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The world of smoke, mirrors and climate change
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TRENDS in Parasitology Vol.17 No.10 October 2001
spleen and liver. Comparable parasite burden in the footpads of mice from all diet groups, and the higher lymph node parasite burden in well-nourished mice compared with malnourished mice, suggested that the higher visceral parasite burden in malnourished mice was a result of a failure in lymph node function rather than a deficit in local NO-mediated parasite killing. Interestingly, parasite visceralization was associated with high PGE2 production and decreased IL-10 levels – conditions that are known to favor tumor cell metastasis and loss of leukocyte adhesion. The authors also suggest that the higher visceral parasite burden in malnourished mice might result from an increased flow of parasitized
leukocytes from the draining lymph node to the spleen, then to the liver, which is enhanced by lymph node PGE2 production and modulated by NO and IL-10. According to the authors, this is the first polynutrient-deficient animal model for human malnutrition, and future studies will show whether these mouse models can reproduce the events observed in human kala-azar. Similarly, the model could be used to study other diseases where malnutrition is a risk factor for disease susceptibility. Finally, the model should also prove whether dietary supplements could be used to control those infectious diseases where malnutrition has been shown to be a risk factor for disease susceptibility4.
466
1 Warburg, A. et al. (1994) Saliva of Lutzomyia longipalpis sibling species differs in its composition and capacity to enhance leishmaniasis. Philos. Trans. R. Soc. Lond. B. Biol. Sci. 345, 223–230 2 Cerf, B.J. et al. (1987) Malnutrition as a risk factor for severe visceral leishmaniasis. J. Infect. Dis. 156, 1030–1033 3 Anstead, G.M. et al. (2001). Malnutrition alters the innate immune response and increases early visceralisation following Leishmania donovani infection. Infect. Immun. 69, 4709–4718 4 Dye, C. (1996) The logic of visceral leishmaniasis control. Am. J. Trop. Med. Hyg. 55, 125–130
Richard Reithinger [email protected]
The world of smoke, mirrors and climate change The increasing trend in reports that relate the emergence and re-emergence of arthropod-borne infectious diseases to changes in climate is becoming as striking as the rise in the number of various diseases that have been studied. Now, Lindgren and Gustafson1 conclude that the increase in the incidence of tick-borne encephalitis (TBE) in Sweden since 1984 is due to climate change (more specifically several temperature variables) and should, therefore, be added to this epidemiological ‘hall of fame’2. There might be some truth to the relationship between climate change and TBE incidence, but metaphorical smoke and mirrors obscure the analysis presented in this study. The ‘smoke’ renders various parts of this study less than transparent. First, temperature thresholds for the development of Ixodes ricinus are cited from studies of the American tick, Ixodes scapularis, thus ignoring a large body of published data on the European cousin. Second, the authors have
ignored recent analyses of the pan-European multi-variable climatic determinants of TBE virus transmission, and predictions of the probable impact in forecast climate change, which matches the observed decrease in TBE incidence along the southern edge of the current European range3. Third, the report confusingly refers to an increasing slope when it presents data for an increasing correlation coefficient. Finally, data from earlier years with very high TBE incidence (1956 and 1958) are omitted without explanation. The ‘mirror’ is needed to appreciate fully the graphs presented in this article. The cardinal sin of mixing a dependent axis (TBE incidence) with an independent axis (number of days in the chosen temperature ranges) masks a visual impact that belies the statistics. In 12 out of the 15 years (1984–1998), increased TBE incidence is not associated with greater numbers of warm spring days or cold winter days than occurred in the 1960–1983 period. Also, three out of
the four highest TBE incidence years during 1960–1983 were associated with less than average warm spring days and more than average cold winter days, which is exactly the opposite of the post-1983 trend! During a time when the government of the world’s largest polluter remains unconvinced of the importance of climate change, we should be striving for more scientific work in this arena that is a little less impeachable. 1 Lindgren, E. and Gustafson, R. (2001) Tick-borne encephalitis in Sweden and climate change. Lancet 358, 16–18 2 Taverne, J. (2001) Malaria, politics and endemicity on the net. Trends Parasitol. 17, 412 3 Randolph, S.E. and Rogers, D.J. (2000) Fragile transmission cycles of tick-borne encephalitis virus may be disrupted by predicted climate change. Proc. Roy. Soc. Lond. Ser. B. 267, 1741–1744
Simon I. Hay [email protected]
Trends in Parasitology : a forum for comment Controversial? Thought-provoking? If you wish to comment on articles published in Trends in Parasitology, or would like to discuss issues of broad interest to parasitologists, then why not write a Letter to the Editor? Letters should be up to 700 words. Please state clearly whether you wish the letter to be considered for publication. Letters are often sent to the author of the original article for their response, in which case both the letter and reply will be published together. Please note: submission does not guarantee publication.
http://parasites.trends.com
1471-4922/01/$ – see front matter © 2001 Elsevier Science Ltd. All rights reserved.
TRENDS in Parasitology Vol.17 No.10 October 2001
spleen and liver. Comparable parasite burden in the footpads of mice from all diet groups, and the higher lymph node parasite burden in well-nourished mice compared with malnourished mice, suggested that the higher visceral parasite burden in malnourished mice was a result of a failure in lymph node function rather than a deficit in local NO-mediated parasite killing. Interestingly, parasite visceralization was associated with high PGE2 production and decreased IL-10 levels – conditions that are known to favor tumor cell metastasis and loss of leukocyte adhesion. The authors also suggest that the higher visceral parasite burden in malnourished mice might result from an increased flow of parasitized
leukocytes from the draining lymph node to the spleen, then to the liver, which is enhanced by lymph node PGE2 production and modulated by NO and IL-10. According to the authors, this is the first polynutrient-deficient animal model for human malnutrition, and future studies will show whether these mouse models can reproduce the events observed in human kala-azar. Similarly, the model could be used to study other diseases where malnutrition is a risk factor for disease susceptibility. Finally, the model should also prove whether dietary supplements could be used to control those infectious diseases where malnutrition has been shown to be a risk factor for disease susceptibility4.
466
1 Warburg, A. et al. (1994) Saliva of Lutzomyia longipalpis sibling species differs in its composition and capacity to enhance leishmaniasis. Philos. Trans. R. Soc. Lond. B. Biol. Sci. 345, 223–230 2 Cerf, B.J. et al. (1987) Malnutrition as a risk factor for severe visceral leishmaniasis. J. Infect. Dis. 156, 1030–1033 3 Anstead, G.M. et al. (2001). Malnutrition alters the innate immune response and increases early visceralisation following Leishmania donovani infection. Infect. Immun. 69, 4709–4718 4 Dye, C. (1996) The logic of visceral leishmaniasis control. Am. J. Trop. Med. Hyg. 55, 125–130
Richard Reithinger [email protected]
The world of smoke, mirrors and climate change The increasing trend in reports that relate the emergence and re-emergence of arthropod-borne infectious diseases to changes in climate is becoming as striking as the rise in the number of various diseases that have been studied. Now, Lindgren and Gustafson1 conclude that the increase in the incidence of tick-borne encephalitis (TBE) in Sweden since 1984 is due to climate change (more specifically several temperature variables) and should, therefore, be added to this epidemiological ‘hall of fame’2. There might be some truth to the relationship between climate change and TBE incidence, but metaphorical smoke and mirrors obscure the analysis presented in this study. The ‘smoke’ renders various parts of this study less than transparent. First, temperature thresholds for the development of Ixodes ricinus are cited from studies of the American tick, Ixodes scapularis, thus ignoring a large body of published data on the European cousin. Second, the authors have
ignored recent analyses of the pan-European multi-variable climatic determinants of TBE virus transmission, and predictions of the probable impact in forecast climate change, which matches the observed decrease in TBE incidence along the southern edge of the current European range3. Third, the report confusingly refers to an increasing slope when it presents data for an increasing correlation coefficient. Finally, data from earlier years with very high TBE incidence (1956 and 1958) are omitted without explanation. The ‘mirror’ is needed to appreciate fully the graphs presented in this article. The cardinal sin of mixing a dependent axis (TBE incidence) with an independent axis (number of days in the chosen temperature ranges) masks a visual impact that belies the statistics. In 12 out of the 15 years (1984–1998), increased TBE incidence is not associated with greater numbers of warm spring days or cold winter days than occurred in the 1960–1983 period. Also, three out of
the four highest TBE incidence years during 1960–1983 were associated with less than average warm spring days and more than average cold winter days, which is exactly the opposite of the post-1983 trend! During a time when the government of the world’s largest polluter remains unconvinced of the importance of climate change, we should be striving for more scientific work in this arena that is a little less impeachable. 1 Lindgren, E. and Gustafson, R. (2001) Tick-borne encephalitis in Sweden and climate change. Lancet 358, 16–18 2 Taverne, J. (2001) Malaria, politics and endemicity on the net. Trends Parasitol. 17, 412 3 Randolph, S.E. and Rogers, D.J. (2000) Fragile transmission cycles of tick-borne encephalitis virus may be disrupted by predicted climate change. Proc. Roy. Soc. Lond. Ser. B. 267, 1741–1744
Simon I. Hay [email protected]
Trends in Parasitology : a forum for comment Controversial? Thought-provoking? If you wish to comment on articles published in Trends in Parasitology, or would like to discuss issues of broad interest to parasitologists, then why not write a Letter to the Editor? Letters should be up to 700 words. Please state clearly whether you wish the letter to be considered for publication. Letters are often sent to the author of the original article for their response, in which case both the letter and reply will be published together. Please note: submission does not guarantee publication.
http://parasites.trends.com
1471-4922/01/$ – see front matter © 2001 Elsevier Science Ltd. All rights reserved.