Epidemics caused by long-distance dispersed pathogens result in some of the most explosive and difficult to control diseases of both plants and animals (including humans). Yet the factors influencing disease spread, especially in the early stages of the outbreak, are not well-understood. We present scaling relationships, of potentially widespread relevance, that were developed from more than 15 years of field and in silico single focus studies of wheat stripe rust spread. These relationships emerged as a consequence of accounting for a greater proportion of the fat-tailed disease gradient that may be frequently underestimated in disease spread studies. Leptokurtic dispersal gradients (highly peaked and fat-tailed) are relatively common in nature and they can be represented by power law functions. Power law scale invariance properties generate patterns that repeat over multiple spatial scales, suggesting important and predictable scaling relationships between disease levels during the first generation of disease outbreaks and subsequent epidemic spread. Experimental wheat stripe rust outbreaks and disease spread simulations support theoretical scaling relationships from power law properties and suggest that relatively straightforward scaling approximations may be useful for projecting the spread of disease caused by long-distance dispersed pathogens. Our results suggest that, when actual dispersal/disease data are lacking, an inverse power law with exponent = 2 may provide a reasonable approximation for modeling disease spread. Furthermore, our experiments and simulations strongly suggest that early control treatments with small spatial extent are likely to be more effective at suppressing an outbreak caused by a long-distance dispersed pathogen than would delayed treatment of a larger area. The scaling relationships we detail and the associated consequences for disease control may be broadly applicable to plant and animal pathogens characterized by non-exponentially bound, fat-tailed dispersal gradients.