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Frequencies of resistance

Table 10. Genes affected by point mutations or other genetic events leading to antibiotic resistance in II. pylori and the frequency of resistance (from Megraud and Lamouliatte [166])... Table 10. Genes affected by point mutations or other genetic events leading to antibiotic resistance in II. pylori and the frequency of resistance (from Megraud and Lamouliatte [166])...
Antibiotic group Genes affected Frequency of resistance, %... [Pg.52]

Low resistance frequency Certain essential genes can be bypassed by inhibition of another gene product. Such situations may result in high frequency of resistance emergence [43,99,100]. [Pg.519]

Goldie and Coldman suggested the following equation ss mathematical model of frequency of resistance occurrence ... [Pg.92]

In resistant populations, the frequency of resistance alleles can be very high. For example, using the real-time PCR amplification of specific allele (rtPASA) method, Kim et al. (2007) showed that the frequency of the pyrethroid resistance allele (Leu-Phe mutation in... [Pg.204]

Population mobility is a very important behavioral factor for resistance development. The influx of migrants tends to dilute the frequency of resistance among survivors of treatments, especially for highly mobile insects such as the fall army worm and velvetbean caterpillar. Computer simulation indicated that a moderate rate of immigration of susceptible individuals could ensure the containment of resistance if the initial population was of low density and if a short-lived pesticide was used in regular treatments. [Pg.219]

The frequency of resistance genes in an unselected population is generally unknown, and there is no efficient way of screening large populations (at least 1 000 000 plants, perhaps much higher) to determine such gene frequencies. Other important information on... [Pg.161]

Few studies have been undertaken of the energetic cost of resistance, the resistance mechanism is often not specified in these studies, and the parameters chosen for measurements vary between studies. Comprehensive information is therefore not available. Still, this kind of information is important for understanding the evolution of resistance and its stability. Most new insecticides, it appears, have a mode of action identical to or extremely similar to one that was used previously. The successful use of new insecticides therefore depends on what kinds and frequencies of resistance genes are already present in insect populations to be controlled. It can be expected that resistance mechanisms that affect fitness will be less stable than those that do not. There is, thus, a need for more studies of the relationships between resistance mechanisms and biotic potential in insects. [Pg.55]

It appears that spider mite resistance, or, more precisely, spider mites which possess heritable, substantial reductions in susceptibility, occur to essentially all of the acaricides widely used in agriculture, and possibly for some newer classes of acaricidal compounds that have not been widely employed to-date. Therefore, for most acaricides it is not a question of whether resistance exists per se, rather it is of greatest relevance to determine if problematic frequencies of resistant mites occur at specific locations and, through research, determine what management efforts will keep frequencies of resistant pests below those which impair field performance of acaricides. [Pg.78]

These factors are very likely to be immigration of susceptible mites and/or reduced fitness of resistant individuals. Secondly, populations of T. urticae were relatively susceptible to dicofol most populations had less than 10% resistant spider mites. Field trials evaluating the performance of dicofol in New York apple orchards possessing different frequencies of resistant mites have shown that dicofol provides very acceptable control on populations possessing up to 20% resistant individuals (H. H. Reissig, Cornell Univ., unpublished data). [Pg.82]

From the standpoint of managing resistance to dicofol in spider mite pests of New York apple orchards, our findings for T. urticae are positive. Most populations had fewer than 10% resistant mites, and our laboratory data indicated that the resistant genotypes of T. urticae are substantially less fit than susceptible ones. Field studies of the critical frequency for dicofol resistance (i.e., the frequency at which resistance results in appreciable reductions in control) indicate that frequencies of resistance must be >20% to impair performance of dicofol treatments. Therefore, dicofol treatments would be expected to provide acceptable control of 9-12 of the 15 T, urticae populations we sampled. However, P. ulmi is the dominant spider mite pest of apple in western New York and, as we have demonstrated, the species most likely to exhibit resistance to dicofol. [Pg.89]

Pyrethroid resistance management programs in the USA are still in the formative stages, but likely will evolve and mature rapidly in response to apparent increases in the relative frequencies of resistant genotypes and in the extent of their geographical distribution. The current strategy has the following elements... [Pg.126]

The relationship between monitoring results and field control is still not clearly understood. The presence of resistance genes in a field population does not necessarily lead to field control failures. The frequency of resistance genes in a field population, the size of the pest population and the level of resistance all interact and must be sufficiently high to result in the occurrence of resistance-induced control failures. Conversely, a field control failure does not necessarily imply insecticide resistance. Numerous biological and operational factors interact to affect the evolution of resistance and the level of field control achieved by a pesticide (22.). ... [Pg.138]

Australia. Pyrethroid resistance in Heliothis spp. was first documented in Australia during the 1982-1983 production season, when field control failures occurred against Heliothis armigera (2). Daly and Murray (341, in a thorough evaluation of hypotheses proposed on the evolution of resistance in Australia, concluded that an increase in the frequency of resistance genes in the Emerald area was a result of interactions between high selection pressure, population density, crop phenology and weather, but the evolution of resistance elsewhere was independent of the situation in Emerald. [Pg.139]


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