Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0519030 (Klebsiella)
 21,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Our objective was to estimate the effects of the first occurrence of pathogen-specific clinical mastitis (CM) on milk yield in 3071 dairy cows in 2 New York State farms. The pathogens studied were Streptococcus spp.,Staphylococcus aureus, Staphylococcus spp., Escherichia coli, Klebsiella spp., Arcanobacterium pyogenes, other pathogens grouped together, and "no pathogen isolated." Data were collected from October 1999 to July 2001. Milk samples were collected from cows showing signs of CM and were sent to the Quality Milk Production Services laboratory at Cornell University for microbiological culture. The SAS statistical procedure PROC MIXED, with an autoregressive covariance structure, was used to quantify the effect of CM and several other control variables (herd, calving season, parity, month of lactation, J-5 vaccination status, and other diseases) on weekly milk yield. Separate models were fitted for primipara and multipara, because of the different shapes of their lactation curves. To observe effects of mastitis, milk weights were divided into several periods both pre- and postdiagnosis, according to when they were measured in relation to disease occurrence. Another category contained cows without the type of CM being modeled. Because all pathogens were modeled simultaneously, a control cow was one without CM. Among primipara, Staph. aureus, E. coli, Klebsiella spp., and "no pathogen isolated" caused the greatest losses. Milk yield generally began to drop 1 or 2 wk before diagnosis; the greatest loss occurred immediately following diagnosis. Mastitic cows often never recovered their potential yield. Among older cows, Streptococcus spp., Staph. aureus, A. pyogenes, E. coli, and Klebsiella spp. caused the most significant losses. Many multipara that developed CM were actually higher producers before diagnosis than their nonmastitic herd-mates. As in primipara, milk yield in multipara often began to decline shortly before diagnosis; the greatest loss occurred immediately following diagnosis. Milk loss persisted until at least 70 d after diagnosis for Streptococcus spp., Klebsiella spp., and A. pyogenes. The tendency for higher producing cows to contract CM may mask its impact on cow health and production. These findings provide dairy producers with more information on which pathogen-specific CM cases should receive treatment and how to manage these cows, thereby reducing CM impact on cow well being and profitability.
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PMID:Effect of pathogen-specific clinical mastitis on milk yield in dairy cows. 1537 15

The objective of this study was to estimate the effects of clinical mastitis (CM) (both with and without specific pathogen identification) occurring in different stages of lactation on length of herd life in two New York State dairy farms. The 2,697 cows in the study were followed for one lactation (the first-occurring one on or after 1 October 1999), until it ended because of a new lactation, culling, or end of study (31 March 2001 in one farm; 31 July 2001 in the other). A Cox proportional hazards model with time-dependent covariates, in SAS((R)), was used to measure, within a lactation, the effect of the first occurrence of CM (without specific pathogen identification) occurring 1--7, 8--66, 67--100, 101--225, or >or=226 days in milk (DIM), on how long cows remained in the herd. For the first occurrence of CM due to Streptococcus spp., Staphylococcus aureus, Staphylococcus spp., Escherichia coli, Klebsiella spp., and 'no pathogen isolated', the intervals were before and after the median DIM of first occurrence of each pathogen. There were too few cases due to Arcanobacterium pyogenes, and 'other pathogens grouped together' to split into intervals, so they were modeled as binary variables, i.e. as they occurred. CM was modeled using time-dependent covariates, to account for its differing effects throughout lactation on culling. Other variables controlled for were herd, parity, calving season, and other significant diseases. In the dataset, the lactational incidence risk of the first occurrence of CM was 18.2%; 20.0% of the cows did not survive the lactation that was studied. The overall annual culling percentage for both herds during the study period (including all cows, whether eligible for the study or not) was 35.6%. For cows with CM without pathogen identification, their highest hazard ratio (HR) of culling occurred from 67 to 100 DIM. All of the pathogens modeled markedly reduced herd life. On average over the entire lactation, cows with Staphylococcus spp. CM had the highest HRs for culling, although there were no significant differences among pathogens (at p=0.0018 (reflecting 28 pairwise comparisons)). For early-occurring (before median DIM of first occurrence) S. aureus CM, the daily rate of change of the HR of culling increased over time. The HRs for culling were particularly high for late-occurring (after median DIM of first occurrence) E. coli and Klebsiella spp. CM early in the interval, but the daily rate of change of the hazard of culling for these two pathogens decreased sharply over time. Treating CM as time-dependent therefore allowed us to measure in greater detail, its varying effects (of when it occurred) on herd life.
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PMID:Effect of pathogen-specific clinical mastitis on herd life in two New York State dairy herds. 1611 78