Abstract
The epidemiology of clinical ketosis, hypocalcaemia and hypomagnesaemia was examined. In addition, the genetic variability of ketosis and parturient paresis was investigated. The data set consisted of the lactation records of 70,775 Finnish Ayrshire dairy cows. Each cow was under observation for 2 days before and for 305 days after calving. Lactation incidence rates (%) were: ketosis 6.0, parturient paresis 3.8, non-parturient paresis 0.6, hypomagnesaemic tetany, outdoor 0.6, and indoor 0.2. These diseases formed 22 % of all first treatments by veterinarians during farm visits. 92 % of the cases of ketosis occurred with 8 weeks of parturition, with the highest occurrence 3–5 weeks after calving. Four % of cases of parturient paresis occurred before, and 45 % within 24 h after calving. When cases were categorized by month of calving the risk of ketosis was higher during indoor feeding (October-April) than during outdoor feeding (May-September). The risk of parturient paresis did not significantly vary with month of calving. The occurrence of ketosis increased with parity up to the 4th and decreased thereafter. The occurrence of parturient paresis increased with parity. Both the increase in herd milk yield and the increase in individual milk yields were positively associated with the occurrence of ketosis and parturient paresis. The cows with a history of the reproductive tract infection had a higher risk of contracting ketosis. Heritability estimates for ketosis in various parity groups were from 1.6 % to 4.1 % on the binomial scale (corresponding to 7.3 %–14.4 % on the normal scale), and for parturient paresis from 3.5 to 10.5% (corresponding from 18.3 % to 27.4 %). The genetic correlation between ketosis and parturient paresis, and these and current milk production for all material were insignificant.
Keywords: disease documentation, heritability, ketosis, parturient paresis, nοn-parturient paresis, hypomagnesaemic tetany, dairy cows
Sammanfattning
Epidemiologin av klinisk ketos, hypokalcemi och hypomagnesemi undersöktes. Den genetiska variationen av ketos och kalvningsförlamning undersöktes också. Dataset innehöll laktationsresultaten från 70775 finska Ayrshire kor. Varje ko observerades från 2 dagar före till 305 dagar efter kalvningen. Lactation incidence rate var: ketos 6,0, paresis puerperalis 3,8, icke-puerperal pares 0,6, hypomagnesemi under betesperiod 0,6 och under stallperiod 0,2. Dessa sjukdomar omfattade 22 % av alla, första veterinärbehandlingar på gårdarna. 92 % av ketosfallen infäll inom 8 veckor efter kalvningen. Den högsta frekvensen konstaterades 3–5 veckor efter kalvningen. 4 % av kalvningsförlamningarna inföll förkalvningen och 45 % inom 24 timmar efter kalvningen. Ketosrisken var högre under stallperioden (oktober-april) än under betesperioden (maj-september), när materialet klassificerades efter kalvningsmånaden. Paresrisken varierade inte signifikant efter kalvningsmånaden. Ketosfrekvensen ökade med laktatioinsperioder ända till fjärde kalvningen och minskade därefter. Paresrisken ökade med åldern. Hög mjölkproduktion hos både besättning och enskilda kor hade ett positivt samband med förekomsten av ketos och pares. Kor med tidigare infektion i reproduktionsorgan hade en högre risk att insjukna i ketos. Ärftligheten för ketos i olika laktationsperioder var från 1,6 % till 4,1 % i den binomala skalan (motsvarar från 18.3 % till 27,4 %). Genetisk korrelation mellan ketos och pares och mellan dessa och mjölkproduktion varierade oregelbundet i olika laktationsperioder och en korrelation med hela materialet var osignifikant.
Full Text
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Acknowledgments
The authors thank Pol. Lic. Juni Palmgren for advice on logistic regression, and the Agricultural Data Processing Centre for supplying computer facilities for statistical analysis.
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