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It is important to realize that guidelines cannot always account for individual variation among patients. They are not intended to supplant physician judgment with respect to particular patients or special clinical situations. Infectious Diseases Society of America considers adherence to these guidelines to be voluntary, with the ultimate determination regarding their application to be made by the physician in the light of each patient's individual circumstances.Coccidioidomycosis, also known as San Joaquin Valley fever, is a systemic infection endemic to parts of the southwestern United States and elsewhere in the Western Hemisphere. Residence in and recent travel to these areas are critical elements for the accurate recognition of patients who develop this infection. In this practice guideline, we have organized our recommendations to address actionable questions concerning the entire spectrum of clinical syndromes. These can range from initial pulmonary infection, which eventually resolves whether or not antifungal therapy is administered, to a variety of pulmonary and extrapulmonary complications. Additional recommendations address management of coccidioidomycosis occurring for special at-risk populations. Finally, preemptive management strategies are outlined in certain at-risk populations and after unintentional laboratory exposure.

In this issue of Clinical Infectious Diseases, we are provided glimpses into 2 California pediatric groups that report their experiences with the more severe spectrum of coccidioidomycosis as it affects children. Levy et al describe the use of voriconazole and caspofungin as combination salvage therapy for 9 children since 2003. In their experience, the eventual outcomes in these patients are encouraging. As they have carefully detailed, the clinical course of each patient differs widely. The only commonality seems to be that their doctors were convinced that current treatment was failing. The target of caspofungin and other echinocandins is a subunit of the β-1,3glucan synthase and the gene encoding the subunit is essential to Coccidioides species [1].Moreover, there is experimental evidence of caspofungin’s therapeutic effect in mice [2, 3]. On the other hand, there is virtually no experience with caspofungin use as single-drug therapy for coccidioidomycosis, and Stevens et al recently published a series of adult patients salvaged with posaconazole alone [4]. In the other report, McCarty et al describe 33 pediatric patients who were admitted to a hospital in California’s Central Valley for coccidioidomycosis over a 21month period beginning in January 2010. The variety of illness that these children had was broader but still included 8 patients in whom initial therapy with liposomal amphotericin B was considered to have failed. Interestingly, although McCarthy is an author on both papers, posaconazole with caspofungin was not a secondor even a third-line treatment in the second report. As pointed out in both reports, most of the medical literature dealing with coccidioidomycosis neglects the disease in pediatrics. Even so, how to best treat the most difficult cases is no better understood in adults than it is children. However, for providers with extensive experience with managing such patients, it is abundantly evident that the best patient outcomes emerge from the orchestration of several different elements. This often takes time and does not receive appropriate reimbursement, because coordination of care is something that is just assumed to happen. In this commentary, I would like to put the selection of antifungal agents in the context of the other elements critical to management. An important element in minimizing the morbidity of coccidioidal infections and often missing in the most serious cases is early detection. This is a problem in the weeks or months prior to the appearance of destructive lesions or an eventual hospitalization. In the report by McCarty et al, for example, delays ranged up to 4 months from initial onset of symptoms. Delayed diagnosis occurs partially because currently available diagnostic tests can be falsely negative early in infection [5]. For example, when the professional baseball player Conor Jackson developed coccidioidal pneumonia in 2009, it took more than a month and 3 serum serologies to be ordered before a diagnosis could be made [6]. However, more commonly delays happen because clinicians fail to consider or test for this diagnosis, even within regions endemic for coccidioidomycosis [7]. For example, Arizona state statistics indicate a very low rate of reported coccidioidomycosis in the young as compared to seniors [8]. However, withinmedical practices serving young adults, in whom coccidioidomycosis is routinely considered as a cause of community-acquired pneumonia, case rates equal or exceed those in the elderly [9]. This is not just an issue for infectious diseases and pulmonary medicine specialists. It begs for standard practices to be adjusted by primary care clinicians where Coccidioides is endemic or when patients have traveled to such places. For anyone wishing to refresh their understanding of when to look for early coccidioidal infection, the Valley Fever Center Received 14 February 2013; accepted 19 February 2013. Correspondence: John N. Galgiani, MD, Medical Research Bldg, Rm 119, 1656 E Mabel St, Tucson, AZ 85724 (spherule@u.arizona.edu). Clinical Infectious Diseases © The Author 2013. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved. For Permissions, please e-mail: journals. permissions@oup.com. DOI: 10.1093/cid/cit117

Coccidioidomycosis is the oldest of the major mycoses, on the basis of reports in the literature. The first case was reported in 1892 and occurred in an Argentine soldier. Thus, last year represented the centennial of its discovery. The case was erroneously reported as that of mycosis fungoides. Soon there followed reports from San Francisco describing the disorder as a protozoan infection. It was not until the work of Ophuls in the early part of this century that the disease was properly classified as a mycosis and the causative organism identified as Coccidioides immitis. In the late 1930s, Gifford recognized that the organism that she recovered from the sputum of many patients suffering from a well-known, selflimited pulmonary infection known as San Joaquin Valley fever was the same as the agent described by Ophuls in his report of frequently fatal coccidioidal granuloma. C. E. Smith and his colleagues, under the auspices of the Armed Forces Epidemiological Board, defined the clinical syndrome of primary and disseminated coccidioidal disease during the Second World War. They outlined the area of endemicity, recognized that there were distinct racial differences in the occurrence of dissemination, and developed a series of highly sensitive and specific immunologic diagnostic tests. Their work established a scientific basis of research that, with the isolation of the antibiotic amphotericin B, led to the therapeutic era. The addition of the imidazole group of drugs to the armamentarium followed, and the introduction in the 1980s of the orally active azole derivatives opened yet another era of therapy for coccidioidomycosis.