ARCHIVE FILE
This article was published in 1961
See the original document
INSTITUTE OF INSPECTORS OF STOCK OF N.S.W. YEAR BOOK.
Post-Caponisation Leg Weakness
M. LINDTNER, D.V.Sc., Veterinary Research Officer, Veterinary Research Station, Glenfield
Leg weakness on a large scale involving chemically caponised birds was recently observed in the broiler industry. This condition appears approximately 10-14 days after the inoculation of hormonal preparations. The birds tend to sit down at every opportunity and refuse to move unless disturbed.
Clinical observation reveals an apparent leg weakness in the joints, although the symptoms simulate an early neuro-lymphomatosis as far as jerky gait and trembling of the legs on standing is concerned. No alterations of the joints are seen or palpated, and the only significant finding at post-mortem examination is a spontaneous detachment of the cartilages from the epiphyses which occurs when the joints are dislocated. That this condition is due to caponisation is evident from the history and from the interpretation of hormonal action.
Preparations used for caponisation belong to the Estrin group of ovarian hormones which are responsible for development of secondary female characters in caponised birds. When an excessive level of these hormones is introduced into the body a severe effect is produced upon all other endocrine glands. The most significant response in this case is the cessation of secretion of the growth hormone by the hypophysis. This results in the suspension of chondrioblast (sic) formation, hence lack of multiplication of maturing cartilage cells leading to thinning of the cartilage layers. Since these cells are important producers of the phosphatase enzyme which plays an important part in the calcification process, the weakness of cartilage is understood. Parathyroids, too, seem to be depressed leading to alteration of calcium-phosphorus metabolism and consequently reducing the calcification process.
Since Vit. D appears to control the condition it could be suspected that perhaps Vit. D deficiency could be the cause of the whole problem. However, in Vit. D deficiency the cartilage is thickened, not thinned as in this case, the thickening being the result of compensatory proliferation of cartilage due to calcium-phosphorus disbalance. Vit. D has to some degree a similar action to parathyroid hormone so it could be supposed that treatment with high doses of this vitamin is itself a compensatory action for parathyroid deficiency.
The mechanism of post caponisation leg weakness is, without a doubt, much more involved and complex than discussed here, however, for practical purposes it would suffice to recognise that the condition could be corrected by Vitamin D treatment.
The suggestion would be to keep the birds on Vit. D fortified diet during the 14 days period after caponisation.