Going Light In Young Finches
1st February 2011, 6:52 pm
.Most, if not all, breeders of our native finches will be familiar with the wasting disease which is generally known in the fancy as “going light”. It affects young birds during or shortly after they are weaned.
Going Light in young Finches and how to manage it.
By Dave Henderson.
What are the symptoms?
The classic symptoms are the young bird appearing slightly puffed up with the feathers across the whole body having a slightly raised appearance. The bird will usually sit listlessly and there will be little movement evident. Feeding is difficult and although the bird will often sit for hours on or in the food dish, occasionally nibbling at seeds, it is unable to swallow them. Likewise, the bird will often be unable to drink. Some birds which show the full blown symptoms of the disease will die very quickly. Others can hang on for days before succumbing. In my experience it is very rare for any young bird showing these symptoms to survive. If a young bird completes it’s moult without being visually affected by the disease then it is unlikely to suffer from it as an adult. The critical time therefore is the period between fledging and completion of the moult.
In my experience more or less all of our species of finch can be affected by this disease. The mortality of young greenfinches is very well documented but linnets, twites, crossbills, siskins, redpolls and bullfinches can all suffer as well.
What’s the cause?
Work done by the Viguie’ laboratories in France during the late 1970’s suggested that the disease was caused by a protozoan. These are microscopic parasites which cause a multitude of diseases in many different species of birds, animals and reptiles. In humans they are best known as the cause of malaria: a disease which accounts for around two million human deaths annually across the world.
In 1981 Viguie’ proposed that the disease was called by a protozoan known as Lankesterella. They called the disease Lankesterellosis. They suggested that the disease may have been transmitted via red mite although they also acknowledged at the time that the disease could also be evident in the absence of mite.
A few years later, an English vet, Dr John Cooper, using a very powerful form of microscope (known as an electron microscope) established that the disease was in fact caused by a tissue borne protozoan known as Atoxoplasma. Under the microscope he observed that the parasite was able to form cysts within the tissues of the birds’ body which may have explained why adult birds appear to be able to carry the disease without it causing them any apparent harm. He called the disease Atoxoplasmosis.
Atoxoplasma are a type of coccidia. Coccidia cause diseases in mammals, birds and reptiles. In birds, the coccidia can be split into two distinct groups. The Isospora tend to affect smaller birds such as finches whilst the Emeria tend to affect larger birds such as poultry and game birds. Atoxoplasma are a specific type of Isosporal coccidian.
So it is possible that when referring to the “going light” disease people can call it Coccidiosis, Atoxoplasmosis or Isosporosis. To all intents and purposes all three terms mean the same thing!
Coccidia are similar to bacteria in that they are single celled organisms. Most bacteria multiply by simply dividing in two over and over again. A single bacterial cell becomes 2, then 4, then 8 and so on. Coccidia are different in that they have much more complex life cycles. Part of their lifecycle can involve the formation of “eggs” which are known as oocysts. The coccidian cell multiplies inside the tissues of the adult bird and the oocysts are passed out with the birds droppings. These oocysts are microscopic and cannot be seen by the naked human eye. They can form a protective coating around themselves and are capable of surviving on the surfaces of an aviary or cage for months if not years. It is the presence of the oocysts within the aviary that cause the problem.
How is the disease passed between birds?
As already mentioned, the parasite can live within the tissues of adult birds without causing the birds any harm. However, during the summer months, when the air temperature is warm, the parasite will multiply and the oocysts will be dispersed across the aviary surfaces. The adult birds, at this stage, don’t pass the disease onto the young chicks whilst they are still in the nest. The youngsters are fed by regurgitation by the adults and it’s likely that they also pass on some immunity to the disease via their crop milk.
However, once the youngsters leave the nest, they start to pick for themselves. They are more than likely to ingest some oocysts when they are feeding as they are liable to pick up food from any of the aviary surfaces. As the oocysts enter the young birds’ gut they undergo development during which they damage the lining of the gut. This damage can be so severe that the bird is unable to eat or drink hence the onset of the acute symptoms of the disease. Many of the birds’ other organs such as the liver, spleen, kidneys and brain can also be damaged beyond repair. This is the reason why young birds which show the acute symptoms of the disease rarely recover. The damage is already done when you first notice the bird looking sick.
I’ve often wondered if some of the problems we see in our birds is caused by a sub-clinical form of coccidiosis. That is to say a mild form of the disease where the primary symptoms aren’t evident. It’s possible that twisting or twirling for example could be caused by coccidial damage to the brain?
What’s the best way to control the disease?
The key thing to accept with this disease is that no drug has yet been discovered which is capable of entirely wiping it out from a flock of birds. The main reason for this is the complex nature of the parasites’ lifecycle. The Sulphonamide antibiotics, also known as the “sulpha drugs” are capable of preventing the disease from developing in young birds(and therefore protecting them) but not of eradicating it.
The sulpha drugs were discovered during the 1930’s. They were first used to treat coccidiosis in poultry in the 1950’s but the notion of using them in native finches didn’t kick off until the 1970’s. Their use revolutionised the breeding results of native bird breeders and greatly helped the development of aviary bred strains of native finches.
The original drug which was used from the 1970’s was Sulphamezathine®. This in fact was a brand name. The actual drug it contained was sulphadimidine. Almost 40 years later this is still the drug of choice, at least among UK fanciers, albeit under a different brand name. Over the years we’ve also seen the drug marketed under the brand names Bimadine® and Vesadin®. In recent years the brand now used is Intradine®. The other three Sulphamezathine®,Bimadine® and Vesadin® are no longer available having been discontinued by their manufacturers.
How do the Sulpha drugs work?
The vitamin folic acid is necessary for the synthesis of DNA and RNA and therefore the growth and multiplication of cells. Mammals, including humans, don’t synthesise their own folates but instead absorb them from their diet. However, bacteria and protozoa make their own. Sulphonamides interfere with this folate production and this makes them ideal drugs for halting the multiplication of protozoa. The sulphonamides don’t directly kill the protozoa but instead act to prevent them from growing and multiplying.
How should the Sulpha drugs be used?
In birds the Sulpha drugs are best used as prophylactics. That is to say, they are best used to prevent rather than cure the disease. As young finches appear to have little, if any, immunity to the disease the drug is best given BEFORE any symptoms are evident.
In the poultry industry small doses of sulphonamides (often added to the feedstuff in parts per million) are given to the young birds until they have moulted out. Experience has shown that this is also the best technique to use in native finches as well.
I’ve been using sulphadimidine for over 20 years and found it to be very effective. My method is to draw some neat Intradine® 33% injection into a 5ml syringe. I then add 6 drops of this into each drinker in each aviary. The drinkers I use are old margarine tubs which hold exactly 500mls (half a litre) of water when filled to the brim. The birds both drink from and bathe in these drinkers. I use the drug in the water 5 days on (weekdays) and 2 days off (weekends).
I start adding the drug to the drinking water in each aviary on the day the first chick leaves the nest. Once the chicks from a nest are fully supporting themselves I remove them from their aviary and put them in a treble breeding cage inside my birdroom for a period of time. During all the time they are in cages, the drug regime is continued. Obviously, the adults still in the aviary will be going down for another round and the drug will be kept back from them until their next round of chicks pops the nest at which point in time I’ll start to give those chicks the drug regime as well. Once the breeding season is finished, I return all the young birds back into aviaries in groups of five or six and continue with the drug treatment until they have finished moulting (around the end of September) at which point I stop giving them the drug.
I never moult young birds and adults together in the same aviaries. The reason for this is that it lessens the likelihood of the adults passing on coccidian oocysts to the young birds during the moulting period. I moult birds in groups of adults OR groups of youngsters but never both together. I never give the drug to the adult birds when they are moulting because they don’t need it.
What supportive measures should be taken?
It goes without saying that it is good practice to try to keep the birds living quarters as clean as possible throughout the breeding and moulting periods. In particular it would be advisable to keep the feeding stations and seed containers etc clean in an attempt to reduce the number of oocysts in the vicinity of where the birds are feeding.
Oocysts appear to be very resistant to disinfectants etc. Probably the only sure way to remove them is to pass the tip of a blow torch across the hard surfaces of the aviaries and cages. I do this every year when I prepare my aviaries prior to setting my birds up for breeding.
One of the best ways to kill oocysts in an aviary was to paint the inside with creosote once a year. Creosote contains phenols which are very caustic and will burn oocysts as well as mite etc. However, recent legislative changes have resulted in creosote being banned in the UK. Although a substitute product is available it seems less effective (and is much more expensive) than the original.
Which is the best Sulpha drug to use?
This really is a matter of personal choice.
There are a number of sulpha drugs on the market. I’ve already mentioned sulphadimidine (Intradine®) which is probably the most popular drug used in the UK. Another popular drug is sulphadimethoxine which is available under the brand name Coxi-Plus® and can be obtained in the form of a powder for addition to drinking water. One drug which is popular on the Continent is sulphachloropyrazine which is available under the brand name ESB3® again in the form of a powder. The last named drug is probably the best of the three for treating coccidiosis in adult birds.
The principle difference in these drugs is the length of time they are metabolised and excreted by the body.
Sulphadimidine is the shortest acting, of the three with sulphachloropyrazine the longest acting one.
All of these drugs, especially in liquid form tend to be broken down when exposed to sunlight and/or water. The water molecules actually split the drug molecule ( a chemical reaction called hydrolysis) and energy from sunlight speeds this reaction up. These drugs should all be kept in their original containers in a cool, dark cupboard. There’s a good reason why Intradine® is manufactured in brown glass bottles!!!
Intradine® injection when fresh is a clear liquid with a very faint yellowish colouration. When it has been hydrolysed it turns a brown colour almost like concentrated urine. In this state it is ineffective and should be discarded.
One point to watch out for with Intradine® is that due to it’s low solubility the drug will tend to solidify around the cap of the container in which it is housed. In this form it appears as a white, chalky powder. It is simply the dehydrated dry form of the drug. In addition, it has a very high freezing point and if kept in a cupboard in an unheated birdroom in the winter it’s not unsual for a furry type solid to start appearing inside the bottle. This is merely the drug solidifying having reached it’s freezing point. It will go back into it’s liquid form again as soon as the bottle in brought back into normal room temperature.
There are other sulphonamide drugs on the market, some of which are available in combination with other drugs. One drug which is popular with some fanciers is sulphaquinoxaline (brand name Embazin®) because as well as being able to control protozoal infections it also reputedly kills mite. Quite what it’s pharmacological mode of action is in killing mite is unclear. Embazin® is not marketed in the UK and needs to be obtained from abroad.
Do the Sulpha drugs have any side effects?
There is considerable speculation among native bird breeders regarding whether or not Sulpha drugs cause infertility in birds. I’ve been using it for over 20 years. I’d honestly say my greenfinches aren’t as fertile as I’d like them to be. However, I put this down to the fact that I have decent quality show birds and as everyone knows, big birds are generally more difficult to breed due to their heavier feather among other things. Personally I don’t think sulpha drugs cause infertility. If they did we’d have no show birds left! In any case we tend to use the in very small doses and for only a part of the year.
The Sulphonamide antibiotics were used in humans for many years mainly to treat urine infections. However, they are rarely used nowadays because of their side effects. In humans they cause blood dyscrasias. That is they cause complications with blood cells which can manifest itself as anaemia.
They are also capable of crystallising out in urine (a condition known as crystaluria) and this can result in kidney damage.
The sulphonamide drugs generally have poor solubility and they don’t dissolve well in acids. As birds excrete uric acid I think there is a very real possibility of these drugs crystallising in the kidneys and as a result causing serious harm to birds particularly if high doses are used over a prolonged period of time.
Therefore the aim with these drugs should be to use as low a dose as possible for as short a time as possible.
This is another reason why I tend to use sulphadimidine rather than some of the longer acting sulphonamides.
In summary?
Newcomers to the native bird scene will often go through their first breeding season without using any sulpha drugs and end up breeding a fair number of birds which survive into adulthood. The reason this happens is that in new aviaries it takes time for the oocysts to build up and as such the first crop of youngsters can survive unscathed.. This can lead the breeder into a false sense of security. However, if drugs aren’t used in the second breeding season , the effects can be devastating with a very high rate of mortality resulting in a very demoralised breeder. Hopefully this article will give newcomers some insight into the cause of mortality in young finches and how to go about managing it.
Please do your research before trying anything different. FinchG
