DESORDENES METABOLICOS

Presentación del tema: "DESORDENES METABOLICOS"— Transcripción de la presentación:

1 DESORDENES METABOLICOS

2 Genome-wide assessment of worldwide chicken SNP
genetic diversity indicates significant absence of rare alleles in commercial breeds (2008 by The National Academy of Sciences of the USA- Breed utilization, genetic improvement, and industry consolidation are predicted to have major impacts on the genetic composition of commercial chickens. Consequently, the question arises as to whether sufficient genetic diversity remains within industry stocks to address future needs. With the chicken genome sequence and more than 2.8 million single-nucleotide polymorphisms (SNPs), it is now possible to address biodiversity using a previously unattainable metric: missing alleles. To achieve this assessment, 2551 informative SNPs were genotyped on 2580 individuals, including 1440 commercial birds. The proportion of alleles lacking in commercial populations was assessed by (1) estimating the global SNP allele frequency distribution from a hypothetical ancestral population as a reference, then determining the portion of the distribution lost, and then (2) determining the relationship between allele loss and the inbreeding coefficient. The results indicate that 50% or more of the genetic diversity in ancestral breeds is absent in commercial pure lines. The missing genetic diversity resulted from the limited number of incorporated breeds. As such, hypothetically combining stocks within a company could recover only preexisting within-breed variability, but not more rare ancestral alleles. We establish that SNP weights act as sentinels of biodiversity and provide an objective assessment of the strains that are most valuable for preserving genetic diversity. This is the first experimental analysis investigating the extant genetic diversity of virtually an entire agricultural commodity. The methods presented are the first to characterize biodiversity in terms of allelic diversity and to objectively link rate of allele loss with the inbreeding coefficient.

3 DESORDENES METABOLICOS Factores pre disponentes
Son precipitados por muchos factores: Medio ambiente, ingredientes alimenticios, y principalmente por un metabolismo y productividad incrementada: * Pollos machos de 3 kg de peso vivo a los 42 dias de edad. * Pavitos obtienen 1 kg de ganancia de peso vivo por semana de edad. * Ponedoras comerciales son capaces de poner 330 huevos en 365 dias

4 DESORDENES METABOLICOS Factores pre disponentes
These make up the largest group of poultry diseases classified as metabolic disorders and cause more economic loss than infectious agents. Poultry metabolic diseases occur primarily in two body systems: (1) CARDIOVASCULAR AILMENTS, which in broiler chickens and turkeys are responsible for a major portion of the flock mortality; (2) MUSCULOSKELETAL DISORDERS, which account for less mortality, but in broilers and turkeys slow down growth (thereby reducing profit), and cause lameness, which remains a major welfare concern. In addition, conditions such as osteoporosis and hypocalcaemia in table-egg chickens reduce egg production and can kill. A causa del avance en la selección genética, manejo y nutrición, los pollos y pavos comerciales modernos de hoy día tienen una tasa de rápido crecimiento, y alta eficiencia en conversión alimenticia y tasa metabólica. Estas características promueven un INCREMENTO DE LA INTENSIDAD DEL SISTEMA CARDIOVASCULAR (Porqué?) PREDISPONIENDO A LAS AVES A DESORDENES METABÓLICOS tal como fallas ventriculares, síndrome ascítico, arritmias cardiacas, desordenes cardiopulmonares y muerte súbita.

5 Metabolic Challenges: Past, Present, and Future - S
Metabolic Challenges: Past, Present, and Future - S. Leeson Department of Animal and Poultry Science, University of Guelph, Ontario, Canada N1H 2W J. Appl. Poult. Res. 16:121–125

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7 DESORDENES METABOLICOS Síndrome de muerte súbita
Afecta pollos de engorde de rápido crecimiento. Más en machos. 21 A 28 días de edad Sin signos clínicos Pocos cambios patológicos.

8 DESORDENES METABOLICOS Síndrome de muerte súbita
Causas y factores relacionados: En la actualidad, la avicultura comercial tiene un carácter intensivo, empleando animales de gran potencial genético y elevadas exigencias en instalaciones, alimentación, sanidad y manejo. La fragilidad metabólica y mayor propensión al estrés del pollo parrillero afectan la salud productiva

9 DESORDENES METABOLICOS Síndrome de muerte súbita
Anticoccidiales ionóforos Dietas con carbohidratos como fuente de energía. Alta densidad de la dieta Bajos niveles de calcio Lactato deshidrogenasa. Niveles de biotina, piridoxina y tiamina bajos y otras vitaminas en niveles altos Biotina. Taurina Tipo de grasa Textura de la dieta. Programa de luz.

10 DESORDENES METABOLICOS Síndrome de muerte súbita
Tratamiento y prevención: No hay tratamiento único. Restricción alimento para regular el rápido crecimiento. Programas de luz. Evitar el uso de ionóforos. Niveles adecuados de vitaminas.

11 DESORDENES METABOLICOS Síndrome de muerte súbita
Signs Sudden death in convulsion, most are found lying on their back. Post-mortem lesions Intestine filled with feed. Haemorrhages in muscles and kidneys. The atria of the heart have blood, the ventricles are empty. Serum accumulation in lung (may be little if examined shortly after death). Livers heavier than those of pen-mates (as a percentage of bodyweight.). Diagnosis Birds found on back with lack of other pathology. Treatment None possible. Prevention Lowering carbohydrate intake (change to mash), feed restriction, lighting programmes, low intensity light, use of dawn to dusk simulation and avoidance of disturbance.

12 DESORDENES METABOLICOS Síndrome de hígado graso
What causes fatty liver syndrome? The principal cause is thought to be an excessive calorie intake, but it may also be related to exposure to the mycotoxin aflatoxin, calcium deficiency and stress. An incorrect protein: energy balance may be to blame. Some strains of laying hen appear to be more susceptible. Birds within a flock that are most affected tend to be the higher producing hens. Fatty liver syndrome has been seen in conjunction with cage layer fatigue. Causa de hipoglucemia, incapacidad de llevar a cabo la gluconeogénesis como consecuencia de una baja actividad de la piruvato descarboxilasa PIRUVATO CARBOXILASA Tratamiento: Suplementación con biotina Dieta con alto contenido proteico o lipídico

13 DESORDENES METABOLICOS Síndrome de hígado graso hemorragico
Excesiva acumulación de grasa en el hígado asociado con varios grados de hemorragia. Afecta gallinas ponedoras, reproductoras pesadas y reproductoras de pavos. Animales en jaula y alimentadas con dietas con alto contenido de energía. Hígado agrandado y friable, crestas pálidas. Ovoposición , factor que induce hemorragia y muerte Balance positivo de energía Altas productoras. Causas: Balance de energía Peso de ave Temperatura ambiental Bajos niveles de proteína Colina y vitamina B12. Prevención y tratamiento : Evitar estrés calórico. El balance proteína- energía. Uso de productos granos de destilería y harina de pescado. Uso de grasa en lugar de carbohidratos como fuente de energía para reducir el metabolismo hepático. niveles de vitaminas hidrosolubles y liposolubles.

14 DESORDENES METABOLICOS Síndrome de hígado y riñón graso
Pollos jóvenes Deficiencia de biotina Estrés. Acumulación de grasa alrededor de hígado y riñones. Letargia y muerte. Muerte por hipoglicemia.. Acetil CoA carboxilasa y piruvato carboxilasa. Dietas altas en trigo Integridad intestinal. Dietas de reproductoras. Nivel de proteína en las dietas. TRATAMIENTO: Nivel de biotina 0.2 mg de biotina por Kg de alimento. Nutrición de reproductoras. Aumentar niveles cuando se usan sulfas y dietas bajas en proteína. Evitar estrés

15 Síndromes parecidos pero no parecen estar relacionados bioquímicamente
Síndrome de hígado graso hemorrágico (SHGH) Gallinas ponedoras enjauladas Acumulación de grasa en hígado asociado a hemorragia Prevención: control del balance energético (masa corporal) Síndromes parecidos pero no parecen estar relacionados bioquímicamente 1) Síntomas: Letargo Síndrome de hígado y riñón graso (FLKS) Pollos de engorde Acumulación de grasa alrededor de hígado y riñones 2) Etiología: Edad Temperatura Dieta: - insuficiencia de biotina (coenzima de piruvato descarboxilasa) - pobres grasas y proteínas ↓ actividad PIRUVATO CARBOXILASA 3) Características bioquímicas: ↓ actividad enzimas gluconeogénicos en hígado Hipoglucemia ↑ lípidos en hígado y riñón ↑ ácidos grasos libres y TAG en sangre

16 DESORDENES METABOLICOS Desordenes esqueléticos

17 CONDRODISTROFIA (PEROSIS)
Deficiencia de colina y manganeso. Desorden de la placa de crecimiento de los huesos largos. Perosis, dislocación del tendón. Varus y valgus DESORDEN ó DEFICIENCIA?

18 OSTEOPOROSIS Osteoporosis in laying hens is defined as a decrease in the amount of fully mineralized structural bone, leading to increased fragility and susceptibility to fracture. It contrasts with another cause of bone mineral loss, osteomalacia, in which defective mineralization of bone tissue occurs, with thick seams of poorly mineralized organic matrix. Both conditions will lead to poor quality bone, but osteomalacia is primarily associated with nutritional deficiencies of calcium, phosphorus, or vitamin D, whereas osteoporosis is an altogether more complex problem. Osteoporosis, cage layer fatigue and poor shell quality have a common cause, i.e. insufficient available calcium for the support of bone metabolism or egg shell deposition. Osteoporosis in laying hens is a condition that involves the progressive loss of structural bone during the laying period. This bone loss results in increased bone fragility and susceptibility to fracture, with fracture incidences of up to 30% over the laying period and depopulation not uncommon under commercial conditions.

19 OSTEOPOROSIS o FATIGA DE JAULA EN PONEDORAS

20 DISCONDROPLASIA TIBIAL
(OSTEOCONDROSIS) La discondroplasia tibial (TD) forma parte de un conjunto de alteraciones esqueléticas de las aves de corral producidas en forma intensiva, que entrañan disminución de la performance del lote, del rendimiento individual y del bienestar animal. Es un desorden del desarrollo, caracterizado por la permanencia de cartílago anormal en el extremo proximal de la tibia. Si bien las lesiones moderadas no impiden que los pollos lleguen al alimento y al agua; el dolor, asociado a las lesiones severas, puede motivarlos a echarse y por consiguiente a disminuir el consumo. Un estudio secuencial llevado a cabo en dos líneas comerciales de distinta predisposición a desarrollar TD sugirió que, en el caso en estudio, la TD estaba relacionada a una predisposición al raquitismo y asociada a bajos niveles del metabolito activo de la vitamina D3 (el 1,25(OH)2vitamina D3) en la circulación sanguínea, en el período de mayor crecimiento de la tibia. En un sentido amplio este desorden del desarrollo está determinado genéticamente e influido por el manejo a través de factores tales como: nivel de actividad, composición de la dieta y método de alimentación.

21 La TD es un desorden del desarrollo, caracterizado por la permanencia de cartílago anormal en el extremo proximal de la tibia. La mayor frecuencia de esta afección en el tibiotarso se ha relacionado con la elevada actividad metabólica que este hueso presenta hacia la tercer semana de edad, producto de su rápido crecimiento. Ocurre en pollos, pavos y patos como resultado de una falla en la maduración de los condrocitos que están proliferando en el disco de crecimiento. Esta falla impide la penetración vascular y, por lo tanto, la normal producción de hueso (Sanotra et al., 2001). Cuando se practican cortes sagitales o coronales del extremo proximal de la tibia, se observa una placa de cartílago que ensancha la metáfisis (Figura 1). Figura 1. Tibias de Pollos. Cortes Sagitales de los Extremos Proximales. Izquierda: discondroplasia grado 3; Derecha: cartílago epifisiario normal

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23 The rapid growth rate in broilers is associated with tibial dyschondroplasia (TD). Reducing the growth of broilers can reduce the incidence of TD but this is not an economic solution

24 PICAJE - CANIBALISMO What causes cannibalism?
Cannibalism often starts as feather pulling or picking while the birds are only a few weeks old or as investigative pecking at any age. These behaviours can escalate to aggressive pecking, particularly if injury occurs. Scientific study has shown that any or a combination of stressors can also serve as triggers leading to serious aggressive pecking and cannibalism. These stressors include crowding, bright light intensity, high room temperature, poor ventilation, high humidity, low salt, trace nutrient deficiency, insufficient feeding or drinking space, nervous and excitable birds (hereditary), external parasites, access to sick or injured birds, stress from moving, boredom and idleness, housing birds of different appearance together and birds prolapsing during egg-laying.

25 Prevention and treatment of cannibalism :
Good husbandry practices should aim to minimise the stressors listed above as potential causes for cannibalism. Some strains of birds have been shown to have a higher tendency towards developing aggressive pecking behaviour and so strains that are more placid should be preferred. Bright light is a known factor leading to cannibalism but control of lighting levels in some poultry housing systems can be very difficult if not impossible, such as in free range systems. Where outbreaks of cannibalism have occurred in a flock, or where there is a reasonable concern that management strategies can not be guaranteed to prevent an outbreak, then beak trimming of the birds may be used as a control measure. Trimming of the sharp tip of the upper, and sometimes also lower, beak reduces the damage that is caused by aggressive pecking. The spread of the behaviour may be able to be controlled if the injured and the aggressive birds can be rapidly identified and removed from the flock. Provision of escape areas may also help in floor-housed flocks. Other control methods that have been tested include the use of spectacles to prevent forward vision, bits that prevent complete closure of the beak and coloured contact lenses to prevent the identification of blood on another bird. There is evidence that cannibalism may be alleviated through the use of high fibre diets. It is believed that high fibre diets enhance gut development and gizzard function, which in turn help reduce aggressive behaviour in hens

26 DESORDENES METABOLICOS ASCITIS

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29 Figura 1. Aspecto macroscópico de un
animal en el que se aprecia buen estado de carne y severa ascitis compuesta por material de aspecto gelatinoso.

30 Figura 2. Aspecto macroscópico de los
pulmones que muestran coloración oscura debido a congestión severa y múltiples áreas redondeadas de color blanquecino o blanco-rojizo.

31 DESORDENES METABOLICOS ASCITIS
The ascites syndrome, a metabolic disorder that accounts for OVER 25% OF OVERALL MORTALITY, has become the most noticeable, non-infectious cause of loss in the broiler industry worldwide[1]. There are many factors that cause ascites, for example, high altitude, rapid growth rate, limiting lung volume, the provision of high energy rations and pelleted diets, cold, poor ventilation, the presence of respiratory disease, high sodium and low dietary phosphorus levels, hepatotoxins, mycotoxins and furazolidone in the feed, vitamin E and Se deficiencies and stress. Among so many causes, which one is the main trigger is still questionable. It was reported that low temperature was an easy and economical method to trigger ascites. One report has indicated that high nutrient metabolic rate could cause ascites, however high levels of the hormones (T3 and T4) in the plasma are related to nutrient metabolism. Ascites is a complex problem caused by many interacting factors such as genetics, environment and management. Many nutritional, medicinal and management strategies have been proposed to alleviate the problem. HIGHER LEVELS OF DIETARY VITAMIN C and E ALONG WITH SELENIUM YEAST MIGHT BE BENEFICIAL, presumably because of their role in improving cellular integrity. Oils rich in n-3 fatty acids have been shown to reduce pulmonary hypertension and, consequently, ascites incidence. The potential use of flax oil has already been demonstrated, whereas the effects of other oils rich in n-3 fatty acids (fish, linseed and canola oils) remain to be investigated. The assessment of the effects of dietary electrolyte balance on ascites incidence seems to be a promising field of research in broiler nutrition. In general, reducing the dietary level of salt (NaCl) and adding bicarbonates to the diet and drinking water have been proposed as potential .cost-effective. methods to reduce ascites incidence.

32 The use of nutrients/drug agents that increase the vascular capacity of the lungs or decrease the pulmonary vascular resistance may help to alleviate the problem, but economic and local feed regulations might restrict such use. Diuretics have also shown positive effects, presumably because there is a reduction of sodium and fluid retention in the body; litter humidity however must be closely monitored if diuretics are continuously administered. As the high metabolic rate (fast growth) is a major factor contributing to the susceptibility of broilers to ascites, early-age feed or nutrient restriction (qualitative or quantitative) or light restriction in order to slow down the growth rate seem practically viable methods, since final body weight is not compromised. Optimization of the house temperature and ventilation in cold weather seem helpful practices to decrease ascites incidence. Under practical conditions, it might be interesting to test the additive effects of different approaches when used in combination. It can be concluded that the addition of vitamin C to the diet clearly counteracts the increase in ascites mortality due to low ambient temperature or to dietary T3 supplementation. Further studies are needed to elucidate the exact underlying physiological mechanism.

33 EROSION DE MOLLEJA Mycotoxinas. Cobre. Aminas biogenicas.
Harina pescado (Gizzerosine) Torta de Soya de mala calidad? Adenovirus. Otrors factores: Otor factores capaces de producir erosion de molleja, pero no frecuentemente en condiciones comerciales , se incluye la inanicion alimenticia y deficiencia de AA’s azufrados

34 DESORDENES EN VACUNOS Introduction:
Management of the dry cow plays an important role in the control of metabolic disorders near or at calving time. Calving and the first month after freshening are critical times for the dairy cow. The major disorders affecting the fresh cow are usually the result of nutrition and feed management problems. Metabolic disorders are completely interrelated and tend to occur together The main metabolic disorders of the fresh cow (at calving time) are: - Milk fever - Udder edema - Ketosis - Fat cow syndrome - Retained placenta - Displaced abomasum - Rumen acidosis - Laminitis

35 CETOSIS BOVINA Hipoglucemia. Vacas lecheras (10-60 días después del parto) 1) Síntomas: Pérdida de peso / pérdida de apetito Disminución severa en la producción de leche Parálisis parcial ↑ritmo respiratorio Aliento y orina con olor dulzón (acetona) 2) Características bioquímicas: Hipoglucemia Cuerpos cetónicos en sangre, orina y leche 3) Etiología: Gran demanda de glucosa para formación de leche

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37 El peculiar metabolismo energético de los rumiantes
Celulosa TAG glicerol Glucosa Degradación bacteriana Proteínas aminoácidos FFA Butirato Acetato Propionato Fermentación bacteriana Tejidos CUERPOS CETÓNICOS Absorción en el rumen Obtención energía Hígado y tejidos Obtención energía y acetil-CoA Tejidos Obtención energía Hígado Gluconeogénesis Sangre Niveles glucosa sangre Sistema nervioso Lactosa (leche) GLUCOSA Tratamiento: Inyección intravenosa de glucosa Precursores gluconeogénicos Corticoesteroides (favorecen uso de aminoácidos gluconeogénicos)

38 TOXEMIA DE GESTACION Típica ovejas gestando. Hipoglucemia 1) Síntomas:
Depresión y tendencia a la inmovilidad Pérdida de reflejos y marcha dificultosa. Pérdida de apetito Incapacidad de levantarse y muerte 2) Características bioquímicas: Hipoglucemia Cuerpos cetónicos en sangre y orina 3) Etiología: Factores: Escasez de alimento Estrés (meteorología adversa) Más de un feto Causa: gran demanda de glucosa por parte de los fetos Muerte fetos por hipoglucemia Descomposición fetos Toxinas Gluconeogénesis materna 4) Tratamiento: Inyección glucosa Precursores gluconeogénicos Interrumpir la gestación

39 FIEBRE DE LA LECHE Productores de leche. Hipocalcemia. Costosa de tratar 1) Síntomas: Pérdida de apetito Estreñimiento Dificultad para caminar y levantarse ↓temperatura corporal (extremidades) Arrastre patas traseras Inconsciencia y muerte 2) Características bioquímicas: ↓calcio en sangre 3) Etiología: Causa desconocida Alimentos ricos en calcio (al final de la gestación) Alimentos ricos en potasio (impide movilización de calcio óseo) calcio producción leche calcio producción leche Dieta Dieta Hueso Hueso 4) Tratamiento: Inyección solución calcio

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