Efficacy of netobimin against naturally acquired helminth infections in cattle.
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Biomedical subjects
Publications and source records attributed to Z Johnson.
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A community-based cross-sectional survey of behavioural risk factors for premature mortality was carried out on a group of 354 adults aged 25-44 from previously identified high-mortality 'black-spots' in Dublin who were compared with 333 others from low-mortality areas. In the black-spot areas, 50.9% of respondents were current smokers versus 28.5% in low-mortality areas and 14.6% took 'sufficient' exercise versus 31.4% in low-mortality areas. People living in black spots were also less likely to make 'healthy' dietary choices than those in low-mortality areas. There is a higher prevalence of behavioural risk factors for premature mortality among young adults living in electoral wards/district electoral divisions (DEDs) with high standardized mortality ratios (SMRs) from all causes than among those in areas with low SMRs. A health promotion programme aimed at increasing exercise levels, reducing smoking and encouraging healthy eating should be aimed at young adults in DEDs with high SMRs.
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Turkeys were raised under parasite-free conditions until 25 days of age at which time the birds were administered infective ova of Capillaria obsignata, Heterakis gallinarum, and Ascaridia dissimilis. At 28 days postinfection, four groups of birds were placed on rations medicated with fenbendazole at 15,30,45, or 60 ppm. These rations were given ad libitum for 6 consecutive days. At 31 days postinfection, five additional groups of birds were placed on rations medicated with fenbendazole at 15,30,45,60 or 120 ppm. These latter rations were given ad libitum for 3 consecutive days. One group of turkeys served as an unmedicated, infected control. Treatment group size ranged from 17 to 19 birds. All birds were necropsied 5 days after the medicated rations were withdrawn and nematode recovery was performed. Control birds harbored an average of 3.29 A. dissimilis, 12.06 H. gallinarum, and 65.94 C. obsignata. All but one of the fenbendazole-medicated groups showed 100% removal of A. dissimilis. The exception was that group that received fenbendazole at 15 ppm for 6 days, and that showed a 98.5% efficacy. The removal rate for H. gallinarum ranged from 78.6% (15 ppm for 3 days) to 100% (120 ppm for 3 days and 45 ppm for 6 days). The C. obsignata infections proved dose-limiting, with a removal rate ranging from 30.8% (15 ppm for 3 days) to 97.8% (45 ppm for 6 days).
Little information on the health of populations living in small geographic areas of Ireland is available and it is therefore difficult to clearly identify small communities whose health is significantly below average. The aim of this study was to identify areas within Dublin having above average death rates by application of the technique of small area analysis. By using mortality and census data and by calculating standardised mortality ratios, a number of electoral wards/district electoral divisions in Dublin with significantly elevated mortality rates from all causes and from specific disease groups were identified. In general these were in inner city areas and new suburbs to the north and west of the city. A considerable proportion of the excess mortality can be attributed to conditions amenable to preventive measures. Before specific intervention is attempted, local investigation by Directors of Community Care/Medical Officers of Health will be necessary in order to confirm the findings and to identify factors which may be amenable to prevention. If intervention is attempted it should be carefully planned and should be implemented on a pilot basis initially.
Body weight and nine body measurements were recorded on 79 mature Kedah-Kelantan cows at two locations. The Kedah-Kelantan is an indigenous cattle of Malaysia. A principal component analysis was used to study size and shape as indicated by the dependence structure among measurements. The total variation among measurements associated with the first principal component which was interpreted as a measure of general size was 40.8%. The second principal component contrasted cows tall at the withers, and deep at the chest with top line sloping downward and under line sloping upward from front to rear with those having less wither height and chest depth and straighter lines. This contrast accounted for 14.3% of the variation in body dimensions. The third principal component contrasted long, narrow, and deeper cows with a more compact type. This contrast accounted for 10.7% of the variation in body dimensions.
Spontaneous phage A25-resistant (A25(R)) mutants of group A streptococci, strain K56, were isolated. The mutant cultures were unable to adsorb phage particles and hyperproduced M protein. Trypsin-digested A25(R) cells regained the ability to adsorb phage particles, but failed to become infectious centers. This failure indicated that the mutation created a double barrier to phage growth: (i) receptors were masked by M protein; (ii) irreversibly adsorbed phage were unable to multiply. Spontaneous variants of one A25(R) mutant, shown to be M negative (M(-)) by electron microscopy, serological tests, and sensitivity to phagocytosis, rapidly adsorbed phage and were able to become infectious centers. Therefore, it was concluded that the mutant phenotype, A25(R), arose by a single mutation and genes coding for this trait and M protein synthesis were either genetically linked, controlled by a common gene or were biochemically interdependent. The A25(R) phenotype was unstable and, as expected for plasmid-coded properties, acridine orange induced segregation of this phenotype. The parental M(+), A25-sensitive (A25(S)) cultures proved to be a mixed population. Infection at various multiplicities indicated that this culture was composed of phage A25(S) cells and cells more resistant to infection. Morphological comparison of thin sections of A25(R) and A25(S) cells by electron microscopy demonstrated striking differences. The A25(R) culture was composed entirely of cells uniformly covered with M protein, whereas the A25(S)M(+) wild-type culture was a mixed population, the majority of cells devoid of M protein. Phagocytosis by human blood enriched the culture for the latter cell type, suggesting that differences in phage sensitivity in the wild-type culture were also determined by the presence or absence of M protein. Thus M protein can serve a dual function for the streptococcal cell by allowing it to avoid infection by bacteriophage and ingestion by human leukocytes.
The M antigen, a primary determinant of virulence in group A streptococci that is expressed biologically as resistance to phagocytosis, is known to undergo a variety of phenotypic changes both in vivo and in vitro. These changes are nonrandom and can occur at a high frequency. Using the previously described relationship between the serum opacity reaction (associated with certain strains) and the presence of the M antigen, the phenotypic instability of the M antigen was analyzed. The results support the conclusion that M protein synthesis and the serum opacity reaction are directly or indirectly controlled by the same gene or by genes which are linked and can segregate as a unit. Moreover, growth conditions and the curing agents rifampin and ethidium bromide had a discernible influence on the segregation of clones unable to exhibit serum opacity factor and to resist phagocytosis by human leukocytes. Serial transfer of stationary-phase cultures of four strains of group A streptococci significantly increased the number of colonies negative for the serum opacity reaction and the M antigen. For two of four strains both ethidium bromide and rifampin also increased the segregation of colonies with this phenotype. In light of these experiments and the necessary controls, the possible influence of plasmids or bacteriophage in regulating M protein synthesis is discussed.