CDC Finds Invasive Mold Disease Is Underrecognized

CDC ran active, laboratory-based surveillance — searching lab records directly rather than waiting for doctors to report cases or for billing codes to capture them.

The report, Active Surveillance for Invasive Mold Disease — Four Hospitals, Atlanta, Georgia, 2020–2024, appeared in CDC’s MMWR Surveillance Summaries on July 30, 2026. It was carried out through the Georgia Emerging Infections Program at three laboratories serving four Atlanta hospitals: two academic hospitals and their associated outpatient clinics, one federal hospital, and one community hospital.

That configuration matters, and several early write-ups got it wrong — including some that described “two academic and two community hospitals.” The federal hospital is a distinct setting with a distinct patient population, and any attempt to generalize the numbers has to account for the actual mix.

Rather than relying on diagnosis codes, investigators searched microbiology records for positive mold cultures and positive Aspergillus galactomannan tests. Every flagged patient was then reviewed against clinical history, imaging, tissue findings, laboratory results, recognized host risk factors, the treating physician’s diagnosis, treatment given, and outcome.

The reason for that labor-intensive approach is stated plainly in the report: invasive mold disease is not a nationally notifiable condition in the United States. No central system receives every diagnosed case. Symptoms are nonspecific, cultures are often negative in true infection, and a positive culture can just as easily represent harmless colonization or laboratory contamination.

Investigators flagged 968 patients as potential cases.

After review, 449 met the surveillance definitions for invasive mold disease — slightly under half. The annual count was steady across the five years, roughly 81 to 100 cases per year. This was not a sudden outbreak; it was a persistent burden that nobody had measured locally before.

The three classification tiers are not equivalent, and this is the detail most coverage dropped. 89 cases were “proven” — strong evidence such as fungus recovered from a normally sterile site, or fungal invasion demonstrated in tissue. 142 were “probable” — recognized host risk plus compatible clinical or imaging findings plus mycologic evidence. 218 met a broader surveillance definition — they did not satisfy every formal research criterion, but clinicians diagnosed and treated them, or the patient died within three days of the specimen being collected. Eighteen of those were included solely because the patient died before mold-active treatment could begin.

The broader group should not be dismissed — these were real patients whose doctors judged them infected. But it should also not be described as 218 additional biopsy-confirmed infections, because it isn’t.

Almost everyone in this study had a seriously compromised immune system, a major underlying illness, or both.

Within the 449 cases: 59% had used immunosuppressive medication, 27% had received a solid-organ transplant, 22% had a blood cancer, 18% had end-stage kidney disease, 9% had prolonged neutropenia, 6% had cirrhosis, and 6% had severe burns. Lymphopenia and chronic lung disease were also common.

The COVID-19 subgroup is one of the sharper results. Fifty-eight patients (13%) had current or recent COVID-19. Their 90-day mortality was 66%, against 41% in everyone else — a statistically significant gap. The proportion of cases involving COVID-19 peaked at 23% in 2021 and fell to 5% by 2024. The study cannot prove COVID-19 caused the fungal infections; severe viral illness, corticosteroid treatment, prolonged ICU stays, and ventilation all overlap as risk factors and cannot be separated here.

The 45% figure is all-cause mortality, and the distinction is not a technicality. Among patients with adequate follow-up, 45% died from any cause within 90 days. About 30% died during the hospital stay itself.

These patients frequently had cancer, transplants, kidney failure, cirrhosis, severe burns, COVID-19, or life-threatening critical illness. The study did not adjudicate each death and assign a cause. The accurate statement is that invasive mold disease occurred in a population with extremely high mortality. The inaccurate statement — and the one circulating — is that mold killed 45% of them.

The most defensible wording, if you are sharing this: “Among patients with sufficient follow-up, 45% died from any cause within 90 days.” It is not softer than the truth. It is the truth.

Each of the following has appeared somewhere in coverage or social commentary since publication. None is supported by the paper.

It means insisting on precision — which protects you, and costs you nothing.

There is a temptation, when a major federal agency finally publishes something alarming about mold, to treat it as vindication. It isn’t, and claiming it is carries a real cost. People with MCS already spend years being disbelieved by clinicians, insurers, and disability adjudicators. A community that overstates what a study shows hands those same people a reason to dismiss the next accurate claim. The most valuable thing this site can be is the place where the numbers are right.

MCS is not established as a state of immunosuppression, and it is not listed by CDC as a risk factor for invasive mold disease. The mechanisms behind MCS remain debated in the clinical literature — which does not make the symptoms less real or less disabling, and does not mean environmental control is optional.

Mold and dampness are worth taking seriously on their own terms. CDC and NIOSH associate damp buildings with respiratory symptoms, asthma, allergic rhinitis, hypersensitivity pneumonitis, eczema, and irritation. Those are documented health effects that do not require anything to be growing in your tissue. You do not need this study to justify getting a leak fixed.

One genuine overlap deserves attention: a person with MCS may separately have a transplant, a blood cancer, be on long-term corticosteroids or biologics, or live with severe lung disease, diabetes, or kidney disease. In that situation the elevated infection risk comes from that condition or treatment — not from the MCS label — and it deserves its own conversation with a clinician. For more on how mold exposure may act as an initiating event for chemical sensitivity, see our page on mold, CIRS and chemical sensitivity.

Collapsing these into one category is how both minimization and overdiagnosis happen. They have different mechanisms, different tests, and different treatments.

Find the water and remove the material. Visible mold or a persistent musty smell is reason enough to act — you do not need a test first, and a test does not change the fix.

The response to a damp or moldy building starts with moisture, not with testing. Visible mold or a persistent musty odor is reason enough to find the water source and remove contaminated material. CDC and EPA generally do not recommend routine air testing to decide whether a visible problem needs fixing, and there are no federal health-based airborne mold limits for homes.

1. Stop the leak, condensation, drainage failure, or humidity problem.
2. Dry wet materials quickly; remove what cannot be fully cleaned and dried.
3. Isolate larger work areas and keep contaminated dust out of the HVAC system.
4. Use qualified remediation help for extensive, hidden, recurring, sewage-related, or HVAC-contaminated problems.
5. Do not rely on killing mold — dead mold and fragments still provoke reactions.
6. Do not substitute bleach or another biocide for moisture correction and physical removal.
7. Keep immunocompromised people, and people with significant lung disease, asthma, or severe mold allergy, away from cleanup entirely.
8. Verify the work against dryness, removal, cleanliness, and correction of the cause — scaled to the size of the job.

For a fuller treatment of testing choices, interpreting results, and hiring a remediator, see our mold testing and remediation guide.