top of page
bc header

Journal Library

The Border Canary – Breeding itself into extinction?


A dramatic and pessimistic statement, perhaps, but away from the show bench, the problem of low fertility and failure to get those young which are hatched to weaning would seem to be the most talked about issue within the Convention. In this short article I hope to discuss some of the problem surrounding this situation, suggest some of the causes and offer some insight perhaps into what I believe can be done to reduce the incidence. Regrettably, what I am not able to do is to give you a solution to preventing infertility within your stud.


Let us look at the possibilities in order, starting with clear eggs. Ok, it’s not hard to understand that if the timing of mating, or to be more precise, the timing of pairing up, is not right when one or other of the birds is not in full breeding mode, then mating will not take place and fertilization will not take place. Clear eggs will be the result. This is not the whole story of course, because mating can take place and fertilization may still not occur, or fertilization may take place (and this can be shown by microscopic examination of the membrane surrounding the egg yolk and the holes left by penetrating sperm observed and counted), but no embryo develops. What is happening here? Perhaps the male bird has a low sperm count, or poor quality semen, or perhaps there is a genetic incompatibility between the birds. It is possible that the hen is at fault and that embryonic development does not proceed due to problems on her side. Once again these may be genetic, or nutritional, or disease based, or possibly due to ingested toxins. Whatever the reasons, one would not expect any of these situations to affect more than a limited number of birds within a handful of studs.


Next there is dead-in-shell (DIS). Firstly, what do we mean by DIS? The accepted definition is that of late embryonic death, by which we mean death of an embryo or chick within a few days, perhaps 48hours, of hatching. Death of a developing embryo mid-term is uncommon.


So what are the levels of DIS that are being experienced? Reports that I get are that it is reaching up to 50% in some studs (but see my later comments). Let me try and put this problem into perspective. Infertility in all its forms is a natural occurrence in all living things. In wild birds an infertility level, that is, both clear eggs and those that are fertile failing to hatch, of around 12% is suggested as normal. Whilst of low levels, DIS does occur in wild birds. The other extreme is the level sometimes experienced in commercial poultry hatcheries which can suffer dead-in-shell losses of almost epidemic proportions. It is because of the high economic impact that such situations have on the poultry industry and therefore the necessity to discover a reason, that we have information as to some of the causes of DIS.


So what are the possible causes of DIS? Some we can mention and then dismiss as the small ‘sporadic’ cases which occasionally affect wild and captive birds and would constitute the ‘normal’ level of DIS. These could be mal-presentations of the embryo within the egg, such as a head under a wing for example, preventing the chick from successfully breaking into the airspace and effectively drowning, (uncommon in canaries I think, but then who looks?). Accidental (or occasional deliberate) trauma to the egg can occur allowing excessive water-loss and the chick to dehydrate. Abnormal development, due to genetic incompatibility, does happen. Some of these lethal gene combinations which lead to metabolic malfunctions or developmental abnormalities require embryonic development to proceed to certain stage before they manifest themselves. Some may cause DIS or lead to early chick death post hatch (corona x corona parings in Glosters for example). These could all be considered as ‘normal’ and presumably accepted by the fancier as ‘mother nature’ at work.


Then there are those causes which one feels could result in larger than unexpected levels of DIS, and certainly they get a lot of ‘air play’. Firstly, abnormal incubation. Too hot - too cold; too wet-too dry. This is the area where most of the ‘excuses’ for DIS within the Fancy come from. (Far better to blame the weather and the birds than to level criticism at ones own failings!) Are these fluctuating environmental conditions really to blame?  For incubation and successful hatching to occur it is essential that there is controlled water-loss from the egg. This is achieved through water vapour loss through the pores of the eggshell. The nature of the shell permeability and the humidity of the nest-site environment are the means by which this is controlled. The relative humidity surrounding eggs during natural incubation is in the range of 30–50%. Humidity in the nest during natural incubation is higher than that which results if ambient air was heated to incubation temperature, indicating that the sitting bird conserves humidity around the eggs; that is, the hen bird regulates the humidity to control the rate of water-loss from the eggs. Only in extreme cases is the bird-room temperature likely to have any significant influence on the level of dead in shell.


What about chilling? Chilling following nest desertion will obviously stop development and result in embryonic death but this is crucially time dependent. Remember we are talking about the last couple of days of incubation for it to result in classical DIS. And, of course, all the chicks in the nest will die not a selected few. It is not impossible for a hen to hatch chicks out of synch (if allowed to sit-as-she-lays) and this may contribute to the last laid eggs struggling to hatch. More likely is that they will hatch but be ignored or squashed. In my opinion bird-room conditions have very little impact on the level of dead in shell. The bird-room environment is not the environment of the nest. Hatching eggs in an incubator however, is a completely different scenario but not one which need concern canary breeders.


This leaves us with the chick dying from organ or probably more technically correct systems failure. What I mean by this is that at the point at which the chick is getting ready to hatch, the biological systems which are required to ensure viability, the respiratory system, nervous system, circulatory system etc. are compromised; stop functioning and the chick dies.

The causes behind this problem are easily divided (although not quite so easily explained) into two types: infectious and non-infectious. Infectious agents are in practise bacteria, fungi and viruses. To gain entry, infectious agents must either penetrate the egg through the minute pores in the shell or be placed in the egg prior to the secretion of the shell. To do this the agents must be present within the oviduct. Infectious agents, viruses such as avian influenza and Newcastle disease, and bacteria such as Salmonella and E.coli can cause huge losses in poultry hatcheries but are probably of little significance in being the primary cause of DIS in canaries. However, circovirus amongst others may be.

Perhaps some of you have had DIS embryos examined and the pathology results have shown that bacteria were isolated; this is by no means proof that the embryos died from being infected. (See later.)

Non-infectious causes are probably the causes which result in the majority of DIS ‘outbreaks’. All products; nutritional, fluid, hormonal, immunological and genetic, required for optimal growth of the embryo must be in place within the substance of the egg prior to the formation of the shell. Nutritional deficiencies or excesses in the hen’s diet are reflected in the composition of the egg. Whilst all nutritional aspects of the composition of the egg are important, I would like to highlight a group of compounds called antioxidants, which have been widely studied in poultry and to some degree in parrots in relation to hatchability. To understand the importance of these compounds we need to first understand the physiological changes that are taking place in the body of the embryo at the point at which it dies. DIS takes place at the time the embryo switches over from a non-breathing metabolism to breathing oxygen. The embryo breaks into the airspace and effectively in an instant, completely changes the way in which its body functions. 

Huge amounts of energy are required to prepare for hatching and the fuel that is provided within the egg is mainly fats stored in the yolk. Converting these fats to energy using the newly acquired oxygen from the air produces products which are potentially toxic for the embryo’s cells. The antioxidants stored within the egg counteract these toxins and prevent cellular death. Insufficient of these antioxidants leads to the chick effectively ‘pickling’ itself and dying. The antioxidants with which you will be most familiar are the vitamins E, A, C and the range of products called carotenoids (also responsible for imparting the yellow colour to the egg yolk and feathers). Inadequate dietary levels lead to low levels within the egg and can predispose to DIS.

A simple solution, therefore, would seem to be to ensure that breeding hens had high levels of all these antioxidants in their diet and (presumably) partition them in to the egg in adequate amounts. Beware; dietary excesses can be just as much a problem as deficiencies. The egg is a very convenient ‘toxic dump’. Dietary poisons in the form of excess vitamins (A and D in particular) interfere with embryonic cellular development and cause death! Antibiotic and anti-parasitic drug residues are treated similarly, the hen ‘cleansing’ herself and dumping undesirable material into the egg.

What a lack of antioxidants does and so do external toxins, is compromise the immune system of the developing embryo. This predisposes the embryo to attack by opportunistic bacteria, which in a healthy embryo would have been killed off. Post-mortem may turn up these bacteria, but they are not necessarily the primary cause of the DIS. The longer the embryo has been dead before the egg is opened and DIS is established, the more likely the chance of recovering bacteria from that chick. This will often be the case if the embryo appears ‘wet’ when examined. This is the start of autolysis, that is, tissue break down.

So, what’s to do? We would all accept I am sure, a certain level of DIS as natural. Ensure that adequate but not excessive levels of antioxidants in the pre-breeding diet. Avoid toxins such as antibiotics. Investigate abnormal levels (see below) of DIS. This may mean spending some money (redirect some of the money which you all spend/waste on, in my opinion, worthless quackery). But whatever you do, don’t blame the birds. They are doing the best they can with what you give them under the conditions you keep them in.

A personal point of view.


When it comes to the management and breeding of any animal or bird there are those who are better at it than others. This is where the accolade of being a great ‘stocks man’ is born. There are possibly those currently breeding Borders who are saying, “Problem- what problem?” There will also be those who are either giving up the hobby or moving over to ‘easier’ breeds of canaries because of their frustration at not been able to breed their birds. The problems outlined above are general in their approach. They apply equally to all bird types, to Fifes and Glosters just as much as Borders, but to my knowledge these branches of the Fancy do not (yet) seem to be having a big problem.


Is the Border a special case? Well the fancy thinks it has a fertility problem – from an excessive number of clear eggs through to DIS. (Chick deaths are another issue). Some would argue it ‘knows’ it has a problem! Everyone would seem to have a point of view to offer or a sob story to tell and yet as far as I am aware, no-one has been motivated enough to investigate the issue on a collective level. The ‘problem’, if indeed one exists, is based on anecdotal, as opposed to


If you, the breeders, choose to do nothing, then you must accept the situation. If you are not prepared to accept it then there is a need to be proactive. The Convention (and the Fancy in general) will be best served, I believe, if this is done collectively.

I will leave you with a final comment; the level of DIS in the Borders that I bred in the late nineties and early noughties was very low, under 5%. None of these birds were fit for the show-bench. Perhaps this is the crux of the problem – or there again, perhaps not.


Brian Stockdale BVM&S MRCVS



The Author.


Brian Stockdale is a Veterinary Surgeon based in the Midlands and a visiting lecturer at Nottingham Veterinary School. He has kept and bred many species of birds including Borders. He has given papers on various aspects of avian biology and disease at Conferences in Europe and has contributed chapters to books on avian nutrition and management and regularly writes in Cage and Aviary Birds.

The following item is one which appeared in "The Border Conventional Journal"




To Subscribe To The Journal See Journal Subscriptions

bottom of page