summarizing the metabolic diseases as a main influence on reproductive failure

Summarizing the metabolic diseases as a main influence on

reproductive failure

Paola AmodeoRegional Breeders Association of LombardyCrema– ItalyS.A.T.A. Bovine Nutrition [email protected]

October 25-26 2011 Dott. Paola Amodeo - SATA Bovine Specialist 2

Can genetical selection of dams & sires stop the fertility downbound

trend?

It can help but it is surely not the main drive

Management and nutrition have still a lot to do and say about it


Strong milk producers have worse fertility?

It is all a management challenge


Why should we care?D

ays

in m

ilk

More costs:Dead cows and urgent cullings Better culling value,

voluntary culling

Da

ysin

milk

More costs:Dead cows and urgent cullings Better culling value,

voluntary culling

Post partum involuntary culling(even more expensive for first calving cows)


Why should we care?


Transition cow metabolic diseases lead to reproductive failure

We must search for the causes of such diseases and losses Cow comfort (housing, space, grouping) Environmental (heat stress) Nutritional : mainly related to NEB in

the transition period Seems to be a very important area


Dairy Cow Transition

We are not dealing with macroscopic and gross nutrition mistakes on animal requirements or on macro and micro mineral umpairing as it used to be

Now the problem is more subtle and maybe more sneaky

At the moment it is the main area on which all researchers and nutritionists are concentrating their efforts


Strong physiological changes from dry cow (pregnancy) to lactation

Suppression of appetite

Immune system Suppression

Higher risk for fatty liver, DA, RP, Ketosis and milk fever + masitis and metritis (infectuous)

Fertility culling risk


Main Goal: Control fat mobilization through the transition period to decrease DMI

depression and immune suppression from high non esterified fatty acids

(NEFA)

Latest theory of feed intake control to formulate diets for transition cows

(M.S.Allen and B.J. Bradford – Michigan

State University)


Hepatic Oxidation Theory (HOT)Food intake is controlled by fuels

oxidation in the liver through a system of connections to the

hepatic vagus nerve

Firing rate of the nerve determined by liver oxidation of fuels wich produces ATP: Higher firing rate= hunger Lower firing rate= satiety Higher ATP= more oxidation=lower firing

rate=satietyWe still do not know how ATP concentration

influences firing rate of hepatic vagus nerve


Fuels for oxidation in ruminants are:

Fatty acids (from diet and/or body reserves)

Propionate (by microbial fermentation)

Lactate (by muscles and gut tissues from glucose)

Amino acids (from protein degradation)


…Fatty acids…

NEFA from body fat mobilization (readily oxidized) suppress DMI in the transition period

Fat mobilization is affected by plasma insulin concentration High insulin = fat synthetis Low insulin = fat mobilization


But plasma Insulin decreases by 50% in the pre calving weeks

Lower insulin=more fat mobilization= higer NEFA

Moreover we have a decreased tissue sensitivity to insulin (insulin resistance )

Lower glucose utilization (which remains

constant despite declining of feed intake) so use of NEFA by muscles increases


…At calving..

Plasma glucose concentration drops dramatically at calving

Plasma insulin and insulin tissue sensitivity remain low

Plasma NEFA concentration remain high for several weeks Ketones in plasma

DMI decreases Risk of fatty liver no new glucose production No insuling produced in the pancreas


Mechanism of intake regulation according to the hepathic oxidation theory

Allen et al 2009


NEFA and transition diseases risk

High NEFA in the 2 weeks before calving is associated with

2 to 4 times increased risk of LDA (Cameron et al, 1998; LeBlanc et al, 2005; Opsina et al, 2010)

1.8 times increased risk of retained placenta (RP) (LeBlanc et al 2004)

2 times increased of culling before 60 days in milk (DIM) and 1.5 times increased risk of culling over the whole lactation (Duffield et al, 2005)

Reduced milk yield (Carson, 2008; Opsina et al, 2010)


BHBA and Transition diseases

Subclinical ketosis (BHBA > 1200 – 1400 mol/L) in early lactation is associated with

3 to 8 times increased risk of LDA (Duffield, 1997; Geishauser et al, 2000b; LeBlanc et al 2005)

Decreased probability of pregnancy at first AI (Walsh et al, 2008)

Decreased milk production (Duffield, 2009)

Increased duration and severity of mastitis (Suriyasathaporn, 2000


Suggested herd goals for NEFA and Ketons


AVOID NEB! (Negative Energy Balance)

It suppresses immune function It promotes metabolic disorders It potentially explaines the relationship

between infectious and non infectuous transition disorders

Important role of inflammation response in infectuous diseases as well as metabolic disorders (B.Bradford-Kansas State University)


Inflammation Responsefrom infectuous disorders

Activated immune cells release of nitric oxide, prostaglandins and citokines

Citokines stimulate systemic inflammatory responses (>Temp,<DMI)

Citokines activate production of acute phase proteins (haptoglobin and serum Amyloid A by the liver

•Mammary and uterin infections Local and systemic inflammation

•Coliform MastitisEndotoxines, cytokines

and acute phase proteins•Metritis

High plasma haptoglobin prior to clinical signs of metritis

These non specific inflammatory responses promote development of metabolic disorders by decrease in DMI

and unpair metabolic functions


Inflammation-based pathogenesis of transition cows disorders

Wide evidence of link between inflammation and transition disorders, unpaired repro efficiency, lower plasma calcium concentrations

Metabolic Disorders derive also from inflammation caused by Infections (se above) Oxidative stress (lipids meet ROS (reactive oxigen

species) and produce lipid peroxides Endotoxins from the gut (sub acute ruminal acidosis?


Consequences of such inflammation

Disruption of normal metabolism Induction of metabolic diseases Suppression of immune function

by oxidative stress which damages lipids, proteins and DNA of immune cells


…in summary….

A combination of insults including infection, chronic inflammation in obese cows an lipid peroxide formation promotes systemic inflammation during transition

Inflammation impairs immune function making cows more susceptible to infectuous disorders and to metabolic disorders


…what can we do?

Antioxidants: Vit E and Selenium Contribute to ROS neutralization (both) Decrease production of inflammatory

cytokines (only Vit E) Effects on immune function (only Vit E) Raccomended doses

VIT E = 1500 UI/d in close-up cows Organic Selenium (if deficient) 0,3 ppm/d

(FDA limit)


…what can we do?

Antioxidant Beta Carotene Its concentration dicreases during

transition Recommended dose 600mg/d Can replace Vit A in transition


…what can we do?

Metabolic modifiers: PPAR Agonists of peroxisome receptors Decrease Plasma NEFA concentration Promote fatty acid oxidation in liver Limit triglyceride accumulation and

production of lipid peroxides

NOT APPROVED!


…what can we do?

Choline Limits peroxides formation by

decreasing plasma NEFA and clearing triglycerides from the liver

In the rumen protected form it may contribute to immune functions


…what can we do?

Anti inflammatory agents: NSAIDs (non-steroid anti-inflammatory drugs)

Prevention of hypoglicemia Effective at reducing body temperature Do not consistently improve recovery from

infections Better activity against metabolic disorders Aspirin: lower production of haptoglobine

Future research needed


Nutritional strategies for Transition cows

Late lactation and far off Dry Cows

Limit mobilization of body fat by controlling BCS during late lactation

Feed high NDF, low energy in dry cows

Feed low concentration of high fermentable starch in dry cows



Close-up

Feed high fill, moderate energy diets in close-up cows (Drackley, Overton) control energy intake reduce fat depots sustain plasma glucose through calving increase amount of ruminal digesta

which dicreases risk of DAs increase bufferuing capacity (acidosis) increase acetate production, dicreases

propionate production



Close-up

Correct choice of forages Low potassium content if grasses Not too high NDF fermentability Wheat straw has a slow rumen passage and

slows down diet passage rate (mat) also increasing digesta retention

FATs: should not be fed Can depress feed intake and increase fat

oxidationException: Ω3???? Perhaps antiinflammatory


Overall goals for energy intake of both far-off and close-up cows

Far off cows (dry off until ~ 3 weeks precalving ~18 Mcal of NEL per day

Close-up cows (last 3 weeks before calving) ~19 Mcal of NEL per day

Vary energy density of diets based upon group DMI If energy intake low, increasing energy density may help If energy intake too high, bulk up the diet to control

energy intake

The ONLY way to minimize management/facility-induced variation in feed intake among cows is to ensure that the group is FULLY FED


Drakley’s guidelines for dry cow diets2006


Drakley’s guidelines for closee-up cow diets2006

Low K only Full anionic

NEL, Mcal/lb 0.66 to 0.68 NEL, Mcal/kg 1.45 to 1.50 Metabolizable protein, g/d 1100 to 1200 NFC, % 30 to 34 Starch, % 17 to 20 Dietary Ca, g/d 100 140 Dietary Ca, % 0.90 1.2 Dietary P, % 0.30 to 0.35 Mg, % 0.40 to 0.42 Cl, % 0.3 0.8 to 1.2 K, % < 1.3 < 1.3 Na, % 0.10 to 0.15 S % 0.20 0.3 to 0.4 Added Se, ppm (organic) 0.3 Vitamin A (IU/d) 100000 100000 Vitamin D (IU/d) 30000 30000 Vitamin E (IU/d) 1800 1800 Prefer use of organic trace elements, including organic Se



Fresh cows (0-14 days post partum)

Avoid highly fermentable starch sources (high propionate production stimulation of oxidation of Acetyl CoA suppress feed intake)

Dry Corn is best (provide glucose precursors and less propionate)

As gut fills begins to dominate feed a less filling and more fermentable diet


Next problem….

How can we move from theory to practice?

Thanks for the attention

summarizing the metabolic diseases as a main influence on reproductive failure

Documents

bovine nutrition

fuels oxidation

higher firing rate

hungerlower firing rate

fatty liver

liver oxidation of fuels

hepatic vagus nervefiring

main influence