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 SNP

genetic 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.

DESORDENES METABOLICOSFactores pre disponentes

• Son precipitados principalmente por:- Alta Intensidad metabolica, y- Alta Productividad:Pollos machos de 3 kg de peso vivoPollos machos de 3 kg de peso vivoa los 42 dias de edad, Pavitosobtienen 1 kg de ganancia de pesovivo por semana de edad,Ponedoras comerciales son capacesde poner 330 huevos en 365 dias

• Otros factores: Medio ambiente,ingredientes alimenticios, etc.

*

DESORDENES METABOLICOSFactores pre disponentes

• 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 tasametabólica.

• Estas características promueven un

� These make up the largest group of poultry

diseases classified as metabolic disordersand cause more economic loss thaninfectious agents.

� Poultry metabolic diseases occur primarily in

two body systems:

(1) CARDIOVASCULAR AILMENTS, which in• 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.

(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. Leeson

Department of Animal and Poultry Science, University of Guelph,

Ontario, Canada N1H 2W1 - 2007 J. Appl. Poult. Res. 16:121–125

DESORDENES METABOLICOSSíndrome de muerte súbita

Afecta pollos de engorde de rápido crecimiento.

Más en machos.

21 A 28 días de edad

Sin signos clínicos

Causas y factores relacionados:

• En la actualidad, la avicultura comercial

tiene un carácter intensivo, empleando

animales de gran potencial genético ySin signos clínicos

Pocos cambios patológicos.

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

DESORDENES METABOLICOSSíndrome de muerte súbita

• Anticoccidiales ionóforos

• Dietas con carbohidratos como fuente de

energía.

• Alta densidad de la dieta

• Bajos niveles de calcio

• Lactato deshidrogenasa.• 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.

• Restricción alimento para regular

el rápido crecimiento.

• Programas de luz.

• Evitar el uso de ionóforos.

• Niveles adecuados de vitaminas.

DESORDENES METABOLICOSSíndrome 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. • 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.

DESORDENES METABOLICOSSíndrome de hígado graso

• What causes fatty liver syndrome?• The principal cause is thought to be an

excessive calorie intake, but it may alsobe related to exposure to the mycotoxinaflatoxin, calcium deficiency andstress.

Causa de hipoglucemia, incapacidad de llevar a cabo la

gluconeogénesis como consecuencia de una baja actividad

de la piruvato descarboxilasa

PIRUVATOCARBOXILASA

stress.• An incorrect protein: energy balance may

be to blame. Some strains of laying henappear to be more susceptible.

• Birds within a flock that are most affectedtend to be the higher producing hens.Fatty liver syndrome has been seen inconjunction with cage layer fatigue.

Tratamiento: Suplementación con biotina

Dieta con alto contenido proteico o lipídico

DESORDENES METABOLICOSSíndrome 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.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.

DESORDENES METABOLICOSSíndrome 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

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

DESORDENES METABOLICOSDesordenes esqueléticos

Problemas podales

artritis osteopatías

osteítis osteodisplasiasosteodistrofias

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 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

DISCONDROPLASIA TIBIAL

(OSTEOCONDROSIS)

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.

• 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 deresultado 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

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 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

PICAJE - CANIBALISMO

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.

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 alsobirds 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

DESORDENES METABOLICOSASCITIS

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.

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.

DESORDENES METABOLICOSASCITIS

� 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,

� 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 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 neededmortality due to low ambient temperature or to dietary T3 supplementation. Further studies are 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 importantrole 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

DESORDENES EN VACUNOS

• 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

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

ULTIMO TRABAJO

• Informe de peso de pollos y gallinas del

experimento

• Informe de actividad en el experimento