Microbiology of EFB
Simply put, European Foul Brood is caused by the bacterium Melissococcus pluton. This bacterium is carried from larva to larva on the mouthparts of the nurse bees. Cleaning bees mouthparts become contaminated as they polish the cells between brood cycles and the whole lot will be spread through the colony during the processes of grooming, food sharing and communication. Of course, diseases of all types can be spread between hives by robbing or drifting bees and the beekeeper also helps with colony manipulations, management practices and comb exchanges between colonies. Pollination, migratory beekeeping and sales of bees can spread diseases over a wide area.
Unlike AFB, where the bacteria are invariably found in pure culture because of the antibiotic released by the bacteria as they sporulate, the presence of secondary bacteria are another feature of EFB. ' Bacterium Acromobacter euridic' is most common and is thought to accelerate the death of infected larvae while Melissococcus faecalis (Sour brood) is characterised by its sour smell. Where EFB has become well established you may find the secondary bacteria Paenibacillus alvei also characterised by an appalling smell. When this is present larvae may die after the cell has been sealed giving rise to dark, perforated and sunken cappings resembling AFB. The vital difference is that, although the cell contents are brown and gooey, they do not form a decent rope when tested with the matchstick. They do however form rather sticky scales although these can be distinguished from AFB because of the variable colour and because they can be removed from the cell. The presence of these bacteria can indicate that the disease is of long standing and that antibiotic treatment is unlikely to be effective.
Practical consequences of biology
Melissococcus pluton is a sneaky little organism with one or two quirks that make EFB more difficult to diagnose and control than other bee diseases.
. The pathogen acts as a parasite competing with the larva for its food.
. When there is enough food infected larvae survive to pupate.
. Signs of disease are not always expressed although the bacteria remain within the colony.
These points have profound practical consequences for beekeepers.
The bacteria multiply in the mid gut of an infected larva where they compete for the larval food supply, in effect they act as parasites rather than pathogens. As long as there is plenty of food there will be enough to meet the demands of both the larvae and the bacteria. The developing larvae will survive and the colony won't show any outward signs of disease. However, if the available food is only just enough the bacterial competition will cause the larva to die of starvation and signs of European Foul Brood become obvious. The fact that the bacteria compete with the bee larva for food and if there are enough bacteria and not enough food, the larva will die of starvation is a very important point to bear in mind. Understanding this explains some of the difficulties that can arise in the detection and control of EFB. The age of the larvae at infection can also affect the development of the disease. Small inoculations of bacteria in older larvae will not have time to develop sufficiently for disease signs to show before pupation.
Bees remove sick and dying larvae from the hive, which consequently greatly reduces both the level of bacteria present and the numbers of larvae displaying clinical signs of disease. Perversely, it is the larvae surviving to pupate that ensure infective bacteria remain in the colony. The reason is rooted in the larval anatomy. Prior to pupation larvae have a blind gut - so stuff can go in but not come out. Bacteria may invade and develop in the larval gut but will not be released into the comb. As it prepares for pupation the ends of larval gut join allowing the contents to be voided into the cell and contaminating the comb with infective bacteria.
Two important practical consequences arise for the beekeeper from the interaction of bees and bacteria.
. It will not always be possible to see signs of EFB in the colony. This doesn't necessarily mean it has gone. It has a 'now you see it now you don't' reputation. As long as there is plenty of food coming in to the colony then there will be enough for both the larva and the bacteria to survive. In this circumstance there will be few, if any clinical signs. Remember too, it is the survival of infected larvae that perpetuates the disease. Where there is not enough food, e.g. at times of dearth or where there is rapid brood rearing and bees are only just able to keep up with demand for larval food, disease signs will show. The bees recognise the sick larvae and dispose of them outside the hive with their bacterial contamination still safely locked inside their blind gut. The clinical signs of disease will disappear and the levels of bacteria present will be greatly reduced. Disease signs may be obvious and widespread at one inspection but have completely vanished by the next. In fact this is one of the bees natural control mechanisms for this disease and demonstrates how closely the EFB bacteria and the bees' life histories are inter-linked and how comfortably this pathogen is adapted to its host. It also has consequences for the timing of antibiotic applications.
Once EFB has been present in a colony a reservoir of bacteria will remain in the comb with the potential for re-infecting the colony at a later date. The levels of bacteria in the colony will
rise and fall and disease signs may or may not show but there will always be some bacteria remaining unless the beekeeper intervenes to do something about it. This can occur even if the comb has been removed from the colony for a time. Professor Heath showed quite clearly that combs stored for several years can still contain viable EFB bacteria. It is this ability for sub-clinical levels of bacteria to remain in the comb that makes it so difficult for the beekeeper who is unfortunate enough to have European Foul Brood to control it - let alone get rid of it completely.
The best time to look for EFB, at least if you want to find it, is when brood rearing is at its maximum and food availability is only just sufficient for a healthy larva to survive and pupate. Remember that EFB bacteria act as parasites so, for an infected larva, there will not be enough food to go round, it will die and the disease signs will show up. This will usually be in late May or early June depending on the size of the stock and where you live. Inspections that are not timed to look in a colony when EFB symptoms are likely to be visible are useless as far as EFB control is concerned. It is also hopeless looking for EFB when there is little or no unsealed brood for instance when requeening or swarming has occurred.
Remember that even where there are no visible symptoms that the bacteria may still be present in the hive and is likely to be so if there has been a history of disease in the colony, the brood frames, or the area. It may be in a subclinical state or surviving as lurking bacteria waiting for the right conditions to show disease signs again. Bacteria in honeybee colonies can stay in this 'lurking' state for many years with no apparent ill effect on the bees and may show up when conditions are right as an apparently spontaneous outbreak.
Herein also lies another debate. Are the bacteria naturally ubiquitous in the environment and therefore normally present in every bee colony or are they only there after the colony has been infected with disease? Each of these ideas, or models, will have a different consequence for the practical beekeeper. If the bacteria is there in every colony what triggers the disease and how can we control it? If it is not ubiquitous but remains perhaps as a bacterial or subclinical infection after a disease outbreak then how do we get rid of it once and for all? Experiments from Cardiff University point to the bacteria being ubiquitous in the environment. In my own experience as a bee inspector (which is practical not scientific) I am not alone in believing that I have never seen a spontaneous case of EFB.
Plus..........
http://web.oie.int/fr/normes/mmanual/A_00122.htm
