Valley fever: a fungus in the dust, and a map that keeps growing

Topic: Valley fever (coccidioidomycosis): a dust-borne fungal infection with an expanding range · Since 1990 · Grounded citations only · Published 2026-08-09

Start here: what Valley fever is

Valley fever — medically, coccidioidomycosis — is a lung infection you catch by breathing dust. There is no person-to-person spread, no insect vector, no contaminated food. The reservoir is soil.

Two closely related soil fungi cause it: Coccidioides immitis and Coccidioides posadasii, which were recognized as separate species only in 2002, distinguished by DNA polymorphisms and by growth differences on high-salt media, with C. posadasii being the non-California population [1] [2]. Both are thermally dimorphic, and that two-form life cycle is the whole story of how they infect people. In soil the fungus grows as filaments (hyphae) that fragment into tough, easily airborne spores called arthroconidia. When soil is disturbed — by wind, construction, farming, digging, driving — those spores go into the air, and a person breathes them in. Inside the warm lung the fungus switches form entirely: each arthroconidium swells into a spherule, which fills with hundreds of endospores and then ruptures, releasing them to form new spherules [3] [4] [5]. That parasitic form exists only in the host, and it is why the body's usual antifungal defences work poorly against it [6].

Where it is. The endemic region is the arid and semi-arid southwestern United States — Arizona, California's Central and San Joaquin Valleys, Nevada, New Mexico, Utah — extending into parts of Mexico, Central and South America [7] [8] [9]. Risk follows dust exposure, so the burden falls on people who work outdoors and disturb soil: agricultural and construction workers, and anyone downwind of them.

What it does. Most people who inhale the spores are fine — infection is often asymptomatic or resolves on its own. Of those who get sick, the usual presentation is a community-acquired pneumonia: cough, fever, fatigue, chest pain, sometimes a rash and joint aches severe enough to have earned the old name desert rheumatism. A minority progress to severe pulmonary disease, and a smaller minority to disseminated infection, where the fungus spreads beyond the lung to skin, bone, joints, and — the most feared destination — the meninges around the brain and spinal cord [7] [10] [11].

Why it matters, and why it is in the news. Three reasons, and each is developed below.

1. It is routinely missed. In a prospective study of adults presenting with a new lower-respiratory syndrome in an endemic area, Valley fever was serologically confirmed in 16 of 55 people (29%) — and 81% of those with Valley fever had been given antibacterial drugs, which do nothing to a fungus. Symptoms alone had "insufficient predictive value… to guide clinicians without specific laboratory tests" [12]. Without deliberate testing, the true frequency is underestimated by public health statistics. 2. Case counts are rising. Reported infections have "increased dramatically over the past decade" [13], with Arizona surveillance documenting a rise from 33 to 43 cases per 100,000 population between 1998 and 2001 alone [14]. 3. The map is moving. A climate niche model projects that under a high-warming scenario, by 2100 the area of climate-limited endemicity will more than double, the number of affected states will rise from 12 to 17, and cases will increase by 50%, expanding north into Idaho, Wyoming, Montana, Nebraska, and the Dakotas [15].

Three pillars follow — measurements, medicines, and progress — with a simple simulatable climate model between the first two that explains the mechanism behind the third.

Pillar 1: measurements and diagnosis

The spectrum you are trying to place a patient on

Diagnosis in Valley fever is really two questions at once: is this Coccidioides? and how far has it gone? The IDSA guideline organizes its recommendations along exactly that spectrum, "from initial pulmonary infection, which eventually resolves whether or not antifungal therapy is administered, to a variety of pulmonary and extrapulmonary complications" [7]. That clause — resolves whether or not antifungal therapy is administered — is the single most important clinical fact about the common form of this disease, and it shapes the treatment section below.

The stages, in plain terms:

Serology: the test that carries most of the weight

Because culture is slow and hazardous to laboratory staff and biopsy is invasive, the workhorse is antibody testing, and its logic has been stable for decades [3] [20].

The two antibody classes answer different questions:

In practice a sensitive enzyme immunoassay (EIA) is used to screen, with immunodiffusion and CF used to confirm and characterize [20].

The feature that makes CF uniquely valuable is that it is quantitative. The result is a titre — the greatest serum dilution at which the reaction still occurs, reported as 1:2, 1:4, 1:8, 1:16 and so on, each step a doubling. Because titre tends to rise with the burden and extent of infection, it functions as a severity and progression marker rather than a yes/no answer: a rising titre on serial testing signals progressive or disseminated disease, a falling titre signals response to treatment, and a high titre prompts a search for dissemination. That prognostic use is why serology has "assisted in the diagnosis and prognosis of coccidioidomycosis for a half-century" [3] [7].

The important caveat is that serology depends on a working immune system. In a review of 1,797 serologic tests from 298 immunocompetent and 62 immunosuppressed patients, immunosuppressed people had lower seropositivity rates for every test type during the first year — though they can mount a response, and combining multiple test methods improved detection in that group [20]. The patients at highest risk of severe disease are therefore the ones most likely to test falsely negative.

Antigen detection helps where antibodies fail. A Coccidioides antigen EIA detected antigenuria in 70.8% of patients with more-severe coccidioidomycosis while remaining absent in 99.4% of healthy individuals and patients with non-fungal infections, with cross-reaction against other endemic mycoses in 10.7% — useful specifically for rapid diagnosis of severe forms [21]. Culture and molecular methods remain definitive, and molecular identification of thermally dimorphic fungi has moved steadily from classical to nucleic-acid-based approaches [22] [23].

Why so much is missed

Underdiagnosis is not a subtle effect. A cohort study of community-acquired pneumonia patients in southern California found that "limited and delayed testing probably leads to underdiagnosis among non-Hispanic black, Filipino, or Hispanic patients and among high-risk groups, including persons in whom antimicrobial drug therapy has failed" [24]. Combined with the finding that roughly a third of endemic-area pneumonias may be Valley fever [12], the practical recommendation follows directly: if a patient who lives in or has travelled to a Coccidioides-endemic region develops pneumonia, the diagnostic evaluation should routinely include testing for this organism [12].

Centerpiece: a simple simulatable climate-incidence model

Everything about the resurgence and the expanding map rests on a claim about climate driving incidence, and that claim has been modelled explicitly.

The mechanism has a nickname: "grow and blow." Wet conditions let the fungus grow in the soil and build biomass; a later dry, dusty, windy period aerosolises the arthroconidia and delivers them to human lungs. Because those are two separate steps separated in time, the relationship between rainfall and cases is lagged.

Write incidence in season t as the sum of an antecedent-growth term and a concurrent-dispersal term:

I(t) = β₀ + β_grow · P(t − L) + β_blow · D(t)

where P is antecedent precipitation, D is a concurrent dry/dusty dispersal index, and L is the lag.

Grounding. The model form, the lag, and the relative importance of the two terms are all taken from the climate–coccidioidomycosis modelling literature rather than invented here. Analysing Pima County, Arizona, and explicitly testing hypotheses "linking climate and dust to fungal growth and dispersion," Comrie found that precipitation during the normally arid foresummer 1.5–2 years before the season of exposure is the dominant predictor of the disease in all seasons, accounting for half of the overall variance, while dispersion-related conditions predicted incidence in fall, winter and the arid foresummer — and that "cross-validated models combining antecedent and concurrent conditions explain 80% of the variance" [25]. A follow-up assessment confirmed that roughly 80% of the variance in seasonal incidence can be explained by "precipitation and dust-related climate scenarios prior to and concurrent with outbreaks" [26]. Earlier Arizona work using Poisson regression on surveillance data had already found combinations of climatic and environmental factors highly correlated with seasonal case counts [14].

Parameters, honestly. The lag used in the figure, 21 months, is the midpoint of that grounded 1.5–2 year window. The coefficients β₀, β_grow, β_blow and the climate series P(t) and D(t) are illustrative and flagged — deterministic sinusoids standing in for a real regional record, not data from any location. The one quantitative link back to the source is enforced rather than asserted: the coefficients are set so that the antecedent-precipitation term carries about half the variance of the predicted series, which the script computes (49.7%) and checks against the published "half of the overall variance" finding [25].

0 12 24 36 48 60 72 84 96 months 0.0 0.5 1.0 1.5 2.0 2.5 3.0 3.5 antecedent precipitation, arbitrary units Grow and blow: incidence tracks rain from 1.5-2 years earlier 0 2 4 6 8 10 12 14 predicted incidence, arbitrary units lag 1.6 yr GROW: wet season builds fungal biomass BLOW: dry, dusty season aerosolises the spores
Computed illustration of the lagged "grow and blow" climate-incidence relationship, I(t) = b0 + b_grow*P(t-L) + b_blow*D(t). The shaded blue trace is antecedent precipitation - an annual cycle under a four-year wet/dry oscillation; the red line is predicted incidence. The lag L is 21 months, the midpoint of the GROUNDED 1.5-2 year window over which antecedent precipitation is the dominant predictor of disease. The incidence peak driven by the wettest antecedent season arrives 1.6 years after that rainfall peak - shorter than the 21-month input lag, because the concurrent dry-season dispersal term pulls the peak earlier. Coefficients and the synthetic climate series are ILLUSTRATIVE, not data from any location; they are constrained so the antecedent-precipitation term carries about half the variance of the predicted series (computed: 49.7%), reproducing the published finding that antecedent precipitation accounts for half the overall variance (Comrie 2005 [W2081710608]; Talamantes et al. 2007 [W2007281007]).

What the model explains. Three things that are otherwise puzzling.

First, why a wet winter is bad news two years later rather than immediately. The delay is the fungus growing before anything can blow.

Second, why both wet and dry matter, in that order. Regional analyses bear this out with real data: across Arizona, California, Nevada, New Mexico and Utah for 2000–2015, incidence was greater "in areas with warmer air temperatures and drier soils," the mean annual cycle "peaked following periods of low precipitation and soil moisture," but year-to-year, autumn incidence in California's San Joaquin Valley was higher "following cooler, wetter, and productive springs" [27]. Soil-moisture records make the same point directly, relating incidence in Arizona and California to soil moisture from previous summers [28].

Third, why a warming, drying climate expands the disease. If the endemic range is set by a climate envelope — warm enough, dry enough, with enough seasonal rain to grow the fungus — then shifting that envelope shifts the map, which is precisely what the niche-model projection of a doubled endemic area and 12→17 affected states encodes [15].

Limits. A two-term linear model with one lag is a teaching object. Real analyses use distributed lags across many months rather than a single L, and generalised additive models rather than a straight line [29]; the effective lag varies by region and season [27] [25]; and the model says nothing about where the fungus actually lives in the soil, which remains a genuine gap — environmental detection is difficult and patchy [13].

Pillar 2: medicines

Treatment in Valley fever is unusually stratified: for the most common presentation the right answer is often nothing, and for the most severe it is forever.

Most primary infections need no antifungal. The IDSA guideline is explicit that initial pulmonary infection "eventually resolves whether or not antifungal therapy is administered" [7]. Management for an otherwise healthy person with uncomplicated pneumonia is therefore observation with structured follow-up — serial serology and imaging to confirm resolution rather than progression — plus symptomatic care. The reason this matters is that azoles are not free: they run for months, interact with other drugs, and carry hepatic and teratogenic risk. Treating everyone would harm more people than it helps.

Azoles are the mainstay when treatment is warranted — for prolonged or severe pneumonia, for patients at high risk of dissemination, and for extrapulmonary disease. Fluconazole and itraconazole are the standard oral agents; they work by inhibiting fungal lanosterol 14α-demethylase, blocking ergosterol synthesis and so damaging the fungal cell membrane. Newer triazoles have activity against Coccidioides as well, and the treatment guidelines have been revised across two decades of accumulating azole experience [7] [30] [13] [31] [32]. Notably, in the Kern County study, oral antifungal therapy before hospitalization was associated with reduced risk of coccidioidomycosis pneumonia, suggesting that early treatment of high-risk groups may prevent severe disease [16].

Amphotericin B is reserved for severe and rapidly progressive disease. It binds ergosterol directly and punches pores in the fungal membrane — the oldest and still one of the most reliable antifungal mechanisms, sixty years on [33] [34] [35]. Its problem has always been toxicity, especially to the kidney, which is why lipid formulations were developed and are now standard where the drug is needed [36] [37] [38] [39].

Coccidioidal meningitis requires lifelong therapy. This is the sharpest statement in the whole review and it rests on direct evidence. Fluconazole works: in 50 consecutive patients with active coccidioidal meningitis treated with 400 mg daily for up to four years, 37 of 47 evaluable patients (79%) responded [40], and itraconazole showed similar utility in chronic disease [41]. But response is not cure. In a study of 18 patients in whom azole therapy was stopped after apparent remission, 14 of 18 (78%) relapsed — 15 of the relapses meningeal — and relapse occurred anywhere from 0.5 to 30 months after stopping, with no pre-stop feature (which azole, how long, CSF indices) distinguishing those who relapsed from those who did not [42]. The title of that paper is the clinical bottom line: Is it ever safe to stop azole therapy for Coccidioides immitis meningitis? The answer, in practice, is no. Where azoles fail, options include intrathecal amphotericin B and, in case reports, echinocandins [43].

There is no licensed human vaccine. This is the largest gap in the field, and it has been recognized as such for decades — a review two decades ago argued that a coccidioidomycosis vaccine "is justified and attainable" [44], and the case-control work on severe disease ends by noting that high-risk persons "may benefit from vaccination once an effective CM vaccine is available" [16]. It remains unavailable. Progress and obstacles are covered below.

Pillar 3: progress — climate, expansion, and what is being built

The range is expanding, and the driver is climate

The projection is the headline: under a high-warming scenario, by 2100 the climate-limited endemic area more than doubles, affected states go from 12 to 17, and cases rise by 50%, with expansion north into Idaho, Wyoming, Montana, Nebraska, South Dakota and North Dakota — while precipitation limits spread further east [15]. That projection is a climate niche model fitted to contemporary climate and incidence data and then driven with Earth system model output, so it inherits both the strengths and the uncertainties of that approach.

Drought turns out to be a distinct driver, not just "dryness." The most rigorous recent analysis used California census-tract surveillance data from 2000 to 2020, generalised additive models with distributed monthly lags on precipitation and temperature, and an ensemble prediction algorithm to estimate the counterfactual incidence that would have occurred without drought. Across 81,448 reported California cases, it estimated 1,467 excess cases in the two years following the 2007–2009 drought and 2,649 drought-attributable excess cases following the later drought — set against the context that California is in "the driest multi-decadal period since 800 CE, exacerbated by anthropogenic warming" [29]. Drought followed by rain is the grow-and-blow cycle operating on a multi-year scale.

The dust side has hardened too. Reconstructing long-term dust climatology from continuous aerosol observations across the western United States for 1988–2011, investigators reported "direct evidence of rapid intensification of dust storm activity over American deserts," with the frequency of windblown dust storms increasing 240% from the 1990s to the 2000s — in contrast to declining trends in Asia and Africa — linked to Pacific sea-surface temperature variability, and then examined the relationship between that dust trend and Valley fever [45] [46] [47]. Coccidioidomycosis is now routinely cited among the diseases whose burden climate change aggravates, and among the fungal pathogens whose emergence climate is driving [48] [49] [50].

Vaccines: real progress, still no product

The immunology is encouraging and the endpoint remains out of reach. Protection against Coccidioides is cell-mediated, and vaccine-induced protection against the three systemic mycoses endemic to North America was shown in mice to require Th17 cells [51] — a mechanistic target rather than a guess. Host-response and vaccine-development work has been reviewed repeatedly across two decades [52] [53] [13], and recombinant antigen candidates have been evaluated as monovalent, divalent and chimeric constructs [54]. New vaccine platform technologies developed for other pathogens are an obvious opportunity here [55] [56]. But the honest summary is the one the field itself gives: the search for a preventative vaccine is ongoing [13].

Diagnostics and drugs in the pipeline

Diagnostics are moving toward faster, less antibody-dependent methods: antigen EIA for severe disease [21], and molecular identification of thermally dimorphic fungi shifting from classical to nucleic-acid-based approaches [22] [23] [57]. The broader challenge of diagnosing invasive fungal infection quickly is an active field in its own right [58].

Drugs. Beyond the azoles, nikkomycin Z — a chitin synthase inhibitor, attacking a target absent from human cells — has been the long-standing hope, with a recent assessment asking directly whether it is "ready to meet the promise" [59] [60] and experimental work evaluating frequent oral dosing in a central-nervous-system coccidioidomycosis model, aimed squarely at the meningitis problem [61].

Genomics underpins much of this. Comparative genomic analysis of Coccidioides and its relatives [62], population genomic sequencing revealing recent hybridization and transposon control [63], and genome-wide association approaches now being applied to the fungus itself [64] are building the target list. Work on the developmental switch — the genes governing spherule remodelling and endospore formation, and regulators such as Ryp1 — targets the transition that makes this organism pathogenic in the first place [5] [4] [65].

Dig deeper in lmmol

  • The health reviews index collects the other conditions in this series. Valley fever shares its central logic with black lung: an environmental exposure measured in dust, a dose that depends on what the air is carrying, and prevention that means controlling the exposure rather than curing the damage.
  • STAT1 does not yet have a static page in this graph, but it is the entity to look up next: gain-of-function mutations in it cause disseminated coccidioidomycosis, which is the clearest human evidence that Th1/interferon-γ immunity is what contains this fungus [19].
  • For entities without a linked static page here, use lmmol's graph index, all diseases, or all proteins rather than guessing an entity URL.

Key papers

  1. W4242945259: Molecular and Phenotypic Description of Coccidioides posadasii sp. nov., Previously Recognized as the Non-California Population of Coccidioides immitis (cited 397×)
  2. W2152146814: Climate and acute/subacute paracoccidioidomycosis in a hyper-endemic area in Brazil (cited 77×)
  3. W2121842229: Serology of coccidioidomycosis (cited 366×)
  4. W2102705829: Gene expression in human fungal pathogen Coccidioides immitis changes as arthroconidia differentiate into spherules and mature (cited 44×)
  5. W3024343424: Defining Critical Genes During Spherule Remodeling and Endospore Development in the Fungal Pathogen, Coccidioides posadasii (cited 35×)
  6. W568600803: Coccidioides Endospores and Spherules Draw Strong Chemotactic, Adhesive, and Phagocytic Responses by Individual Human Neutrophils (cited 67×)
  7. W2479157738: 2016 Infectious Diseases Society of America (IDSA) Clinical Practice Guideline for the Treatment of Coccidioidomycosis (cited 608×)
  8. W4206301643: Coccidioidomycosis: epidemiology (cited 253×)
  9. W3129795073: Endemic and Other Dimorphic Mycoses in The Americas (cited 63×)
  10. W2013871628: Coccidioidomycosis (cited 264×)
  11. W2143083649: Epidemiologic, Clinical, and Diagnostic Aspects of Coccidioidomycosis (cited 262×)
  12. W2131843801: Coccidioidomycosis as a Common Cause of Community-acquired Pneumonia (cited 289×)
  13. W2129525280: Recent Advances in Our Understanding of the Environmental, Epidemiological, Immunological, and Clinical Dimensions of Coccidioidomycosis (cited 280×)
  14. W2170086004: An Epidemic of Coccidioidomycosis in Arizona Associated with Climatic Changes, 1998–2001 (cited 150×)
  15. W2970573935: Expansion of Coccidioidomycosis Endemic Regions in the United States in Response to Climate Change (cited 226×)
  16. W2159910402: Risk Factors for Severe Pulmonary and Disseminated Coccidioidomycosis: Kern County, California, 1995-1996 (cited 231×)
  17. W1601510919: Coccidioidomycosis in Liver Transplant Recipients in an Endemic Area (cited 70×)
  18. W1556581972: The Utility of Diagnostic Testing for Active Coccidioidomycosis in Solid Organ Transplant Recipients (cited 59×)
  19. W2134194869: Signal transducer and activator of transcription 1 (STAT1) gain-of-function mutations and disseminated coccidioidomycosis and histoplasmosis (cited 242×)
  20. W2016227754: Serologic testing for symptomatic coccidioidomycosis inimmunocompetent and immunosuppressed hosts (cited 163×)
  21. W2099295865: Diagnosis of Coccidioidomycosis with Use of the <i>Coccidioides</i> Antigen Enzyme Immunoassay (cited 175×)
  22. W4402319660: Diagnosis of Human Endemic Mycoses Caused by Thermally Dimorphic Fungi: From Classical to Molecular Methods (cited 7×)
  23. W2099114511: Molecular diagnostics of infectious diseases (cited 304×)
  24. W2792695318: Testing for Coccidioidomycosis among Community-Acquired Pneumonia Patients, Southern California, USA1 (cited 21×)
  25. W2081710608: Climate Factors Influencing Coccidioidomycosis Seasonality and Outbreaks (cited 162×)
  26. W2007281007: Assessment of Climate– Coccidioidomycosis Model (cited 44×)
  27. W2792699090: Coccidioidomycosis Dynamics in Relation to Climate in the Southwestern United States (cited 123×)
  28. W2594168789: Relating coccidioidomycosis (valley fever) incidence to soil moisture conditions (cited 62×)
  29. W4302018471: Effects of precipitation, heat, and drought on incidence and expansion of coccidioidomycosis in western USA: a longitudinal surveillance study (cited 91×)
  30. W2164174337: Practice Guidelines for the Treatment of Coccidioidomycosis (cited 280×)
  31. W2104445943: Comparison of In Vitro Activities of the New Triazole SCH56592 and the Echinocandins MK-0991 (L-743,872) and LY303366 against Opportunistic Filamentous and Dimorphic Fungi and Yeasts (cited 577×)
  32. W2357730895: Isavuconazole Treatment of Cryptococcosis and Dimorphic Mycoses (cited 220×)
  33. W3126290817: Sixty years of Amphotericin B: An Overview of the Main Antifungal Agent Used to Treat Invasive Fungal Infections (cited 367×)
  34. W2121842516: Amphotericin B: spectrum and resistance (cited 472×)
  35. W2061894085: It only takes one to do many jobs: Amphotericin B as antifungal and immunomodulatory drug (cited 310×)
  36. W2144030592: Amphotericin B Lipid Complex for Invasive Fungal Infections: Analysis of Safety and Efficacy in 556 Cases (cited 626×)
  37. W2149546447: A Double‐Blind, Randomized, Controlled Trial of Amphotericin B Colloidal Dispersion versus Amphotericin B for Treatment of Invasive Aspergillosis in Immunocompromised Patients (cited 334×)
  38. W2997896219: Lipid Systems for the Delivery of Amphotericin B in Antifungal Therapy (cited 202×)
  39. W2172068234: Comparative Efficacy and Distribution of Lipid Formulations of Amphotericin B in Experimental<i>Candida albicans</i>Infection of the Central Nervous System (cited 374×)
  40. W2011031248: Fluconazole Therapy for Coccidioidal Meningitis (cited 208×)
  41. W2052469869: Itraconazole Therapy for Chronic Coccidioidal Meningitis (cited 152×)
  42. W2065870824: Is It Ever Safe To Stop Azole Therapy for <i>Coccidioides immitis</i> Meningitis? (cited 206×)
  43. W2149812263: Treatment of meningeal coccidioidomycosis with caspofungin (cited 35×)
  44. W2035624263: Prospects of vaccines for medically important fungi† A vaccine against coccidioidomycosis is justified and attainable (cited 99×)
  45. W2606775993: Intensified dust storm activity and Valley fever infection in the southwestern United States (cited 279×)
  46. W4285731816: Dust Storms, Valley Fever, and Public Awareness (cited 44×)
  47. W4360603582: Health and Safety Effects of Airborne Soil Dust in the Americas and Beyond (cited 123×)
  48. W4290673830: Over half of known human pathogenic diseases can be aggravated by climate change (cited 958×)
  49. W3157952205: Climate change and the emergence of fungal pathogens (cited 380×)
  50. W3017538594: Climatic changes and their role in emergence and re-emergence of diseases (cited 447×)
  51. W2108822061: Vaccine-induced protection against 3 systemic mycoses endemic to North America requires Th17 cells in mice (cited 231×)
  52. W2153910927: Coccidioidomycosis: Host Response and Vaccine Development (cited 212×)
  53. W2071499523: Advances in combating fungal diseases: vaccines on the threshold (cited 222×)
  54. W2176670588: Evaluation of Two Homologous Coccidioides Posadasii Antigens as Recombinantly Expressed Monovalent, Divalent, and Chimeric Vaccine Candidates (cited 0×)
  55. W2891486793: New Vaccine Technologies to Combat Outbreak Situations (cited 595×)
  56. W3089805074: Emerging Concepts and Technologies in Vaccine Development (cited 327×)
  57. W2948495375: Recent trends in molecular diagnostics of yeast infections: from PCR to NGS (cited 133×)
  58. W4381250317: Diagnosis of invasive fungal infections: challenges and recent developments (cited 340×)
  59. W3097240824: Nikkomycin Z—Ready to Meet the Promise? (cited 77×)
  60. W2061931513: Comparison of susceptibility of fungal isolates to lufenuron and nikkomycin Z alone or in combination with itraconazole (cited 20×)
  61. W4401715932: Evaluation of nikkomycin Z with frequent oral administration in an experimental model of central nervous system coccidioidomycosis (cited 3×)
  62. W2169900015: Comparative genomic analyses of the human fungal pathogens <i>Coccidioides</i> and their relatives (cited 333×)
  63. W2170082195: Population genomic sequencing of <i>Coccidioides</i> fungi reveals recent hybridization and transposon control (cited 196×)
  64. W4412014516: “Select and Resequence” Methods Enable a Genome-Wide Association Study of the Dimorphic Human Fungal Pathogen <i>Coccidioides posadasii</i> (cited 1×)
  65. W4225503377: The WOPR family protein Ryp1 is a key regulator of gene expression, development, and virulence in the thermally dimorphic fungal pathogen Coccidioides posadasii (cited 27×)