1 MB Consult Limited, Bingley, UK; 2 Bayer HealthCare AG, Animal Health Division, Leverkusen, Germany
Keywords: antibiotics , animal husbandry , resistance
Sir,
We would like to comment on the paper by Delsol et al.1 with respect to the rather misleading conclusions which in our opinion cannot be supported by the data as presented.
There are a number of inconsistencies within the paper; however, we would like to draw attention to the lack of detail regarding statistical analysis of the presented data. In paragraph two of the results it is stated that, "Treated pigs inoculated with cyclohexane-resistant S. Typhimurium DT104 (group 2) and treated pigs inoculated with gyrA mutant S. Typhimurium DT104 (group 3) consistently shed higher numbers of Salmonella than the treated pigs from their respective control groups (P<0.01 for both)". This would certainly not be true for the gyrA mutant S. Typhimurium DT104 (group 3). For more than half the experimental period, Figure 1 shows that at some time after day 14 and likely before day 21, the treated animals were shedding fewer Salmonella than the untreated animals. The point was also made that for group 2, the Salmonella counts were 100-fold higher in treated than untreated pigs for 2 weeks post-treatment. This does not appear to be the case at day 14, although in the absence of tabulated data it is difficult to be sure. Furthermore, the statistical analysis does not address whether there are any statistical differences in counts of treated and untreated animals in both groups 2 and 3 at 35 days. This is highly relevant to the conclusions that are made by the authors, "In conclusion, our study has provided direct evidence that enrofloxacin-treated pigs could be entering abattoirs with higher numbers of quinolone-resistant zoonotic bacteria than untreated pigs, increasing the risk of these entering the food chain."
This conclusion cannot be supported by the data, as at the end of the study period the level of colonization in the treated pigs and the controls did not appear to differ. Additionally, the authors have failed to relate the experimental conditions to current understanding of development of the gastrointestinal flora in the pig and to commercial practice within the pig industry. The experiment was completed at approximately 13 weeks, whereas under commercial conditions, pigs are slaughtered at 5.56 months of age, i.e. at 2325 weeks of age, which is 1012 weeks later than the age at which the experimental trial was finished. It is therefore erroneous and highly misleading to state that this trial gives direct evidence that enrofloxacin-treated pigs could be entering abattoirs with higher numbers of quinolone-resistant bacteria compared with untreated pigs thereby increasing the risk of quinolone-resistant zoonotic bacteria entering the food chain.
The authors make no reference to the fact that the trial was performed in young weaner pigs, at an age at which the intestinal flora is still very immature. Indeed, Belil et al.2 make the point that there is little information about the age of contamination by ubiquitous Salmonella serotypes of growing pigs in subclinically infected herds and that longitudinal studies following the bacteriological and serological status of pigs should be carried out to determine the typical age of contamination. This is crucial because it is well accepted that the gastrointestinal flora of the young animal changes over time. Smith & Crabb3 showed this as far back as 1961, and more recently Katouli et al.,4 using techniques that measured the metabolic potential of the faecal flora of pigs, showed a continuously changing flora as animals aged, although in this study analysis did not continue for more than 3 months. Understanding the development of the gastrointestinal flora and associated immunological changes in growing pigs is fundamental to making conclusions which extrapolate from a limited study such as that of Delsol et al.1 to implications for public health. In a detailed longitudinal study to describe the serological response to Salmonella enterica in growing pigs, Bel
il et al.2 showed that seroconversion occurred during the last third of the fattening phase, from 140 days to slaughter age whilst in contrast shedding was reported during the first half of the fattening period suggesting Salmonella shedding precedes seroconversion.
We make these points to illustrate the complexity of the situation and to ask that the authors re-consider their data in the overall context of an understanding of gastrointestinal development and of practices within the pig industry. This is especially important when making comments concerning public health.
Acknowledgements
Peter Silley acts as a Consultant to Bayer HealthCare AG, Animal Health Division.
Footnotes
* Corresponding author. Tel: +44-1274-551818; Email: p-s{at}mbconsult.com
References
1
.
Delsol, A. A., Woodward, M. J. & Roe, J. M. (2004). Effect of a 5 day enrofloxacin treatment on Salmonella enterica serotype Typhimurium DT104 in the pig. Journal of Antimicrobial Chemotherapy 53, 3968.
2
.
Belil, P. A., Chauvin, C., Proux, K. et al. (2003). Longitudinal serological responses to Salmonella enterica of growing pigs in a subclinically infected herd. Preventive Veterinary Medicine 60, 20726.[CrossRef][ISI][Medline]
3 . Smith, H. W. & Crabb, W. E. (1961). The faecal bacterial flora of animals and man: its development in the young. Journal of Pathology and Bacteriology 82, 5366.[ISI]
4 . Katouli, M., Melin, L., Jensen-Waern, M. et al. (1999). The effect of zinc oxide supplementation on the stability of the intestinal flora with special reference to composition of coliforms in weaned pigs. Journal of Applied Microbiology 87, 56473.[CrossRef][ISI][Medline]
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