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.
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.
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.
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
Cells Examined | 8846 | 3283 | 6104 | 1118 |
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 Mite | 85% | 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:
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.
The development of guidelines for the use of non-regulated
chemical products presently being used against the varroa mite.
Mechanisms to ensure the responsible use of chemical
measures.
The development of cultural (non-chemical) control measures
against varroa, to supplement chemical control.
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.
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