sou · GLB3132d1 · 1998-01-01 00:00:00 — Increased prevalence in medicated group in 2 experiments, no statis- tical difference in 2 experiments Increased prevalence and duration of shedding in medicated groups et al, 1985 chickens Various, natural No statistical difference between All groups except one of the controls also received monensin Manning et al, 1994 Increased prevalence of salmonella All birds kept on used shedding in medicated group 4ABELL 6))) &ORTS¤TTNING et al, 1981 Prolonged salmonella shedding in Nurmi and Rantala, Reduced prevalence and amount of salmonella shedding in medicated Small or no increase in prevalence of shedding in groups fed virginiamycin or bacitracin. increase in most groups fed Possibly identical to one of the experiments reported by Leuchtenberger Increased prevalence of salmonella shedding in medicated groups Increased prevalence and duration of shedding in groups fed or no increase in Effect of infectious dose, poultry breed and feed type also investigated Troutt et al, 1974 Diminished clinical signs in 1 Arrows indicate conclusions as drawn by the authors regarding effect of on colonisation; denotes no difference, denotes a decrease, indicate an increase in shedding time and/or prevalence when medicated groups were compared to control groups The interest in these studies has mainly been focused on prevalence and duration of salmonella shedding in experimentally infected animals. Most studies have been conducted for 40-50 days and evaluated at the end of the study period. Roughly, 18 experiments show non-significant results, 14 experiments indicate an increase in prevalence/duration of salmonella shedding among medicated animals, and 4 trials indicate a decrease in shedding by medicated animals (see table 4.VIII). Only one study (, 1989) established a dose-dependent response, to in-feed avoparcin. Three studies (Nurmi and Rantala, 1974; , 1989; , 1991) evaluate the amount of organisms shed. Two indicate a possible decrease in numbers shed by bacitracin-fed animals and two an increase in the amount shed by animals receiving avoparcin. However, none of these studies investigate the amount of organisms shed over time. Regarding changes in the infectious dose, or increased susceptibility of infected animals, the prevalence of salmonella in the different experimental groups shortly after infection may give a hint. One study, by and (1980) clearly showed, by dose-titration, a decrease (from 104 to 103) in the infectious dose necessary for colonising avoparcin-fed birds as compared to non-medicated birds. Some substances do appear to affect the course of salmonella infection within an animal herd. and co-workers (1981) used an inoculation dose optimised to achieve colonisation of about of the animals, which resulted in a faster spread of the infection, with an earlier peak of the epidemic curve, in birds receiving either avoparcin or virginiamycin, compared to the control group. At day 47, the prevalence of salmonella in samples from live birds was larger in the control group than in the medicated groups, but the prevalence of salmonellae in caecal contents after slaughter was larger in the medicated groups. This illustrates that there is sometimes a difference between the epidemic curves of the control group and the medicated group. Comments on study design One problem with many of the studies in the table above is that the groups of animals are too small. Population size and density are important factors influencing the spread and persistence of an infection within a herd (, 1977). Studies performed on small groups of chickens are not necessarily applicable to real poultry flocks with tens of thousands of birds. The need for a study design as realistic as possible must be balanced against the need for a controlled environment. Practices vary in animal husbandry and what is a realistic study design in one part of the world may be unrealistic in another area. For example, (1983) conducted a series of studies on the effect on salmonella shedding if chickens were raised on clean or used and found a higher prevalence of shedding among birds raised on clean . As evident from table 4.VIII, most investigators use 3.Typhimurium for the experimental inoculation, and most strains are laboratory mutants resistant to nalidixic acid. It is unclear whether the results obtained with such strains are applicable to all salmonella serovars. Further, the properties of an old laboratory strain are not necessarily comparable to wild strains. Enteritidis is currently the main cause of poultry-derived salmonellosis in humans. As this serovar has a distinctly different behaviour compared to 3 Typhimurium in the host animals in natural infections (and Lovell, 1991), separate studies should be conducted. Similarly, for swine, other serovars may be of interest. Titration of infectious dose and of dose-response relationships is an essential part of risk assessment (see chapter 8). This type of investigation is crucial when determining causal relationships and also for explaining the seemingly conflicting results obtained in different studies. If the doses used are close to the threshold value of response/no response, different studies are bound to show equivocal results. In all dose-response experiments, (1989) found significant increases in salmonella shedding by chickens in all groups receiving concentrations of avoparcin from 15 ppm. For lower concentrations, variable results were obtained. This explains the contradictory results obtained in studies where 10 ppm has been used. Doses used for inoculation are often large enough to cause colonisation of almost every animal in the control groups. While this allows for a maximum number of animals to monitor the shedding time, differences in susceptibility or epidemic curves are impossible to detect. From a statistical point of view, these studies were designed to demonstrate differences between experimental groups, not to prove the absence of differences. In the former type of experiments, the null hypothesis is that there is no difference. In such cases, most statistical analyses use figures for significance and power that accept a risk of falsely rejecting the null hypothesis (type I error) and a risk of falsely maintaining the null hypothesis (type II error). Consequently, results calculated under these assumptions cannot simply be reversed to argue that the null hypothesis is true. When trying to prove safety, the allowances for type I and type II errors should be reversed. Alternatively, other statistical methods can be used, such as the detection level (a parameter indicating the minimum effect that could have been detected) suggested by (1995). In addition to various 3ALMONELLA spp., colonisation of the animals with other zoonotic and animal pathogens could also be affected. is known of such effects in relation to pathogens such as #AMPYLOBACTER spp., 9ERSINIA spp., verotoxin-producing %SCHERICHIA COLI, #LOSTRIDIUM PERFRINGENS, 3ERPULINA HYODYSENTERIAE and ,AWSONIA INTRACELLULARIS Increased presence in the animal intestine of these bacteria could have serious consequences for either human or animal health. No studies specifically addressing this topic have been found. 4.8.3Other alterations of the microflora Resistant bacteria may carry other traits that are disadvantageous for the host, such as other resistance genes, or virulence genes. An increase of the population of naturally resistant bacteria following exposure to antibacterial substances can be expected. Moreover, the prevalence of species with a high capacity for acquisition of resistance genes can be expected to increase. Although this may indirectly lead to an overall increase in resistance, this issue has not attracted much attention. In an earlier cited study by Kaukas and co-workers (1988 , see 4.3.1), the feeding of increased the proportion of % FAECIUM. As this species was generally more resistant than the other enterococcal species, the increased in groups fed . Resistance to the antibiotics studied is mainly conferred by acquired resistance genes in % FAECIUM cause disruption of the intestinal microflora which may increase the susceptibility to colonisation by enteric pathogens. Avoparcin enhances intestinal colonisation with salmonella. Some other also affect salmonella colonisation. Information on enteric pathogens other than salmonella is scarce. Published studies do not directly address the influence of on contamination of food of animal origin with zoonotic pathogens. Well-designed studies, and use of appropriate statistical methods, are needed in this area. Use of results in dissemination of resistance to and related substances. Resistance against can and does transfer between different bacteria and between different human and animal hosts. The use of will thereby contribute to the increase of the environmental pool of resistance genes. The relative importance of this contribution for the increased resistance in animal and human pathogens cannot be determined. In a situation where the substance in question is not used for therapy, the bulk of the resistance genes will be directly attributable to usage. At least two of the formerly primarily used as are today options for new therapeutical drugs. The possible effects of on prevalence of food-borne pathogens in animal products have not been fully addressed. For salmonella, the effects would be expected to be more important in areas where the prevalence is low, or where control programs are in force. Regarding other pathogens, such as #AMPYLOBACTER spp. and 9ERSINIA spp., no information has been found. EFFLUX - transportation of a substance out of the bacterial cell, mostly by a membrane "pump" CHROMOSOME - circular DNA structure, the major part of the bacterial genome CO RESISTANCE - simultaneous resistance to several different antibacterials by different mechanisms, encoded by different genes CO TRANSFER - simultaneous transfer of different resistance genes, located on the same mobile element CONJUGATION OR CONJUGAL TRANSFER - direct transfer of plasmids or transposons between different bacteria via cell-cell contact CONJUGATIVE PLASMIDS AND TRANSPOSONS - mobile DNA elements that carry genes encoding the mechanisms for their own conjugal transfer CONSTITUTIVE EXPRESSION - the gene product is synthesised regardless of the presence of an inducer CROSS RESISTANCE - resistance to different antimicrobials by the same resistance mechanism DELETION - disappearance of DNA within or between genes sequence that encodes a single protein; promoter plus open reading frame - gene lacking promoter, that encodes a specific mechanism, and can be inserted into integrons - several genes located together, forming a functional gene with products acting together to exert an effect INDUCIBLE RESISTANCE - the product of the resistance gene is only synthesised in the presence of the inducing substance, usually the antimicrobial that the resistance mechanism counteracts INSERTION - addition of DNA within or between genes INTEGRON - small mobile element carrying gene cassettes and genes encoding its own transfer and insertion into the bacterial genome, as well as genes encoding rearrangement, expression and uptake of gene cassettes INTERGENIC SEQUENCE - DNA sequence separating functional genes MULTIRESISTANCE - resistance to a large number of different antimicrobials by various resistance mechanisms encoded by different genes MUTATION random change in DNA sequence, can change the amino acid of an encoded protein OPEN READING FRAME (ORF) - DNA sequence that encodes a single protein OPERON - gene plus the operator controlling its expression PHAGE - virus that infects bacteria and inserts its own DNA into the bacterial genome PLASMID - extrachromosomal small, covalently closed, usually circular DNA element that can replicate autonomously and be transferred between bacteria RIBOSOME - cytoplasmic structure where protein synthesis takes place through translation of mRNA TRANSDUCTION - phage mediated gene transfer TRANSFORMATION - gene transfer via bacterial uptake of free, extracellular DNA TRANSPOSON - small, mobile DNA element that carry one or several genes, plus genes encoding for its on transposition between various locations in the bacterial genome !ARESTRUP & - , 1995. 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