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A Review of Some Developmental Anomalies in Domestic Species in North Central Region of Nigeria-Contributions of Normadism and Climate Changes in Embryo-toxicicitity  

Michael Samuel1 , Wanmi N.1 , Usende L.2 , Ozegbe P.C.2
1 Departments of Veterinary Anatomy, College of Veterinary Medicine, Federal University of Agriculture Makurdi, Benue state, Nigeria
2 Veterinary Anatomy, Faculty of Veterinary Medicine, University of Ibadan, Nigeria
Author    Correspondence author
Animal Molecular Breeding, 2016, Vol. 6, No. 1   doi: 10.5376/amb.2016.06.0001
Received: 12 Oct., 2015    Accepted: 27 Nov., 2015    Published: 01 Jan., 2016
© 2016 BioPublisher Publishing Platform
This is an open access article published under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Preferred citation for this article:

Samuel O.M., Wanmi N., Usende L., and Ozegbe P.C., 2016, A Review of Some Developmental Anomalies in Domestic Species in North Central Region of Nigeria-Contributions of Normadism and Climate Changes in Embryo-toxicicitity, Animal Molecular Breeding, 6(01): 1-7 (doi: 10.5376/mpb.2016.06.0001)

Abstract
This review of literatures on some developmental anomalies in domestic animals reported in the middle belt region of Nigeria seeks to evaluate the contributions of embryo-toxic contributions of environmental factors in syndromic monsters among domestic species. Three cases were considered including a rare case of Amelia brachiomelia monobrachium in a doe-goat, congenital bovine fetal Anasarca (calf) and Dicephalic, Dithoracic, Abdominopagus, Ischio-omphalopagus Tetrabrachius Tetrascelus (lamb) in Benue state. This survey evaluated each dysmorphologies in an embryologic perspective in an effort to reveal unexplored areas which may illuminate on possible pathogenetic pathways and may substrate in ameliorating the frequency of occurrence of developmental errors. The investigation concludes an enhanced possibility of genetic disposition to mutative threshold by selection through methylation repression of gene transcription in early embryo stage of affected species to result in DNA character damage and that more investigation in this regards is necessary. By season of occurrence, unpredictable climate situations, sustained high temperature deviations and phytoteratogens in alternative diets during extended dry periods may aggravate the pathogenesis of hereditary dysgenesis.                                                  
Keywords
Goats; Congenital abnormalities; Amelia; Brachiomelia monobrachium; Congenital bovine fetal Anasarca; Conjoined twins; Ecotoxicology; Climate phenomenon

Introduction

Genetic constitution in man and animals forms the basis of hereditary disorders (Binanti and Riccaboni, 2011; Olopade et al., 2011) while character damages in affected genomic architecture forms a substrate for observed phenotypic expressions (Nodem and de Lahunta, 1985; Gilbert, 2006) in a morphologically abnormal individual. Dysmorphologies; caused by genetic events such as gene mutations, chromosomal aneuploidies and translocations are called malformations (Szczerbal et al., 2006). These malformations often appear as syndromesinvolving severally evolved embryonic systems in which abnormalities are observed concurrently (Bowers, 2011).
 
Hereditary defects of limbs probably arise from aplasia of limb buds from about the fourth to eighth week of gestation (Corbera, 2002). The congenital absence of one or more limbs in tetrapods is a rare anomaly known as abrachia, and used to designate agenesis of either or both thoracic limbs, whereas apodia refers to agenesis of both pelvic limbs. A missing limb is defined as monobrachia or monopodia (Leipold et al., 1983; Leipold, 1997; Szczerbal et al., 2006) initiated at the instance of retinoic acid-activated Hox genes (Newth, 1978; Gilbert, 2006) by Tbx5 and Tbx4 proteins expression in limb fields (fore and hind limbs respectively) in an early-stage embryo. Synthesis may be attenuated by certain chemical compounds (De Lahunta, 1983; Stratford et al., 1996) occurring. Conjoined twinning is often associated with pathogenetic discrepancies involving two more or less developed organisms as a consequence of incomplete cleavage at primitive streak stage (Noden and De Lahunta, 1985) or a secondary union of two separate monozygotic embryonic discs in one of only eight specific sites dorsally or ventrally joined to the neural tube (Kaufman, 2004) at 13-14days after fertilization (Kaufman, 2004) and exclusively associated with 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 attributable to anomalous fetuses in farm animals forms 30% of losses (Samuel et al., 2013)
 
Olsen and Miller (1958); Bancrroft and Gamble (2007) suggested that bovine congenital fetal anasarca could arise from chromosomal aneuploidy characterized by late gestation abortions (Coates et al., 1988; Tickle, 2003).  As a component of hydrops fetalis (Machado et al., 2002), and a heritable condition common in Ayrshire and Swedish lowland breeds of cattle but has been reported in Humans (Karen and Melisa, 2011).
 
6 Discussions
Conjoined twinning; Based on body region of connection are classified as craniopagus, cephalopagus, thoracopagus, omphalopagus, pyopagus, ischiopagus and rachipagus (Duhamel, 1966) had been reported to be an outcome of fission-fusion theory  with a higher probability of fission failure (Spiers et al., 2014; Lanteri et al., 2012).
 
About 2% of human infants are born with a readily observable anatomical abnormality (Bowers, 2011) including missing limbs and occurs as disruptions to genetic instructions (Devanathan et al., 1990; Samuel et al., 2015). Co-option (recruitment) of existing genes and pathways for new functions is a fundamental mechanism for creating new phenotypes (Binanti and Riccaboni, 2011), Duplication and divergence at gene level may allow these to assume divergent functions (Szczerbal et al, 2006). Stability defects in the expressivity of genes (Szczerbal et al, 2006) responsible for the development of limbs could be incriminated in the pathogenesis of this type of phocomelia observed (Smolec et al., 2011; Olopade et al., 2011). Findings on the present cases are consistent with previous reports in ewes, buffaloes and Does (Milton et al., 1989, Devanathan et al., 1990; Laiju et al., 2012).
 
Some birth defects are produced by mutant genes or chromosomes, while others by toxic, viral, environmental or a combination of these factors that impede development (Kaufman, 2004; Devanathan et al., 1990). Neural crest cells are precursors of pigment cells (Saperstein, 2002) which seem deficient in the areas around the skin covering the undeveloped limb suggests the likelihood of commencement of such impairments at gastrulation and organization stage in the embryo (Bowers, 2011).
 
Exogenous disruptors including chemicals, viruses, radiations hyperthermia and toxic plants may act as substrate in allometric growth impairments of body parts in in-born developmental errors (Newth, 1978; Conlon and Raff, 1999). Phocomelia has prior been reported to be associated with ingestion of pthalidomides in the first trimester of gestation (Gilbert, 2006). Phytoteratogens, in a similar manner by placental crossing causes deleterious effects through embryonic demise and could be species specific (Knight and Walter, 2012) but milder in late embryonic life. Veratrum californicum (Jervine, cyclospermine, swainsonine and anagyrine an alkaloid of quinolizidine) inhibit cholesterol synthesis and as well incapacitates Sonic hedgehog functionality leading to cyclopia and arthrogryposis in lambs and goats (Binns et al., 1972; Hiraga and Dennis, 1993). Inorganic crop fetilizers applied to forages fed to pregnant animals may be incriminated. Observed developmental errors demonstrated by phenotypic incompetence occasioned by anatomic deformities of tissues/organs may compromise viability (Dyce et al., 2002). Two separate reports, Czarnecki (1976) globossus amorphous fetus in cattle, Nottidge et al.,(2007) cranio-thoracopagus (Monocephalus thoracopagus tetrabrachius) in dogs, inherited abnormalities has been attributed to environmental factors such as extreme temperatures, consumption of toxic substances such as herbicides at onset of planting/breeding seasons and long period of drought.
 
Precautionary mechanisms to serve as preventive measures in the etiology of such mutilating conditions should be directed towards genetic engineering and safe farm practice with prompt report of occurrences for investigation of probable etiology, migrations of herdsmen with breeding stocks should be discouraged/provided transit route camps with adequate feed supplies. Furthermore, in abnormal weather events with sustained daily mean temperature departures of 1.9-2.9°C (NIMET, 2010) for over two months and prolonged dry period supplemental feeding of pregnant does may discourage the use of alternative diets through which unwholesome plants are browsed. Feeding of stored feed rations often moldy should be discouraged in breeding seasons despite preponderance of low grade dietary alternatives (Terje et el., 1996) in inter-tropical discontinuities and resultant fluctuations dry spell periods (NIMET, 2010).
 
Breeding from such dams should be discouraged while adequate record keeping for epidemiological surveys will militate against future occurrences (Nottidge et al., 2007).
 
Research gaps observed in the developmental progression of monstrosities may be bridged through Karyotyping of breeding stocks. Knowledge of novel biogenetic surveillance technique in reproduction is necessary for integration of anatomical information about congenital anomalies and its consequences in epidemiological surveys for restructure in medicine.
 
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