veterinary Teratologia

Introduction to the teratología: the study of the congenital veterinary medicine malformations

Index

1. Introduction
2. Classification of the congenital malformations
3. Environmental causes of congenital malformations
4. Mechanisms of production of congenital anomalies in the animals
5. Interactions between causes and mechanisms in the congenital anomalies

1. Introduction

The reproduction process is the one that assures the continuity the Earth life. The organisms have a great structural and functional complexity, a plot of interactions and regulations that allow them to live in an atmosphere that varies continuously. That complexity of the multicellular organisms begins to be generated during the embryonic development when, from an only cell, cigota, is constructed an organism made up of million cells that interact.
Part of the success of the survival of the embryos during its development depends on which they count on the suitable genetic information and an optimal atmosphere, without injurious influences. Before alterations in the genetic material or the presence of injurious agents, it is probable that congenital alterations in the development or malformations happen. Some congenital malformations cause the embryonic death, others are not diagnosed but until the birth and many they are not recognized in the neoborn ones, but that are discovered in later stages of the life.
The normality of an animal new born depends on a correct association between its weaves and of which these constitute organs with capacity to develop different functions. A normal organism is therefore a ?multicellular society? whose components are also normal and interact correctly. The origin of that ?society?, as already we studied, is, initially, a unique cell: cigota. The embryonic development is not more than the passage from the unicellular stage to a multicellular stage, where each component has specialized. The analysis of the implied biological mechanisms in the diversification of cells and weaves already has been analyzed when dealing with the ?biological mechanisms the development?. A revision of this subject is necessary, as well as of the cellular characteristics and functions, since the normal embryogenesis and their alterations can be included/understood from those contents.

What are the congenital malformations or anomalies?
The congenital malformations or anomalies are the structural or functional presents at moment of the birth and originated in a fault in the formation of one or more constituent alterations or defects of the body during the embryonic development.
The term ?congenital? talks about to the characteristics acquired during the embryonic development. Such characteristics can or not be hereditary. When saying ?components of the body?, reference to different levels from organization becomes, from the molecular one to the organic one.
The scientific discipline in charge of the study of the congenital malformations denominates Teratología.
The congenital term indicates existing conditions in the birth or before this it happens. It excludes, therefore, the morphologic abnormalitys caused by traumatismos for which the denomination of ?injury? is used, and the damages produced by bacterial or virales affections that settle down once the organ already has formed. For example, an animal can be born with hepatitis and their liver to present/display the characteristic injuries. It will be spoken then of a ?fetal disease? and a ?fetal injury?.
Teratógenos is those agents who can induce or increase the incidence of the congenital malformations when they are administered or they acted in a pregnant animal.
The discussion exists on if all present anomaly to the birth is a ?teratogénico change?. Traditionally they have been different like teratogénicos changes to those produced during the organogenesis and toxicológicos changes to which they affect systems total or partially formed. In addition, the intrauterine deaths and the reabsorciones not always are including like teratológicos effects. In order to include to all the affections that can happen during the development it has preferred the denomination of toxicología of the development or embriotoxicidad.

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2. Classification of the congenital malformations

The study of the malformations and the determination of its causes have medical and economic importance. One has settled down, for example, that between 10 to a 12% of pigs and a 15% of potrillos, die in the first 48 hs. of life as a result of congenital anomalies. The incidence of congenital anomalies to the birth can be from the 1.2 to 5.9%.
The embryonic and fetal development can be altered by different external factors (radiations, heat, toxic substances, virus) or internal (genetic or chromosomic alterations). Also joint the congenital defects can be the result of of factors both related: the genic heap (genome) and the environmental factors.

Congenital malformations of genetic and chromosomal origin
The alterations in the genetic material of an organism can affect a gene (congenital malformations of genetic or precise origin), to several genes (poligénicas congenital malformations), or to the chromosomes (congenital malformations of chromosomal origin).

Congenital malformations of genetic origin
The properties of a protein depend on the amount, quality and ordering of the amino acids that constitute it. The order of the amino acids in the protein molecule is determined by tripletes of bases in the corresponding gene. Many amino acids can be codified by more of triplete of the DNA. Each base can be replaced by anyone of the other three being able to happen that:

The substitution determines the appearance of triplete different from the original one but that it corresponds with he himself amino acid. In this case the protein will maintain its sequence normal of amino acids and the modification of the genetic code does not become evident.
The substitution of a base determines the appearance of triplete that codifies a different amino acid. The incorporation of that new amino acid in the protein molecule can not alter its properties or determine its abnormal behavior.
It can happen that the substitution of a single base turns to triplete that normally corresponds with an amino acid, ?triplete of completion?. In this case, the protein molecule codified by the altered gene will be transcribed solely until the place in which triplete of abnormal completion has formed.
Congenital errors of the metabolism
Many alterations caused in the presence of enzymatic anomalies of genetic origin exist. All is originated in the presence of an abnormal gene, that determines a fault in the enzymatic synthesis. One of the most common alterations is the accumulation of a substance that normally is degraded by an enzyme, or the absence of a product by abnormalitys in the enzyme that catalyzes its synthesis. The enzymatic activity depends on different factors, among them its three-dimensional, conditional structure by the distribution of amino acids throughout the molecule.

How can be altered the genes?
The genetic anomalies appear the process as resulting from of mutation. A mutation is a change in the sequence of bases of the DNA that can determine a modification in the characters of an organism and, if the alteration affects the DNA of the germinal cells, can be transmitted to the descendants (it sees ?radiations?). Different molecular forms from the mutations exist, between which it is possible to mention: the replacement of a base by another one, the deleción of a portion of DNA, the investment of a portion of he himself and the insertion of new bases.
The fundamental cause in the production of mutations is the ionizing radiations (to see more ahead), but also many chemical substances are able to produce them, like also biological agents.
A gene whose presence determines the death of the organism, in an early or delayed stage of its development, denominates lethal gene.
The anomalies by genetic causes have happened to occupy the attention of the veterinarians in the deposits before the diminution of the infectious, parasitic and nutricionales diseases due to the handlings and suitable diagnoses.

Congenital malformations of chromosomal origin
Each chromosome is formed by numerous genes and, as we saw, the simple substitution of a base in a gene can have injurious effects for the organism. The alteration of a whole chromosome can be lethal or cause of severe anomalies. The chromosomic alterations can be classified in: 1. - alterations in the number of chromosomes; 2. - modifications in the structure; or 3. - mosaic chromosomal and chimeras.

Alterations in the number of chromosomes.
The numerical alterations of the chromosomes can imply to autosomas or the sexual chromosomes.
Alterations in the number of autosomas
When failing the separation of the homologous chromosomes during the meiosis originates gametas, and therefore, cigotas, with chromosomes of more or less. The organisms with a chromosome of denominate trisómicos more and those where it lacks a chromosome call monosómicos. A gameta with the double of the normal number of chromosomes can happen that the separation of a complete group of chromosomes fails, originating itself. If so gameta it is united with other than it contains the normal number of chromosomes, the resulting embryo will have three groups of homologous chromosomes instead of two, having denominated it to it triploide. If two are united gametas with the double of the normal number of chromosomes, the resulting embryo will be a tetraploide (four groups of homologous chromosomes). These cases where they exist one or more additional groups of chromosomes, are known with the name of poliploides.

Alterations in the number of sexual chromosomes
When the lack of disjunction affects the sexual chromosomes, we can be with males whose chromosomic formula is ?the normal number of autosomas XXY?, in which case will be sterile or with females with ?I number normal of autosomas X0? or ?the normal number of autosomas XXX?. In both cases one is generally sterile individuals.

Structural modifications
These abnormalitys can take place during the movements and changes that undergo the chromosomes during the meiosis. It can happen the rupture and loss of a portion of the chromosome, denominated deleción. The deleciones are thus, alterations that consist of the elimination of more or less great segments of a chromosome. It can also happen that a segment of a chromosome is duplicated and, therefore, exists duplication of the genes that contains, or the order of the nucleótidos ones can be invested to a segment, altering.
The traslocaciones consist of the union of a chromosome or from he himself, to another chromosome. In many cases the presence of a traslocación does not produce fenotípicas anomalies in an organism, if the amount of genetic material continues being the same one. These cases denominate ?balanced traslocaciones?. If the individual has chromosomic traslocaciones in the germinal cells, exists the possibility that some of their descendants has a trisomía of the traslocado chromosome. During the formation of the germinal cells by meiosis two possibilities exist. One is that the normal chromosome is located in one of gametas and the traslocado one in another one. The other possibility is that the normal chromosome and the traslocado one go to the same gameta, originating itself after the fertilization a trisomía.

Chromosomal mosaics
They exist individual whose cells do not have all the same chromosomic constitution, to these cases denominates ?mosaics?. An example of mosaic individuals is generated when during the first embryonic segmentation a lack of disjunction takes place. Both blastómeros resultants present/display different number of chromosomes, occurring cellular place to two lineages or different lines.

Mechanisms of production of chromosomic anomalies
In anyone of the two divisions that conform the meiosis a fault in the separation of the homologous chromosomes can happen such, being abnormal the distribution from between the cells daughters. This abnormality denominates ?not-disjunction? or ?not-separation?. For example, if not-disjunction in a chromosome takes place during the espermatogénesis, the final result will be the production of two spermatozoa that lacks that chromosome and two that contains it by double game. If one of the spermatozoa that the fecund excessive chromosome to a normal ovocito has, cigota resulting is trisómica.
The chromosomic anomalies that happen after the fertilization have a high probability of originating individuals with a chromosomal mosaic. The lack of separation of chromosomes can happen in anyone of the mitóticas divisions, for example during the segmentation. It is improbable that the anomaly happens in all blastómeros the embryonic cells or. If it affects to some of them, can originate three different cellular lines: the normal ones, the trisómicas and the monosómicas. In many cases these are not able to survive, reason why the embryo turns out to be a mosaic conformed by normal and trisómicas cells.
The chimeras are resulting embryos of the fusion of two embryos of different chromosomic constitution. Experimentally the fusion of blastocistos of mammals has been obtained. These embryos manage to be developed normally, although if one of the components is XX and the other XY appears intersexuality pictures.
In the normal bull calves the chromosomic identification of the females is 60XX and of the males 60 XY. But in some females, calls freemartin is a mixture of 60XX in some cells and 60XY in others. These cases have been observed in twin females of a male when their placentarias circulations have megred. Also one assumes that. In case of unique gestation, it happened fusion of early embryos. This type of chimeras has been observed also in pigs, goats and ewes.

The causes of chromosomic anomalies
A correlation between the age of the mother at the moment of the conception and the appearance of some chromosomic anomalies has settled down. In the case of the human species trisomías of the autosómicos pairs have been observed 13 and 18 and of the sexual chromosomes in gametas or embryos of greater individuals of 40 years.
The irradiation of the organism is another causal one of chromosomic anomalies. Experimentally, cells in vitro have been radiated during the G1 stage of the cycle and the same ones have developed anomalies when arriving at phase M, that is to say, when they are divided. One assumes that these anomalies reflect alterations physical-chemistries in the chromosomes, that would prevent their normal separation during the mitosis.
The chemical substances that interfere in the DNA synthesis and alter their structure also produce chromosomic anomalies. The virus is able to cause ruptures of chromosomes.

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3. Environmental causes of congenital malformations

It was indicated previously that the mutations can take place spontaneously or be induced. In this last case, the agents who cause mutations denominate mutágenos and they are classified in:
a. - agents of physical type, like the radiations alpha, beta, gamma, X, ultraviolet, etc., which produce chromosomic ruptures or injuries.
b. - agents of chemical type, like some substances of the smoke of the cigarette, vegetal drugs and components.
c. - agents of type biological, like certain virus who affect the genetic material of the cell to which they parasitan.
d. - nutricionales and metabolic agents.
e. - autoimmunity reactions.
f. - factors associated to the maternal age.

To the producing agents of mutations and that are located or they originate in the external atmosphere the embryo denominates environmental teratogénicos agents.

Characteristics of the environmental teratogénicos agents
1. - the teratogénicos agents can affect the embryo directly, or do it through modifications in the mother or the placenta.
The placenta is the organ that ties to the developing organism with the mother and, through her, with the outer atmosphere. The embryo nourishes and eliminates products of its metabolism by means of the molecule passage by the placenta. Toxic substances exist that cross the placentaria barrier and act directly on the embryo. Also have been other substances that alter the placentaria circulation and with no need cause fetal alterations to enter the body of the developing organism. It has been postulated that some teratogénicos agents could affect to the embryo by means of the production of alterations in the metabolism of the mother.

The environmental teratogénicos agents can be innocuous for the mother.
Many medicines do not produce undesired effects in the adults but they are teratogénicos. The greater susceptibility of the embryos to the toxic effect of environmental agents is explained on the base of two mechanisms: 1 - the embryos are ?immature more?, from the metabolic point of view, that the adults. For example, only one reduced fraction of hepáticas enzymes in charge to eliminate drugs is present in the organisms developing. 2 - a minimum metabolic alteration, that in an adult one causes ?a fleeting? malaise, can interfere with in the embryo with a mechanism of the development, causing an irreversible damage.
The period of development in which a teratogénico agent acts on the embryo determines which are the affected organs.
The mechanisms of the development that participate in the formation of an organism are similar and depend on the cellular metabolism. If a substance that blocks necessary metabolic roads for the cellular division is administered during a period of the development, those organs will be affected for which the mitosis, then particular, are essential. Of this it can be deduced that most of the teratogénicos agents produce different malformations according to the moment from the development in which they act.
A same congenital malformation can be produced by different environmental teratogénicos agents.
If a metabolic process is essential for the development of an embryonic organ, any environmental agent who alters it will produce an anomaly in that organ.
The teratogenicidad of an environmental agent depends on the dose administered to the mother.
Experimentally it is observed that any drug, in high dose, produces congenital malformations.
The teratogénica action of an environmental agent depends on the ?genetic constitution? of the organism on which it acts.
When administering itself laboratory a teratogénica animal substance is verified that, in certain doses, this one produces malformations only in 50% of the embryos (teratogénica dose 50). When it is tried a teratogénica drug in different species is observed that the sensitivity of the drug is different for each one from them. They exist individual with enzymatic deficiencies that make them particularly susceptible to the effects of a substance.
The effects of a teratogénico agent can happen unnoticed at the moment of the birth.
Some visible congenital malformations externally or that produces functional alterations series, are detected to the birth. Many others are diagnosed during the later periods. For example, certain cerebral injuries are detected in the maturity by faults in the conduct (neurological maturation).
Periods of the development do not exist in which the embryo is free of being affected by teratogénicos agents.
The most sensible period to the action of teratogénicos agents corresponds with the first stages of the development and, mainly, the organogenesis. Nevertheless, some substances are teratogénicas in the stages more outposts.
The environmental teratogénicos agents can produce fenocopias, that is to say, identical congenital anomalies to the originated ones by abnormal genes.
If an abnormality in the gene To determines the absence of enzyme B, this absence can cause a malformation through the lack of synthesis of substance D, from a precursor C. the presence of an agent able to inhibit to enzyme B produces equal effect, although the enzyme has formed normally.

Environmental teratogénicos agents
Radiations
The ionizing radiations are classified in two categories. First gamma radiations are the electromagnetic waves (and
x-rayses), and second are the corpuscular ones (radiations alpha, the neutrons and the radiations beta). One denominates them ionizing because, when acting on the matter, they such produce impacts in the atoms that constitute it, expelling from protons or electrons, altering therefore the balance of loads that normally maintain to atoms in a state of electrical neutrality. When a radiation alters some of the atoms that constitute a protein molecule, it determines his ionization and the molecule becomes strange for the cell. The injurious effects depend on the amount of received radiation. If she is low, probably it will affect few proteins and the cell will put into action repairing mechanisms, being the reversible damage. A ?threshold? exists therefore that will have to be exceeded so that the damage is irreversible. Another type of molecule for whose alteration a threshold does not exist is the desoxirribonucleico acid (ADN). If the impact of the radiation causes the rupture in a certain place of the molecule, this can, in certain cases, to repair itself completely. But that repair can take place of erroneous way. For example, which the two helices are united to each other of crossed way, altering the genetic code, which will imply an alteration in the protein codified by that segment. All alteration in the code takes to the appearance of abnormal genes.
The classic tríada one of the anomalies by radiation in the domestic animals includes: 1 - retardation of the extrauterine growth intra or, 2 - embryonic, fetal or neonative death and 3 - congenital malformations. The central nervous system is the affected structure more in the mammals.

Chemical agents
The chemical agents constitute the group of ampler potential teratógenos, as much as therapeutic agents as environmental. In general, the therapeutic doses do not cause alterations.
The exhibition to toxic substances like the selenium, the tetanic toxin, the sulfonamides (antibiotic), produces increase of congenital anomalies. Vegetables exist that, to the being consumed by gestantes females, produce anomalies. For example the Veratrum californicum produces craneales and cerebral malformations. In bovines young born with deformities of the spine and the joints of the carpus and tarso as a result of the consumption has been observed of cicuta (Conium maculatum) by their mothers between days 55 and 75 of gestation.

Infectious agents
The virus. The virus can affect the cells of two different ways. On the one hand, they can proliferate within the cells producing its later rupture and, by another one, incorporate its genetic information, determining the intracellular protein synthesis that leads to an alteration of the metabolism. A requirement so that the embryos are affected by the virus is that in the mother one takes place ?viremia?, that is to say, a generalization of the infection by virus. Cases exist where the virus does not cause alterations in the mother and, nevertheless, they seriously affect the embryo. The determination of the viral origin of an alteration in the embryos can be made solely by means of isolation of the virus of embryonic weaves or by means of serológicos studies.
The parasitic infections. The known case more is the one of the toxoplasmosis. This parasite causes, when affecting to embarrassed women, cases of mental retardation.

Nutricionales and endócrinos factors
The maternal nutrition has an important effect on the prenatal development. The vitamin deficiency A (vitamin deficiency A), generates lip leporino, ocular, cardiovascular, urinary and genital defects in pig, rats and rabbits. The hipervitaminosis To, produces malformations in hamster, rabbit, cobay, rat, mouse and pig. The vitamin deficiency D causes skeletal alterations and dental abnormalitys.
The iodine deficiency in the diet causes ?cretinismo?. The gland thyroid begins to accumulate iodine towards half-full of the gestation. That mineral arrives at the embryo through the placenta and, if its concentration is low in the maternal blood by nutricional deficiency, also he will be deficient in the embryo. This causes deficiency of tiroideas hormone production that determines mental retardation and enanismo.
Many alterations in the development are fitted within the denominated ?malformations of multifactorial cause?. This denomination indicates that it is not an only gene or a chromosome altered the people in charge of his appearance, but the joint operation of several different genes on which leading environmental factors act.

Environmental temperature
The hypertherm in the pregnant domestic animals is cause of anomalies of the central nervous system and the eye. Between the environmental causes that entail hypertherm is to lock up to a pregnant female in a car exposed to the sun. The febrile diseases during the preñez also constitute a embriotoxicidad risk.
The experimental hypotherm in rats, gestantes mice and hamsters causes defects in the central nervous system and the skeletal development.

The environmental contamination
The contamination of the atmosphere produced by the resulting remainders of industrial procedures, combustion product accumulation, indiscriminate use of plaguicidas, etc. is being constituted in one of the main problems for all the species. Although it has not been determined stops most of the polluting agents a teratogénico effect, is not illogical to suppose that they have it.

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4. Mechanisms of production of congenital anomalies in the animals

In previous paragraphs the primary causes have considered that generate malformations, being indicated to the genetic, environmental factors or their joint operation. The mechanisms by means of which those factors can alter the normal development of an embryo are such that they determine this development. Since we have already studied, five basic mechanisms for the embryogenesis exist: induction, cellular differentiation, cellular death, growth and cellular motilidad.

Faults in the induction: many embryonic components are developed by the inductive action of preexisting structures. The induction mechanism can fail of two ways, by deficiency or excess.
Absence or deficiency of induction: the new component (organ) does not form. To this alteration agenesia is denominated. When the lack of induction is not complete, it can happen that the induced organ initiates its development, being a partial structure and giving rise to one disgenesia.
Example: normally, notocorda exerts an inductive effect on the suprayacente ectoderm, causing its transformation in neuroectodermo. The cephalic part of this neuroectodermo will give origin encéfalo. If the inductive action of notocorda in the cephalic end of the embryo is absent, agenesia encephalic or ?anencefalia? will take place.

Excess of induction: if the organ or inductive structure exerts its action of exaggerated way or it appears by duplicate, a duplication of the induced organ takes place.
Example: a pair of conduits, denominated exists ureterales conduits, that they induce to an area of gononefrótomo to be different itself in the kidneys (and straight left). If for some reason, the ureteral conduit straight appears double, will induce to the formation of two kidneys of that side of the body, being generated a ?renal duplication?.

Faults in the cellular death: the normal occurrence of cellular death during the development is a mechanism genetically programmed denominated apoptosis. Many embryonic conduits present/display, in some stage of their development, a phenomenon of multiplication of their cells of internal coating, which leads to the obliteración or the temp closing of its lumen. Normally it happens apoptosis of many of the cells that proliferated and the light of the conduit reappears. An anomaly is that the death does not happen or does it of incomplete way. In the first case, the light of the conduit does not reappear, being left this one obliterated totally and taking place a denominated malformation atresia. When the apoptosis is incomplete, the light of the conduit is minor who the normal one and to this narrowing denominates estenosis.
Example: the light of the intestine of the embryos presents/displays areas closed by the cellular proliferation that reopen during the gestation. If the reapertura does not happen atresia generates one ?intestinal?, and if the opening is incomplete, a ?intestinal estenosis?.

Faults in the growth: during the morfogénesis of an organism changes of form and position occur that can, primarily, to attribute itself to rates of different mitóticas divisions for different cellular groups. This way it happens a growth differential of the components of the embryo. Alterations in the global growth of an organ can happen, conducive to that he himself is too great or small. In the first case the area code will be put in front ?macro?, and in the second ?micro-?.
Example: if the language grows exaggerated it speaks of ?macroglosia?, and if she is minor who the normal thing, it is ?microglosia?.
Another form of alteration of the growth is a fault in the coordination of the speed in which it happens.
Example: paladar forms from two outlines that grow from the lateral ones of the dorsal region of the mouth to megring in the mean line of the ceiling of the mouth. If the outlines grow more slowly than the normal thing, the fast growth of the rest of the head leads to a lack of fusion in the mean line of both processes, being a called malformation ?palatal fissure?.
Some shifts of position of the organs in the body occur to the growth differential of the corporal regions as resulting from. If the organs do not occupy the normal anatomical place, it is spoken of ectopía.
Example: the kidneys form initially in the pelvic region and, by growth differential of the abdominal region, they end up occupying a lumbar position. When it fails its displacement happens ?ectopía renal?.

Faults in the cellular motilidad: the displacement of cellular groups during the development is a common phenomenon. The migrantes cells constitute inductive factors of the weaves at which they arrive or of the organs of which they are neighboring in his definitive position. When it does not happen the migration of cells is absent the component or inductive organ, being generated one agenesia or one disgenesia.
Ejemplo: las células germinales primitivas o gonocitos (precursoras de las gametas) se originan fuera del cuerpo embrionario, a nivel del endodermo del saco vitelino. Durante el desarrollo migran hacia unas estructuras denominadas crestas genitales en el interior de la cavidad abdominal y allí inducen a los tejidos circundantes a la formación de la gónada. Si tal migración no ocurre, se presenta una anomalía llamada "agenesia gonadal".

Fallas en la diferenciación celular: los mecanismos biológicos de inducción, migración, muerte celular y crecimiento son considerados como aspectos de la diferenciación celular. Las fallas más notorias en la diferenciación celular son aquellas donde:
Se ve alterado el funcionamiento celular. Tales serían los casos de células encargadas de elaborar sustancias con función hormonal y que, por distintos motivos no elaboren o no liberen al medio su producción.
Se ve alterada la capacidad de respuesta celular. En estos casos las células que deberían responder ante el estímulo de un agente inductor no lo hacen.
Ejemplo: en los testículos se presentan unas células (células intersticiales o de Leydig) responsables de la elaboración de hormonas denominadas andrógenos. Las demás células de la gónada y de los órganos accesorios deben responder a la acción inductora de los andrógenos para diferenciarse correctamente. Si estas células son incapaces de responder al estímulo hormonal, se presenta una anomalía conocida como "síndrome del testículo feminizante".

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5. Interacciones entre causas y mecanismos en las anomalías congénitas

Los factores genéticos y ambientales se pueden combinar para determinar la aparición de anomalías. Por ejemplo, agentes ambientales como las radiaciones, la anoxia, las drogas antimetabólicas, los virus y los anticuerpos producen la muerte de grupos celulares o interfieren en el metabolismo celular, reduciendo las mitosis de las estructuras en crecimiento. Las anomalías congénitas producidas por la interacción de genes anormales y agentes ambientales perjudiciales se denominan "de causa multifactorial" o "multifactoriales".
Los factores genéticos actúan de manera más generalizada que los ambientales. Dado que los genes controlan la síntesis de proteínas y a través de ellas gobiernan la vida celular, es evidente que la alteración en uno o más genes habrá de interferir en cualquiera de los cinco mecanismos biológicos del desarrollo. Por ejemplo, la síntesis de sustancias inductoras, la de componentes estructurales para la diferenciación celular, los componentes metabólicos que desencadenan la muerte celular, las características físico-químicas de las membranas que dirigen la migración de células y las proteínas contráctiles que la facilitan, la duración del período G1 de la mitosis, son todos aspectos de la actividad celular regulados por genes.

Alteraciones en el desarrollo de los animales domésticos asociadas con anomalías congénitas
Interrupción de la gestación o aborto: se denomina aborto a la expulsión del embrión o feto durante el período del desarrollo en el que todavía no es viable. Cuando el feto es expulsado en un período en que puede sobrevivir se habla de parto prematuro.
Los abortos espontáneos se producen generalmente en el primer tercio de la gestación y suelen corresponderse con embriones o fetos que presentan malformaciones. También existen factores ambientales que desencadenan abortos espontáneos, tales como traumatismos, infecciones, deficiencias nutricionales y alteraciones endócrinas de la hembra gestante. Estos factores pueden actuar directamente sobre el feto o alterando las condiciones necesarias para su supervivencia (aporte de oxígeno, nutrientes, etc.).
Existen casos donde el embrión queda retenido en el útero por períodos más o menos largos. En estos casos puede ocurrir que el feto y sus envolturas adquieran consistencia dura, conformando una estructura denominada litopedion, o de aspecto laminar: feto papiráceo.

 

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