Coccidioidomycosis and COVID-19 Co-Infection, United States, 2020

Alexandra K. Heaney; Jennifer R. Head; Kelly Broen; Karen Click; John Taylor; John R. Balmes; Jon Zelner; Justin V. Remais

Disclosures

Emerging Infectious Diseases. 2021;27(5):1266-1273. 

In This Article

Possible Effects of Co-infection on Disease Progression

Severe COVID-19

Underlying respiratory illness is a major risk factor for severe COVID-19 (Appendix references 60,64). The Centers for Disease Control and Prevention reported that among COVID-19 patients in the United States with available data on concurrent conditions, 9.2% had a chronic lung disease such as chronic obstructive pulmonary disease, asthma, or emphysema; chronic lung disease was the most common concurrent condition after diabetes (Appendix reference 81). The prevalence of chronic lung disease is higher among hospitalized patients (15%) and highest among patients in the intensive care unit (21%) (Appendix reference 81). Several studies of COVID-19 patients in China have also shown elevated rates of death and severe disease among those with underlying chronic respiratory conditions (Appendix references 64,82,83). Acute coccidioidomycosis is often self-limiting, but ≈3%–5% of patients have a chronic pulmonary form of the illness (Appendix references 84,85). The evidence that chronic lung disease increases risk for severe COVID-19 suggests that patients with chronic pulmonary coccidioidomycosis might be predisposed to severe COVID-19.

Coccidioidomycosis Reactivation

Infection with COVID-19 might reactivate disease in a coccidioidomycosis patient whose illness has progressed to a chronic but inactive state. After an initial Coccidioides infection resolves, the fungus can remain in the lungs in a latent state and become reactivated under certain conditions (Appendix references 86–93). Coccidioidomycosis reactivation has been reported among pregnant women, especially those who previously had disseminated coccidioidomycosis (Appendix reference 94). Patients with organ transplants, which usually require immunosuppressive medications, also have higher rates of coccidioidomycosis reactivation (Appendix references 87–92). SARS-CoV-2 infection has been associated with immune dysregulation, including lymphopenia (Appendix reference 95), which might lower the host's ability to regulate Coccidioides infection (Appendix reference 96). Although no studies have reported coccidioidomycosis reactivation in COVID-19 patients as of February 2021, emerging evidence suggests that COVID-19 infection might accelerate the reactivation of latent tuberculosis (L. Pathak, unpub. data, https://www.biorxiv.org/content/10.1101/2020.05.06.077883v2). In addition, dexamethasone, a medication recommended for patients with severe COVID-19, increases the risk for severe coccidioidomycosis (Appendix references 97,98).

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