Subclinical Ketosis Types, Impacts, and Risk Factors
The transition period, three weeks before and after calving, is arguably the most important time in a cow's life. After calving, the cow has an increased energy requirement for milk production, but her feed energy intake is reduced. This results in negative energy balance (NEB), which is associated with an increased risk for metabolic disorders, such as hyperketonemia, or ketosis. Subclinical ketosis results from prolonged negative energy balance in the absence of clinical signs of ketosis.
During this time cows are also at risk of developing associated periparturient diseases, such as retained placenta, metritis, displaced abomasum, lameness, and clinical ketosis. It was documented that around 30 to 50 percent of dairy cows develop metabolic or infectious diseases following calving (LeBlanc, 2010).
Under these conditions production performance decreases, herd health status deteriorates, and risk for early culling increases. All these factors add significant costs to the producer.
Hyperketonemia as a component of subclinical ketosis (SCK) is a major cow health issue on dairy farms universally. It was estimated that the global prevalence is over 20 percent (Overton, 2017). In the U.S. the SCK prevalence ranges from 5 – 80 percent (Armstrong, 2020), with an average of 28.9 percent at 5 days in milk (DIM) (Oetzel, 2013). In some European countries, the prevalence of SCK ranges from 11.2 – 36 percent within 2-15 DIM, and 32 – 49 percent within 7-21 DIM, with the highest prevalence in France, the Netherlands, Germany, and Italy (Lei and Simoes, 2021).
Types of Ketosis
Clinical or spontaneous ketosis - is caused by poor energy supply in early lactation and occurs between 3 – 6 weeks postpartum, close to the peak of lactation when milk production exceeds the amount of glucose available (Kronfeld, 1982). Glucose precursors from the diet are not sufficient and cows are in a state of chronic hypoglycemia. Cows with spontaneous ketosis do not develop the ‘fatty liver syndrome’. The key solution to this disorder is to review the diet for adequate supplied energy.
Subclinical ketosis or hyperketonemia - fatty liver complex is the most prevalent ketosis on dairy farms. It is caused by fatty liver disease at the beginning of lactation before or at birth, due to the excessive mobilization of body fat (Lei and Simoes, 2021). Usually, it occurs between 5 to 15 days but can linger up to 21 days. The earlier in the lactation it occurs the more severe it is. Obese cows or heifers at calving are likely to develop this type of ketosis. The key solution is a balanced diet through dry and close-up periods and low stress. Â
Dietary ketosis – occurs when poorly fermented wet grass or legume silages with high levels of butyric acid (>0.5 to 1% of DM) are fed to the cows in large quantities. In wet or poorly ensiled grasses aerobic fermentation by butyric acid-producing bacteria overwhelms the lactic acid-producing bacteria and can result in a high butyric acid content. Producers can check the buy acid forage level in the forage analysis report. The key solution is to avoid feeding butyric acid-laden silage to transition cows.
Negative Impacts of Subclinical Ketosis
Cows with SCK do not show any of the signs that are exhibited during clinical ketosis (markedly decreased milk production, decreased feed intake, dry manure, rapid loss of body condition, and in exceptionally severe cases, neurological signs such as leaning or walking against the stall front, licking, or chewing (LeBlanc, 2015)). These cows do have the usual appetite without reducing DMI (Zhang, 2020). However, they do manifest lower production and lower reproductive performance and are likely to develop periparturient diseases.
 Studies reported overall economic losses in the range of $129 to $289 per case of SCK (Liang et al., 2017; McArt et al., 2015) primarily due to milk losses, feed costs, increased postpartum diseases, replacement costs, and premature culling. However, if subclinical ketosis is concurrent with a second or third disease condition the costs can almost double. Overall economic losses were estimated about 50 percent higher for multiparous vs primiparous cows (Lei at al, 2021; McArt et al., 2015; Liang at al., 2017).
Lei et al. (2021) estimated that in 100 cow dairy with 21.8 percent prevalence of SCK, the losses range from $4, 4425 to $6,000 per year.
Milk yield reduction can vary from 2.2 lbs to 5.3 lbs/day/cow (4.4% - 7%) between hyperketotic and non-ketotic cows during the first week after calving (Oetzel, 2013).
Differences in milk yield losses depend on the severity and onset of SCK. Modest vs. severe SCK reduced milk yield by 13.2 lbs/d/cow for the first 30 DIM (McArt, 2012). Cows with SCK onset 3-7 DIM produced about 4.6 lbs/d/cow less for the first 30 DIM than cows with SCK onset between 8 and 16 DIM (McArt et al., 2012).
Cows with untreated SCK have a three times higher chance of being removed from the herd during the first 30 DIM due to being sold or dying (McArt et al., 2012). Early SCK detection with propylene glycol oral treatment reduces this risk significantly.
Subclinical ketosis has a profound effect on the risk for subsequently displaced abomasum (DA), cows with SCK are 3-19 times more likely to develop DA (Ospina, 2010; Oetzel, 2013). The earlier the SCK ketosis develops in lactation (3-5 DIM vs. 6-16 DIM) the more likely for cows to develop DA (Oetzel, 2013).
Cows with SCK have 1.1 - 7.2 times greater odds of developing metritis (Duffield, 2009; Ospina, 2010) due to impaired immune function; 1.4 times greater odds of developing endometritis; 4-6 times higher risk of clinical ketosis; increased severity and duration mastitis; 1.2 – 1.7 times less likely to conceive at first breeding and consequently decreased pregnancy rates (LeBlanc, 2015; McArt et al., 20212b).
Subclinical Ketosis Risk Factors
Nutritional factors have been thought of as the root and solution to SCK problems. Balanced nutrition, adequate energy supply, and dry matter intake during the dry period, transition, and early lactation have undeniable roles. However, researchers in Wisconsin assessed that only 15 – 20% of the transition cow issues, including SCK, were caused by nutrition. Factors of biological or environmental and/or management origin contribute to the occurrence of SCK on dairy farms as well.
Recent research suggests that the biological factors are not necessarily related to the adipose tissue metabolism during the transition period, but rather to the immune system utilization of glucose during inflammation. It has been postulated that inflammation before calving accentuates the reduction in feed intake, stimulates increased adipose tissue mobilization, creates an additional drain for glucose, and thus subsequently promotes ketone synthesis inducing the state of hyperketonemia (Horst et. al., 2021).
The management factors that create less than desirable conditions for the cows are qualified as stressors. These stressors usually limit DMI and rumination time.
Biological Factors
Breed – Jerseys herd have a higher prevalence of ketosis (11.4 – 25%) as opposed to Holstein (0-28%) (Chandler et al., 2018).
Body condition – cows or heifers with high body condition scores (BCS >4) at calving associated with overfeeding during the dry period are critical risk factors for developing SCK (Leslie et al., 2000).
Days in Milk - a higher prevalence of SCK occurs in the first two weeks of lactation, a period after which there is a significant decline in prevalence. Others observed the peak of prevalence at 5 DIM (McArt et al., 2012).
Parity – it was suggested that for Holstein cows higher lactation has a direct link to a higher occurrence of SCK. However, a higher prevalence of SCK in Jersey cows occurs in primiparous. (Chandler, 2018).
Season Differences– Some authors reported Spring as the most problematic season for SCK in general, while others suggested that Summer may be the highest for SCK prevalence due to heat stress, suppressed feed intake, low silage quality, and overall reduced management intensity (Leslie at al., 2000; Lei and Simoes, 2021).
Management Factors
Herd size – large herds have a generally lower prevalence of SCK than smaller herds. Large herds implement better strategies for grouping cows according to milk productivity which allows for better nutrition management for each group. (Lei and Simons, 2021).
Sufficient buck space, overcrowded pens, co-mingling cows and heifers, an excessive number of group changes, heat stress, and hardness of standing surface were identified as significant contributors to SCK incidence (Nordlund, 2010).
References
Armstrong J. How to manage subclinical ketosis (SCK) on your dairy, U of Minnesota Extension, 2020.
Chandler, T.L.; Pralle, R.S.; Dórea, J.R.R.; Poock, S.E.; Oetzel, G.R.; Fourdraine, R.H.; White, H.M. Predicting hyperketonemia by logistic and linear regression using test-day milk and performance variables in early-lactation Holstein and Jersey cows. J. Dairy Sci. 2018, 101:2476–2491.
Duffield, T. 2000. Subclinical ketosis in lactating dairy cattle. Vet. Clin. North Am. Food Anim. Pract. 16:231-253.
Horst, E. A., Kvidera S. K., and Baumgard, L. H. The influence of immune activation on transition cow health and performance—A critical evaluation of traditional dogmas. J. Dairy Sci. 2021, 104:8380-8410.
LeBlanc, S. J. 2010. Monitoring metabolic health of dairy cattle in the transition period. J. Reprod. Dev. 56:S29–S35
LeBlanc, S. 2015. Managing Ketosis in the Transition Cow for Health and Reproduction. Dairy Cattle Reproduction Council Proceedings, Buffalo, NY. 94-101.
Lei M. A. C., Simoes J. 2021.Ketosis Diagnosis and Monitoring in High-Producing Dairy Cows. Dairy.
 Liang, D.; Arnold, L.M.; Stowe, C.J.; Harmon, R.J.; Bewley, J.M. Estimating US dairy clinical disease costs with a stochastic simulation model. J. Dairy Sci. 2017, 100, 1472–1486
Leslie K. E., Duffiled T.F., Schikken Y. H. , LeBlanc S. J., The Influence of Negative energy on Udder Health, National Mastitis Council Regional Meeting Proceedings (2000)
McArt, J. A., D. V. Nydam, and G. R. Oetzel. 2012a. Epidemiology of subclinical ketosis in early lactation dairy cattle. J. Dairy Sci. 95:5056-5066.
McArt, J. A., D. V. Nydam, and G. R. Oetzel. 2012b. A field trial on the effect of propylene glycol on displaced abomasum, removal from herd, and reproduction in fresh cows diagnosed with subclinical ketosis. J. Dairy Sci. 95:2505-2512.
McArt, J.A.A.; Nydam, D.V.; Overton, M.W. 2015.Hyperketonemia in early lactation dairy cattle: A deterministic estimate of component and total cost per case. J. Dairy Sci. 2015, 98, 2043–2054
Nordlund K. Five Keys to Preventing Poor Transition Cows. Hoard’s Dairyman, April 25, 2010 .
Oetzel, G. R. 2013. Understanding the Impact of Subclinical Ketosis. Department of Medical Sciences, University of Wisconsin, Madison 53706.
Ospina, P. A., D. V. Nydam, T. Stokol, and T. R. Overton. 2010. Evaluation of nonesterified fatty acids and beta-hydroxybutyrate in transition dairy cattle in the northeastern United States: Critical thresholds for prediction of clinical diseases. J. Dairy Sci. 93:546-554.
Overton, T.R., McArt J.A.A., Nydam D.V. A 100-Year Review: Metabolic health indicators and management of dairy cattle. DJDS 100: 10398-10417, 2017
 Zhang, G.; Ametaj, B.N. Ketosis an old story under a new approach. Dairy 2020, 1, 5.










