pathogens are involved in winter losses. We hypothesized that pathogens may reduce the life expectancy of individual winter bees to a point that the critical size threshold of a cluster to survive winter would be reached leading to the collapse of the colony. To test this hypothesis, a monitoring experiment on 29 colonies has been performed in winter 2007/2008 in Switzerland where levels of three pathogens including Deformed wing virus (DWV), Acute bee paralysis virus (ABPV) and Nosema ceranae, Varroa destructor (Vd) infestation, and life expectancy of individuals workers were measured. The results show that neither ABPV nor Nosema ceranae could be incriminated as a deadly factor in this study. Conversely, both DWV and Vd, in this order, reduced significantly life expectancy of winter workers. Furthermore, the number of DWV-infected bees in colonies, which didn`t survive winter, was significantly higher than in colonies which survived. The data of this study are in contrast with the intriguing Colony Collapse Disorder in the U.S, for which Varroa destructor and DWV were poor correlates with CCD risk. Finally, the results suggest that reduced life expectancy of individual bees is one proximate mechanism of colony winter losses and Varroa destructor remains one of the main culprits.

PREVALENCE OF VIRAL SEQUENCES IN HONEY BEES FROM THE UMASS APIARY-

 Buranda,b, J.P., A. Dea & R. Zhengc - Honey bees (Apis mellifera), from hives maintained in an apiary on the University of Massachusetts-Amherst campus were analyzed over a two year period for the presence of viral pathogens. Individual bees from these hives were found to be infected with one or more of the 4 honey bee viruses: Black queen cell virus (BQCV), Deformed wing virus (DWV), Sacbrood virus (SBV) and Lake Sinai virus (LSV-1). The prevalence of each of these viruses varied both within a hive and between hives throughout the season. In both years DWV was the most prevalent of the viruses and, as expected, was found in all the hives. Generally, the level of DWV was low or not detected early in the season rising to levels as high as 80% of the bees in a hive being infected by this virus at the end of season. BQCV was the second most prevalent virus and was also found in all the hives in both seasons. Although generally present at low levels, BQCV did reach levels as high as 50% in one hive. SBV was also found in all of the hives sampled in 2010 and 2011 and was found in almost half the bees sampled from one hive in August in 2010 and in a different hive in 2011. LSV-1 was found at low levels in almost all the hives sampled.


PREVALENCE OF VIRAL SEQUENCES IN HONEY BEES FROM THE UMASS APIARY-

Buranda,b, J.P., A. Dea & R. Zhengc 

Honey bees (Apis mellifera), from hives maintained in an apiary on the University of Massachusetts-Amherst campus were analyzed over a two year period for the presence of viral pathogens. Individual bees from these hives were found to be infected with one or more of the 4 honey bee viruses: Black queen cell virus (BQCV), Deformed wing virus (DWV), Sacbrood virus (SBV) and Lake Sinai virus (LSV-1). The prevalence of each of these viruses varied both within a hive and between hives throughout the season. In both years DWV was the most prevalent of the viruses and, as expected, was found in all the hives. Generally, the level of DWV was low or not detected early in the season rising to levels as high as 80% of the bees in a hive being infected by this virus at the end of season. BQCV was the second most prevalent virus and was also found in all the hives in both seasons. Although generally present at low levels, BQCV did reach levels as high as 50% in one hive. SBV was also found in all of the hives sampled in 2010 and 2011 and was found in almost half the bees sampled from one hive in August in 2010 and in a different hive in 2011. LSV-1 was found at low levels in almost all the hives sampled.


Dynamics of Persistent and Acute Deformed Wing Virus Infections in Honey Bees, Apis mellifera
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3280512/

NOSEMA

A new study concerning nosema and it's interaction with pesticides and fungicides. Well worth the read IMO. Below is an excerpt from the study:

http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0070182#authcontrib

147 of the 630 bees (23.3%) fed Nosema spores became infected. 22 of the 35 pesticides (62.9%) found in our pollen samples had relative risk values significantly different from 1 (Table 2). 8 pesticides (22.9%) were associated with increased Nosema prevalence, while the remaining 14 were associated with decreased Nosema prevalence. Two of the three detected pesticides applied by beekeepers to control hive mites (marked with a * in Table 2) had a relative risk larger than two, indicating Nosema prevalence in bees fed pollen containing those chemicals (DMPF and fluvalinate) was more than double the Nosema prevalence in bees that did not consume these chemicals. Of the seven pesticides found in pollen from over half, or at least four, of the crops, the majority were associated with higher Nosema prevalence in bees that consumed them. Both control diets had relative risk values not significantly different from one.
A pollen sample’s fungicide load significantly affected Nosema prevalence among bees fed that pollen (Fig. 5; GLMM, likelihood ratio test: χ = 5.8, df = 1, p = 0.02), but pesticide diversity did not (χ = 1.7, df = 1, p = 0.19). A bee’s source colony, included as a blocking variable, also did not affect Nosema prevalence (χ = 2.0, df = 2, p = 0.36). Replacing fungicide load with chlorothalonil load obtained the same result (chlorothalonil load: χ = 5.3, df = 1, p = 0.02; pesticide diversity: χ = 1.5, df = 1, p = 0.23; source colony: χ = 2.0, df = 2, p = 0.36; fungicide load model AIC = 612.71, chlorothalonil load model AIC = 613.15). Chlorothalonil was also the most abundant fungicide in our samples, and comprised 50.0±10.2% (mean ± se) of the per sample total fungicide load.

Older Study:
A total of 705 individual bees were analyzed from five colonies over three seasons in 2010. bees analyzed were sampled from the honey supers because we found no significant difference in infection levels among different groups of bees sampled   Overall, colonies were found to be infected with N. ceranae. In the spring, all colonies were found infected with an average N. ceranae copy number of 8,007. In the summer, 80% of colonies were found infected with an average N. ceranae copy number of 37,057.   Only one colony was found infected in the fall; however, only one bee from this colony was positive for N. ceranae infection with an average copy number of 70.3. All other samples were negative (n = 249).   These findings bring into question whether a hive that has been deemed highly infected has been diagnosed as such because of an overall high infection level or because of sampling practices in which a minority of bees were highly infected but the remainder exhibited only low-level infections or no infection. 

Insects 2012, 3, 1143-1155; doi:10.3390/insects3041143

Individual Variability of Nosema ceranae Infections in Apis mellifera Colonies Author to whom correspondence should be addressed; E-Mail: traverb@vt.edu

MUTUALISTIC SYMBIOSIS BETWEEN A PARASITIC MITE AND A PATHOGENIC VIRUS UNDERMINES HONEY BEE IMMUNITY AND HEALTH

Whole article here:  http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4812730/


Abstract

Honey bee colony losses are triggered by interacting stress factors consistently associated with high loads of parasites and/or pathogens. A wealth of biotic and abiotic stressors are involved in the induction of this complex multifactorial syndrome, with the parasitic mite Varroa destructor and the associated deformed wing virus (DWV) apparently playing key roles. The mechanistic basis underpinning this association and the evolutionary implications remain largely obscure. Here we narrow this research gap by demonstrating that DWV, vectored by the Varroa mite, adversely affects humoral and cellular immune responses by interfering with NF-κB signaling. This immunosuppressive effect of the viral pathogen enhances reproduction of the parasitic mite. Our experimental data uncover an unrecognized mutualistic symbiosis between Varroa and DWV, which perpetuates a loop of reciprocal stimulation with escalating negative effects on honey bee immunity and health. These results largely account for the remarkable importance of this mite–virus interaction in the induction of honey bee colony losses. The discovery of this mutualistic association and the elucidation of the underlying regulatory mechanisms sets the stage for a more insightful analysis of how synergistic stress factors contribute to colony collapse, and for the development of new strategies to alleviate this problem.



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