In the interests of full record-keeping... And because I don't want to pretend to myself either...
Something was badly wrong with the chick, but even after an amateur post mortem I still can't be sure what it was. It didn't appear to be coccidiosis as there were no signs of pinpoint haemorrhage along the intestine; that was a big surprise. However the intestines seemed to contain food at the same degree of digestion pretty much all the way along (chick starter — a uniform pasty grey). He was also remarkably thin.
His gizzard and proventriculus were misshapen, and both were lax and floppy, especially at the junction between the two. His liver was very faintly marbled rather than uniform in colour, though this was subtle. His kidneys looked perfectly healthy and there were no obvious signs of infection; his lungs looked quite normal. However his heart looked distinctly pale and seemed to contain little actual muscle, and there seemed to be some watery fluid around the heart.
All in all, he was a very sick bird.
It's impossible for me to know what happened, but I did find something that mentioned most of the above symptoms: www.wattnet.com/Archives/Docs/701pi36.pdf?CFID=25710...
The article mentions that gizzard and proventriculus malformations and floppiness can relate (among other environmental and contagious conditions) to the breakdown of amino acids in meat meal or other animal protein meals, which produces toxins. These toxins in themselves apparently harm the digestive process, and may have some relationship to the proliferation of enteritic viruses.
'High levels of DBAs [Dietary Biogenic Amines] like histamine, 3HT, 5HT, histidine, dopamine, gizzerosine and serotonine, can be found in dietary constituents such as tankage fish meal, corn screening, soyabean meal, vitamin premixes, fats, poultry meal, meat and bone meal. The biogenic amines are [...] considered toxic to animals.'
The condition has apparently also been known as 'malabsorption syndrome, infectious proventriculitis, infectious runting syndrome, pale bird syndrome and stunting syndrome'.
Looking up malabsorption syndrome elsewhere, I get:
It seems that malabsorption syndrome involves the full gamut of causes: viral; genetic; and management. Is that a way of saying nobody knows? Even so, on the management side I feel quite guilty. Once again I find myself abhorring meat meal and wishing there was something better, even as I can't know if this was the main problem.
So what should I do? The 30 broiler chicks are peeping happily in the shed and eating ordinary medicated chick starter. The plan was to gradually introduce sprouts and cracked grains (with protein) over the following week, and do everything the same as for my light sussex. But with one bird out of twelve showing a serious condition that may be due to contagion or may be due to management, I have to question which way to go. And to complicate things further, it may be that the diet was perfectly fine and the birds were genetically predisposed. Remember, only half the eggs hatched, and many had weak legs and signs of fluff/feather abnormalities right from day of hatch.
Perhaps it's best to remind myself why I chose to make my own mixes: commercial foods contain synthetic vitamins and some of these appear, to my reading, to have negative health consequences for people. Even organic feeds may at present contain artificial methionine. I do still want to limit the use of synthetic feeds if I can.
So here's a plan, with minor changes to what I've done so far:
Chick starter for 1 week, pure (with some kefir for probiotics).
Chick starter + cracked grains, sprouts, yeast, lucerne, chopped greens, kefir whey and fresh protein (e.g. mincemeat) for 1 week (half-half) but no meat meal.
Whole sprout/yeast/lucerne/greens/protein diet from week 2 onward, and again no meat meal.
This will be expensive as I have to buy mincemeat from a butcher (typically, $7 per kg). It's very hard to get fresh unpreserved mince more cheaply than that. But I have to get the protein percentages right.
The benefit of not changing absolutely everything this time around (for instance not throwing in the towel and going back to commercial feeds fully) is that I can gain a better idea whether meat meal is a possible culprit. I can't be 100% sure because the current chicks have different genetic makeup to the light sussex, but I can probably settle my own mind to a large degree. At least, if I notice any chicks that are weaker, paler or unthrifty, I'll have a fair idea it isn't the meat meal. And then it may be time to reassess the whole diet.
Meanwhile, plan B (which isn't an alternative but an adjunct): find a cheaper, better, safer protein source for long term home chick raising. Well, that's already been on the back burner. But maybe it's time to kick along a little...