- Email: [email protected]
Response to John Egerton's letter
Preventive Veterinary Medicine 117 (2014) 314
Contents lists available at ScienceDirect
Preventive Veterinary Medicine journal homepage: www.elsevier.com/locate/prevetmed
Reply to Letter to the Editor Response to John Egerton’s letter Dear Editor, Our study followed one flock that had virulent footrot (“SFR”) and so we are discussing the initiation and development of footrot. We are not discussing interdigital dermatitis in a flock in the absence of Dichelobacter nodosus as described by Parsonson et al. (1967), as mentioned in John Egerton’s letter. With regard to previous work (Egerton et al., 1969; Roberts and Egerton, 1969), the conclusions about the crucial role of Fusobacterium necrophorum in SFR are based on histological qualitative observations lacking definitive bacterial identification, and isolation work, which is intrinsically biased and not always representative of populations in situ. We do not disagree with much of John Egerton’s letter, but generally it is of little relevance to our argument. The sheep in our study were from a commercial farm in the UK and so would have had a typical interdigital skin microbial community and been exposed to the normal risks of physical damage to the skin, associated with this environment. These per se do not cause footrot. We did not interfere with this process and do not disagree that damage to the skin and bacteria on the foot are involved in susceptibility to footrot, however, we consider that our conclusions hold. D. nodosus load was significantly associated with the development of both clinical stages of footrot, whilst F. necrophorum load was not. We present the relationship for when footrot occurs, not explanations for why sheep may be more or less susceptible to footrot. We would not find a significant association with D. nodosus load and disease if, the DNA detected came solely from non-viable organisms, or if as Egerton suggests, weekly samples were too far apart in time and swab samples were not representative. All of these facts would have led to random error rather than a statistical association. A false association could occur if there was bias, this is discussed in our paper and we see no reason for bias to have occurred.
DOIs of the original articles: http://dx.doi.org/10.1016/j.prevetmed.2014.03.004, http://dx.doi.org/10.1016/j.prevetmed.2014.08.019. http://dx.doi.org/10.1016/j.prevetmed.2014.09.001 0167-5877/© 2014 Elsevier B.V. All rights reserved.
Finally, we disagree with the last paragraph of John Egerton’s letter. We present data that are consistent with the findings of Kennan et al. (2001, 2010); that D. nodosus has a causal association with footrot. We do not agree that it is necessary to introduce D. nodosus to healthy uncontaminated skin, in order to demonstrate cause: in fact, this is an artificial situation that does not reflect the natural state of sheep feet nor the opportunistic nature of many pathogens. Indeed, F. necrophorum is also unable to cause inflammation when introduced to healthy skin of healthy feet (Parsonson et al., 1967). Longitudinal epidemiological studies, like ours, provide a route to examine complex endemic diseases such as footrot and elucidate key drivers when disease is spreading naturally, not through artificially damaged and infected feet. References Egerton, J.R., Roberts, D.S., Parsonson, I.M., 1969. The aetiology and pathogenesis of ovine foot-rot. I. A histological study of the bacterial invasion. J. Comp. Pathol. 79, 207–217. Kennan, R.M., Dhungyel, O.P., Whittington, R.J., Egerton, J.R., Rood, J.I., 2001. The Type IV fimbrial subunit gene (fimA) of Dichelobacter nodosus is essential for virulence, protease secretion, and natural competence. J. Bacteriol. 183 (15), 4451–4458. Kennan, R.M., Wong, W., Dhungyel, O.P., Han, X., Wong, D., Parker, D., Rosado, C.J., Law, R.H.P., McGowan, S., Reeve, S.B., Levina, V., Powers, G.A., Pike, R.N., Bottomley, S.P., Smith, A.I., Marsh, I., Whittington, R.J., Whisstock, J.C., Porter, C.J., Rood, J.I., 2010. The subtilisin-like protease AprV2 is required for virulence and uses a novel disulphide-tethered exosite to bind substrates. PLoS Pathog. 6 (11), e1001210. Parsonson, I.M., Egerton, J.R., Roberts, D.S., 1967. Ovine interdigital dermatitis. J. Comp. Pathol. 77, 309–313. Roberts, D.S., Egerton, J.R., 1969. The aetiology and pathogenesis of ovine foot-rot. II. The pathogenic association of Fusiformis nodosus and F. necrophorus. J. Comp. Pathol. 79, 217–227.
Luci Ann Witcomb UCL School of Pharmacy, University College London, 29-39 Brunswick Square, London WC1N 1AX, United Kingdom E-mail address: [email protected] 23 August 2014
Contents lists available at ScienceDirect
Preventive Veterinary Medicine journal homepage: www.elsevier.com/locate/prevetmed
Reply to Letter to the Editor Response to John Egerton’s letter Dear Editor, Our study followed one flock that had virulent footrot (“SFR”) and so we are discussing the initiation and development of footrot. We are not discussing interdigital dermatitis in a flock in the absence of Dichelobacter nodosus as described by Parsonson et al. (1967), as mentioned in John Egerton’s letter. With regard to previous work (Egerton et al., 1969; Roberts and Egerton, 1969), the conclusions about the crucial role of Fusobacterium necrophorum in SFR are based on histological qualitative observations lacking definitive bacterial identification, and isolation work, which is intrinsically biased and not always representative of populations in situ. We do not disagree with much of John Egerton’s letter, but generally it is of little relevance to our argument. The sheep in our study were from a commercial farm in the UK and so would have had a typical interdigital skin microbial community and been exposed to the normal risks of physical damage to the skin, associated with this environment. These per se do not cause footrot. We did not interfere with this process and do not disagree that damage to the skin and bacteria on the foot are involved in susceptibility to footrot, however, we consider that our conclusions hold. D. nodosus load was significantly associated with the development of both clinical stages of footrot, whilst F. necrophorum load was not. We present the relationship for when footrot occurs, not explanations for why sheep may be more or less susceptible to footrot. We would not find a significant association with D. nodosus load and disease if, the DNA detected came solely from non-viable organisms, or if as Egerton suggests, weekly samples were too far apart in time and swab samples were not representative. All of these facts would have led to random error rather than a statistical association. A false association could occur if there was bias, this is discussed in our paper and we see no reason for bias to have occurred.
DOIs of the original articles: http://dx.doi.org/10.1016/j.prevetmed.2014.03.004, http://dx.doi.org/10.1016/j.prevetmed.2014.08.019. http://dx.doi.org/10.1016/j.prevetmed.2014.09.001 0167-5877/© 2014 Elsevier B.V. All rights reserved.
Finally, we disagree with the last paragraph of John Egerton’s letter. We present data that are consistent with the findings of Kennan et al. (2001, 2010); that D. nodosus has a causal association with footrot. We do not agree that it is necessary to introduce D. nodosus to healthy uncontaminated skin, in order to demonstrate cause: in fact, this is an artificial situation that does not reflect the natural state of sheep feet nor the opportunistic nature of many pathogens. Indeed, F. necrophorum is also unable to cause inflammation when introduced to healthy skin of healthy feet (Parsonson et al., 1967). Longitudinal epidemiological studies, like ours, provide a route to examine complex endemic diseases such as footrot and elucidate key drivers when disease is spreading naturally, not through artificially damaged and infected feet. References Egerton, J.R., Roberts, D.S., Parsonson, I.M., 1969. The aetiology and pathogenesis of ovine foot-rot. I. A histological study of the bacterial invasion. J. Comp. Pathol. 79, 207–217. Kennan, R.M., Dhungyel, O.P., Whittington, R.J., Egerton, J.R., Rood, J.I., 2001. The Type IV fimbrial subunit gene (fimA) of Dichelobacter nodosus is essential for virulence, protease secretion, and natural competence. J. Bacteriol. 183 (15), 4451–4458. Kennan, R.M., Wong, W., Dhungyel, O.P., Han, X., Wong, D., Parker, D., Rosado, C.J., Law, R.H.P., McGowan, S., Reeve, S.B., Levina, V., Powers, G.A., Pike, R.N., Bottomley, S.P., Smith, A.I., Marsh, I., Whittington, R.J., Whisstock, J.C., Porter, C.J., Rood, J.I., 2010. The subtilisin-like protease AprV2 is required for virulence and uses a novel disulphide-tethered exosite to bind substrates. PLoS Pathog. 6 (11), e1001210. Parsonson, I.M., Egerton, J.R., Roberts, D.S., 1967. Ovine interdigital dermatitis. J. Comp. Pathol. 77, 309–313. Roberts, D.S., Egerton, J.R., 1969. The aetiology and pathogenesis of ovine foot-rot. II. The pathogenic association of Fusiformis nodosus and F. necrophorus. J. Comp. Pathol. 79, 217–227.
Luci Ann Witcomb UCL School of Pharmacy, University College London, 29-39 Brunswick Square, London WC1N 1AX, United Kingdom E-mail address: [email protected] 23 August 2014