Signs of "Line Breeding"?

What happens to that population, inevitably, is three things:

1) You lose fertility and fecundity (both the ability of the male and female to produce offspring and the numbers of those offspring who are born). That's very obvious in chicken strains, where low hatchability and low egg production and, in many strains, low vigor of newly hatched chicks plague many of the show-bred birds.

I wonder how the (very vigorous) flock of Heritage Barred Rocks from late 1800s - early 1900s still exists today, with no "new blood" added.​
 
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I don't know that flock, so I can only comment generally, but if you start off with a large enough unrelated group and you keep them breeding as widely as possible you can keep them going in a healthy way. If your founding group is 500 very loosely related birds, for example, and you close the population at that size, they can keep going quite well. It's when you take one pair, or one trio, or ten or twenty birds, and close your gate behind them for the next ten years - which is a practice some of the old German breeding books recommend - that you end up having to combat the major issues.

Similarly, it can be a big problem when the entire variety, even if it's thousands of birds now, was based on just one pair originally. Some of the colors in the different breeds are like that. It may LOOK like a big population, but in fact they're all just siblings, genetically.

Inbreeding depression is not something I made up to ruin anybody's day; it's a very well known phenomenon and it is what WILL happen.

It's also important to realize that a heck of a lot of the stuff we do when we "linebreed" has absolutely nothing to do with what actually works scientifically; it's an equal helping of the old European rules made up at the turn of the last century, which were completely focused on appearance and not on function or health or longevity, and the house-witch legends that get added as time goes by. When you have somebody saying that the best way to breed is to start with a pair and breed each back to its parent for a certain number of generations and then combine those "lines" at a certain point, or anyone saying that the male line should be structured differently from the female line, or someone saying that a pure strain that has never had any other blood added is more valuable than a mixed one, no matter the quality of the individual birds, that's the old Euro strategies. When you hear someone saying that the best match is to take a female back to her maternal grandfather (or anything mentioning the phase of the moon - tons of those around) or any other kind of "best" pairing (that somehow always applies regardless of the individual animals involved), or "males bring color but females bring type," those are just eye of newt or knock-on-wood practices.

There's nothing wrong with any of that, of course - nothing wrong with breeding in the new of the moon by selecting the great-grandfather of your tail-line pullets and making sure he's got a certain color in his hackles but it doesn't matter if they do, or any one of a thousand breeding strategies - and it may even work for you. Plenty of those sayings got started because they worked unexpectedly well, and the breeder thought it was because he or she followed a certain rule instead of because that particular pairing was just really good. What is not so cool is perpetuating them as best practices for others, especially if it leads to somebody being labeled as a better breeder or a worse breeder because of it.
 
if i understand it corectlyu he might be white but still could b a splash
L&Schickens :

pips&peeps :

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You got your birds from a different breeder than the OP and I.

I know Lisa, and she would want to know that there is a problem. I think she just acquired the birds last year, so this is her first breeding season with them. I am sure that she will be working on fixing it in her stock.

I have not told Lisa about my webbibg problem. I like her adn didn't want to hurt her feelings. BUT I have a true WHITE Marans cockerel and when I asked about him to her she said he was splash. I have since sent more pictures of him to her and he is no splash, he is white. He also has very little feathering on his legs. I also have a cockerel with no tail. I almost think some of my eggs were out of Marans hens, but by an Auracana roo of hers. She has not replied to my e-mails about the white roo. I guess I should tell her about the webed feet and bad toes I got, but I don't really want money back or anything like that.​
 
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I (respectfully) disagree. Fanciers from many many years ago used this method without problems.


Thought I would share some information on nutrition and breeding with you all....

By Mark Pattison, Paul McMullin, Janet M. Bradbury

Nutrition and Hatchability

The importance of the nutrition of the dam is indicated by the fact that the egg must contain all the nutrients needed by the embryo.

Development in the egg and for a week or more after hatching is, as far as fat soluble vitamins and some other factors are concerned, reliant upon supplies from the yolk. Hence, deficiency signs in newly hatched chicks (and often within the next 7 - 10 days) usually reflect a breeder feed inadequacy rather than a relationship with the starter feed.

It is difficult to affect the relative protein, fat, and carbohydrate content of an egg via the diet of the hen, but the concentration of the vitamins and trace elements in her blood and tissues directly influences that in her egg. Hence, analyses of egg yolk to determine vitamin and other deficiencies in the breeder may be the preferred and more direct route than blood or tissue sampling of the relevant hens.

Even at acceptable rates of hatchability a proportion of dead-in-shell embryos may exhibit nutritional signs, as detailed above, as a result of individual variations of metabolism.

It is of basic importance to realize that hens can produce eggs with dietary levels of vitamins that will not allow the eggs to hatch (except in the case of Vitamin A deficiency, in which the cessation of production occurs first).

Nutrient deficiencies may give rise to malformed embryos or reduction in hatchability, but it may be difficult to identify by the examination of the embryo the nutrient deficiency responsible for the poor hatchability, since the time of embryonic death will often depend on the degree of deficiency involved. Thus, it has been shown by experiment with pantothenic acid that, while in extreme deficiency hatchability may be totally suppressed, in milder deficiencies a peak of early mortality (1-4 days) occurs but later peaks change according to the amount of pantothenic acid in the diet. Most water-soluble vitamins have a similar effect.

In practice the nutrient deficiencies most likely to give rise to reduced hatchability, unless adequate breeder supplements are used, are Vitamin B2 (riboflavin), and some others of the B group (eg biotin), Vitamin E, manganese, zinc, phosphorus.

Early death may be related to:
* Biotin
* Vitamin E deficiency (vascular lesions).

Later death (ie later and around mid-term) may be related to:
* Riboflavin (anaemia, oedema, micromelia, mesonephros degeneration, and clubbed down)
*Phosphorus (no specific abnormalities)
*Zinc inadequacies (faulty trunk, limb, beak, brain and eye development - abnormalities associated with development of the skeletal mesoderm).

Death during the last few days and at hatching, may be related to deficiencies of the following:
*Vitamin B2 (clubbed down, curled toe, micromelia, degeneration of the myelin sheath of peripheral nerves, degeneration of embryonic Wolffan bodies)
*Biotin chondrodystrophy, syndactyly, characteristic skeletal deformities, ataxia, and chondrodystrophy in newly hatched chicks)
*Folic Acid (chicks may be of normal appearance but die soon after pipping; in severe depletion chondrodystrophy, syndacryly, and parrot beak)
*Vitamin B12 (malposition, myoatrophy, chondrodystrophy, oedema, hemorrhage)
*Manganese (chondrodystrophy, parrot beak, globular head, cervicothoracic oedema, retarded down feather and body growth, micromelia and ataxia in newly hatched chicks) - bone formation defects are probably associated with abnormal mucopolysaccharide in the organic matrix of bone. Vitamin B12 and manganese deficiencies may be associated with extreme reduction in hatchability.

Nutritional deficiencies may be direct (ie due to inadequate supply in the feed). This can be the result of nutrients not being added, badly mixed or badly stored feed. Alternatively, dilution by post-manufacture addition of cereals to formulated rations can be implied.

Indirect deficiencies can be caused by antagonists such as mycotoxins, inadequate absorption (eg parasitism or disease), underconsumption (eg overcrowding), or the results of an inappropriate drug inclusion.

While "nutritional deficiency lesions" are commonly seen in dead-in-shell embryos, incorrect feed manufacture is now seldom incriminated and definitive deficiencies of single nutrients are rare. Instead, a miscellany of lesions suggestive of a number of nutrient shortfalls is the commoner finding. It has also been reported that syndromes, which seem to mimic the signs of certain deficiencies, may be evident despite adequate supplies of that nutrient in the feed (eg a clubbed down syndrome has been seen in flocks well supplied with Vitamin B2).

Definitions for some that may not know:

chondrodystrophy: A disturbance that affects the development of the cartilage of the long bones and that especially involves the region of the epiphysial plates, resulting in arrested growth of the long bones.

myoatrophy: atrophy or wasting away of the muscles.

syndactyly: A condition in which two or more of the toes are joined (fused) together.

oedema: The presence of an excessive amount of fluid in or around cells, tissues or serous (resembling, producing, or containing serum) cavities of the body.

micromelia: abnormally small and imperfectly developed extremities.

ataxia: shaky and unsteady movements or loss of the ability to coordinate muscular movement.
 
thanks for some interesting reading here!

i am just curious what might be the best way to add some of those 'missing' vitamins and minerals if you are noticing any of those deformities or conditions happening in chicks! especially the biotin!
 
Chickie'sMoma :

thanks for some interesting reading here!

i am just curious what might be the best way to add some of those 'missing' vitamins and minerals if you are noticing any of those deformities or conditions happening in chicks! especially the biotin!

Biotin is a B vitamin. It is known as vitamin B7, or occasionally as vitamin H.
There are many common foods that are rich in biotin, including egg yolks, milk, poultry, fish, broccoli, spinach, and cauliflower.

There are poultry vitamins and minerals available to add to their water. I use human vitamins, too.​
 
If you're interested in reading more about inbreeding depression in chickens, here are some articles:

Inbreeding and fertility in Leghorns: http://www.ncbi.nlm.nih.gov/pubmed/10465386
Another
leghorn population, this one closed after only two roosters and five hens were brought in (this would be similar to what a lot of show lines are structured like): http://www.ncbi.nlm.nih.gov/pubmed/3413010

One
of the reasons it's so important to look at the statistics very objectively is that human nature is to justify the means according to the desirable ends. If you're consistently winning, you define that as success, even if you're only getting two eggs a week. If you're getting super dark eggs, that's a success, even if your hatchability is at 60%. And by saying that I'm not singling out any particular breeder - I mean that's what we ALL do. So since the exhibition poultry fancy tends to define a successful "old line" as one being very consistent and extreme in type, we tend to look at those old lines and say that the breeder was doing great work. But there could still be a huge amount of inbreeding depression going on, with the attendant lower fertility and hatchability.
 
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Thank you for the articles. I guess we can find articles to sway opinions, either way.

Part of your article said .....

There was a significant effect of inbreeding on reproduction traits in line EW attributable to the inbreeding of the hen, embryo and mate. No such effect was observed in the other lines. 5. In all lines inbreeding tended to reduce egg number and delay sexual maturity. In general, all lines reacted differently to inbreeding.
 
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EW was the egg weight line. That particular line was pushing for extra heavy eggs and doing so by hyper-inbreeding the chickens. It had very high death rates before hatching. The "no such effect" refers only to the hatching death rates - the other lines didn't show that particular effect. But they all had reduced egg numbers and later maturity.

Here are more, if you're interested:

Inbreeding effects: http://www.ncbi.nlm.nih.gov/pubmed/6634593 (they use the term "selected" to mean "culled to emphasize that trait")
How to save endangered chicken breeds (this is a VERY good one - note all the references on the established dangers of inbreeding and the emphasis on not inbreeding the remaining members of the breeds): http://www.kongressband.de/wcgalp2010/assets/pdf/0422.pdf
Inbreeding
over a long period of time (40 years) of a laying strain: http://www.ncbi.nlm.nih.gov/pubmed/1893259

The
dangers of inbreeding are population genetics 101. It's not like I went and combed through a million articles on how great inbreeding is to find a few on it being dangerous - the literature is pretty much unanimous that it's as bad an idea in chickens as it is in any other organism, if what you care about is the long-term fitness of the entire population. Inbreeding works miracles to set an extremely consistent body type, so if that's the goal then inbreeding will get you there faster than anything else, and will keep you there. But you pay the price in terms of the health (and ability to survive long-term) of the overall population. To strain a metaphor, inbred populations are hothouse flowers - showy, bright, unusual, consistent, and difficult to maintain. Diverse populations are cockroaches - able to weather any challenge, likely to be around forever, not terribly fancy or consistent, but fertile as heck.

The challenge for the breeder is to figure out what their goals and their definition of success is, and try to do as much good as possible, create as productive an animal as possible (whatever your definition of productive is), while doing as little harm as possible. For some breeders the only thing they are willing to accept is consistent results on champion row. In that case they may choose to inbreed like crazy. Others may want maximum lifespan, maximum hatchability, maximum parasite resistance, and not really care whether it looks more like a cochin or like a rock. They are going to be the ones inbreeding the very least. The key for all of us is to not define breeder A as the "good" one and breeder B as the "bad" one. The chickens themselves probably like breeder B best! Good and bad breeding is not about the fact that he can get a perfect necklet on a barred breed and she can't. Good and bad breeding is about treating animals well while meeting your goals, understanding and being able to articulate the tradeoffs and benefits of each decision, and supporting those who come after you. You can be a brilliant breeder of barnyard mutts or a terrible breeder of champions, and certainly the other way around as well.

But - whatever anyone decides - they should know that actions have prices, and inbreeding always and consistently does.
 

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