DESORDENES METABOLICOS-2012-I [Modo de

DESORDENES METABOLICOS-2012-I [Modo de

UNIVERSIDAD NACIONAL “SAN LUIS GONZAGA “ – DE ICA
FACULTAD DE MEDICINA VETERINARIA
DEPARTAMENTO DE PRODUCCION ANIMAL
CURSO DE NUTRICION ANIMAL-2011-II
DESORDENES METABOLICOS
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)
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.
DESORDENES METABOLICOS
Son precipitados por muchos factores:
Medio ambiente, ingredientes alimenticios,
principalmente
por
un
metabolismo
y
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
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.
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.
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
SINDROME de MUERTE SUBITA
SINDROME DE MUERTE SUBITA
Afecta pollos de engorde de rápido crecimiento.
Más en machos.
21 A 28 días de edad
Sin signos clínicos
Pocos cambios patológicos.
Causas
y
relacionados:
factores
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
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.
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.
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.
SINDROME DE HIGADO 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.
PIRUVATO
CARBOXILASA
Causa
de
hipoglucemia,
incapacidad de llevar a cabo la
gluconeogénesis
como
consecuencia de una baja actividad
de la piruvato descarboxilasa
Metabolismo hepático durante ayuno
Tratamiento:
Suplementación con biotina
Dieta con alto contenido proteico o lipídico
SINDROME DE HIGADO 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.
SINDROME DE HIGADO Y RIÑON 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 enjauladas
Síndromes
Acumulación de grasa en hígado asociado a hemorragia parecidos pero no
Prevención: control del balance energético (masa corporal) parecen estar
relacionados
Síndrome de hígado y riñón graso (FLKS)
bioquímicamente
Pollos de engorde
Acumulación de grasa alrededor de hígado y riñones
1) Síntomas: Letargo
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
DESORDENES ESQUELETICOS
Problemas podales
artritis
osteítis
osteopatías
osteodistrofias
osteodisplasias
condrodistrofia
discondroplasia
raquitismo
Varus y valgus
osteomalacia
espondilolistesis
Necrosis cabeza del fémur
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?
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.
OSTEOPOROSIS o FATIGA DE JAULA EN
PONEDORAS
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.
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 Figura 1. Tibias de Pollos. Cortes Sagitales
que ensancha la metáfisis (Figura 1).
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
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.
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
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.
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.
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.
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
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
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
El peculiar
Celulosa
metabolism
o energético
Degradación bacteriana
de los
rumiantes
Glucosa
TAG
Proteínas
glicerol
FFA
Fermentación bacteriana
aminoácidos
Acetato
Butirato
Propionato
CUERPOS
CETÓNICOS Obtención
energía
Absorción en el rumen
Hígado y
tejidos
Tejidos
Hígado
Gluconeogénesis
Obtención
energía y
acetil-CoA
Obtención
energía
Tratamiento:
Tejidos
GLUCOSA
Sangre
Niveles glucosa sangre
Sistema nervioso
Lactosa (leche)
Inyección intravenosa de glucosa
Precursores gluconeogénicos
Corticoesteroides (favorecen uso de aminoácidos gluconeogénicos)
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
4) Tratamiento:
Descomposición
fetos
Toxinas
Inyección glucosa
Precursores gluconeogénicos
Interrumpir la gestación
Gluconeogénesis
materna
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)
Dieta
Hueso
Dieta
calcio
producción
leche
Hueso
4) Tratamiento: Inyección solución calcio
calcio
producción
leche