Varroa and the health of a honey bee colony

What varroa is

Varroa destructor is an external parasitic mite about 1.5 mm across — large enough to see, and enormous relative to a bee. Its original host is the Asian honey bee, Apis cerana, with which it has coexisted for a very long time and which has behavioural defences against it. Sometime in the twentieth century it jumped to the western honey bee, Apis mellifera, which had no evolved defences at all, and it has since spread to almost every part of the world where honey bees are kept. Australia held out until 2022.

The mite reproduces inside sealed brood cells. A female enters a cell containing a larva just before the workers cap it, lays eggs, and her offspring feed on the developing bee. When the bee emerges, the mites emerge with it. This is why varroa populations track brood rearing, and why a colony's mite load grows exponentially through a season.

Why it is worse than a parasite should be

A mite feeding on a bee is damaging. A mite acting as a hypodermic needle between bees is catastrophic, and that is the real mechanism. Varroa transmits and amplifies viruses — deformed wing virus above all — and it does so in a way that bypasses the bee's ordinary defences. Colonies collapse from viral disease vectored by varroa far more often than from the direct feeding damage.

Two corrections worth making explicitly. First, varroa feeds primarily on the bee's fat body, an organ analogous to a liver, rather than on haemolymph as was believed for decades — which explains why the damage to immunity and overwintering ability is so much greater than the volume of fluid taken would suggest. Second, a colony that looks strong in autumn can be dead by February, because the mites damaged the long-lived winter bees the colony's survival depends on. Untreated colonies commonly die in their second or third winter rather than immediately.

How it is managed

• Monitoring first. Alcohol wash, sugar roll or drop counts on a sticky board give a mite load per hundred bees. Treating without measuring is how resistance develops and how colonies are lost anyway.
• Organic acids — oxalic acid and formic acid — which are effective, cheap and have not generated widespread resistance. Oxalic acid works best when there is no sealed brood for mites to hide in.
• Thymol and other essential-oil-based treatments, temperature-sensitive but useful in the right window.
• Synthetic acaricides such as pyrethroids and amitraz, which work and to which varroa has repeatedly developed resistance where they have been used as a sole strategy.
• Biotechnical methods: drone brood removal, which exploits the mites' preference for drone cells, and induced brood breaks that interrupt the reproductive cycle.
• Breeding for resistance. Varroa-sensitive hygiene and similar traits are real, heritable and being selected for, and this is the only approach that offers a permanent answer rather than an annual one.

The other pressures, in proportion

Varroa is the largest single problem but not the only one. American and European foulbrood are serious bacterial brood diseases, notifiable in many jurisdictions. Nosema is a gut parasite. Small hive beetle and the tropilaelaps mite are spreading pests. Pesticide exposure, particularly to systemic neonicotinoids, causes sublethal harm to foraging and navigation that is well documented. And forage scarcity — the monoculture problem — leaves colonies nutritionally stressed and less able to withstand everything else.