Honeybees of South Africa

Honeybees of South Africa

South Africa is home to two sub-species or races of honeybees which are indigenous to the country: Apis mellifera Scutellata (or “African bee”) and Apis mellifera Capensis (or “Cape bee”).  The Cape bee is generally confined to the western and southern Cape regions particularly referred to as the Fynbos region running in an imaginary line between Vredendal on the western Atlantic coastline across to Willowvale on the eastern Indian Ocean coastline.  The African bee covers the region to the north of this area although there is hybrid zone overlapping the two regions where A.m. capensis and A.m. scutellata hybridize.

The African bee is an aggressive bee with a hardy strain and capable of producing large crops of honey.  It has more of a yellow striped abdomen compared to A.m. capensis.  Only the queens are fertile; worker bees are infertile when the queen is present.  However the worker bees have the ability to lay unfertilised, drone eggs.  The queens are prolific layers and during strong honey flows the colony builds up rapidly.  The African bee was introduced to the Brazilian bee industry in the mid 1950’s and immediately adapted to its surrounds, hybridizing with the locally introduced European bees.  These bees became known as the infamous “African Killer Bees” which have steadily moved northwards up into the United States.

1A healthy colony of A.m. scutellata

(source: P. Kruger: Department of Entomology, University of Pretoria)

2

Scutellata worker bees with queen.  Spot the braula (bee louse) on the worker bee next to the queen. (Source: P. Kruger: Department of Entomology, University of Pretoria)

The Cape bee tends to be a more docile bee (although can also become aggressive when provoked), distinguished from the African bee by a darker abdomen and are sometimes referred to as “black bees”.  It has a unique characteristic in that the worker bees (females) have the ability to produce both male and female offspring and thus able to re-queen a colony which has become queenless.  The downside of this characteristic is that it has the ability to parasitise scutellata colonies.  Capensis laying workers invade and subsequently begin to lay their own eggs, challenging the scutellata queen’s ability to control the colony.  The original colony becomes overtaken by Cape bees and will collapse.  Signs of a Capensis invasion are: multiple eggs observed in cells, (may even be laid on top of pollen), raised capping of brood cells, reduced activity within the hive, and non-aggressive bees.

3

Capensis worker bees with queen.  Note the braula (bee louse) on the queen and worker bees attempting to clean her. (Source: Internet – Unknown).

4

Cape bees and African bees together.  The cape bees have darker bodies whereas the scutellata bees have orange bodies. 

(Source: P. Kruger: Department of Entomology, University of Pretoria).

capensis_eggsMultiple capensis eggs laid inside a scutellata queen cell – prima facie evidence of a capensis invasion!!!

5A colony of Cape bees.  From a distance they are hardly distinguishable from African bees. ; but if you look closer you can see they are “black bees”. 

(Source: K. Crous: Department of Entomology, University of Pretoria)

Bee Diseases, Pests and Parasites

Dr H Human and Prof C.W.W Pirk, SIRG, University of Pretoria

Knowledge about the various bee diseases, pests and parasites are an important aspect of beekeeping management/ practises.  Brood and / or adult bees can be affected.  Certain diseases and conditions have distinctive symptoms in contrast to viruses that do not produce distinctive signs in the field.  Some of these diseases, pests and parasites can be avoided while others can be dealt with through early detection.

Healthy brood

A healthy brood comb is usually compact and eggs, larvae or pupae can be seen in nearly all the cells from the centre of the comb outwards.  Unsealed brood has a pearly white colour and sealed brood will have even cappings of a uniform colour.

Unhealthy brood

The brood comb of diseased colonies often has a spotted pattern (pepperbox appearance).  The cappings may appear sunken or even punctured and the colour can be darker.  Sometimes dried out remains are present on the bottom or sides of cells.

The following diseases, parasites and pests will be discussed
Bacterial diseases:
American foulbrood (AFB)
European foulbrood (EFB)
Fungal diseases:
Chalkbrood
Stonebrood
Nosema
Viral diseases:
Deformed wing virus (DWV)
Kashmir, Acute bee paralysis virus and Israeli acute paralysis virus (ABPV, IAPV)
Sacbrood
Parasitic Mites:
Varroa
Tracheal
Pests:
Small hive beetles
Wax moths

Bacterial diseases

American foulbrood (AFB)

Infection is caused by the spore-forming bacterium Paenibacillus larvae.  This disease can result in severe colony losses.  It affects only the brood, is highly contagious and extremely difficult to eradicate.  The bacterial spores can remain viable for up to 60 years and are extremely resistant to heat extremes and chemicals.

Infected larvae die and a distinctive foul smell develops upon decomposition.  At this stage the remains can be drawn out as a string (i.e. extend up to 10-30mm).  There after the remains dry out to dark and highly infectious foulbrood scales that remain in the cell.  Infected colonies have scattered and uneven brood patterns with dark, greasy looking, sunken cappings.

pic1

Picture 1. Scattered and uneven brood pattern of AFB infected colony. pic2Picture 2. Ropiness can be demonstrated in AFB infected larvae.

European foulbrood (EFB)

This brood disease is caused by the non-spore forming bacterium Melissococcus pluton.  It affects open brood and is common during spring when brood rearing is at its height.  Colonies may be severely weakened.  EFB is considered a less serious disease than AFB but high losses have been recorded.  Infected larvae appear coiled/ twisted in their cells with a brownish colour and normally die when they are 4-5 days old.  Sometimes one can detect a sour odour.

pic3Picture 3. Colour change of larvae with EFB.

Fungal diseases

Chalkbrood

This is a disease affecting sealed brood and is caused by the fungi Ascosphaera apis.  The presence of chalkbrood is influenced by climatic factors, which influence the temperature and humidity in the hive, especially when it is cooler and wet.  This fungus can affect a single colony or an entire apiary or even regions in “chalkbrood years”.  At first larvae are covered with a fluffy, whitish fungus growth.  After death the larvae become mummified and have a chalk-like appearance; the colour varying from white, to grey to finally black,

pic4Picture 4. Chalkbrood mummies

Stonebrood

Even though this disease is considered to be extremely rare, it has recently been confirmed in bees in the Gauteng region.  This disease is caused by the fungi Aspergillus flavus, A. fumigatus and/ or, A. niger.  The spores can easily be transmitted.  Stonebrood is pathogenic to larvae, pupae and adult bees and can cause respiratory diseases in humans and other animals.

Early stage of stonebrood infection is difficult to detect but after death larvae become very hard and are difficult to crush.

Nosema

Nosemosis is a common disease of adult honeybees, caused by the microsporidian Nosema apis or Nosema ceranae.  Although N. ceranae is not associated with dysentery, it has been linked to colony losses and is often associated with other diseases such as viruses.  Infected bees suffer from severe dysentery, subsequently resulting in starvation and a shortened lifespan.  Reliable diagnostic symptoms are lacking, however heavily infected bees have swollen and greasy looking/ shiny abdomens and are unable to fly.  They may crawl at the entrance or stand trembling on top of the frames.  There may be dysentery spots on the hives, frames and landing boards with dead bees at the entrance.

Viruses

Honeybee health can be dramatically affected by viral diseases that are linked to Varroa mites.  Varroa mites are known to favour the outbreak of viral diseases.  Viruses may be present in hives without any clinical symptoms that only becomes visible after stressors have weakened the colony.  Viruses are difficult to distinguish from each other and molecular tools (PCR – polymerase chain reaction) are required to identify them.  There are no noticeable or reliable symptoms with the exceptions of Deformed wing virus (DWV) and Sacbrood.

Deformed wing virus (DWV)

This virus causes bees to grow ragged wings that are incapable of flight. These bees die off naturally or are removed from the colony within 2-3 days after emergence.

Sacbrood

Sacbrood is a common brood disease caused by the virus Morator eatotulas.  Infected larvae die and tissue disintegrates into a brown watery solution held together by the larva’s outer skin.  The virus is probably fed to larvae by nurse bees and thereafter contaminates the cleaning bees.  This disease does not cause serious colony losses and may appear at any time during brood rearing season although it is most common during the first half of the season and usually subsides after honey flow starts.

pic5Picture 5. Larvae infected with sacbrood.

Parasitic Mites:

Varroa destructor

These are external parasitic mites that feed of the haemolymph (blood) of developing and adult bees.  Examples of the damage caused by these mites are morphological deformation, reduced lifespan, weakening of the immune system and transmission of secondary diseases (e.g. bacteria and viruses such as DWV, Kashmir Bee Virus and Acute Bee Paralysis Virus).  Varroa mites are one of the most serious pests of European bees worldwide; if infested colonies are left untreated by the beekeepers, the mites will kill the colony within 2 to 3 years.  The mites need brood to reproduce and they find drone cells more attractive to breed in than worker cells.

pic6Picture 6. Varroa destructor mites on pupae and adult bees.

Honeybee tracheal mite (HBTM) – Acarapis woodi

Tracheal mites are endoparasitic mites and only parasitise the adult bees, affecting their trachea or respiratory system.  Heavy infestation results in sick bees that do not work as hard or live as long as healthy bees, subsequently causing weakened colonies and increased mortality.  Due to their small size, these mites can’t be seen with the naked eye and are difficult to detect.  Few tracheal mite problems have been reported worldwide in recent years.

pic7Picture 7. Tracheal mites in honeybee trachea.

Pests:

Small hive beetle (SHB) – Aethina tumida

Small hives beetles are endemic to sub-Saharan Africa.  African bees are able to keep the beetles in check but weakened colonies may lose control over their beetle populations.  The colonies will then abscond and leave the infested nest site behind.  However, they have recently been introduced in Northern Africa, Australia, Hawaii and North America where it developed into a pest resulting in devastating infestations.

Small hive beetles feed on bee brood and food reserves and reproduce within hives, but as soon as the larvae reach the wandering stage, they crawl out of the hives to pupate in the soil, (within 20 m of the hive).
pic8Picture 8. Small hive beetle larvae (wandering stage) and adult SHB emerging from soil.

Wax moth – Galleria mellonella

Wax moths are known to cause serious damage in hives after the bees have been driven out or in comb stores.  Burrowing larvae leave silk trails behind and can, in extreme cases, destroy the entire comb, with only a matted mass of silk and other debris remaining.  Moths’ larvae destroy the comb and gnaw wooden material as they get ready for pupation.  Their cocoons are very sturdy.  Strong colonies are not susceptible to damage since they can control the population of moths.  The wax moth is adapted to warm climates and generate less damage in cold regions or at higher altitude.

pic9Picture 9. Frame with wax moth damage.

pic10Picture 10. Adult wax moth and wax moth cocoons.

Acknowledgements
We wish to thank Dr V. Dietemann and Dr P. Kryger for their contributions.

Further reading:
Alippi, A. M. (2007) Evidence for plasmid-mediated tetracycline resistance in Paenibacillus larvae, the causal agent of American Foulbrood (AFB) disease in honeybees Veterinary Microbiology 125: 290–303.

Charrière JD, 2007. Protection des rayons contre la teigne Galleria Mellonella. ALP Forum 45, 8pp.

Charrière,J.D.; Dietemann,V.; Schäfer,M.; Dainat,B.; Neumann,P.; Gallmann,P. 2011. Leitfaden Bienengesundheit des Zentrums für Bienenforschung. ALPForum 84, from the Swiss Bee Research Center

de Graaf D.C. et al. (2006) Diagnosis of American foulbrood in honey bees: a synthesis
and proposed analytical protocols. Letters in Applied Microbiology 43: 583–590 .

De Rycke, P. H. (2002) The possible role of Varroa destructor in the spreading
of American foulbrood among apiaries Experimental and Applied Acarology 27: 313–318,.

Ellis, J.D., (2003). The ecology and control of the Small hive beetle (Aethina tumida) PhD thesis Rhodes University.

Fera National Bee Unit (NBU) (2010) The Small Hive Beetle a serious threat to European apiculture. This document is also available on BeeBase (National Bee Unit) website, www.nationalbeeunit.com

Genersch, E. (2008) Paenibacillus larvae and American Foulbrood –long since known and still surprising J. Verbr. Lebensm. 3: 429 – 434.

Hood, W.M. (2004). The Small hive beetle, Aethina tumida: a review. Bee World, 85: 51-59.

Human, H. et al. (2011) The honeybee disease American foulbrood – An African perspective African Entomology 19(3): 551–557.

Kryger P, Human H, 2010. Manual on Honey bee diseases. For SABIO BEECON 2010

Neumann, P., Elzen, P.J., (2004).  The biology of the Small hive beetle (Aethina tumida, Coleoptera: Nitidulidae). Gaps in our knowledge of an invasive species. Apidologie 35: 229-247.

Schäfer, M.O. et al. (2009) Small hive beetles, Aethina tumida, are vectors of Paenibacillus larvae. Apidologie available online www.apidologie.org

Schäfer et al 2008 A scientific note on quantitative diagnosis of small hive beetles,
Aethina tumida, in the field Apidologie 39: 564–565

Williams JL, 1990. Insects: Lepidoptera (Moths) In: Honey Bee Pests, Predators, and Diseases (Morse R and Nowogrodzki R, Eds.), second edition. Cornell University Press,