PROBLEMS OF PREGNANCY
A number of factors can influence embryonic development. The conceptus
may be exposed to harmful agents during the pre-attachment, embryonic or
fetal stages of development, and vulnerability to these agents varies with
these different stages. For example, during the pre-attachment stage the
embryo is very resistant to teratogens and the zona pellucida is an efficient
barrier to many viruses. By contrast, the embryonic stage, with rapid cell
growth and differentiation, is most susceptible to teratogens. Furthermore,
each organ has a critical period of development.
FERTILISATION FAILURE AND EMBRYONIC/FETAL LOSS:
In polyoestrous species embryonic loss can be suspected when there is an
irregular extension of the interoestrus period. Furthermore, in polytocous
species, like the pig, embryos may be lost without termination of pregnancy.
Fetal loss occurs before fetal maternal recognition, and therefore does not
involve the elongation of the life of the corpus luteum, is referred to as early
embryonic death (EED). Loss after the life of the corpus luteum has been
extended is termed late embryonic death (LED). In mares, most loss occurs
between days 10 and 14 post-service; in beef cattle it is before day 15 postservice. In sheep most losses occur between days 15 and 18 post-service.
Failure of maternal recognition of pregnancy will cause early embryonic
loss, and the animal returns to oestrus at normal intervals (<25 days). Late
embryonic loss occurs after maternal recognition of pregnancy, and animals
may show their next heat 25 to 40 days after the previous heat.
Causes of embryonic/fetal loss:
1-Extreme environmental temperatures.
 Cattle that are mated in a high environmental temperature and kept
there after service exhibit a high rate of embryonic death.
 The dominance of the large preovulatory follicle is suppressed by
heat stress, and the steroidogenic capacity of theca and granulosa
cells is compromised.
 Progesterone secretion by luteal cells is lowered during the
summer in hot climates.
 Cows subjected to chronic heat stress this is also reflected in a
lower plasma progesterone concentration.
 Heat stress has also been shown to impair oocyte quality and
embryo development, and increase embryo mortality. In addition to
the immediate effects of heat stress. These include altered follicular
dynamics, suppressed production of follicular steroids and lower
quality of oocytes and developing embryos. This may explain why
poor fertility may persist for some time after periods of heat stress.
 Poor pregnancy rate is a problem when European cattle are
introduced into hot countries where they are exposed to ambient
temperatures above 30°C; it is quite likely that increased embryonic
death is part of the reason. There is little doubt that genetic factors
are involved in this as in other aspects of heat tolerance. Crosses
between indigenous heat tolerant breeds and European breeds are
more heat tolerant than the imported animals and they are more
fertile. The position is less clear with extreme cold, but there are
indications that a corresponding adverse effect occurs. The problem
could arise during unusually cold periods in temperate climates
where housing tends to provide cover rather than warmth.
2-Metritis/endometritis:
Metritis or endometritis in varying degrees of intensity is a common
condition causing infertility in cattle. Where caused by infection it can be
divided into non-specific, exemplified by Arcanobacterium pyogenes
infection, and specific, typified by Tritrichomonas fetus and Campylobacter
fetus infection. There are also a number of infections that are difficult to
classify such as bovine herpes virus-1 (BHV-1), Ureaplasma spp. and
Haemophilus somnus. Non-specific metritis is the result of either massive
infection or of the infective organisms taking advantage of a deficient
uterine defence mechanism, usually caused by damage at and after calving.
Non-specific infection can be facilitated by the synergistic action of different
organisms, for example A. pyogenes and Fusobacterium necrophorum.
Specific infections colonize the undamaged uterus. Two important specific
infective agents are C. fetus and T. fetus. Campylobacteriosis is spread
venereally and causes a mild endometritis in infected females that have not
had previous experience of the condition. It has been shown in slaughter
experiments that in infected animals fertilization rate is normal and that the
infertility is due in the main to embryonic death within three weeks of
conception. Loss of the embryo is likely to be due to interference with the
uterine environment. Another infectious agent that is introduced from the
vagina into the uterus at insemination, but not at natural service, is
Ureaplasma,
which
causes
a
purulent
metritis
and
infertility.
Haemophilus/Histophilus also causes vaginitis and reduced fertility. For
detailed discussion of a wide range of infectious agents.
Infectious conditions can cause infertility in at least four ways:
1-The febrile reaction raises the temperature of the uterus. Bluetongue is an
example of a disease that causes a high temperature resulting in loss of the
embryo at about the time of hatching from the zona pellucida, about day 10–
12 after service.
2- The organism infects the uterus and causes metritis, which presumably
interferes with embryo nutrition and may also infect the embryo. Examples
are BHV-1 virus and Chlamydiales infections. mild endometritis causes
embryonic death whereas purulent metritis
may be interference with
spermatozoa survival .
3-Infection of the conceptus can cause its death. The thought that embryo
transfer could transmit infectious diseases from the sire or the dam is
worrying. In theory, bacterial and fungal infections are less likely than viral
infections to be carried by embryos.
4-Endotoxins produced by Gram-negative infections can increase PGF2a
production and cause premature luteolysis.
3-Maternal endocrine environment:
 Low plasma concentrations of progesterone resulted in the development
of a stronger luteolytic signal. This was taken as an explanation for the
fact that cows with lower plasma concentrations of progesterone post
insemination are more prone to embryo loss than those with higher
progesterone levels.
 Interferon tau (IFN-t) . Successful maternal recognition of pregnancy
in cows depends on the presence of a sufficiently well developed
embryo producing sufficient quantities of IFN-t
4-Aged gametes:
Fresh chilled semen ages after several days and the inseminated cows have
a lower pregnancy rate almost certainly due to both reduced fertilization rate
and increased loss of embryos. There is no evidence of adverse effects from
ageing of frozen semen stored in liquid nitrogen. Fertilization of ageing eggs
following ovulation of persistent dominant follicles is also likely to result in
an increased amount of early embryonic death.
5-Local trauma:
This cause of loss affects the late embryo and early fetus. One source of
local trauma to the pregnant uterus is
 the hand of a person carrying out manual pregnancy diagnosis, or some
other palpation of the uterus . The technique, which was carried out on
two days, involved palpation of fetal fluid, identification of the amniotic
vesicle and slipping of the chorioallantoic membranes.
 with good transrectal ultrasound examination technique such losses
should now be largely preventable.
6- Genetic factors: In some cattle, in the process of cell division,
translocation of parts of certain chromosomes without loss of genetic
material has taken place, a condition that is passed on to future generations.
These individuals can be identified by cytogenetic examination of
leukocytes. When semen from bulls with a translocation is used for
insemination there is a slight increase in the incidence of return to service,
which is believed to be the result of embryonic death, presumably because of
lack or excess of some genetic material due to abnormal division at meiosis.
It is also probable that many genetically abnormal embryos are lost early in
development, with the advantage that the dam can return to normal breeding
at the earliest opportunity.
Some factors almost certainly cause an increased return to service via an
unknown mechanism. An example is the etiological relationship between
loss in body condition from calving to service and associated poor
pregnancy rate. The possible sites where inadequate nutrition may have
detrimental effects on reproductive function include:
1- The hypothalamus/pituitary gland to impair gonadotrophin release.
2 -The ovaries, possibly resulting in altered follicular growth patterns and
reduced quality of oocytes and subsequent reduced embryo survival.
3 -Inadequate uterine environment resulting in impaired embryo survival.
Genetic factors causing embryonic loss include single-gene defects,
polygenic abnormalities and chromosomal anomalies. A few single-gene
mutations are lethal and result in the death of the conceptus. If the gene is
dominant, a single copy may be sufficient to cause death, whilst in other
instances it is only the homozygous state that is lethal (e.g. the dominant
Manx gene (M) in the cat). Recessive genes only exert their effect in the
homozygous state. Not all genetic defects are lethal. Some abnormal fetuses
survive to term, which is biologically and economically wasteful. Therefore,
carrier animals should be eliminated from the breeding programme wherever
possible. Traditional methods of test mating to identify animals which are
carriers of a recessive gene (backcross to the recessive) are laborious and in
some cases not justified on welfare grounds. The mule is a cross between a
female horse and a male donkey, and the hinnies are a cross between a
female donkey and a male horse. The males of both crosses show
abnormalities of chromosome pairing at the pachytene stage of meiotic
prophase, and little or no mature spermatozoa are produced. Thus the males
are infertile. Females are also affected during the fetal development of the
germ cells, and most oogonia die as they are entering meiosis. However,
sometimes a mature follicle is present in the adult, and, rarely, confirmed
foalings have been reported in both mules and hinnies.