How to treat negative energy cows?


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What is Negative Energy Balance?
•Difference between energy intake from feed and energy required for body maintenance, production and gestation (Alawneh et al.2012; Heuer.,2000).

•High producing dairy cows mobilize their body fat, and to some extent, protein reserves in order to sustain their milk production which leads animals to enter a state of NEB.
(Knop and Cernescu.2009; Zurek et al.1995).

NEBAL in Dairy Cows
•The primary challenge faced by cows is a sudden increase of nutrient requirements for milk production at a time when dry matter intake (DMI) and nutrient supply lags behind.
•High nutrient demands for galactopoesis are accompanied with mobilization of body reserves to support milk production. Thus the cows enter a physiologically unavoidable negative energy balance status (Grummeret al., 2004; Ingvartsen, 2006)

Onset of Early Lactation
It is characterized by:
↓ Dry Matter Intake
↓ Energy Availabilty
↑ Milk Production
↑ Energy Demand
Transition Period In Dairy Cow:

3 weeks before to 3 weeks after calving (Drackley, 1999).
Harmonal Shift
•Progesterone P4 ↓ ⇒ E2 ↑ ⇒ Fat Mobilization ↑ , DMI ↓

(Drackley et al., 2005;Ingvartsen, 2006).
NEB results in:
•NEB leads to metabolic and microbial diseases such as milk fever, endometritis, ketosis, displaced abomasum and retained placenta (Drackley,1999; Duffield and Herdt, 2000).

•Senatore et al. (1996) noted that first lactation cows experiencing NEB have delayed ovulation.
•Disproportional energy metabolism (fatty liver, Ketosis, SARA) •Disturbed mineral utilization (Milk fever,sub-clinical hypocalcemia) •Perturbed immune function (Retained placenta, metritis, mastitis).
•Kestosis is the imbalanced use of body fat characterized by hypoglycemia and hyperketonemia. (Kehrli et al., 2006)
•Insufficient blood glucose levels induce a decline in plasma insulin, and mobilization of triacylglycerol deposits as NEFA (Block and Sanchez, 2000).
•Complete oxidation of NEFA generates acetyl coenzyme A used to generate energy via the Krebs cycle.If the Krebs cycle gets overloaded the acetyl Co A is diverted to produce ketones (acetoacetic acid, acetone,and -hydroxybutyrate or BHB). If ketones are elevated,clinical ketosis ensues (Block, 2010).
•When switching from a dry-period to an early lactation diet, the mucosa of the rumen will not have adapted yet, as the papillae are too short and the resorbing surface too small to deal with the sudden increase of short-chain fatty acids (SCFA) levels (Nordlund et al., 1995).
It results in Sub-acute ruminal acidosis (SARA).
Milk fever
•Low energy balance disturbs mineral utilization that results in hypocalcemia that leads to milk fever.
•Left-displaced abomasum (LDA) is a disorder that occurs mainly in high producing dairy cows postpartum (Geishauser, 1995).
•Nearly 50% of the LDA cases are accompanied by NEB (Heuer, 2000).
•There is a link between feed intake and subsequent developmentof metritis (Huzzey et al., 2007, 2009).
•Cows with severe metritis eat 2–6 kg DM less than healthy cows in the 2–3 weeks preceding the clinical signs of metritis (Huzzey et al.,2007).

•Endometritis is associated with reduced feed intake, severe negative energy balance, and disturbed immune function (Urton et al., 2005;Hammon et al., 2006; Huzzey et al., 2007).
•It commonly occurs in high producing dairy cows more than 26 days postpartum (Sheldon et al., 2006b).

•Rop is sequelae of disproportional energy metabolism and perturbed immune function.
•Decreased neutrophil function as cause of retained placenta in dairy cattle.

(Kimura, K., Goff, J.P., Kehrli Jr., M.E., Reinhardt, T.A., 2002.)
•A study of effects of NEB on udder inflammation in Holstein dairy cows concluded that animals in severe NEB that had increased SCC in milk (van Straten et al.2009).

•SCC in milk, which can act as an indicator of subclinical mastitis, was observed to be higher in animals with four and more lactations (Syridion et al.2012).
•Animals in a state of NEB eventually lose weight, this could also contribute to the development of lameness. It has been demonstrated that animals with excessive weight loss postpartum had an increased risk of subsequent lameness. (Alawneh et al.2014).
Possible Nutritional Strategies to combat NEB

•The NRC (National Research Council, 2001) guidelines suggest that approximately 1.25 Mcal/kg of net energy for lactation (NEL) has to be fed from dry off until approximately 21 d before calving, and that a diet contain-ing 1.54 to 1.62 Mcal/kg of NEL has to be fed during the last 3 wk preceding parturition.
•Dann et al.(2003) reported that supplying excessive energy to dairy cows during the early dry period may have detrimental carryover effects during the subsequent early lactation period.

1.Increasing DMI
• ↓ Starch content ⇨ ↑ DMI (Allen et al., 2009).
•Caution is advised when formulating early lactation diets to resume ovarian activity since highly fermentable starch diets fed immediately after calving may decrease DMI and prolong NEB (Allen et al.,2009).

2.Carbohydrate based formulation of Prepartum Diet
•Rabelo et al. (2003) says diets higher in non- fiber carbohydrates (NFC) content must be fed prior to calving to promote development of ruminal papillae for adequate absorption of volatile fatty acids produced during ruminal fermentation.
•These increased amounts of propionate support hepatic gluconeogenesis and the production of microbial protein, providing the diet contains sufficient rumen-degradable protein, which in turn satisfies protein requirements for maintenance, pregnancy, and mammogenesis.

Hayirli and collaborators (2002) reported that prepartum DMI was positively correlated with NFC content of the prepartum diet.

3.Fat supplementation in transition diet
•CLA supplementation increases DMI and some of the negative acute phase proteins such as albumin and cholesterol (Trevisi and Bertoni,2008; Esposito et al., 2013).
4.Rumen Protected Choline
•Yields of milk and fat-corrected milk have generally increased in response to feeding rumen-protected choline during the transition period.
•(Hartwell et al., 2000; Piepenbrink andOverton, 2003; Pinotti et al., 2003; Scheer et al., 2002)
•There is a need for nutrition strategies which reduce susceptibility to production diseases.
•Reliable tools to assess the immune status of the cow must be developed to explain the immune responses of peripartal disorders.

•Senatore, E. M., W. R. Butler, and P. A. Oltenacu. 1996. Relationships between energy balance and postpartum ovarian activity and fertility in first lactation dairy cows. J. Anim. Sci. 62:17–23.
•Drackley, J.K., 1999. Biology of dairy cows during the transition period:the final frontier? J. Dairy Sci. 82, 2259–2273.
•Duffield, T., Herdt, T., 2000. Subclinical ketosis in lactating dairy cattle.Vet. Clin. N. Am. Food Anim. Pract. 16, 231–253.
•Ingvartsen, K.L., 2006. Feeding-and management-related diseases in thetransition cow: physiological adaptations around calving and strate-gies to reduce feeding-related diseases. Anim. Feed Sci. Technol. 126,175–213.
•Grummer, R.R., Mashek, D.G., Hayirli, A., 2004. Dry matter intake andenergy balance in the transition period. Vet. Clin. N. Am. Food Anim.Pract. 20 (3), 447–470.

•Nordlund, K.V., Garrett, E.F., Oetzel, G.R., 1995. Herd-based rumenocente-sis: a clinical approach to the diagnosis of subacute rumen acidosis.Compend. Contin. Educ. Pract. Vet., 17

•Geishauser, T., 1995. Abomasal displacement in the bovine – a review oncharacter, occurrence, aetiology and pathogenesis. J. Vet. Med. A 42,229–251.

•Heuer, C., 2000. Negative Energy Balance in Dairy Cows: Prediction, Con-Q5sequences, Prevention. Utrecht University

•Allen, M., Bradford, B., Oba, M., 2009. The hepatic oxidation theory of thecontrol of feed intake
•Trevisi, E., Bertoni, G., 2008. Attenuation with acetylsalicylate treatmentsof inflammatory conditions in periparturient dairy cows. In: Aspirinand Health Research Progress. Nova Science Publishers, Hauppauge,NY, USA, pp. 23–37.