The Veterinary Journal 188 (2011) 122–124

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The Veterinary Journal

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Short Communication Prevalence of subclinical in dairy herds

Timothy A. Reinhardt a,*, John D. Lippolis a, Brian J. McCluskey b, Jesse P. Goff a,1, Ronald L. Horst a,2 a Periparturient Diseases of Cattle Research Unit, USDA-Agricultural Research Service, National Animal Disease Center, Ames, IA 50010, USA b Centers for Epidemiology and Animal Health, USDA-APHIS, Fort Collins, CO, USA article info abstract

Article history: The prevalence of subclinical hypocalcemia in the transition cow is unknown. Cows with subclinical Accepted 29 March 2010 hypocalcemia have no clinical signs of hypocalcemia but may be more susceptible to other diseases. The objective of this study was to determine the prevalence of subclinical hypocalcemia in the US dairy herds. As a part of the United States Department of Agriculture’s National Animal Health Monitoring Sys- Keywords: tem 2002 Dairy study, serum samples were collected from 1462 cows within 48 h of parturition. The fever samples were sorted by number: 1st (n = 454), 2nd (n = 447), 3rd (n = 291), 4th (n = 166), 5th Hypocalcemia (n = 72), and 6th (n = 32). Subclinical hypocalcemia (<2.0 mM) increased with age and was present in Subclinical hypocalcemia 25%, 41%, 49%, 51%, 54%, and 42% of 1st–6th lactation cows, respectively. Cows with serum con- Dietary cation anion difference (DCAD) Anion–cation balance centrations >2.0 mM had significantly lower serum non-esterified fatty acids indicating better energy Non-esterified fatty acids (NEFA) balance than those with subclinical hypocalcemia. Subclinical hypocalcemia may make cows more sus- ceptible to secondary diseases but more research will be required to determine if this is true. Published by Elsevier Ltd.

Clinical hypocalcemia (milk fever) in dairy cows is an econom- et al., 2007). Data were analyzed by ANOVA using a factorial design ically important disease and significantly increases a cow’s suscep- in the JMP statistical package (SAS Institute). The main effects were tibility to mastitis, retained fetal membranes, displaced lactation number and clinical signs of milk fever. Means and SEM abomasum, dystocia and ketosis, which can reduce a cow’s produc- are reported for all data. Means separation was conducted by the tive life (Curtis et al., 1983, 1985). Hypocalcemia reduces the abil- method of Tukey. ity of immune cells to respond to stimuli (Kimura et al., 2006) thus The overall incidence of milk fever found from the NAHMS 2002 contributing to infections, such as mastitis. Hypocalcemia reduces Dairy study was 5%, which aligns with the 5–7% incidence of clin- smooth muscle contraction, which results in reduced rumen and ical hypocalcemia reported by others (DeGaris and Lean, 2008; abomasal motility leading to displaced abomasum and reduced Goff, 2008; Mulligan and Doherty, 2008). Fig. 1 shows the inci- feed intake (Goff, 2008). Its effects on muscle contraction prevent dence of subclinical and clinical hypocalcemia by lactation num- efficient teat closure, which contributes to mastitis (Goff, 2008). ber. The Merck Veterinary Manual defines normal blood calcium The objective of this survey was to determine the prevalence of in the cow as 2.1–2.8 mM3 and subclinical hypocalcemia was de- subclinical hypocalcemia in dairy herds. As a part of the United fined as serum calcium <2.0 mM as this is below the normal refer- States Department of Agriculture’s (USDA) National Animal Health ence range. Subclinical hypocalcemia increased with age and was Monitoring System (NAHMS) 2002 Dairy study, serum samples present in 25%, 41%, 49%, 51%, 54%, and 42% of 1st–6th lactation were collected from 1462 cows within 48 h postpartum, represent- cows, respectively. Furthermore, 47% of all cows in their second lac- ing 480 dairy herds from 21 States. The National Animal Disease tation or greater had varying degrees of subclinical hypocalcemia Centers (NADC) Animal Care and Use Committee approved all ani- that in some cases is severe enough to alter physiological and im- mal studies and procedures. Specific management data were col- mune functions (Kimura et al., 2006). lected where available including whether a cow was treated for Figs. 2A–C show the mean serum calcium, 1,25(OH)2D and clinical milk fever. Samples were assayed for calcium, 1,25- NEFA concentrations by age/lactation number. There was a signif- dihydroxyvitamin D (1,25(OH)2D), and non-esterified fatty acids icant decline in serum calcium concentrations as the lactation (NEFA) as described elsewhere (Prapong et al., 2005; Melendez number increased from 1st to 4th. This reflects the effects of age, and the increased number of cows which had subclinical hypocal- cemia (Fig. 2A). The serum calcium concentrations in 5th–6th lac- * Corresponding author. Tel.: +1 515 337 7540. tation cows were not significantly different from 3rd to 2nd E-mail address: [email protected] (T.A. Reinhardt). 1 Present address: Department of Biomedical Sciences, College of Veterinary Medicine, Iowa State University, Ames, IA 50010, USA. 2 Present address: Heartland Assays, Ames, IA 50010, USA. 3 See: http://merckvetmanual.com/mvm/htm/bc/tref7.htm.

1090-0233/$ - see front matter Published by Elsevier Ltd. doi:10.1016/j.tvjl.2010.03.025 T.A. Reinhardt et al. / The Veterinary Journal 188 (2011) 122–124 123

Fig. 1. Serum calcium concentrations were plotted for 1462 cows. All serum samples were collected within 48 h postpartum by lactation number: 1st lactation Fig. 3. Mean postpartum NEFA concentrations for normal calcemic cows, serum cows (n = 454), 2nd lactation cows (n = 447), 3rd lactation cows (n = 291), 4th Ca > 2.0 mM with subclinical hypocalcemic cows which had serum Ca > 2.0 mM lactation cows (n = 166), 5th lactation cows (n = 72), and 6th lactation cows (n = 32). (mean ± SEM, Ca < 2.0 mM, n = 630 and Ca > 2.0 mM, n = 832)). **P < 0.001. The percent of cows by lactation number that experienced a clinical milk fever episode which was treated or were subclinically hypocalcemic are shown in the graph. lactation cows, respectively. This was most likely due to the low

cow numbers in these two age groups. Mean serum 1,25(OH)2D concentrations rose significantly as calcium declined (Fig. 2B) but this rise plateaued beyond 3rd lactation cows. These data suggest that this normal homeostatic response to hypocalcemia may have limits with the animal’s age and may therefore contribute to great- er or prolonged hypocalcemia in older animals. Fig. 3 shows that cows with serum calcium >2.0 mM had lower serum NEFA concen- trations postpartum then cows with serum calcium <2.0 mM (P < 0.001), which indicates that normocalcemic cows are in better energy balance than in subclinical hypocalcemic cows. This link between subclinical hypocalcemia and higher serum NEFA pro- vides further evidence as to why both clinical and subclinical hypo- calcemic cows are probably at greater risk for diseases and why we should therefore be concerned about the prevalence of subclinical hypocalcemia in dairy herds. The take home message with the data available is simply that postpartum blood calcium is below the normal range in many more cows than we have previously appreciated. We speculate that this may have some health effects (Curtis et al., 1983, 1985) due to calcium’s central role in many cellular functions (Kimura et al., 2006; Goff, 2008). The high prevalence of subclinical hypo- calcemia should be viewed as a potential health risk to the transi- tion cow that requires further research.

Conflict of interest statement

None of the authors of this paper has a financial or personal relationship with other people or organizations that could inappro- priately influence or bias the content of this paper.

References

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