Hostname: page-component-7479d7b7d-fwgfc Total loading time: 0 Render date: 2024-07-12T07:30:23.987Z Has data issue: false hasContentIssue false
  • English
  • Français

Infertility and neonatal mortality in the sow II. Experimental observations on sterility

Published online by Cambridge University Press:  27 March 2009

R. W. Pomeroy
R. W. Pomeroy
Affiliation:
School of Agriculture, University of Cambridge and AgriculturalResearch Council
Get access Rights & Permissions [Opens in a new window]

Extract

1. Sixty-two commercial sows with a history of sterility were served either less than 7 days or between 12 and 21 days before slaughter and the ovaries examined at autopsy. Thirty-eight sows had apparently normal ovaries and twenty-four abnormal ovaries. Of the sows with normal ovaries, seven out of ten served within 7 days of slaughter were pregnant, but only four out of twenty-two served between 12 and 21 days were pregnant. Two sows were not served because they did not come into oestrus. Of the sows with abnormal ovaries only one out of nineteen which had been served was pregnant. Thus in sows with apparently normal ovaries it is suggested that the main cause of sterility is embryonic mortality, whereas in sows with abnormal ovaries the main cause is lack of fertilization.

2. Sterility associated with cystic ovaries was studied in inbred sows and the oestrous cycle in such sows was found to be irregular, usually with an abnormally long dioestrous interval. There were no cases of nymphomania associated with cystic ovaries.

3. The ovaries of ten sterile sows were examined by successive observational laparotomies. In some cases cysts were present together with apparently normal ovulations and it is suggested that the cysts developed from follicles which failed to rupture. In other cases cyclical growth and regression of cysts occurs without ovulations, whereas in others where the cysts are very large (30-50 cm. in diameter) the cysts may be permanent structures. Sows with large multiple cysts frequently show no signs of oestrus and it seems likely that the breakdown in the ovulation process starts with irregular ovulations and tends to proceed towards the development of these large multiple cysts.

4. Intravenous injections of Prolan (l.h.) had no effect on the ovarian cysts. Implantation of stilboestrol tablets reduced the cystic condition but the treated sows did not come into oestrus although corpora lutea were found in the ovaries at autopsy. Intramuscular injections of stilboestrol also reduced the cystic condition and in one case a sow actually became pregnant.

5. No response was obtained to p.m.s. injections in sows in which the ovaries had reverted to an infantile condition.

6. Cystic ovaries were produced by subcutaneous injections of progesterone and these closely resembled those found in sterile sows. The ovaries of gilts with progesterone-induced cysts tended to revert to normal after the cessation of the injections but the fertility of the gilts was low due to failure of fertilization.

7. Preliminary attempts to graft ovaries met with little success probably due to immunological reaction against and imperfect vascularization of the grafts. Further attempts were postponed pending the results of trials with sheep using a different grafting technique.

8. Evidence as to the effect of fatness in causing sterility in gilts was obtained from the records of the National Pig Breeders' Association. Two overfat experimental gilts which did not come into oestrus were found to have apparently normal ovaries at autopsy and a third came into oestrus and was mated after a period on a submaintenancediet, but though it ovulated normally the ova were unfertilized.

Type
Research Article
Information
The Journal of Agricultural Science , Volume 54 , Issue 1 , February 1960 , pp. 18 - 30
Copyright
Copyright © Cambridge University Press 1960

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

REFERENCES

Baker, L. N., Ulberg, L. C., Grummer, R. H. & Casida, L. E. (1954). J. Anim. Sci. 13, 648.CrossRefGoogle Scholar
Brambell, F. W. R. & Mills, I. H. (1947). J. Exp. Biol. 24, 192.CrossRefGoogle Scholar
Hammond, J. (1955). Brit. Med. Bull. 11, 165.CrossRefGoogle Scholar
Harris, M. & Eakin, R. M. (1949). J. Exp. Zool. 112, 131.CrossRefGoogle Scholar
Heuser, C. H. & Streeter, G. L. (1929). Contr. Embryol. Carneg. Inst. 109, 20.Google Scholar
Laing, J. A. (1949). J. Comp. Path. 59, 97.CrossRefGoogle Scholar
Marshall, F. H. A. & Jolly, W. A. (1907). Trans. Roy. Soc. Edinb. 45, 83.CrossRefGoogle Scholar
Marshall, F. H. A. & Peel, W. R. (1910). J. Agric. Sci. 3, 383.CrossRefGoogle Scholar
Nalbandov, A. V. (1952). Fertil. Sterility, 3, 100.CrossRefGoogle ScholarPubMed
Parkes, A. S. & Smith, A. U. (1953). Proc. Roy. Soc. B, 140, 455.Google Scholar
Perry, J. S. & Pomeroy, R. W. (1956). J. Agric. Sci. 47, 238.CrossRefGoogle Scholar
Pomeroy, R. W. (1960). J. Agric. Sci. 54, 1.CrossRefGoogle Scholar
Robinson, G. E. Jnr. & Nalbandov, A. V. (1951). J. Anim. Sci. 10, 469.CrossRefGoogle Scholar
Tanabe, T. Y. & Casida, L. E. (1949). J. Dairy Sci. 32, 237.CrossRefGoogle Scholar
Ulberg, L. C., Grummer, R. H. & Casida, L. E. (1951). J. Anim. Sci. 10, 665.CrossRefGoogle Scholar
Warwick, A. C., Grummer, R. H. & Casida, L. E. (1949). J. Anim. Sci. 8, 569.CrossRefGoogle Scholar
Wilson, R. F., Nalbandov, A. V. & Krider, J. L. (1949). J. Anim. Sci. 8, 559.CrossRefGoogle Scholar