All About Acarine (Acarapis woodi (Rennie))

From Bee Craft October 2011

Pam Gregory, MSc, NDB

This mite lives in the respiratory system of adult bees

Trachea with acarine mites visible through the walls

AFTER THE long drawn out and complicated diseases investigated in earlier articles, acarine is a mercifully straightforward one. The tautologically named acarine mite (or tracheal mite in the United States) is, as its more precise American name suggests, a mite parasitic on adult bees that affects the breathing tubes (or tracheae).

Isle of Wight Disease?

It was first described in 1921 when attention had turned, as it has now, to the causes of the devastating colony losses that were occurring at that time. Consequently, this newly discovered mite was generally accepted at the time to be the cause of the so-called ‘Isle of Wight’ disease (the 1920s CCD equivalent). However, this blame does not stand up to scrutiny and ‘Isle of Wight’ disease is now thought to be due to a more complex combination of factors.

This microscopic mite is widespread around the world. It measures 150 x 65 mm and belongs to the class Arachnida. The mites invade the bee’s thoracic breathing tubes, notably the large prothoracic tracheae. The mites are found in a ratio of 3 females to 1 male and each female will lay between 5 and 7 eggs that emerge after about 14 days. The young mites then creep out from the thoracic spiracles (breathing tube openings). These emerging mites spread around the hive by clambering onto the thoracic hairs of newly hatched young bees, attracted by their breathing movements.

A mite reaching out for a passing young bee

Bees more than 9 days old are not normally affected and neither are queens. If on rare occasions queens are infected they remain productive for their normal life span. It is not really clear why this age related infectivity should be the case. Some have suggested that the hairs on the main thoracic spiracles become stiffer over time and the young mites are unable to push their way through into the thoracic tracheae, which sounds plausible at least.

Unlike the other spiracles, the prothoracic spiracle has an operculum (or covering flap) that does not fully close, which may be why this spiracle is more susceptible to infection. There are no outward signs of acarine mites and their main effect is to shorten the life of the bee. This can slow colony development in the spring although the mites do not appear to have much effect in summer. Infected queens may live for many years. There is a popular, but incorrect, supposition that crawling and ‘K-winged’ bees are indicative of acarine mites (or acarosis). Internally, infected tracheae appear dark brown, as a result of being jammed full of mites and mite debris and seem to be more brittle than unaffected tracheae that would normally be white.

Like nosema, acarine will get worse during adverse weather conditions (especially during the early spring or in wet summers) when the bees are confined for long periods in close proximity to each other and the mites can spread easily from old to young. Colonies normally clear up of their own accord once the weather improves. Infected overwintering bees will die out more quickly once warm spring weather arrives, being replaced by a new and uninfected generation of bees. Older bees will be the foragers that will be out of the hive when the weather is good, thus reducing the time they are in contact with young bees. They will also die away from the hive, removing any minor reservoir of infectivity. Nonetheless, a severe acarine infestation can kill a colony

Microscopic Examination

The size of sample needed to find at least one infected bee per sample

Acarine infestation is identified using a low-powered dissecting microscope of 10x magnification. A sample of about 30 bees is dissected to inspect physically the large prothoracic tracheae for signs of mites. I have included a table (above) used by the MAFF/ADAS bee laboratories that I have from when I worked there, to determine a suitable size sample.prothoracic tracheae for signs of mites. I have included a table (above) used by the MAFF/ADAS bee laboratories that I have from when I worked there, to determine a suitable size sample.

From this it can be seen that in the usual sample size of 30 mites you can be 99% certain of finding the mite if 15% of bees are infested or 95% certain to find it if only 10% of the bees have mites.

An acarine mite
in a trachea

For the dissection, the dead bee is pinned at a convenient angle, legs upwards, onto a cork and the head removed to expose the first pair of tracheae. The chitinous ‘collar’ at the front of the thorax is also removed so that both of the tracheae are exposed for examination. If mites are present either one or both tracheae will be discoloured, from light brown to black depending on the severity of the infection. The normal colour is creamy white.

If you are really keen to see the mites close up and personal the trachea can be dissected out and placed onto a slide with a drop of water and a coverslip. Inspection of this slide under a compound microscope (x40 magnification will be enough) will reveal mites at all stages; adults, developing nymphs and eggs. It is a tedious job dissecting a 30 bee sample from each of your hives, especially if you have lots, but local associations sometimes have microscope days to do this. I imagine in the future that easier, molecular assay diagnostic methods could be developed – but also that there is little commercial imperative to do so.

Genetic Resistance

Dissection of thoracic tracheae. Normal (left), infected (right)

Bailey and Ball indicate the longest kept records in the world for levels of acarine infestation were for England and Wales between 1947–1980. These dates suggest they are Ministry of Agriculture Fisheries and Food (MAFF) records starting after the second world war, at the instigation of the NAAS (National Agricultural Advisory Service), and finishing at the time when acarine and nosema diagnosis moved from being a free service to a paid one. The records show declining infestation during the recording period. This is thought to be related to the development of greater genetic resistance. However, it does also coincide with a period of reducing bee densities because of lessening interest in beekeeping.

Both colony density and apiary size have since been shownto be related to a number of disease problems, notably acarine and chronic bee paralysis virus (CBPV).

Nonetheless, there are well documented differences in susceptibility to the acarine mite between different races of bees so genetic resistance to the mites does exist. I recently came across a report of the International Bee Research Association (IBRA) Sixth European Honey Bee Conference in July 2002 which stated that no cases of acarine had ever been found in the Apis mellifera macedonica indigenous to a specific area of Greece. This local honey bee ecotype has a much smaller prothoracic spiracle than either A mellifera carnica (dark European) or A mellifera ligustica (Italian) races. The size of the operculum was directly related to the prevalence of acarine in each race.

The native Apis mellifera mellifera is reputed to be more resistant while A mellifera ligustica (the yellow Italian/New Zealand strains) has a reputation for being particularly susceptible to acarine mites. However, even within races there will also be significant variability in genetic resistance to disease. All this adds weight to arguments for the preservation of ecotypes and biodiversity in honey bees and the development of bees adapted to local environments.


In the past the most outrageous things were used to try and kill acarine mites. The best known is Frow Mixture – a concoction of nitrobenzene, safrole and petrol! Trying to purchase these ingredients today would likely bring you under suspicion of being a terrorist or worse.

Other substances such as oil of wintergreen (methyl salicylate) or menthol were used as well as disinfectant, garlic, formalin or salt and more recently Folbex (chlorobenzilate) or Folbex VA (bromopropylate). Fortunately for the green image of honey the latter are no longer used or even available in the UK.

It is rational to expect that varroacides will help to reduce acarine infestation too. The National Bee Unit tell me that thymol will have an effect on acarine and in some countries this is openly stated. It is also likely that the pyrethroids and Apivar will also have an effect as they are broad miticides but in all cases it will depend on the size and timing of the dose whether they make contact with the acarine mites.

Varroa mites significantly increase the pathogenicity of viruses and there has been some discussion whether acarine mites can have the same vector effect. Bailey and Ball (1991) consider that they definitely do not and I have not come across any particular evidence for this idea anywhere.

So, with no real treatment available and a high potential for developing genetic resistance, if the bees are heavily infected with acarine, it is probably best just to let them die out. Genetic resistance is best developed by breeding from resistant colonies and despatching those that are susceptible. Beowulf Cooper (founder of British Isles Bee Breeding Association, BIBBA) and others more recently suggest that ‘Winter losses are a national asset’ being an essential contribution to selecting for hardy, thrifty, disease resistant native bees. If that seems just too callous and the conditions are right then a possible alternative is to requeen them with a queen of a more resistant strain

References and Further Reading

Bailey, L and Ball, BV, 1991. Honey Bee Pathology. 2nd edition. Academic Press. Harcourt Brace, London.

Morse RA (ed) 1978. Honey Bee Pests, Predators and Diseases. 1st Edition. Comstock Publishing Associates, Cornell University Press, Ithaca, USA.

Morse, RA and Nowogrodzki, R (eds) 1990. Honey Bee Pests, Predators and Diseases. 2nd Edition. Comstock Publishing Associates, Cornell University Press, Ithaca, USA.

Cooper, BA. 1986. The Honeybees of the British Isles. BIBBA, Derby.

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