Factors Affecting Ketosis on a Large Southern Ontario Dairy Farm
Melissa L. Davies
Ontario Veterinary College, University of Guelph, Ontario
Tavistock Veterinarians, Tavistock, Ontario
Abstract
Subclinical ketosis is an important metabolic disease in transition dairy cows, which can lead to a decrease
in milk production and increased incidence of diseases such as retained placenta, metritis, fatty liver and
mastitis. Heat stress and feeding of a ration that contains butyric acid are two factors that could result in an
increase in herd prevalence of subclinical and clinical ketosis. This study on a dairy herd in Southern Ontario
examined the correlation of elevated ambient temperature, feeding silage containing high levels of butyric acid
on the herd prevalence of ketosis. In this herd the increased baseline prevalence of ketosis in fresh cows, along
with the variability of herd prevalence between tests was attributed to elevated ambient temperatures and
feeding of silage containing high levels of butyric acid.
Introduction
Subclinical ketosis (SCK) has been defined as a condition marked by increased levels of circulating ketone
bodies without the presence of clinical signs of ketosis (1). SCK causes economic losses in dairy herds directly
by decreasing milk production and indirectly by increasing the risk for displaced abomasum and other
periparturient diseases. Not only can SCK be a result of numerous disease processes that drive down feed
intakes but it can also initiate further intake suppression, potentially resulting in other disease events such as
displaced abomasum, fatty liver, endometritis, mastitis, retain placenta, or infertility. The first few weeks of
lactation are associated with a negative energy balance and low dry matter intake (DMI), with a peak intake at
eight to ten weeks post-calving. The resulting low serum concentrations of glucose and insulin can lead to the
mobilization of body fat stores for use as energy causing a release of non-esterified fatty acids (NEFAs) into the
blood stream, which in turn increases serum β-hydroxybutyrate (BHBA) (2).
The fresh cows included in this study calved between July 8th and August 30th, 2010 on a 150 cow, wellmanaged Holstein dairy herd in Southern Ontario. The cows are milked in a double 12 parallel parlour and
housed in a 4 row free-stall mattress barn. Herd production in June, 2010 was 36Kg 3.5% BF and 3.1% protein
with a pregnancy rate of 21%. Dry cows are housed in the free-stall barn and then moved to the close-up straw
pack 3 weeks prior to expected calving. Immediately after calving, the dams are moved to the fresh pen, where
they remain for a minimum of fourteen days, until moving to the free stall barn with the milking herd. The fresh
pen is a straw bedding pack with self-locking headgates and a slatted floor along the feed bunk. The fresh cows
were fed a haylage, corn silage, straw, protein supplement and mineral ration and the dry cows were fed straw,
corn silage, protein, and mineral ration. Any animal that required treatment for ketosis after fourteen days fresh
remained in the fresh pen until deemed “healthy” upon which they were moved to the free stall barn.
The cows, one to fourteen days fresh, were tested bi-weekly for fourteen days (minimum 4 tests/cow) for
ketosis using a milk Keto-Test strip (Elanco Animal Health, Greenfield, IN) in addition to a basic physical exam
including rectal temperature. For each cow, fresh milk was placed directly onto the pad of the Keto-Test strip,
excess milk was shaken off and the strip was read after sixty seconds. A result of 100 µmol/L of BHBA was
diagnosed as subclinical ketosis and the cow was treated by drenching with 300mL of glycol or Ketamalt
(Bimeda®-MTC Animal Health Inc. Cambridge, Ontario)). A result of 200 µmol/L of BHBA or greater was
treated with intravenous dextrose and Vitamaster (Vétoquinol Canada Inc. Lavaltrie, QC) along with pumping
of water mixed with a fresh cow energy blend, and Ketamalt.
Results
Prevalence of Ketosis
This study was completed at this particular farm due to the high incidence of ketosis and the decrease of
milk production from thirty six to thirty two kilograms. The prevalence of ketosis in the fresh cows was
determined for each test date and was examined over the period of two months: July and August. The Elanco
Animal Health data sheet offers tools for investigation and implementation of action to reduce ketosis. One
suggestion is that a herd ketosis prevalence of 20% should be the goal of most dairy farms (3). They have also
set criteria that, if met, reveal the suspicion of a possible ketosis issue in the herd which may warrant further
examination (Elanco Animal Health). One of Elanco Animal Health’s criteria for investigation of ketosis is the
discovery of a herd prevalence that was three standard deviations above the 20% prevalence goal on one test
date. This herd met the criteria with three peaks greater than three standard deviations (Fig 1). This indicated
that there was a ketosis issue in the fresh cows. These peaks occurred on July 19th (71%), July 28th (78%), and
August 5th (88%), and were preceded by multiple days with maximum ambient temperatures above 26°C
(Environment Canada; Appendix I).
Another interpretation guideline set by Elanco Animal Health states that an investigation is required if
eight consecutive herd test results were above the 20% prevalence mark. On this dairy farm, all of the test dates
resulted in a herd prevalence of 30% or higher (Fig 1) (Elanco Animal Health).
Figure 1: Herd prevalence of ketosis over fifteen test dates. The target herd prevalence of 20% has
been starred and is marked as zero standard deviation (SD; red numbers). A standard deviation of
three has also been marked. A vertical black line between test numbers 7 and 8 separates the tests
completed in July and August, respectively.
Laboratory Data
Feed samples were collected in response to a decrease in butter fat, DMI and milk production. The
samples were submitted to for laboratory analysis; which revealed a butyric acid level of 5.7% x 4.5kg DM.
This feed had been fed to the fresh cows from July 1st to the beginning of September.
To examine if the elevated herd prevalence of ketosis was due to a close up dry cow issue, blood samples
were drawn from all the cows in that pen on one test date. The blood was submitted to the laboratory to
evaluate the NEFA level and all cows were within normal limits.
Disease Incidence
During the two month period in the fresh cow group there were two deaths; one from rupture of pelvic
ligaments that was euthanized and one death from unknown causes. A necropsy was carried out on the cow that
died from an unknown diagnosis; however, the decomposition was too severe to interpret the findings. There
was a slightly increased incidence of metritis in the fresh cows; especially the cows that were positive on the
Keto-Test strip.
Discussion
Silage containing Butyric Acid
Clostridial fermentation of silage can lead to the production of butyric acid and protein degradation
products causing the feed to have a unique odor which is easy to detect. Published papers describing the feeding
of silage containing butyric acid indicate that daily levels of over 50-100g/head/day can cause ketosis and levels
over 200g/head/day may lead to severe ketosis (5,6,7,8). About 750g of butyrate is produced by the ruminal
bacteria each day, and is used as metabolic energy for the muscles of the rumen; however, any excess butyrate is
converted to serum BHBA, a volatile fatty acid, which increases the risk of developing ketosis (9). Silage
containing butyric acid must not be fed in significant quantities to lactating animals, especially those cows in
early lactation and close to calving. Instead, the producer can either: divert, dilute, or destroy the contaminated
silage. Silage with low levels of butyric acid can be used to feed replacement heifers, late lactation cows, or faroff dry cows, but levels need to be monitored as it could impair DMI in these groups. Any feed containing over
2% butyric acid on a dry matter basis should be destroyed (9).
The level of butyric acid in the silage in this study equates to 250g/head/day, which is above the level
suggested for causing severe ketosis. The reason the silage on this farm underwent abnormal fermentation that
created butyric acid was that the first cut haylage was harvested and ensiled at 27% dry matter, which is
extremely wet. This level of butyric acid can account for the herd prevalence of ketosis being greater than the
goal of 20% in eight consecutive tests. It cannot, however, be the sole reason for the ketosis issue on this farm
due to the presence of the dramatic peaks and troughs seen on the graph of herd prevalence (Fig 1). If this
silage was the only contributing factor to the prevalence of ketosis in the fresh cows, the recorded herd
prevalence should not vary so dramatically over such a short time period. In August the prevalence of ketosis in
the herd slowly decreased which is in part because as the silage was fed from the bunker the level of butyric
acid decreased. Also since the NEFA results from the dry cows were within normal limits it was ruled out that
the elevated herd ketosis prevalence was a dry cow issue as well as the fact that the dry cows were not fed the
haylage containing the butyric acid.
Heat Stress
Heat stress is a major factor that can negatively affect milk production in dairy cows, especially highproducing animals in early lactation. Roenfeldt (10) stated that the thermoneutral zone (TNZ) occurs when
ambient temperatures are between 5°C and 25°C. When the environmental temperature is above this level the
cow enters a state of heat stress due to the fact that she is not able to adequately decrease her temperature via
thermoregulatory mechanisms. The shift in the dairy industry to higher producing cattle has potentially
indirectly contributed to the sensitivity of cows to thermal stresses. As milk production increases, the cow must
consume more nutrients, resulting in an increase in metabolic heat production. This, in turn, makes her more
susceptible to heat stress at a lower ambient temperature (11). A cow responds to heat stress using numerous
mechanisms, such as, increasing her respiratory rate and rectal temperature, panting, drooling, sweating,
reducing her milk production, and decreasing DMI (11). Heat stress can be reduced by installing methods to
cool the cows more effectively such as, sprinklers at the feed bunks and in the parlor, appropriately placed fans,
open curtains, avoidance of over-crowding pens, etc.
The ambient temperature in Southern Ontario during the months of July and August 2010 reached record
highs; therefore, heat stress was a significant concern among Ontario dairy producers throughout those months.
As ambient temperature changes daily it potentially is the cause of the large peaks seen on the prevalence graph
(Fig 1). The peaks correlate to multiple days of 26°C or greater temperatures causing a decrease in DMI and an
increase in ketosis (Environment Canada).
The summative effects of heat stress and the feeding of silage containing butyric acid created an
underlying ketosis concern on this particular dairy farm. However, during the period of high ketosis prevalence
it was through consistent monitoring of the fresh cows with the KetoTest strips and treatment of positive cows,
the incidence of disease as a result of severe clinical ketosis was averted in most cases. Monitoring of fresh
cows for ketosis is a valuable tool and allows for treatment of subclinical cows in the hopes of improving their
milk production before a dramatic decreases occurs and to avoid other medical conditions and associated
treatments.
Acknowledgments
The author would like to thank the producer who allowed the study to be conducted on-farm and the
bovine veterinarians at Tavistock Veterinarians especially Dr. Wayne Shewfelt for his guidance, support, and
advice. Thank you.
References
1. Duffield, T. 2000. Subclinical ketosis in lactating dairy cattle. Pages 231-253 in Vet. Clin. North Am. Food
Anim. Pract, Vol. 16, Metabolic Disorders of Ruminants. T. H. Herdt, ed. W.B. Saunders, Philadelphia
2. Radostits OM, Gay CC, Hinchcliff KW, Constable PD. Veterinary Medicine: A Textbook of the Diseases of
Cattle, Sheep, Pigs, Goats and Horses, 10th ed. London: WB Saunders, 2008; pp.1661-1667.
3. Duffield T. 2004. Identifying High Risk Herds. Proceedings of the WBC Congress, Québec, Canada.
4. Tveit B, Lingaas F, Svendsen M, Sjaastad O. 1992. Etiology of Acetonemia in Norwegian Cattle. 1. Effect
of Ketogenic Silage, Season, Energy Level, and Genetic Factors. J Dairy Sci. 75:2421-2432.
5. Lingaas F, Tveit B. 1992. Etiology of Acetonemia in Norwegian Cattle. 2. Effect of Butyric Acid, Valeric
Acid, and Putrescine. J Dairy Sci 75:2433-2439.
6. Schultz LH. 1971. Management and Nutritional Aspects of Ketosis. J Dairy Sci. 54: 962-973.
7. Mills SE, Beitz DC, Young JW. 1986. Charcterization of Metabolic Changes During a Protocol for Inducing
Lactation Ketosis in Dairy Cows. J Dairy Sci. 69:352-361.
8. Oetzel GR. 2007. Herd-Level Ketosis – Diagnosis and Risk Factors. Preconference Seminar 7C: Dairy Herd
Problem Investigation Strategies: Transition Cow Troubleshooting. Proc AABP. 67-91.
9. Roenfeldt S. 1998. You Can’t Afford to Ignore Heat Stress. Dairy Manage. 35(5):6-12.
10. Kadzere CT, Murphy MR, Silanikove N, Maltz E. 2002. Heat Stress in Lactating Dairy Cows: a Review.
Livestock Production Science. 77:59-91.
Appendix I
(Environment Canada)