Conclusion and Future Directions
Over the last 30 years, reported cases of valley fever have increased dramatically (Sondermeyer et al. 2013; Huang et al. 2012; Hector et al. 2011; Lewis et al. 2015; Twarog and Thompson 2015).
Data show that strains recovered in a recent study of Arizona isolates were highly variable with no clonal structure; therefore, a pathogenic clone was not responsible for the rise in cases (Jewell et al. 2008). A central question regarding the increase of disease remains unanswered. Possible non-mutually exclusive causes include climate change, increased host susceptibility, and changes in reporting and awareness. Another complication is the high levels of recombination, admixture, and genetic diversity and an as yet undiscovered sexual life cycle that could produce an alternative infectious morphology: the ascospore. Genetic variation in the fungus and ability to adapt to novel hosts and colonize new environments are additional unanswered questions. The potential emergence of antifungal resistance is cause for concern, and the lack of early accurate diagnosis and treatment recommendations for humans is troublesome. Furthermore, treatment and diagnostic development for our four-legged friends is based on clinical trials in humans. Thus, many clinicians are forced to use “wait and see” approaches to treatment. Greater research effort to understand the organisms as well as the disease is needed, particularly in response to the potential for the disease to expand into new areas.Acknowledgments This work was supported in part by the Arizona Biomedical Research Commission grant (ABRC/ADHS 14-082975).
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