Abstract Aim The distribution of Yersinia pestis, the pathogen that causes plague in humans, is reliant upon transmission between host species; however, the degree to which host species distributions dictate the distribution of Y. pestis, compared with limitations imposed by the environmental niche of Y. pestis per se, is debated. We test whether the present‐day environmental niche of Y. pestis differs between its native range and an invaded range and whether biotic factors (host distributions) can explain observed discrepancies. Location North America and Central Asia. Major taxa studied Yersinia pestis. Methods We use environmental niche models to determine whether the current climatic niche of Y. pestis differs between its native range in Asia and its invaded range in North America. We then test whether the inclusion of information on the distribution of host species improves the ability of models to capture the North American niche. We use geographical null models to guard against spurious correlations arising from spatially autocorrelated occurrence points. Results The current climatic niche of Y. pestis differs between its native and invaded regions. The Asian niche overpredicted the distribution of Y. pestis across North America. Including biotic factors along with the native climatic niche increased niche overlap between the native and invaded models, and models containing only biotic factors performed better than the native climatic niche alone. Geographical null models confirmed that the increased niche overlap through inclusion of biotic factors did not, with a couple of exceptions, arise solely from spatially autocorrelated occurrences. Main conclusions The current climatic niche in Central Asia differs from the current climatic niche in North America. Inclusion of biotic factors improved the fit of models to the Y. pestis distribution data in its invaded region better than climate variables alone. This highlights the importance of host species when investigating zoonotic disease introductions and suggests that climatic variables alone are insufficient to predict disease distribution in novel environments.