DESORDENES METABOLICOS

Breed utilization, genetic improvement, and industry conso lidation arepredicted to have major impacts on the genetic composition o f commercialchickens. Consequently, the question arises as to whether s ufficient geneticdiversity remains within industry stocks to address future needs. With thechicken genome sequence and more than 2.8 million single-nu cleotidepolymorphisms (SNPs), it is now possible to address biodive rsity using apreviously unattainable metric: missing alleles . To achieve this assessment,2551 informative SNPs were genotyped on 2580 individuals, i ncluding 1440commercial birds . The proportion of alleles lacking in commercial populations

Genome-wide assessment of worldwide chicken SNPgenetic diversity indicates significant absence of rare

alleles in commercial breeds (2008 by The National Academy of Sciences of the USA-www.pnas.orgcgidoi10.1073pnas.0806569105)

commercial birds . The proportion of alleles lacking in commercial populationswas assessed by (1) estimating the global SNP allele frequen cy distributionfrom a hypothetical ancestral population as a reference, th en determining theportion of the distribution lost, and then (2) determining t he relationshipbetween allele loss and the inbreeding coefficient. The results indicate that50% or more of the genetic diversity in ancestral breeds is ab sent incommercial pure lines. The missing genetic diversity resulted from the limitednumber of incorporated breeds. As such, hypothetically com bining stockswithin a company could recover only preexisting within-bre ed variability, butnot more rare ancestral alleles. We establish that SNP weigh ts act as sentinelsof biodiversity and provide an objective assessment of the s trains that aremost valuable for preserving genetic diversity. This is the first experimentalanalysis investigating the extant genetic diversity of vir tually an entireagricultural commodity. The methods presented are the first to characterizebiodiversity in terms of allelic diversity and to objective ly link rate of allele losswith the inbreeding coefficient.

� Son precipitados por muchos

factores:

Medio ambiente, ingredientes

alimenticios, y principalmente por un

DESORDENES METABOLICOSFactores pre disponentes

alimenticios, y principalmente por un

metabolismo y productividadincrementada:

* 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

� 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 eficienciaen conversión alimenticia y tasa metabólica.

DESORDENES METABOLICOSFactores 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:� Estas características promueven un

INCREMENTO DE LA INTENSIDAD DELSISTEMA CARDIOVASCULAR (Porqué?)PREDISPONIENDO A LAS AVES ADESORDENES METABÓLICOS tal como fallas

ventriculares, síndrome ascítico, arritmias

cardiacas, desordenes cardiopulmonares y

muerte súbita.

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 reducingprofit), 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.

Metabolic Challenges: Past, Present, and Future - S. LeesonDepartment of Animal and Poultry Science, University of Guelph,Ontario, Canada N1H 2W1 - 2007 J. Appl. Poult. Res. 16:121–125

Afecta pollos de engorde de rápido crecimiento.

DESORDENES METABOLICOSSíndrome de muerte súbita

Más en machos.

21 A 28 días de edad

Sin signos clínicos

Pocos cambios patológicos.

Causas y factores relacionados:

� En la actualidad, la avicultura comercial

tiene un carácter intensivo, empleando

DESORDENES METABOLICOSSíndrome de muerte súbita

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

� Anticoccidiales ionóforos

� Dietas con carbohidratos como fuente de

energía.

� Alta densidad de la dieta

� Bajos niveles de calcio

� Lactato deshidrogenasa.

DESORDENES METABOLICOSSíndrome de muerte súbita

� 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.

Tratamiento y prevención:

� No hay tratamiento único.

DESORDENES METABOLICOSSíndrome de muerte súbita

� Restricción alimento para regular el rápido

crecimiento.

� Programas de luz.

� Evitar el uso de ionóforos.

� Niveles adecuados de vitaminas.

� 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.

DESORDENES METABOLICOSSíndrome de muerte súbita

� 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.

� 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 mycotoxinaflatoxin, calcium deficiency and stress.

� An incorrect protein: energy balance may

DESORDENES METABOLICOSSíndrome de hígado graso

Causa de hipoglucemia, incapacidad de llevar a cabo la

gluconeogénesis como consecuencia de una baja actividad

de la piruvato descarboxilasa

PIRUVATOCARBOXILASA

� 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 affectedtend to be the higher producing hens.

Fatty liver syndrome has been seen in

conjunction with cage layer fatigue.

Tratamiento: Suplementación con biotina

Dieta con alto contenido proteico o lipídico

� 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.

DESORDENES METABOLICOSSíndrome de hígado graso hemorragico

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.

� Pollos jóvenes

� Deficiencia de biotina

� Estrés.

� Acumulación de grasa alrededor de hígado y riñones.

� Letargia y muerte.

� Muerte por hipoglicemia..

DESORDENES METABOLICOSSíndrome de hígado y riñón graso

� 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

Síndrome de hígado graso hemorrágico (SHGH)Gallinas ponedoras enjauladasAcumulación de grasa en hígado asociado a hemorragiaPrevención: 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 engordeAcumulación de grasa alrededor de hígado y riñones

2) Etiología:2) Etiología:EdadTemperaturaDieta: - insuficiencia de biotina (coenzima de piruvato descarboxilasa)

- pobres grasas y proteínas↓ actividad PIRUVATO CARBOXILASA

3) Características bioquímicas:↓ actividad enzimas gluconeogénicos en hígadoHipoglucemia↑ lípidos en hígado y riñón↑ ácidos grasos libres y TAG en sangre

Problemas podales

artritis osteopatías

osteítis osteodisplasiasosteodistrofias

DESORDENES METABOLICOSDesordenes esqueléticos

condrodistrofia

raquitismo

osteomalacia

discondroplasia

Varus y valgus

espondilolistesis

Necrosis cabeza del fémur

� Deficiencia de colina y manganeso.

� Desorden de la placa de

CONDRODISTROFIA (PEROSIS)

� Desorden de la placa de crecimiento de los huesos largos.

� Perosis, dislocación del tendón.

� Varus y valgus

DESORDEN ó DEFICIENCIA?

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 whichdefective mineralization of bone tissue occurs, with thick seams of poorlymineralized organic matrix.Both conditions will lead to poor quality bone, but osteomalacia is primarilyassociated with nutritional deficiencies of calcium, phosphorus, orassociated with nutritional deficiencies of calcium, phosphorus, orvitamin D, whereas osteoporosis is an altogether more compl exproblem .Osteoporosis, cage layer fatigue and poor shell quality hav e a commoncause, i.e. insufficient available calcium for the support of bonemetabolism or egg shell deposition .

Osteoporosis in laying hens is a condition that involves the progressive loss ofstructural bone during the laying period. This bone loss results in increasedbone fragility and susceptibility to fracture, with fracture incidences of up to30% over the laying period and depopulation not uncommon undercommercial conditions.

OSTEOPOROSIS o FATIGA DE JAULA EN PONEDORAS

� La discondroplasia tibial (TD) forma parte de un conjunto de alteracionesesqueléticas de las aves de corral producidas en forma intensiva, que entrañandisminución de la performance del lote, del rendimiento individual y del bienestaranimal. Es un desorden del desarrollo, caracterizado por la permanencia decartílago 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

DISCONDROPLASIA TIBIAL(OSTEOCONDROSIS)

� Si bien las lesiones moderadas no impiden que los pollos lleguen al alimento y al agua; eldolor, asociado a las lesiones severas, puede motivarlos a echarse y por consiguiente adisminuir el consumo.

� Un estudio secuencial llevado a cabo en dos líneas comerciales de distinta predisposicióna desarrollar TD sugirió que, en el caso en estudio, la TD estaba relacionada a unapredisposición al raquitismo y asociada a bajos niveles del metabolito activo de lavitamina D3 (el 1,25(OH)2vitamina D3) en la circulación sanguínea, en el período demayor crecimiento de la tibia.

� En un sentido amplio este desorden del desarrollo está determinado genéticamente einfluido por el manejo a través de factores tales como: nivel de actividad,composición de la dieta y método de alimentación.

� La TD es un desorden del desarrollo,caracterizado por la permanencia decartílago anormal en el extremoproximal de la tibia. La mayorfrecuencia de esta afección en eltibiotarso se ha relacionado con laelevada actividad metabólica queeste hueso presenta hacia la tercersemana de edad, producto de surápido crecimiento.

� Ocurre en pollos, pavos y patos como� Ocurre en pollos, pavos y patos comoresultado de una falla en la maduraciónde los condrocitos que están proliferandoen el disco de crecimiento. Esta fallaimpide la penetración vascular y, por lotanto, la normal producción de hueso(Sanotra et al., 2001).

� Cuando se practican cortes sagitales ocoronales del extremo proximal de latibia, se observa una placa de cartílagoque ensancha la metáfisis (Figura 1).

Figura 1. Tibias de Pollos. Cortes Sagitales de los Extremos Proximales. Izquierda:

discondroplasia grado 3; Derecha: cartílago epifisiario normal

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

� What causes cannibalism?

� Cannibalism often starts as feather pulling or pickingwhile the birds are only a few weeks old or asinvestigative pecking at any age. These behaviourscan escalate to aggressive pecking, particularly ifinjury occurs. Scientific study has shown that anyor a combination of stressors can also serve as

PICAJE - CANIBALISMO

or a combination of stressors can also serve astriggers leading to serious aggressive peckingand 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.

Prevention and treatment of cannibalism :

� Good husbandry practices should aim to minimise the stressors listed above aspotential causes for cannibalism.

� Some strains of birds have been shown to have a higher tendency towards developing aggressivepecking 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 insome poultry housing systems can be very difficult if not impossible, such as in freerange systems. Where outbreaks of cannibalism have occurred in a flock, or where there is areasonable 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 tipthen beak trimming of the birds may be used as a control measure. Trimming of the sharp tipof the upper, and sometimes also lower, beak reduces the damage that is caused by aggressivepecking.

� The spread of the behaviour may be able to be controlled if the injured and the aggressive birdscan be rapidly identified and removed from the flock. Provision of escape areas may also helpin floor-housed flocks. Other control methods that have been tested include the use ofspectacles to prevent forward vision, bits that prevent complete closure of the beak andcoloured contact lenses to prevent the identification of blood on another bird.

� There is evidence that cannibalism may be alleviated through the use of high fibrediets. It is believed that high fibre diets enhance gut development and gizzard function,which in turn help reduce aggressive behaviour in hens

DESORDENES METABOLICOSASCITIS

Figura 1. Aspecto macroscópico de unanimal en el que se aprecia buen estadode carne y severa ascitis compuesta por

material de aspecto gelatinoso.

Figura 2. Aspecto macroscópico de lospulmones que muestran coloración oscura

debido a congestión severa y múltiplesáreas redondeadas de color blanquecino o

blanco-rojizo.

� The ascites syndrome, a metabolic disorder that

accounts for OVER 25% OF OVERALLMORTALITY, has become the most noticeable,

non-infectious cause of loss in the broilerindustry worldwide[1].

� There are many factors that cause ascites, forexample, high altitude, rapid growth rate,

DESORDENES METABOLICOSASCITIS

� 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 OFDIETARY VITAMIN C and E ALONG WITHSELENIUM YEAST MIGHT BE BENEFICIAL,presumably because of their role in improving

example, high altitude, rapid growth rate,limiting lung volume, the provision of highenergy rations and pelleted diets, cold, poorventilation, the presence of respiratory disease,high sodium and low dietary phosphorus levels,hepatotoxins, mycotoxins and furazolidone inthe 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.

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 dietaryelectrolyte 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.

� The use of nutrients/drug agents that increase the vascular capacity of the lungs or decreasethe pulmonary vascular resistance may help to alleviate the problem, but economic and localfeed regulations might restrict such use. Diuretics have also shown positive effects, presumablybecause there is a reduction of sodium and fluid retention in the body; litter humidity however mustbe closely monitored if diuretics are continuously administered. As the high metabolic rate (fastgrowth) is a major factor contributing to the susceptibility of broilers to ascites, early-age feed ornutrient restriction (qualitative or quantitative) or light restriction in order to slow down the growthrate seem practically viable methods, since final body weight is not compromised. Optimization ofthe house temperature and ventilation in cold weather seem helpful practices to decrease ascitesincidence.

� Under practical conditions, it might be interesting to test the additive effects of different approacheswhen used in combination.

� It can be concluded that the addition of vitamin C to the diet clearly counteracts the increase in� It can be concluded that the addition of vitamin C to the diet clearly counteracts the increase inascites mortality due to low ambient temperature or to dietary T3 supplementation. Further studiesare needed to elucidate the exact underlying physiological mechanism.

� Mycotoxinas.

� Cobre.

� Aminas biogenicas.

� Harina pescado (Gizzerosine)

� Torta de Soya de mala calidad?

� Adenovirus.

EROSION DE MOLLEJA

� 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

� Introduction:

� Management of the dry cow plays an important rolein 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:

DESORDENES EN VACUNOS

calving time) are:

� - Milk fever

� - Udder edema

� - Ketosis

� - Fat cow syndrome

� - Retained placenta

� - Displaced abomasum

� - Rumen acidosis

� - Laminitis

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

CETOSIS BOVINA

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

Celulosa

Tejidos HígadoHígado y

FFAProteínas

aminoácidos

TAG

glicerol

Tejidos

Obtenciónenergía

CUERPOSCETÓNICOS

Glucosa

Degradación bacteriana

ButiratoAcetato Propionato

Fermentación bacteriana

Absorción en el rumen

El peculiar metabolismo energético

de los rumiantes

Tejidos

Obtenciónenergía

HígadoHígado ytejidos

Obtenciónenergía yacetil-CoA

GLUCOSA Sangre

Niveles glucosa sangre

Sistema nervioso

Lactosa (leche)

Tratamiento: Inyección intravenosa de glucosaPrecursores gluconeogénicos

Corticoesteroides (favorecen uso de aminoácidos gluconeogénicos)

Gluconeogénesis

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 orina3) Etiología:

TOXEMIA DE GESTACION

4) Tratamiento: Inyección glucosaPrecursores gluconeogénicosInterrumpir la gestación

Factores: Escasez de alimentoEstrés (meteorología adversa)Más de un feto

Causa: gran demanda de glucosa por parte de los fetos

Muertefetos por

hipoglucemia

Descomposiciónfetos

Toxinas Gluconeogénesismaterna

1) Síntomas: Pérdida de apetitoEstreñimientoDificultad para caminar y levantarse↓temperatura corporal (extremidades)Arrastre patas traserasInconsciencia y muerte

Productores de leche. Hipocalcemia. Costosa de tratar

FIEBRE DE LA LECHE

2) Características bioquímicas: ↓calcio en sangre

4) Tratamiento: Inyección solución calcio

3) Etiología: Causa desconocidaAlimentos ricos en calcio (al final de la gestación)Alimentos ricos en potasio (impide movilización de calcio óseo)

Hueso calcio producciónleche

Dieta

Hueso calcio producciónleche

Dieta