DESORDENES METABOLICOS

UNIVERSIDAD NACIONAL “SAN LUIS GONZAGA “ – DE ICA

FACULTAD DE MEDICINA VETERINARIA

DEPARTAMENTO DE PRODUCCION ANIMAL

CURSO DE NUTRICION ANIMAL-2011-II

DESORDENES METABOLICOS

Breed utilization, genetic improvement, and industry consolidation arepredicted to have major impacts on the genetic composition of commercialchickens. Consequently, the question arises as to whether sufficient geneticdiversity remains within industry stocks to address future needs. With thechicken genome sequence and more than 2.8 million single-nucleotidepolymorphisms (SNPs), it is now possible to address biodiversity using apreviously unattainable metric: missing alleles. To achieve this assessment,2551 informative SNPs were genotyped on 2580 individuals, including 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 frequency distributionfrom a hypothetical ancestral population as a reference, then determining theportion of the distribution lost, and then (2) determining the relationshipbetween allele loss and the inbreeding coefficient. The results indicate that50% or more of the genetic diversity in ancestral breeds is absent incommercial pure lines. The missing genetic diversity resulted from the limitednumber of incorporated breeds. As such, hypothetically combining stockswithin a company could recover only preexisting within-breed variability, butnot more rare ancestral alleles. We establish that SNP weights act as sentinelsof biodiversity and provide an objective assessment of the strains that aremost valuable for preserving genetic diversity. This is the first experimentalanalysis investigating the extant genetic diversity of virtually an entireagricultural commodity. The methods presented are the first to characterizebiodiversity in terms of allelic diversity and to objectively link rate of allele losswith the inbreeding coefficient.

� Son precipitados por muchos factores:

Medio ambiente, ingredientes alimenticios, yprincipalmente por un metabolismo yproductividad incrementada:

DESORDENES METABOLICOS

productividad incrementada:* Pollos machos de 3 kg de peso vivo a los 42 dias deedad.

* Pavitos obtienen 1 kg de ganancia de peso vivo porsemana de edad.

* Ponedoras comerciales son capaces de poner 330huevos en 365 dias

� A causa del avance en laselección genética, manejo ynutrición, los pollos y pavoscomerciales modernos de hoy díatienen una tasa de rápidocrecimiento, y alta eficienciaen conversión alimenticia ytasa metabólica.

� Estas características promuevenun INCREMENTO DE LAINTENSIDAD DEL SISTEMAINTENSIDAD DEL SISTEMACARDIOVASCULAR (Porqué?)PREDISPONIENDO A LASAVES A DESORDENESMETABÓLICOS tal como fallasventriculares, síndrome ascítico,arritmias cardiacas, desordenescardiopulmonares y muertesúbita.

� 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 chickensand turkeys are responsible for a major portion of the flockmortality;mortality;

(2) MUSCULOSKELETAL DISORDERS, which account for lessmortality, but in broilers and turkeys slow down growth(thereby reducing profit), and cause lameness, which remainsa major welfare concern.

In addition, conditions such as osteoporosis and hypocalcaemiain 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

SINDROME DE MUERTE SUBITA

Afecta pollos de engorde de rápido crecimiento.

Más en machos.

SINDROME de MUERTE SUBITA

Más en machos.

21 A 28 días de edad

Sin signos clínicos

Pocos cambios patológicos.

� Causas y factoresrelacionados:

� En la actualidad, la aviculturacomercial tiene un carácterintensivo, empleandoanimales de gran potencialgenético y elevadas exigenciasgenético y elevadas exigenciasen instalaciones,alimentación, sanidad ymanejo.

� La fragilidad metabólica ymayor propensión al estrésdel pollo parrillero afectan lasalud productiva

� 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 altosniveles altos

� Biotina.

� Taurina

� Tipo de grasa

� Textura de la dieta.

� Programa de luz.

�Tratamiento y prevención:

� No hay tratamiento único.

� Restricción alimento � 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.

� Serum accumulation in lung (may be little if examined shortly after death).

� Livers heavier than those of pen-mates (as a percentage of bodyweight.). 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 excessivecalorie intake, but it may also be related to exposureto the mycotoxin aflatoxin, calcium deficiency andstress.

SINDROME DE HIGADO GRASO

stress.

� An incorrect protein: energy balance may be to blame.Some strains of laying hen appear to be moresusceptible.

� Birds within a flock that are most affected tend to bethe higher producing hens. Fatty liver syndrome hasbeen seen in conjunction with cage layer fatigue.

Causa de hipoglucemia,incapacidad de llevar a cabo lagluconeogénesis comoconsecuencia de una baja actividadde la piruvato descarboxilasa

PIRUVATOCARBOXILASA

Tratamiento: Suplementación con biotina

Dieta con alto contenido proteico o lipídico

Metabolismo hepático durante ayuno

� Excesiva acumulación de grasa en el hígado asociado con varios grados de

hemorragia.� Afecta gallinas ponedoras, reproductoras

pesadas y reproductoras de pavos.

SINDROME DE HIGADO GRASO HEMORRAGICO

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� 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.

SINDROME DE HIGADO Y RIÑON GRASO

� 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.� 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.� Nutrición de reproductoras.

� Aumentar niveles cuando se usan sulfas y dietas bajas en proteína.

� Evitar estrés

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: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

Problemas podales

artritis osteopatías

osteítis osteodisplasiasosteodistrofias

DESORDENES ESQUELETICOS

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 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 primarilyassociated with nutritional deficiencies of calcium, phosphorus, orassociated with nutritional deficiencies of calcium, phosphorus, orvitamin D, whereas osteoporosis is an altogether more complexproblem.

Osteoporosis, cage layer fatigue and poor shell quality have 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 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.

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

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 thataccounts 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,limiting lung volume, the provision of highenergy rations and pelleted diets, cold, poorventilation, the presence of respiratorydisease, high sodium and low dietaryphosphorus levels, hepatotoxins, mycotoxinsphosphorus levels, hepatotoxins, mycotoxinsand furazolidone in the feed, vitamin E and

� Se deficiencies and stress. Among so manycauses, which one is the main trigger is stillquestionable. It was reported that lowtemperature was an easy and economical methodto trigger ascites. One report has indicated thathigh 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 manyinteracting factors such as genetics, environment andmanagement. Many nutritional, medicinal andmanagement strategies have been proposed to alleviatethe problem. HIGHER LEVELS OF DIETARYVITAMIN C and E ALONG WITH SELENIUM YEASTMIGHT BE BENEFICIAL, presumably because of theirrole in improving cellular integrity. Oils rich in n-3fatty acids have been shown to reduce pulmonaryhypertension and, consequently, ascites incidence. Thepotential use of flax oil has already been demonstrated,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 electrolytebalance on ascites incidence seems to be a promisingfield of research in broiler nutrition. In general,reducing the dietary level of salt (NaCl) and addingbicarbonates to the diet and drinking water have beenproposed as potential .cost-effective. methods to reduceascites 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)

EROSION DE MOLLEJA

(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

� Introduction:

� Management of the dry cow plays an important role in the control of metabolic disorders nearor 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 managementproblems. 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

DESORDENES EN VACUNOS

� - 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

Obtención

energía

CUERPOSCETÓNICOS

Glucosa

Degradación bacteriana

ButiratoAcetato Propionato

Fermentación bacteriana

Absorción en el rumen

El peculiar metabolismo energético

de los rumiantes

Tejidos

Obtención

energía

HígadoHígado y

tejidos

Obtención

energía y

acetil-CoA

GLUCOSA Sangre

Niveles glucosa sangre

Sistema nervioso

Lactosa (leche)

Tratamiento: Inyección intravenosa de glucosa

Precursores 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 orina

3) Etiología:

TOXEMIA DE GESTACION

4) Tratamiento: Inyección glucosa

Precursores gluconeogénicos

Interrumpir la gestación

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

fetosToxinas

Gluconeogénesis

materna

1) Síntomas: Pérdida de apetito

Estreñimiento

Dificultad para caminar y levantarse

↓temperatura corporal (extremidades)

Arrastre patas traseras

Inconsciencia 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 desconocida

Alimentos ricos en calcio (al final de la gestación)

Alimentos ricos en potasio (impide movilización de calcio óseo)

Hueso calcioproducción

leche

Dieta

Hueso calcioproducción

leche

Dieta