Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (706 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
Infection with a fungus of the genus coccidioides, endemic to the southwestern united states. It is sometimes called valley fever but should not be confused with rift valley fever. Infection is caused by inhalation of airborne, fungal particles known as arthroconidia, a form of fungal spores. A primary form is an acute, benign, self-limited respiratory infection. A secondary form is a virulent, severe, chronic, progressive granulomatous disease with systemic involvement. It can be detected by use of coccidioidin.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Coccidioidomycoses; Coccidioides Infection; Coccidioides Infections; Infection, Coccidioides; Coccidioidomycosis Infection; Coccidioidomycosis Infections; Infection, Coccidioidomycosis; San Joaquin Valley Fever.
Where it fits in the MeSH classification
- Broader topics
- Mycoses
- Narrower topics
- Coccidioidal Meningitis
Related concepts
- Coccidioides
- Southwestern United States
- Rift Valley Fever
- Fungal Spores
- Coccidioidin
Research landscape
PubMed indexes 3,426 records tagged with the MeSH heading “Coccidioidomycosis” (counts retrieved 2026-10-29). 395 of them (11.5%) were published from 2020 onward, and the busiest period so far is through 1999 with 1,939 records.
Reviews account for 505 records (14.7%) and meta-analyses for 1. Randomized controlled trials number 6 (0.2%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 1,939 |
| 2000-2009 | 504 |
| 2010-2019 | 588 |
| 2020 onward | 395 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 505 | 14.7% |
| Meta-analyses | 1 | 0.0% |
| Randomized controlled trials | 6 | 0.2% |
Method: PubMed query "Coccidioidomycosis"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in infectious diseases
Infectious disease evidence combines microbiology, epidemiology and clinical trials. Laboratory studies identify pathogens and how they cause harm; surveillance and outbreak investigations describe who is affected and how infection spreads; trials establish whether treatments and vaccines work. Results depend on place and time, because pathogens evolve and resistance patterns and population immunity change. Check when and where the data were collected, how cases were defined and how up to date the evidence is.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Coccidioides immitis and posadasii; A review of their biology, genomics, pathogenesis, and host immunity | 2018 | Review article Design not recorded in structured metadata | 76 | cc by PMID 30179067 · DOI · PMC6141143 |
| Testing for coccidioidomycosis among patients with community-acquired pneumonia | 2008 | Research article Design not recorded in structured metadata | 76 | cc by PMID 18598625 · DOI · PMC2600364 |
| Coccidioidal pneumonia, Phoenix, Arizona, USA, 2000-2004 | 2009 | Research article Design not recorded in structured metadata | 72 | cc by PMID 19239751 · DOI · PMC2681119 |
| Exhausted T cell phenotypes in disseminated coccidioidomycosis | 2026 | Research article Design not recorded in structured metadata | 1 | cc by PMID 42171605 · DOI · PMC13232714 |
Coccidioides immitis and posadasii; A review of their biology, genomics, pathogenesis, and host immunity [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Coccidioides immitis and C.
- Closing excerpt
- Unfortunately, efforts to develop an effective subunit vaccine have not yet been productive, although two potential live fungus vaccines have been developed.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (150 words)
Coccidioides immitis and C. posadasii are two highly pathogenic dimorphic fungal species that are endemic in the arid areas of the new world, including the region from west Texas to southern and central California in the USA that cause coccidioidomycosis (also known as Valley Fever). In highly endemic regions such as southern Arizona, up to 50% of long term residents have been infected. New information about fungal population genetics, ecology, epidemiology, and host-pathogen interactions is becoming available. However, our understanding of some aspects of coccidioidomycosis is still incomplete, including the extent of genetic variability of the fungus, the genes involved in virulence, and how the changes in gene expression during the organism's dimorphic life cycle are related to the transformation from a free-living mold to a parasitic spherule. Unfortunately, efforts to develop an effective subunit vaccine have not yet been productive, although two potential live fungus vaccines have been developed.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 30179067 · DOI · PMC6141143
Testing for coccidioidomycosis among patients with community-acquired pneumonia [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Coccidioidomycosis is a common cause of community-acquired pneumonia (CAP) in disease-endemic areas.
- Closing excerpt
- testing among CAP patients was infrequent, reportable-disease data, which rely on positive diagnostic test results, greatly underestimate the true disease prevalence.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (149 words)
Coccidioidomycosis is a common cause of community-acquired pneumonia (CAP) in disease-endemic areas. Because testing rates influence interpretation of reportable-disease data and quality of CAP patient care, we determined the proportion of CAP patients who were tested for Coccidioides spp., identified testing predictors, and determined the proportion of tested patients who had positive coccidioidomycosis results. Cohort studies to determine the proportion of ambulatory CAP patients who were tested in 2 healthcare systems in metropolitan Phoenix found testing rates of 2% and 13%. A case-control study identified significant predictors of testing to be age >/=18 years, rash, chest pain, and symptoms for >/=14 days. Serologic testing confirmed coccidioidomycosis in 9 (15%) of 60 tested patients, suggesting that the proportion of CAP caused by coccidioidomycosis was substantial. However, because Coccidioides spp. testing among CAP patients was infrequent, reportable-disease data, which rely on positive diagnostic test results, greatly underestimate the true disease prevalence.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 18598625 · DOI · PMC2600364
Coccidioidal pneumonia, Phoenix, Arizona, USA, 2000-2004 [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Community-acquired pneumonia (CAP) often results in severe illness and death.
- Closing excerpt
- In the absence of distinguishing clinical features, coccidioidal pneumonia can be identified only with appropriate laboratory studies.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (151 words)
Community-acquired pneumonia (CAP) often results in severe illness and death. In large, geographically defined areas where Coccidioides spp. are endemic, coccidioidomycosis is a recognized cause of CAP, but its frequency has not been studied extensively. To determine the frequency of patients with coccidioidomycosis, we conducted a prospective evaluation of 59 patients with CAP in the Phoenix, Arizona, area. Of 35 for whom paired coccidioidal serologic testing was performed, 6 (17%) had evidence of acute coccidioidomycosis. Coccidioidal pneumonia was more likely than noncoccidioidal CAP to produce rash. The following were not found to be risk factors or reliable predictors of infection: demographic features, underlying medical conditions, duration of time spent in disease-endemic areas, occupational and recreational activities, initial laboratory studies, and chest radiography findings. Coccidioidomycosis is a common cause of CAP in our patient population. In the absence of distinguishing clinical features, coccidioidal pneumonia can be identified only with appropriate laboratory studies.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 19239751 · DOI · PMC2681119
Exhausted T cell phenotypes in disseminated coccidioidomycosis [4]
Abstract reading summary — source excerpts
- Opening excerpt
- BACKGROUNDCoccidioidomycosis ranges from self-limiting uncomplicated Valley fever (UVF) in most cases to life-threatening disseminated coccidioidomycosis (DCM) in rare individuals.
- Closing excerpt
- FUNDINGNational Institute of Allergy and Infectious Diseases grants U19 AI166059 and R21 AI149654 and University of California Office of the President grant VFR-19-633386.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (256 words)
BACKGROUNDCoccidioidomycosis ranges from self-limiting uncomplicated Valley fever (UVF) in most cases to life-threatening disseminated coccidioidomycosis (DCM) in rare individuals. A few patterns of immunologic deficits allowing for dissemination have been identified, although the specific defects in most individuals with DCM remain undefined. We hypothesized that chronic antigen exposure in DCM engenders a state of T cell exhaustion.METHODSFrom a cohort of over 300 individuals with confirmed diagnoses of coccidioidomycosis, circulating T cell phenotypes were characterized via flow cytometry and Coccidioides-specific T cell responses were measured by activation-induced marker (AIM) assay.RESULTSMale sex was significantly associated with disseminated disease (OR 2.5, 95% CI 1.5-4.0). A majority (52%) of individuals showed Coccidioides-specific T cell responses in our AIM assay. We noted a significant difference in patients sampled in the first year of diagnosis, where only 8% of patients with DCM had T cell responses during this time, as compared with 44% of individuals with UVF (P = 0.04). Among DCM patients with detectable AIM responses, CD4+ T cells demonstrated an exhausted phenotype with elevated PD-1 expression compared with UVF individuals. In vitro PD-1 blockade augmented IFN-γ production in most tested individuals with DCM.CONCLUSIONThese findings suggest that dissemination may occur in some individuals during a period of impaired antigen-specific T cell activity. Importantly, these responses can be augmented in vitro by PD-1-blocking antibodies, supporting further study of immune checkpoint therapy as an adjunct to antifungal treatment in disseminated coccidioidomycosis.FUNDINGNational Institute of Allergy and Infectious Diseases grants U19 AI166059 and R21 AI149654 and University of California Office of the President grant VFR-19-633386.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42171605 · DOI · PMC13232714
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article 2016 Infectious Diseases Society of America (IDSA) Clinical Practice Guideline for the Treatment of Coccidioidomycosis [5]
- Research article Coccidioidomycosis [6]
- Research article Coccidioidomycosis [7]
- Research article Serology of coccidioidomycosis [8]
- Research article Practice guideline for the treatment of coccidioidomycosis. Infectious Diseases Society of America [9]
- Research article Epidemiology of coccidioidomycosis [10]
References
- Kirkland TN, Fierer J. Coccidioides immitis and posadasii; A review of their biology, genomics, pathogenesis, and host immunity. . 2018. PMID 30179067 · DOI · PMC6141143
- Chang DC, Anderson S, Wannemuehler K, Engelthaler DM, Erhart L, Sunenshine RH, et al.. Testing for coccidioidomycosis among patients with community-acquired pneumonia. . 2008. PMID 18598625 · DOI · PMC2600364
- Kim MM, Blair JE, Carey EJ, Wu Q, Smilack JD. Coccidioidal pneumonia, Phoenix, Arizona, USA, 2000-2004. . 2009. PMID 19239751 · DOI · PMC2681119
- Whitehill GD, Stephens AV, Thauland TJ, Moreno Lastre MA, Tate MM, Beyhan S, et al.. Exhausted T cell phenotypes in disseminated coccidioidomycosis. . 2026. PMID 42171605 · DOI · PMC13232714
- Galgiani JN, Ampel NM, Blair JE, Catanzaro A, Geertsma F, Hoover SE, et al.. 2016 Infectious Diseases Society of America (IDSA) Clinical Practice Guideline for the Treatment of Coccidioidomycosis. Clin Infect Dis. 2016. PMID 27470238 · DOI
- Galgiani JN, Ampel NM, Blair JE, Catanzaro A, Johnson RH, Stevens DA, et al.. Coccidioidomycosis. Clin Infect Dis. 2005. PMID 16206093 · DOI
- Stevens DA. Coccidioidomycosis. N Engl J Med. 1995. PMID 7898527 · DOI
- Pappagianis D, Zimmer BL. Serology of coccidioidomycosis. Clin Microbiol Rev. 1990. PMID 2200605 · DOI · PMC358158
- Galgiani JN, Ampel NM, Catanzaro A, Johnson RH, Stevens DA, Williams PL. Practice guideline for the treatment of coccidioidomycosis. Infectious Diseases Society of America. Clin Infect Dis. 2000. PMID 10770727 · DOI
- Pappagianis D. Epidemiology of coccidioidomycosis. Curr Top Med Mycol. 1988. PMID 3288356 · DOI
About this article
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- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
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- automated source verified; no human expert review has been recorded yet.
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- 1, last updated 2026-10-29.
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Evidence strength
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