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No description available.

A bidirectional selection experiment for increased and decreased somatic cell counts (SCC) in milk was conducted with two selected lines (high line or HSCC, low line or LSCC) and one control line (CSCC) of mice. Distribution of milk SCC in mice was 4 to 5 times the distribution in Holsteins. The shape of the lactation curve of mice was similar to that of Holsteins with maximum yield at day 7 (2.06 gms). The phenotypic regression of lactation milk yield on lactation milk SCC (-0.276) was significant (P < .05) and indicated that dams with higher SCC produce less milk. Small phenotypic correlations of milk SCC with blood SCC (-0.09) and percentage phagocytic cells (-0.06) were found, indicating that these traits are unrelated. A small but significant (P < .05) negative correlation (-0.14), was found between response to endotoxin challenge and milk SCC indicating that dams with inherently higher milk SCC responded less to endotoxin challenge than dams with lower milk SCC. No major pathogens which cause mastitis in cattle were detected in milk of mice. In addition, the bacteria identified (Bacillus sp., Corynebacterium sp. etc) did not cause any serious infections and/or increase in milk SCC in mice. Selection for high and low milk SCC produced a symmetrical response in the two selected lines (HSCC and LSCC), such that after 7 generations of selection, the two lines differed by more than 500,000 cells/ml of milk. A small negative genetic regression ( -0.162) of milk yield on milk SCC suggested a small correlated response in yield opposite in direction from the direct response for milk SCC. Small negative genetic regressions of blood SCC and percentage phagocytic cells on milk SCC ( -0.087 and -3.492) suggested that these three traits are genetically independent. Selection on milk SCC did not result in change either in total leukocytic cells per ml of blood or in percentage phagocytic leukocytes in blood. A negative genetic regression of response to challenge on milk SCC (-3.201) was found suggesting that selection for low milk SCC results in an increase of the ability of the individual mouse to elevate milk SCC after an injection with E. coli endotoxin. However, more data are needed to confirm this conclusion. Phenotypic correlations between milk SCC and several measures of fitness and genetic regressions of these measures on milk SCC were negligible. / Ph. D.

A dairy cow body condition scoring system was devised by the author as a practical means of determining the body condition, or fitness pertaining to the degree of body fat of dairy cows at any point during the lactation cycle. The factors considered were the thoracic and lumbar regions of the vertebral column (chine, loin and rump), spinous processes (loin), anterior coccygeal vertebrae (tailhead), tuber sacrale (hooks), and tuber ishii (pin bones). All factors in the body condition scoring system must be considered while appraising each cow. Each cow was scored on a 1 to 5 scale with 1 indicating severe undercondition and 5 indicating severe overcondition. During an 18-month period, 28 cows in each of 29 Virginia dairy herds were used for obtaining body condition scores, body weight, frame size measurements and blood samples. Herds were chosen according to rolling herd milk production average and cows were chosen at random from within five Estimated Relative Producing Ability groupings to insure a representative sample of herds across and levels of production in Virginia and of cows within each herd. Herds were sampled at 3-month intervals and complete Dairy Herd Improvement Association records were obtained for each cow in each herd. The relationships of dairy cow body weight, frame size measurements, milk production and related parameters, and blood profiles to the body condition scoring system were determined. Body condition using this method was found to be independent of frame size and only moderately correlated with body weight, the number of intercostal spaces and the ratio of body weight to wither height. Body condition was found to be relatively low during early lactation and to increase through late lactation and remain constant during the dry period. Dairy cows of greatest milk production efficiency did not increase significantly in body condition throughout lactation, had fewer days open, but had less persistency of lactation. Dairy cows that increase significantly in body condition throughout lactation were less efficient milk producers, had a greater number of days open, had relatively high body condition scores in late lactation, but had greater persistency of lactation. Blood parameters, although statistically significant in many cases, were found to be of little or no practical value when compared between body condition, stage of lactation, and dairy merit groupings. The dairy cow body condition scoring system is a practical means of quantitating body condition of dairy cows. / Ph. D.

Johne's disease (JD), caused by Mycobacterium avium subspecies paratuberculosis (MAP) is a chronic, debilitating enteritis of cattle, other domestic livestock and some wildlife species. JD was first identified in the late 1800s and today it is a worldwide problem in dairy cattle. Heavily infected cows have reduced milk production, a higher risk of removal from the herd and low slaughter value. Several countries have implemented national level control strategies. In New Zealand, JD was first reported in 1912 and today the prevalence of infected dairy herds is thought to be high. To improve our understanding of the epidemiology of JD and to evaluate the feasibility of a national control strategy, four studies were conducted. The first study was a questionnaire based case-control study to identify associations between management practices and the occurrence of clinical JD on farms from four regions of New Zealand. The second study was on the effect of sub-clinical JD on milk production and the risk of removal from the herd in four dairy herds over four milking seasons. The effect of misclassification of disease status on productivity estimates was also studied. In the third study diagnostic test result data from the productivity study was combined with a novel Bayesian regression model to estimate performance of the ELISA and faecal culture tests as a function of covariates and utilising repeated tests on individual cows. Finally, results from these three studies were used to adapt an existing JD simulation model, 'JohneSSim', to represent the epidemiological behaviour of JD in New Zealand dairy herds. Control strategies for the disease were simulated and evaluated based on their cost effectiveness. Of the 427 farmers responding to the questionnaire, 47% had suspected clinical cases of JD in their herd in the preceding 5 years. Only 13% of suspected infected herds had an average incidence of greater than 0.5 cases per 100 cow years at risk. The disease was not considered a serious problem by 20% of herd managers who reported the presence of disease in the preceding 5 years. The presence of Jersey cows in the herd and the purchase of bulls had strong positive associations with the presence of clinical JD. Grazing calves in the hospital paddock, larger herds, the purchase of heifers, and the use of induction were also positively associated with JD. In the productivity study the herd-level prevalence of JD by ELISA and/or faecal culture ranged from 4.5% (95% CI 2.6-6.9) to 14.2% (95% CI 9.2-20.6). Daily milksolids production by JD positive cows was 0.8% (95% CI -6.1%-4.5%) less than that of JD negative cows. However in herd D, JD positive cows produced 15.5%, (95% CI 6.75%-24.2%) milksolids less than JD negative herd mates daily. This equates to a loss of 53kg of milksolids/305 day lactation, or NZD 265/lactation, given a price of NZD 5/kg of milksolids. In herd D only, the annual hazard ratio of removal for JD positive cows was significantly increased. It was 4.7 times and 1.4 times higher in cows older than 5 years and younger than 5 years. The results were insensitive to misclassification. Analysis of the diagnostic test data demonstrated the strengths of our Bayesian regression model. While overall estimates of sensitivity and specificity by this method were comparable to estimates by existing methods, it showed a broad trend of increasing sensitivity in higher parity groups and higher sensitivity in early, relative to late, lactation. It also showed that estimates of prevalence may in fact decline with repeated, relative to single, testing. Our novel approach demonstrated trends that could not be shown by existing methods, but could be improved by application to a larger data set. Simulation showed that control strategies for JD based on either test-and-cull, vaccination, breeding for genetic resistance, or removal of offspring from clinically affected cows, were not cost effective for the average infected herd. Improvement of the hygiene associated with calf management provided the greatest reduction in the within-herd prevalence of JD. While JD is present in a high proportion of New Zealand dairy herds, the incidence of clinical cases is usually low, and most farmers consider it to be of little importance. However, JD causes significant losses in productivity in some herds. The disease would probably be best controlled on a herd-by-herd basis, given the limited success of national-scale control programs for JD in other countries. The education of dairy farmers regarding risky management practices, and the offer of a risk assessment to farmers wishing to control the disease, would provide a combination of wide reaching and targeted approaches, of low cost, for JD control. It seems likely that JD will persist in some capacity in the years ahead, but will remain of minor concern next to major animal health issues, such as infertility and mastitis. Clarification of the effect of genetic strain on the virulence of MAP may help explain differences in the effect of the disease between herds. This knowledge could then be used to further improve the efficiency of JD control.