Mitchell Rebecca M, Schukken Ynte, Koets Ad, Weber Maarten, Bakker Douwe, Stabel Judy, Whitlock Robert H, Louzoun Yoram
Centers for Disease Control and Prevention, Atlanta, Georgia.
Department of Population Medicine and Diagnostic Sciences, Cornell University, Ithaca, NY, USA.
Vet Res. 2015 Jun 19;46(1):66. doi: 10.1186/s13567-015-0188-x.
The objective of this paper is to study shedding patterns of cows infected with Mycobacterium avium subsp. paratuberculosis (MAP). While multiple single farm studies of MAP dynamics were reported, there is not large scale meta-analysis of both natural and experimental infections. Large difference in shedding patterns between experimentally and naturally infected cows were observed. Experimental infections are thus probably driven by different pathological mechanisms. For further evaluations of shedding patterns only natural infections were used. Within such infections, the transition to high shedding was studied as a proxy to the development of a clinical disease. The majority of studied cows never developed high shedding levels. Those that do, typically never reduced their shedding level to low or no shedding. Cows that eventually became high shedders showed a pattern of continuous shedding. In contrast, cows with an intermittent shedding pattern had a low probability to ever become high shedders. In addition, cows that start shedding at a younger age (less than three years of age) have a lower hazard of becoming high shedders compared to cows starting to shed at an older age. These data suggest the presence of three categories of immune control. Cows that are intermittent shedders have the infection process under control (no progressive infection). Cows that start shedding persistently at a young age partially control the infection, but eventually will be high shedders (slow progressive infection), while cows that start shedding persistently at an older age cannot effectively control the infection and become high shedders rapidly.
本文的目的是研究感染副结核分枝杆菌（MAP）的奶牛的排菌模式。虽然已有多项关于MAP动态的单场研究报告，但尚未对自然感染和实验性感染进行大规模的荟萃分析。观察到实验感染奶牛和自然感染奶牛的排菌模式存在很大差异。因此，实验性感染可能由不同的病理机制驱动。为了进一步评估排菌模式，仅使用自然感染情况。在这类感染中，将向高排菌状态的转变作为临床疾病发展的一个指标进行研究。大多数被研究的奶牛从未出现高排菌水平。那些出现高排菌水平的奶牛，通常不会将排菌水平降至低排菌或无排菌状态。最终成为高排菌者的奶牛呈现出持续排菌的模式。相比之下，具有间歇性排菌模式的奶牛成为高排菌者的概率较低。此外，与年龄较大开始排菌的奶牛相比，年龄较小（小于3岁）开始排菌的奶牛成为高排菌者的风险较低。这些数据表明存在三类免疫控制情况。间歇性排菌的奶牛能够控制感染过程（无进行性感染）。年轻时开始持续排菌的奶牛部分控制了感染，但最终会成为高排菌者（缓慢进行性感染），而年龄较大时开始持续排菌的奶牛无法有效控制感染，会迅速成为高排菌者。
