A 7th revision post for the British Beekeeping Association’s Module 3 Honey bee Pests, Diseases and Poisoning exam, which I’m taking in March. I’m doing the BBKA’s correspondence course, so I have a tutor setting me papers which she then marks. The last question for paper 2 is a very practical one – trying to work out what has caused a colony to die out.
B5. a colony was fed three gallons of syrup in late October during a period of rather damp weather; next Spring it was slow to build up compared with other colonies in the apiary; there were brown stains on the frames and combs; it recovered enough to produce swarm cells in early July but several of the queen cells had dark coloured walls and the occupants died in the propupal and pupal stages; on sunny days several workers could be found crawling outside the hive or clustered together on grass stalks with what appeared to be bloated abdomens; their wings looked somewhat dislocated and they were unable to fly.
a) give reasons to suggest what diseases might be present in this colony
The information that the colony was fed three gallons of syrup during damp October weather and had brown stains on the frames and combs suggests the bees were suffering from dysentery.
Dysentery is not a disease but a symptom of problems in the bees’ excretory systems. It happens when excess water accumulates in the rectum, causing runny poop and increased brown splats around the hive’s entrance as the bees struggle to hold in. It is not a sign of nosema, but can help spread nosema spores if nosema is present.
Defecation on a hive by bees with severe dysentery. From extension.org.
The suspicion that nosema is likely to be affecting the hive comes from the phrase ‘next Spring it was slow to build up’. This is the only observable symptom of nosema. The reason it stalls the progress of colonies is that the germinating nosema spores inside the gut of an infected bee impair the digestion of pollen, shortening the lifespan of the bee. Infection is particularly devastating in younger bees, which will not be able to digest enough pollen to develop their hypopharyngeal glands properly and be able to produce brood food.
- Black queen cell virus
We may have had a brush with this in one of our colonies this year. Back in June, in my post ‘Long live Queen Neroli, our Jubilee Queen’ I recounted how we were worried at finding a queen cell still capped when the queen should have already emerged:
“We asked John Chapple’s advice. He instructed us to shake the bees off the frame and then gently cut the tip of the queen cell off with a hive tool to see what was inside. The queen revealed was obviously a goner, and had been for some time. “I’m no expert” (hah!) John said, “but that looks like black queen cell virus”. Having looked it up at home, this is a virus associated with the spore disease nosema, which is worrying. You can see her tattered wings and black body below.”
Black queen cell virus, which turns queen cell walls dark brown-black and the dead prepupa or pupa inside a yellow colour with a tough skin, is associated with nosema, which may be why the queen cells in the hive we’re investigating have succumbed. The virus can only multiply when nosema is present, and in this case several cells have dark coloured walls. The virus probably enters the developing queen through her gut, so as nosema weakens the gut wall this will allow the virus easier entry than the walls of a healthy gut would.
Our dead queen photographed above is black rather than yellow, so John may have been mistaken about the cause of death being Black queen cell virus.
Normally most honey bee viruses exist in a temporarily inactive state and do not cause signs of disease. However, the presence of other parasites or diseases can activate them. Viruses generally are often transmitted through diseases such as acarine, nosema and varroosis, which act as a vector by in some way facilitating the entry of a virus, or activating previously dormant viruses already present in the host. Varroa is thought to be a particularly common vector and viral replication has been shown to be activated by the presence of varroa. As the mites suck the haemolymph of the bees they also act as tiny hypodermic syringes, injecting the viruses directly into their hosts.
In ‘The Honey Bee Around & About’ by Celia F Davis (2009), she says:
“To a honey bee virus a bee hive must be paradise and when an organism such as Varroa destructor appears on the scene, to act as an efficient vector, it must seem like its Birthday and Christmas rolled into one.” (p39)
- Chronic bee paralysis virus (CBPV)
The beekeeper has noted that “on sunny days several workers could be found crawling outside the hive or clustered together on grass stalks with what appeared to be bloated abdomens; their wings looked somewhat dislocated and they were unable to fly.”
Bloated, distended abdomens (due to a build-up of fluid in the honey stomach) and dislocated wings, causing inability to fly, with crawling on the ground or up plant stems, are symptoms of Chronic bee paralysis virus. There are two main ways the virus can manifest itself in colonies; one causes the problems noted above – abnormal trembling of the body and wings, bees crawling on the ground due to flight inability, bloated abdomens, and dislocated (K letter-shaped, partially spread) wings.
The other form causes hairless, shiny, and black-appearing bees that are attacked and rejected from returning to their colonies by entrance guard bees. The loss of hair is due to their hive mates having nibbled the hairs away. As they are denied entrance to their colony, their flight in front of the hive will be zig-zagging in a similar way to robber bees. These bees will also tremble.
Both forms of symptoms can be seen in bees from the same colony, and may reflect differences among individual bees in inherited susceptibility to the virus (from the Beebase website).
During July the worker bee population would be at its peak. It seems that close contact amongst overcrowded bees can break hairs from the cuticle, allowing CBPV to spread from diseased bees to healthy bees via their exposed epidermal cytoplasm. It is likely that any factors that result in decreased foraging activities and crowded conditions in the bee colonies may lead to disease outbreaks of CBPV. It is also associated with varroa, and probably acarine.
b) how could the presence of the pathogens be confirmed?
Definite confirmation of nosema requires microscopic examination of the abdomens of older adult bees, which can be collected from the hive entrance. Infection is highly variable in a colony, but foragers tend to contain the higher spore loads. Collecting bees leaving to go on cleansing flights rather than returning will be more effective. Send a sample of 30 bees to a microscopist or the UK National Bee Unit service in a small sturdy box (not plastic, which causes rapid sample degradation).
Lab investigation of a sample will also be needed to positively identify bee viruses.
c) how may the beekeeper have been partially responsible for the condition of the colony?
The information given tells us that the colony was fed three gallons of syrup in late October, during a period of rather damp weather. Sugar syrup feeding generally needs to be finished by early October in Britain, as if syrup is fed too late in the year the bees will have insufficient time to evaporate the excess water, and the syrup will be stored and could ferment, causing digestive problems for the bees when they come to feed on it later. Dysentery is caused by excess water accumulation in the rectum, due to diet or if the bees have been unable to fly for several days due to bad weather.
This late feeding of sugar syrup in unsuitable weather by the beekeeper probably caused the bees to develop dysentery and defecate within the hive, spreading nosema spores already present in the hive more quickly. The younger house bees will attempt to clean up the faeces, causing them to come into contact with the nosema spores in the faeces and become infected.
Widespread nosema infection could have weakened the colony, making it slow to build up in the spring and transmitting black queen cell virus to the queens in their blackened cells. This probably also left the colony more vulnerable to varroa and viruses associated with varroa, such as chronic bee paralysis virus. All this exacerbated by an unfortunate feeding choice in the autumn!
d) is there any advantage in uniting this colony to another one; give reasons?
The colony may currently be queenless if it has been unable to produce a healthy queen. If this is the case, uniting it with a queen-right colony will give it a chance of survival. As several workers have been observed unable to fly it is certainly likely to be low in numbers, and may be unable to build up enough stores and new bees to last overwinter without uniting.
There is possibly a genetic susceptibility to Chronic Bee Paralysis Virus, so requeening with a queen from a different strain is often recommended in bad cases. Uniting the afflicted colony to another one would fulfil this.
The disadvantage will be the chance that this colony could infect a healthy one. The beekeeper will have to weigh up whether it is worth the risk.
e) why may it be advantageous to fumigate the combs?
Fumigation would destroy the spores of nosema and several other infectious diseases which might be present on the combs. It is very difficult to treat honey bee viruses, so a good approach is to treat for vectors such as nosema, to try and reduce the exposure of bees to viruses.
Do you agree with this diagnosis? Have you ever come across similar symptoms in your hive?
- Guide to Bees and Honey, Ted Hooper & Margaret Thomas, Northern Bee Books (2010)
- The Honey Bee Around & About, Celia F Davis, Bee Craft Ltd, (2009)
- Keeping Healthy Honey Bees, David Aston & Sally Bucknall, Northern Bee Books (2010), p66
- Mid Atlantic Apiculture Research Consortium (MAAREC), Bee diseases and their control (2005)
- Mid Bucks Beekeepers Association, Module 3 exam notes, p33
- National Bee Unit Beebase website
- Practical Beekeeping, Clive de Bruyn, Crowood Press (1997)
- Scientificbeekeeping.com, Randy Oliver