B. Sheep and cattle

1. Nature of the subfertility
following treatment with progestagen

a. Causes of failure

The prime cause of failure in the sheep, and possibly in
the cow, is failure of fertilization due to an impairment of normal
sperm transport and survival (Table 3). A secondary cause is early
embryonic mortality attributable to late fertilization or to faults
in the female tract.

i. Failure of fertilization. The only convincing evidence
comes from the sheep, primarily because of the large numbers of
animals required for the drawing of valid conclusions based on
quantal data. In cattle, Wiltbank, Shumway, Parker & Zimmerman
(1967) observed a 56 percent fertilization following oral progestagen
as compared with 86 percent in untreated animals (N.S.). However
at 34 days the percentage of surviving embryos in treated cows was
twice that in controls. Previously, the same group (Parker,
Niswender, Slyter, Wiltbank & Zimmerman, 1965) had concluded, from
equally unsatisfactory data, that embryonic mortality was responsible
for the subfertility. A similar conclusion was reached by
Jainudeen & Hafez (1966), based on observations on 13 animals, 9 used
for an estimation of fertilization and 4 for embryo survival
(G G S ET = s 0 2% P A3

Table 4 presents data for 427 ewes which were flushed for ova.
Eggs were recovered from 366, Fertilization rate fell from 86 per-
cent in control ewes to 62 percent in cyclic ewes treated with
various forms of progestagen and to 54 percent in anoestrous ewes
treated with progestagen + PMS. Lambing performance ran parallel
to these data.

ii. Early embryonic mortality. The only data for the cow

appear to be the unconvincing reports of Parker et al (1965) and
Jainudeen & Hafez (1966).

Data for the sheep appear conflicting. Foote & Waite (1965)
reported abnormal ova following progesterone treatment. On the
other hand, Moore, Quinlivan, Robinson & Smith (1967) found no
evidence of faulty ova and concluded that the observed subfertility
following progestagen treatment could be accounted for by failure of
fertilization due to a change in the environment of the tract.

More recently Quinlivan (1967) and Fletcher (1968) have found
evidence of abnormal cleavage of ova and of excessive mortality,
particularly in early lactation. Similar abnormalities have been
observed by Killeen & Moore (1968) following late fertilization of

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