
Our final consideration of chemical agents which pro=- 
duce inhibition is concerned with feed supplements. Ringnose, 
Morgan, and Lease (1941) described experiments in which crude 
cottonseed o11 added to a practical laying ration reduced the 
hatchability of eggs produced. Naber and Morgan (1957) sup- 
plemented a mash with a 5 per cent solution of aA hydrattic 
processed crude cottonseed oil. The result was a reduction in 
hatchability from 90 per cent to 6 per cent. Most of the mortal- 
ity occurred at the fourth day, the next greatest mortality at 
the eighteenth day. A disruption of the extra embryonic circu- 
latory system was noted in the early stages. In the late stages, 
hemorrhages occurred in the blood vessels. 
Another oil, an extract of the nut Stereuli foetida, 
was added as a supplement to the feed by Schneider et a (1961). 
150 mg. of oil in a gel capsule when addea as a supplement to 
the daily feed produced complete suppression of hatchability. 
Of the 23 eggs tested, 80 per cent were dead by the fifth day, 
93 per cent by the tenth day, and 100 per cent by the nineteenth 
day. Lower concentrations of the 011 caused a reduced hatch- 
ability. It was suspected that a Halphen reactive cyclopropene 
fatty acid was the hatch depressing factor as other components 
such as Stereulic acid when tested alone did not produce 
mortality. 
5. Environmental factors. 
The optimal temperature for incubation is 38.5 degrees 
C. for the chicken. Low temperatures limit development. The 
blood system fails to differentiate at 27 degrees C. (Funk and 
Biellier, 1944). At temperatures lower than 27 degrees C., the 
blastoderm fails to develop beyond the primitive streak stage 
(Harrison and Klein, 1954). Eggs subjected to 25 degrees C. 
have embryonic growth rate thirty times slower than at optimum 
temperature. Ten days was the time limit an egg could be held 
at 25 degrees C. and then put into optimum temperature (38.5 
degrees C.) and have normal development. 
High temperatures, on the other hand, increased the 
number of anomalies and the percentage mortality (Deuchar, 1952). 
Ancel (1958) demonstrated that any interruption of the normal 
incubation-development rate for two to three days resulted in an 
increase in mortality and teratogenesis. Further, the stage at 
which cooling takes place determined the numbers and kinds of 
malformation or deaths. 
Dietary deficiencies of laying hens can be responsible 
for anomalies in the developing young. Landauer (1951) and 
Cravens (1952) have summarized the role of vitamin deficiencies 
in the laying hen upon the developing embryo. Most important 
of the vitamins are biotin, nicotinamide, vitamin Bs and Folic 
acid. 
45 
