Animal Molecular Breeding 2016, Vol.6, No.1, 1
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monochorionic monoamniotic placentation (Spencer,
2001), they are usually not viable. A calf with
Anasarca may be prone to dystocia because the
generalized edema will cause the calf to not fit
through the pelvic canal and are often still-born. It is
thought to be inherited as an autosomal recessive trait
(Binns et al., 1972; Leipold, 1997) associated with
chromosomal polysomy resulting in still births
(Coates et al., 1988).
Though, developmental ‘disorder’ review reports are
comparatively scarce in veterinary literatures (Spiers
et al.,
2010) probably due to the multifactorial
etiologic nature of such anomalies (Lanteri et al.,
2012), comparable reports in small ruminants includes
phocomelia in sheep (Sonfada
et al.,
2010),
brachiomelia in West African Dwarf triplet goat
(Olopade
et al.,
2011), Peromelia in a Simmental calf
(Smolec
et al.,
2011) Hemimelia in goat (Mosbah
et
al.,
2012). Dysgenesis of gross tissue and organization
but with microscopic development of the body axis
has been reported in humans (Hassold, 1986) and
animals (Olopade
et al.,
2010).Overbearing influence
of teratogens at various stages of fetal development as
noted by Devanathan et al. (1990) could predispose or
contribute to the etiology of monstrous conditions
showing poorly developed but organized skeletal
system (Merz, 2005) and prominent dyschordia.
1 Literature Review
For the purpose of this review, articles were assessed
on basic searches from data base of PubMed and
BioMed Central using terms such as; congenital
anomalies,
Amelia,
developmental
errors,
Abdominopagus, Ischio-omphalopagus, (Conjoined
twins) congenital anasarca. The articles and books
consulted were from 1951 to 2015. This enquiry aims
to review literature information on the role of
environmental stress factors in formation of genetic
variants disposed to mutative thresholds and an
involvement of apoptotic cell death pathways in DNA
damage control mechanisms.
2 The Environment
Both predictable and unpredictable components of the
environment may become disruptors of development
(Noden and DeLahunta, 1985) relative to period in
gestation, forming cues for response from the
developing embryo. In this regard there is a lack of
coherent literary emphasis on possible roles of
environmental chemicals in developmental process
alterations and as well a consensus on a standard
method of evaluating the teratogenicity of any
substance
(De
Lahunta,
1983;
Saperstein,
2002).Residues of some herbicides/pesticides have
been documented to possess half-lives as long as 10
years and low dose potency to alter specific enzymatic
courses of such process (Gilbert, 2006). In
unpredictable climate situations genetic differences
can predispose susceptibility to teratogens and tilt
gene mutations towards production of more genetic
variants (Hallgrimson et al., 2002; Samuel et al.,
2013).
3 The Embryo
Gilbert, (2006) defined the embryo as an integration
of several proteins (active and inactive forms) created
through spliceocome (snRNA) mediated differential
nuclear ribonucleic acid (nRNA) splicing resulting in
various mRNA types and in a state of dynamic
synthesis and breakdown of cell metabolites (Noden
and DeLahunta, 1985). The series of activation and
inhibitions processes of proteins under instructions
from the nRNA may result in demonstrable dysgenesis
observed in a developing embryo at different stages of
gestation (Binns et al., 1972; Hassold, 1986; Szczerbal
et al., 2006).
4 Etiology
Apoptotic pathway signaling possibility
Functional derangements in bone morphogenetic
protein (BMPs) and tissue growth factors (TGF-β)
family proteins in cell divisions and apoptotic
processes leads to skeletal system deformities (Gilbert,
2006) while a gain-of-function mutation of any of
superfamily
Bcl-2
protein may inactivate
caspace-9,
caspace-3
(different
caspaces
functions in different
cell types) and
Apaf-1
(Apoptotic protein activating
factor) proteins at cellular levels in the presence of
anti-apoptotic factors to result in embryonic survival
whereas death results from mutation inactivation of
Bcl-2
protein (De Lahunta, 1983; Karen and Melisa,
2011).
5 Results
Sex-linked genes in conjoined twining’s has been
reported with about 72% of occurrences being females
(Spencer, 2001). Incidence of reproductive wastage
