Amoeba Disease

This disease of the digestive system of adult honeybees is caused by the protozoan Malpighamoeba mellificae. After ingestion, the cysts of the amoebae germinate and migrate to the Malpighian tubules. After 18 days, the amoebae, after consuming many epithelial cells, form cysts that are soon after liberated from the tubules and then voided.

The disease is spread similarly to Nosema, with which it is often found as a mixed infection. It is not considered to cause colony mortality, but may be serious because it impairs the functioning of the Malpighian tubules, which act as the kidneys of the bee. The diagnosis of the disease can only be done microscopically, but an apparent inability of healthy-looking colonies to build up may indicate infection. No control chemical is registered and good management practices are the only measure to adopt.
 

Malpighamoeba has been found in Zimbabwe, but after two recent extensive surveys it has still not been found in South Africa.


Chalkbrood


Mycelium of the chalkbrood fungus
growing on a larva


Chalkbrood mummies

The occurrence of chalkbrood in South Africa has dramatically increased since the discovery of the parasitic varroa mite. The fungus Ascosphaera apis that causes chalkbrood only attacks larvae. When the spores are ingested, they germinate and mycelia grow through the body penetrating the epidermis and covering the pre-pupa in a short time-span. Spores can also germinate when it lands on the cuticle and penetrate the pre-pupa from the outside.

The larva dies as a result of physical damage and due to the fungus extracting food (nutrients) for itself. The mycelium grows densely, covering the pupa to the extent that it fills the whole cell. When spores form, the mummified larva will become mottled dark green and black-on-white, later turning to completely black. After some time, the pre-pupa dries out into a chalky lump. These mummies fit loosely in the cells from which they can easily be shaken or removed by the bees. These 'popped rice' mummies are usually the beekeeper's first realization that the colony is diseased when they are found in front of the entrance of the infected hives. When crushed between the fingers, the mummies are chalk-like, and hence the name.

There is no chemical to control registered in South Africa for this disease. The colonies will usually get rid of it on their own accord. However, if the infection is severe, it will be worthwhile to replace the brood combs with those from uninfected colonies. The infected combs must be melted down. Colonies should not be placed under undue stress and more bees and brood should be added to weak colonies. Hive ventilation must be good, especially in humid areas because chalkbrood seem to favours damp conditions.

Chalkbrood has been found in all provinces of South Africa and the infections vary within an apiary and area. No colony loss has yet been reported but in heavily infected colonies more then 50% of the brood may die, placing undue stress on the colony. 
 

 

European Foulbrood

This is the most widespread and common brood disease in South Africa. It is not considered to be serious, but in combination with other maladies it may play a significant role in the collapse of a colony. It is caused by the bacterium Melissococcus pluton (formally known as Bacillus pluton and Steptococcus pluton) and mostly affects young unsealed larvae. The bacterium is spread through food transfer from adult to young larva. It is suspected that the bacterium is present in most colonies, but in latent form, not appearing unless stress factors favour an outbreak. The remains of dead larvae are a source of further infection. Viable spores may also be present on the wax and other debris on the bottom of the hive, on the comb, or present in feces of nurse bees.

Once ingested, the bacteria multiply in the gut of the larva, damaging the intestine inner walls and competing with the larva for food. Eventually the larva dies of starvation usually in it's 4th or 5th day when it is still unsealed. A larva that has died of this disease can easily be recognised because the symptoms are quite typical. Severe infection may however, appear similar to the symptoms of another bacterial disease, American Foulbrood (AFB). This is partly due to other bacteria associated with EFB that may alter the typical symptoms. The most common one is Paenibacillus alvei, which also causes a sour odour that can be confused with the 'glue' smell that is typical of American Foulbrood.

A heavily infected colony may be seriously weakened and, in severe cases, may die out. Such severe outbreaks are more prevalent in the areas with long periods of high humidity. International reports indicate that outbreaks occur more readily in colonies used for pollination. This might be as a result of stress placed on pollination units or it may indicate that nutrition plays a role. Other outbreaks occur when the colonies are building up, usually during the first nectar flows. This may be because many larvae are reared and relatively few nurse bees are available to tend them.


Symptoms

Dead or diseased 4-day or 5-day-old larvae that are still coiled ('c'-shaped) in the cells are a typical symptom of an EFB. The dead larvae become soft and dull yellowish in colour, then brown and finally dry to a scale on the bottom of the cell. Larvae that were still coiled will collapse onto the bottom of the cell, but sometimes the larvae died in the upright position and these appear to 'melt' down onto the side of the cells.

When the infection is severe, dead larvae will be seen in many cells on many frames. On a normal brood comb, the different stages of brood appear uninterrupted and as concentric bands or oval patches. EFB breaks the regularity of this brood pattern and different stages of brood are scattered (shotgun pattern) over the comb.

If larvae have been capped before they died, these cappings will appear darker and concave instead of convex. The cappings may also be punctured in the center.

If a dead larva is not removed by the housebees, it will dry to a rubbery dark brown (almost black) scale. A beekeeper will be able to lift this scale out of the cell in one piece. This is different to the scale formed if the larva died of AFB, where the scale is brittle and breaks easily.


The disease in South Africa

Two severe outbreaks have been reported in the past, but mostly individual colonies are reported with severe symptoms. EFB are found in all provinces and infection varies between colonies, apiaries and localities. However, infections seem to be more severe in colonies in the KwaZulu-Natal coastal belt, and Lowveld. The higher humidity, poorer ventilation, or lack of direct sunlight when these colonies are placed in plantations and orchards may be advantageous to EFB.

 

Nosema

Nosema occurs in adult bees and is caused by a one celled organism, Nosema apis. Spores of nosema are ingested with the food and germinate in the midgut of the bee. Each sends out a long thread, known as the polar filament, which penetrates the cells lining the gut. The living 'germ' of the spore passes through this filament and into a gut cell. Here the organism multiplies and soon fills the infected cells with spores.

 

In diseased bees, the cells, which are released into the lumen of the gut, are frequently packed with nosema spores. These spores, on release, may either infect other cells of the gut lining or may pass out of the bee with its waste products. The infected cells in the gut lining upset the metabolism of the bee by interfering with the digestion and absorption processes. The protein reserves of the infected bee are severely reduced and little brood food can be produced. This is probably why about 15% fewer eggs develop into mature larvae at the height of infection.

Infested workers start foraging earlier in their lives than usual and their lives are shorter than average.

Feces of diseased bees in the hive spread Nosema spores to bees cleaning up. Defecation inside the hive is aggravated if the bees are confined by cold or rainy weather or during normal migration practices of the beekeeper. The disease spreads between colonies if infected bees drift into healthy colonies or if robber bees become infected.

 

Symptoms

No definite diagnosis is possible without microscopic examination. The only outward signs of Nosema are a weakening of a colony or failure to build up normally when conditions are favorable. However, in severe cases the diseased bees will soil the hive, inside and at the entrance. Bees may be seen crawling out of the hive with abdomens slightly swollen. Heavily infected bees may give the impression of being clumsy and lethargic.

Although definite diagnosis of Nosema is only possible with microscope examination, there is a method which beekeepers can put to use with a little practice. The last abdominal segment (with the sting) of an adult bee is grasped with a fine pair of forceps and the gut pulled out. In healthy bees the midgut is brownish-yellow or mustard coloured, and its constrictions or rings are clearly seen. In bees that are heavily infected with nosema, the midgut is white and somewhat swollen, obscuring the constrictions.


Nosema in South Africa

In the South Western Cape Nosema manifests itself in spring during poor weather, but also at other times during dearth periods in fine weather, when the bees consumed infected pollen stores. Nosema have been found in all provinces. In the summer rainfall region the infections were higher during the summer when more brood were reared. No colonies were severely infected and no colony deaths could be attributed to nosema.

 

The parasitic mite Varroa destructor

The most serious parasite of honeybees in the 20th century has undoubtedly been the ectoparasitic mite, Varroa destructor (formerly Varroa jacobsoni). Relatively harmless on its natural host, the Eastern honeybee, Apis cerana, the varroa mite has crossed onto the Western honeybee, Apis mellifera, and spread from its Asian origins throughout most of the world. On the commercially important Apis mellifera the varroa mite is not a benign pest, resulting in most cases in the death of the parasitised honeybee colony. In regions of the world where the varroa mite is well established, such as Europe and the USA, wild honeybee populations have all but disappeared as a result of varroa mortality and commercial beekeeping is only possible with the liberal use of anti-varroa pesticides.

 

 

 

Introduction

The most serious parasite of honeybees in the 20th century has undoubtedly been the ectoparasitic mite, Varroa destructor (formerly Varroa jacobsoni). Relatively harmless on its natural host, the Eastern honeybee, Apis cerana, the varroa mite has crossed onto the Western honeybee, Apis mellifera, and spread from its Asian origins throughout most of the world. On the commercially important Apis mellifera the varroa mite is not a benign pest, resulting in most cases in the death of the parasitised honeybee colony. In regions of the world where the varroa mite is well established, such as Europe and the USA, wild honeybee populations have all but disappeared as a result of varroa mortality and commercial beekeeping is only possible with the liberal use of anti-varroa pesticides.

 

Varroa destructor was first found in South Africa in August 1997, the first report of this mite in sub-Saharan Africa. An immediate survey revealed that the mite was common and widespread in both commercial and wild honeybee populations in the Western Cape, but absent from the rest of the country. The South African National Department of Agriculture convened a workshop during which it was concluded, on the basis of international evidence, that there was no prospect of containing the spread of the mite, nor was there a biocontrol agent available that could be used to eliminate varroa. It was accepted that varroa would eventually spread throughout South Africa, and probably throughout sub-Saharan Africa. The time span for this spread in South Africa was estimated to be between 2-7 years, with rapid spread in areas of commercial beekeeping activity and more gradual spread elsewhere. What effect the varroa mite would have on the honeybees of Africa was less certain. The general belief that the African honeybee would be tolerant to the varroa mite as a result of environmental factors or other variables, and that varroa would have little impact on the bees of Africa had to be tested.

 

At least three different aspects should be considered when estimating the impact of the varroa mite on African honeybees.

  1. The general belief that African honeybees, perhaps by virtue of their short post-capping time in brood development which could result in large numbers of unfertilized daughter mites, their hygienic behaviour, and their defensiveness, would prevent varroa from increasing to dangerous levels in the colonies, and hence would be tolerant to the presence of the mite. Support for this view comes from data from North Africa where varroa has seemingly been of little importance, from Brazil where varroa has not been destructive in Africanized bees, and from early work with Cape honeybees (Apis mellifera capensis) which suggested that these bees would be tolerant to varroa. This view would predict that varroa would spread throughout the African honeybee population, but would be little more than an additional arbitrary pest present in the colonies.

     

  2. It has also been suggested that what has made the Africanized honeybees of South America tolerant to the varroa mite is not some behavioural attribute of these bees, but rather that there are a number of different species and populations of mite, and that the one present in South America is not particularly virulent. This view predicts that if the more virulent strain of mite is present in South Africa, then it will result in the type of destruction witnessed in North America and Europe.

     

  3. A third possibility to consider is that not only are the race of honeybee and the strain of varroa mite important in predicting the outcome of honeybee-mite interactions, but also what viruses are present in the honeybee population. There is considerable evidence that colonies infected with varroa eventually collapse as a result of secondary infections, and of these, viruses activated by the presence of the mites are most important. The outcome of this scenario is impossible to predict, as very little is known about the honeybee viruses of South Africa.

    In both of the last two scenarios it would be predicted that resistance or tolerance in the honeybee population would develop, but only after the collapse of the majority of the population. In such a case the resistance developed could potentially be masked by the use of chemical treatment by beekeepers to sustain susceptible colonies and the resistance might not be expected to spread through the population.

    Although it remains to be determined what effect the mite will have on honeybee populations of Africa, the threat was considered to be sufficient to establish a Varroa Working Group comprising of researchers, beekeepers, users of honeybee pollination, and Department of Agriculture officials. This Working Group instituted a Varroa Research Programme to monitor and investigate the mite in South Africa, the preliminary results of which are presented here.


Source of the varroa

It has been found that the varroa mite that has caused devastation to honeybee populations almost throughout the world for the past thirty years is not a single species, but rather a species complex, consisting of at least 18 types of mite. Of these different types and species, only two are able to reproduce on Apis mellifera, and only one, the Korean-Russian type, is responsible for the extreme damage as seen in Europe and the USA. This species has been called Varroa destructor, and this is the type found in South Africa. Circumstantial evidence suggests that the varroa entered South Africa at Simonstad harbor, probably on a swarm onboard a cargo-ship from Europe.


Distribution

In 1997 the varroa mite was to be found only in the Western Cape, but as expected the mite has spread rapidly throughout South Africa, almost entirely as a result of migratory beekeeping activities, and is now present in commercial honeybee colonies in all provinces.

Varroa mites have also been found in wild honeybee colonies where no beekeeping takes place, including the Kruger National Park, Cape Peninsular National Park, Tsitsikamma National Park and the Cedarberg.

 

Impact of varroa  

The comprehensive monitoring of mite levels and colony condition in more than 300 commercial colonies belonging to Cape beekeepers indicated that varroa numbers were strongly negatively correlated with colony size, brood production, and pollen storage. Hence, as varroa numbers in a colony increased, the colony weakened.

There was, however, no clear-cut relationship between varroa infestation rate and colony mortality. Many colonies severely infested with varroa mites have not died during the course of the study, and it is still not known how acutely the mites will impact on the honeybee population of South Africa.

Comparisons between varroacide-treated and nontreated colonies, however, indicate massive differences in colony survival and productivity, in at least some situations.

In colonies that did not succumb in the short-term, high levels of brood mortality was found (as much as 95%), resulting in the gradual collapse of those colonies.

As the parasites spread, colonies with as many as 50 phoretic mites per 100 bees were not uncommon. This represents some 30 000 mites in large colonies, and clearly indicates that the prediction, that certain behavioural attributes of African honeybees would limit varroa population growth has not taken place. However, after three years of varroa mites having been present in a region, mite numbers were greatly reduced. Whether this was because of mite-tolerance developing in the bees, or because the colonies were too weak and with such high levels of brood mortality they could no longer sustain mite population growth, remains to be determined.

It is too early to draw firm conclusions about the impact of the varroa mites on African honeybees. Clearly, a large percentage of colonies are dying, but only time will tell if the African honeybee populations will collapse on the scale witnessed in Europe and North America.

In South Africa the value added to crop production by the commercial pollination of honeybees has been estimated to be in the order of R3.2 billion per annum (Table 1). It is also worth noting that this agricultural output sustains some 250 000 jobs. However, and in contrast to the Americas, perhaps the greatest threat of varroa in Africa is to the wild honeybee populations that pollinate as many as 40-70% of indigenous flowering plants. Should South Africa and the rest of Africa suffer the loss of wild bees witnessed in other parts of the world, this could have significant implications for floral conservation and biodiversity.


Effect on pollination efficiency

A 14% reduction in pollination efficiency was found in colonies that were heavily varroa infested in contrast to varroa-free control colonies, in the pollination of pumpkins. This was despite there being more foraging activity in the varroa-infected colonies, perhaps in an effort to compensate for the reduced efficiency of foraging workers. These results need to be confirmed on other crops to proof general significance.


Secondary bee diseases

Colonies infested with high numbers of varroa exhibit additional problems with other diseases and pests. Poor brood patterns are common in these colonies. Small hive beetles, chalkbrood and Braula coeca appear to be greatly increased in varroa-infected colonies. Chalkbrood, which was previously rarely reported in South Africa, is now widespread and almost ubiquitous. In addition, at least two viruses (Black Queen Cell Virus and Acute Paralysis Virus) have been found to be contributing to honeybee and colony mortality in varroa-infested colonies. There appears to be no correlation between varroa and tracheal mite levels, and tracheal mites remains uncommon.

Colony collapse in the summer rainfall region of the country is extremely rapid, probably due to the combined contributions of varroa and the Cape Honeybee Problem. The relative importance of these two factors must, however, still be determined.

 

Chemical control

Synthetic varroacides have been found to be extremely effective in the control of mites (>98%) whilst alternative chemical controls (e.g. formic acid) have been found to be less effective ( killing only 70%). Two commercial varroacides (Bayvarol® and Apivar®) have been registered for use in South Africa. Most beekeepers, who originally were against the use of any chemicals in their colonies for the control of varroa are now using some varroacide to protect their colonies. Wild honeybees can obviously not be treated with varroacides, and there is great concern amongst beekeepers that the catching of honeybee swarms, the lifeblood of their industry, is on the wane.  

 
 
Dwarf and deformed workers is the result of varroa parasitism
Mite reproduction

Varroa mites are found to successfully reproduce in both worker brood and drone brood in Cape honeybees, with mites being found in 6% of worker cells and 24% of drone cells (sample size 22 000 cells). The reproductive rate in worker brood is calculated to be 1.4 (that is, 0.4 daughter mites produced per cell), and 1.9 in drone brood. Most significantly only one mature mite is present in 56% of varroa-infected cells with emerging worker bees and 27% in drone brood. This mean that reproduction has not been successfully completed, either because the short post-capping period of Cape bees has prevented completion of the mite reproductive cycle, male mite mortality, or the foundress was infertile. 

The data suggest a significant percentage (>27%) of infertile female mites in the population. These infertile mites are probably the result of incomplete reproduction due to the shortened post-capping period found in the worker brood of Cape honeybees. The extremely high numbers of varroa mites found in Cape honeybees (>30 000 in some colonies) indicates however, that although the short post-capping period of Cape bees must limit mite population growth to some extent, it is insufficient to prevent mite levels increasing to harmful levels. This data also indicates that the general presence of drone brood for much of the year is crucial to mite population growth.

 

Reproduction of Varroa destructor in Cape honeybees

White-Eye Worker PupaeWhite-Eye Drone PupaeEmerging Worker BroodEmerging Drone Brood
Cells Examined8846328361041118
Cells with Varroa
5.98%
(0.0 - 42.55)
24.0%
(0.0 - 74.87)
4.83%
(0.0 - 49.33)
33.81%
(0.0 - 84.72)
Number of Adult Mites per Infested Cell
1.24
(0 - 4)
1.83
(0 - 10)
1.74
(0 - 6)
3.48
(0 - 21)
Cells with Only a Single Adult Mite85%73%56%27%
 

 

Hygienic behaviour

A small population of selected Cape honeybee colonies have been tested for hygienic behaviour, as a possible basis for resistance to mites and hence the basis for selection and breeding of varroa resistant Cape honeybees. Hygienic behaviour in these colonies has been found to be extremely variable, both between colonies, and over time, but the Cape honeybee appear to be more hygienic than European races with 100% of dead brood being removed by this unselected population within 48 hours. This hygienic trait, however, seemed ineffectual against varroa mite infestation, and all but 2 of the 20 colonies died within 18 months. At present, there seems to be little correlation between the hygienic behaviour of Cape honeybees and their tolerance to varroa mites and natural resistance to the mites does not appear to be a common trait.


Conclusions

South Africa has the varroa mite that has caused widespread collapse of honeybee colonies throughout the world, and nothing has emerged during the Varroa Research Programme to suggest that the South African situation will be any different. The mite has spread all over the country, including the wild honeybee population, and will eventually be found in all honeybee colonies in a matter of only a few years. Severe colony damage and loss is being witnessed due to the mite and associated secondary diseases.

Left to their own devices African honeybees may be able to accommodate the mite as they appear to have done with other honeybee diseases. It is expected that large numbers of African honeybee colonies will die as a result of varroa, both in the wild and managed bee populations, but thereafter, resistance to the mite is expected to develop rapidly in these populations. As varroa-resistant bees would produce more swarms and drones, the resistance should spread through the population and simply allowing natural selection to take its course should result in African honeybees becoming tolerant to the varroa mite. The economic demand for commercial honeybee colonies will, however, dictate that beekeepers treat colonies with varroacides should honeybee losses become considerable. This will artificially sustain the susceptible honeybee population, and will retard the development and spread of a naturally-selected varroa-resistant population.

Hence, a comprehensive response to the varroa threat is required, involving Integrated Pest Management (IPM) strategies, further research, and regional, governmental and legal strategic actions. Included in this strategy are:

  1. The development of mechanisms or legislation for the regional control and rotation of varroacides with different modes of action, to slow down the development of resistance in the mite population and to prolong effective chemical control.

     

  2. The development of guidelines for the use of non-regulated chemical products presently being used against the varroa mite.

     

  3. Mechanisms to ensure the responsible use of chemical measures.

     

  4. The development of cultural (non-chemical) control measures against varroa, to supplement chemical control.

     

  5. The active development of natural resistance to the varroa mite in the wild honeybee population, by restricting the use of chemical control in certain regions, to facilitate the development of tolerance by natural selection.

    The presence of the varroa mite in Africa clearly represents a severe threat to the beekeeping industry, to agriculture dependent on honeybees for commercial pollination, to the wild honeybee population, and to the conservation of indigenous flora relying on honeybees for pollination. Only time will tell how severe the threat is.

 

Tracheal Mites 

The tracheal mite, Acarapis woodi, causes what is generally referred too as Acarine disease. The adult mites infest the prothoracic tracheae i.e. the first pair found on the thorax, and complete their life cycle there. They feed on the blood (haemolymph) by piercing with their mouthparts through the tracheal walls.

 

There is still some controversy about the damage heavy infestation cause, with some bee pathologists claiming serious primary or secondary damage while others dispute this information. It is hard to believe that a bee, whose tracheae are packed with mites that damage the tracheal walls and soil the tracheal interior, is not influenced negatively. It has also been reported that the bees' wing bases and the muscles and nerves of the wings are damaged because the blood and oxygen supply is reduced. The bees are then unable to fly. Secondary infections may also be more prevalent in infested bees whose damaged tracheal walls provide excess for viruses and bacteria into the thorax of the bee.

 

The mites are tiny and require microscopic examination for undisputed identification. However, heavily infested tracheae can be seen with the naked eye. When the front segment of the thorax of a bee is removed the tracheae are exposed. Healthy tracheae are clear, while infested ones appear brown and may even have black patches of necrotic tissue. Upon examination with a magnifying glass (15 to 20 x magnification) the mites can be seen. Generally it would be advantageous to control mites within a colony. However, this is not as simple as it may seem, because the symptoms are not easily detected, and there is no period or season when mite numbers increase significantly. Infestations have not been correlated with bee race, season, or other environmental factors.


Symptoms

It was generally believed that severely infected bees would loose their ability to fly and crawl out of the hive, but this symptom has been disputed. It has been proven that many infected workers foraged normally. Most bee pathologists agree that the mite is not a serious parasite because it does not cause large-scale bee mortality or any colony losses. But beekeepers may disagree because infested colonies may not produce to their optimum ability, influencing their economic viability.


The mite in South Africa

Trachea mites are found in low numbers in all provinces. Although their numbers apparently increased during winter, the mite population probably remained stable, and the 'increase' can be attributed to the fact that fewer bees are present during the winter.

 

Viruses 

Sacbrood (designated SBV) is probably the best known viral disease because of its well-recognisable symptoms. In the pre-pupa stage, just prior to the cells being capped, when the larvae are in the stretched or upright position infected larvae die. The cell cappings over dead larvae are often perforated and sunken.

 

SACBROOD

Sacbrood (designated SBV) is probably the best known viral disease because of its well-recognisable symptoms. In the pre-pupa stage, just prior to the cells being capped, when the larvae are in the stretched or upright position infected larvae die. The cell cappings over dead larvae are often perforated and sunken.

Viruses multiply in living cells of their host and are therefore difficult to control, because what kills a virus is likely to kill the host cells as well, and therefore the host. Bees probably have some degree of natural resistance to bee viruses otherwise there would be no bees today. Paralysis symptoms usually disappear under favorable weather and foraging conditions. If single colonies should exhibit severe symptoms, the beekeeper will be wise to cull them, and melt all the combs.

Symptoms

The outer skin that loosely surrounds the actual body of the larva fills with a clear liquid, while the underdeveloped head darkens. The white body of the larva become yellowish and shrinks inside the liquid-filled sac. This is more noticeable at the tail end. If the larva is not removed, it will dry into a brittle but easily removable scale. No particular odour is present. If the infection is serious, the brood will have the scattered appearance characteristic of other brood diseases.

The house bees, which are contaminated while removing infected dead brood, probably spread the virus. Serious outbreaks are rare and control measures are usually not necessary. If control does become necessary, strengthening of the colony and requeening are suggested.

Sacbrood in South Africa

In South Africa the disease is rarely reported because only a few sacbrood larvae are usually present in an infected colony. However, it is widespread despite not having been reported as a chronic or serious disease.

PARALYSIS AND OTHER VIRUSES

Viruses most commonly cause paralysis of adult honeybees. Two kinds of viruses that cause paralyses have been identified, namely chronic bee paralysis virus (CBPV) and acute bee paralysis virus (ABPV). A third, Kashmir bee virus (KBV), is very similar to ABPV.

Symptoms of the disease are the inability to fly, as well as uncoordinated and trembling movements of the body. Affected bees are usually found on top of the frames. In severe cases, large numbers of crawling bees are seen on the hive floor and in front of the hive. Death follows within days. The infected bees may be molested by the other bees and become hairless. The symptoms of paralysis are similar to those of Nosema and poisoning by pesticides.

It is still unclear if any of the other viruses found in honeybees are of any consequence. Some have been reported to cause mortality but none to the degree that warrants any special mention. Those described to date are: filamentous bee virus (FBV), Thai sacbrood virus, cloudy wing virus (CWV), bee virus X (BVX), bee virus Y (BVY), black queen-cell virus (BQCV), slow paralysis virus, Arkansas virus and Egypt bee virus (EBV). In South Africa ABPV, BQCV and SBV have been positively identified.

 

Information on other pests and diseases 

Keeping beekeepers and crop producers informed about honeybee pests and diseases is important to create better products and services. Other organisms that are of little economic importance are: Small hive beetle, banded bee pirate, yellow bee pirate, various large hive beetles, parasitic flies, other parasitic mites, other wasps, the Deathshead moth, greater and lesser waxmoth, honeybadgers (ratels), nectar flies, rodents, toads, geckos and lizards, starvation, overheating and chilling, termites, ants, bee scorpions (chalifers), braula (bee louse), and birds. South Africa is still free of American Foulbrood and the parasitic mite, Tropilealaps clarea.

 

 

Details
Contact person:Mike Allsopp
Contact e-Mail:allsoppm@arc.agric.za