Transmission dynamics of Tasmanian devil facial tumor disease may lead to disease-induced extinction

Transmission dynamics of Tasmanian devil facial tumor disease may lead to disease-induced extinction
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DOI:
10.1890/08-1763.1
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发表时间:
2009-12-01
期刊:
影响因子:
4.8
通讯作者:
Lazenby, Billie
Lazenby, Billie
中科院分区:
环境科学与生态学1区
文献类型:
--
作者:
McCallum, Hamish;Jones, Menna;Lazenby, Billie

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除了受到疾病威胁的物种之外,大多数威胁导致宿主物种灭绝的病原体还维持在一个或多个储存宿主上。此外,大多数传统的宿主-病原体理论假设传播与宿主密度有关,因此病原体应该在其唯一宿主之前灭绝。袋獾面部肿瘤疾病是最近出现的一种传染性癌症,导致了大规模的人口下降和对这种最大的幸存有袋类食肉动物未来持续存在的严重担忧。在这里,我们报告了在六个地点进行的标记-再捕获研究的结果,并使用这些数据来估计流行病学参数,这些参数对于准确评估这种疾病的灭绝风险和有效管理这种疾病的威胁至关重要。三个网站进行了监测之前或接近疾病到达的时间,并在其他三个疾病是建立在诱捕开始时,在一个网站至少10年。我们没有发现疾病患病率存在性别特异性差异的证据,也没有证据表明感染力存在一致的季节性变化。在所有地点,尽管导致种群数量大幅下降,但该病仍保持在高流行水平(2-3岁动物>50%)。我们还提供了这种疾病的基本生殖率R-0的第一次估计。使用一个简单的年龄结构的确定性模型,我们表明,我们的研究结果是不一致的传输是成比例的感染主机的密度,但与频率相关的传输是一致的。这一结论得到以下观察结果的进一步支持:在一个人口密度在过去12年中减少了90%的地点,2-3岁儿童的当地疾病患病率仍然超过50%。这些发现为这种宿主特异性病原体将导致塔斯马尼亚魔鬼灭绝的担忧提供了相当大的权重。我们的研究强调了迅速实施监测计划以确定传播如何取决于宿主密度的重要性,并强调需要持续的管理策略,包括无病“保险人口”,沿着持续的实地监测计划,以确认当地人口是否灭绝。
Most pathogens threatening to cause extinction of a host species are maintained on one or more reservoir hosts, in addition to the species that is threatened by disease. Further, most conventional host-pathogen theory assumes that transmission is related to host density, and therefore a pathogen should become extinct before its sole host. Tasmanian devil facial tumor disease is a recently emerged infectious cancer that has led to massive population declines and grave concerns for the future persistence of this largest surviving marsupial carnivore. Here we report the results of mark-recapture studies at six sites and use these data to estimate epidemiological parameters critical to both accurately assessing the risk of extinction from this disease and effectively managing this disease threat. Three sites were monitored from before or close to the time of disease arrival, and at three others disease was well established when trapping began, in one site for at least 10 years. We found no evidence for sex-specific differences in disease prevalence and little evidence of consistent seasonal variation in the force of infection. At all sites, the disease was maintained at high levels of prevalence (>50% in 2-3-year-old animals), despite causing major population declines. We also provide the first estimates of the basic reproductive rate R-0 for this disease. Using a simple age-structured deterministic model, we show that our results are not consistent with transmission being proportional to the density of infected hosts but are consistent with frequency-dependent transmission. This conclusion is further supported by the observation that local disease prevalence in 2-3-year-olds still exceeds 50% at a site where population density has been reduced by up to 90% in the past 12 years. These findings lend considerable weight to concerns that this host-specific pathogen will cause the extinction of the Tasmanian devil. Our study highlights the importance of rapidly implementing monitoring programs to determine how transmission depends on host density and emphasizes the need for ongoing management strategies involving a disease-free "insurance population,'' along with ongoing field monitoring programs to confirm whether local population extinction occurs.