How Do You Get a Fungal Infection? Causes & Risks

Fungal infections happen when fungal organisms gain entry to your body and your defenses fail to clear them. The entry points are surprisingly varied: you can inhale microscopic spores from soil or dust, pick up a skin infection from another person or animal, develop an overgrowth of fungi already living in your body after a course of antibiotics, or introduce a fungus directly through a wound. What determines whether exposure turns into actual disease is usually the balance between the fungus’s ability to invade and your immune system’s ability to fight back, and dozens of factors can tip that balance.

Breathing In Spores From the Environment

Many of the most serious fungal infections start in the lungs, simply because you inhale spores that are floating in the air. Certain fungi, called endemic fungi, live naturally in soil and become airborne when the ground is disturbed. When you breathe those spores in, they can settle in your lungs and cause infection. These organisms can infect perfectly healthy people who happen to live in or visit the right geographic area, though they cause far worse disease in people with weakened immune systems.¹

Histoplasmosis is a good example. The fungus Histoplasma lives in soil enriched by bird or bat droppings, and people get exposed when they disturb that soil through activities like excavation, demolition, farming, or exploring caves. Occupational exposures are frequently linked to histoplasmosis outbreaks.² A landscaper clearing a chicken coop or a construction crew demolishing an old building can kick up enough spores to infect an entire work crew. Valley fever (coccidioidomycosis) follows a similar pattern, with the fungus living in arid soils across the southwestern United States and parts of Latin America. Aspergillus mold spores are essentially everywhere, indoors and out, but cause disease almost exclusively in people whose immune defenses are compromised.³

The distinction matters practically. With endemic fungi, you get infected because you went to the wrong place at the wrong time and breathed in the wrong air. With opportunistic molds like Aspergillus, the spores are in virtually every breath you take; the issue is not exposure but what your immune system does with it.

Skin Contact and Dermatophytes

The fungal infections people encounter most often in daily life are the superficial ones: athlete’s foot, ringworm, jock itch, and nail fungus. These are caused by dermatophytes, a specialized group of fungi that feed on keratin, the tough protein in your skin, hair, and nails. Dermatophytes produce enzymes that break down keratin, which is both how they eat and how they invade.⁴ Common species include Trichophyton rubrum, Trichophyton mentagrophytes, and Microsporum canis.⁵

You can pick up dermatophytes through direct skin-to-skin contact with an infected person, by touching an infected animal, or by walking barefoot on contaminated surfaces like locker room floors and swimming pool decks. The fungi thrive in warm, moist environments, which is why they favor the spaces between your toes, your groin, and the underside of your nails. Their toolkit for infection involves adhesion to your skin surface, secretion of proteases that dissolve keratin, and invasion via fungal filaments that burrow into tissue.⁶

Most dermatophyte infections stay on the surface and are more annoying than dangerous. But in rare cases, especially in people with certain genetic vulnerabilities, the infection can go deep and become invasive. That transition from nuisance to serious disease depends heavily on the immune response, which most people mount effectively enough to confine dermatophytes to the outer layers of skin.

How Your Body Normally Keeps Fungi in Check

Humans have several layers of defense against fungal invaders. The first is temperature: your core body temperature of about 37°C (98.6°F) is too hot for most fungal species to grow. Out of the millions of known fungal species, only a few hundred can tolerate human body heat well enough to cause disease. This thermal barrier is arguably the most important reason mammals have relatively few fungal diseases compared to, say, amphibians or insects.⁷

Beyond temperature, your immune system actively detects and destroys fungi. Immune cells like macrophages and dendritic cells sit at the front lines, especially in your lungs, skin, and gut. These cells carry pattern recognition receptors that detect structural features on fungal surfaces and trigger an immune response.⁸ One particularly important branch of this defense is the IL-17 pathway, which is critical for keeping Candida and other fungi from colonizing your skin and mucous membranes. People born with genetic defects in IL-17 signaling develop chronic, recurrent fungal infections of the mouth, skin, and nails.⁹

The practical takeaway is that most fungal exposure does not lead to disease. You breathe in Aspergillus spores regularly. Candida already lives on your skin and in your gut. Dermatophyte spores are on gym floors everywhere. In a person with a functioning immune system, these encounters are handled routinely. Infection happens when something weakens or bypasses those defenses.

Medications That Open the Door

Several categories of medication can raise your risk of fungal infection, sometimes dramatically. The most widely recognized are immunosuppressive drugs. Glucocorticoids (like prednisone), commonly prescribed for autoimmune conditions and inflammatory diseases, suppress the immune cells that keep fungi under control. In a large time-varying analysis of patients on TNF-alpha inhibitor therapy, periods of glucocorticoid use were associated with roughly 1.8 times the infection risk compared to periods without either glucocorticoids or other immunosuppressants. Non-glucocorticoid immunosuppressants carried an even higher risk, at about 2.3 times.¹⁰

Antibiotics work through a completely different mechanism but still promote fungal disease. They do not suppress your immune system; instead, they wipe out bacteria in your gut that normally keep fungi in check. When those bacterial competitors are removed, Candida albicans can overgrow. This effect has been demonstrated in both animal models and human studies, and it is especially pronounced with antibiotics that target anaerobic bacteria.¹¹ This is the basic reason many people develop oral thrush or vaginal yeast infections after a course of antibiotics: the drugs cleared the bacteria that were keeping Candida populations small.

Chemotherapy, organ transplant anti-rejection drugs, and biologic therapies for conditions like rheumatoid arthritis or Crohn’s disease all carry varying degrees of fungal infection risk. The common thread is that any treatment which suppresses your immune function, especially the white blood cells that patrol for fungi, gives opportunistic organisms a chance to establish themselves.

Diabetes and Metabolic Conditions

Diabetes, particularly when blood sugar is poorly controlled, creates conditions that fungi exploit. High blood glucose impairs the ability of white blood cells to kill invading organisms, and it provides a richer nutrient environment for fungi that feed on sugar. The connection is especially stark with mucormycosis, an aggressive and fast-moving infection caused by molds in the Mucor family. Mucormycosis typically begins in the nose and sinuses after spores are inhaled and is strongly associated with diabetes.¹² The condition gained worldwide visibility during the COVID-19 pandemic, when surges in mucormycosis cases were reported in countries like India, often in patients with diabetes who had also received high-dose steroids.

High glucose also affects Candida infections. Some Candida species ramp up their ability to form protective biofilms in high-glucose environments, making them harder for both your immune system and antifungal drugs to reach.¹³ If you have diabetes and notice recurrent yeast infections, poor blood sugar control is one of the first things worth addressing.

Hospital-Acquired Fungal Infections

Hospitals are paradoxically risky environments for fungal infection. The patients there tend to have weakened defenses, and the medical devices used to treat them can serve as entry points for fungi. Intravenous catheters are a major source. Candida species can form biofilms on catheter surfaces, creating a reservoir of infection that is extremely difficult to treat. These biofilms can tolerate antifungal drug concentrations many times higher than what is needed to kill free-floating Candida cells.¹³ Patients receiving nutrition through an IV are at particular risk because the high glucose content of the fluid enhances biofilm formation.

Construction or renovation near hospitals can also release Aspergillus spores into the air. For immunocompromised patients, even brief spikes in airborne mold spore counts can trigger invasive pulmonary aspergillosis. HEPA filters have been investigated as a protective measure. One retrospective study of COVID-19 patients in Pakistan found that portable HEPA filters were associated with a decrease in invasive fungal infections.¹⁴ However, a separate single-center study in patients with acute myeloid leukemia found no additional benefit of HEPA filtration on top of antifungal prophylaxis.¹⁵ The evidence, in other words, is mixed and probably depends on the patient population and what other preventive measures are already in place.

Candida Auris and Drug Resistance

One of the more alarming developments in fungal disease over the past decade is the emergence of Candida auris, a yeast species that was first identified in 2009 and has since spread to hospitals on every inhabited continent. What makes C. auris unusual is its ability to persist on hospital surfaces for extended periods, its tendency to colonize patients and spread from person to person in healthcare settings, and its resistance to multiple classes of antifungal drugs.¹⁶

Unlike most Candida species, which typically cause infection from your own body’s resident fungi, C. auris behaves more like a hospital-acquired bacterium. It survives on bed rails, doorknobs, and medical equipment, resists standard disinfectants, and tolerates desiccation and high-salt conditions that would kill other fungi.¹⁷ Healthcare facilities dealing with outbreaks have had to implement aggressive contact precautions, enhanced environmental cleaning, and patient screening programs to contain the spread.¹⁸ For the average person outside a hospital, C. auris is not a significant concern, but for critically ill or immunocompromised patients, it represents a genuinely new kind of threat.

Wounds and Traumatic Inoculation

Some fungal infections begin not through breathing or surface contact but through direct introduction into deeper tissue via a wound. This is called traumatic inoculation, and it is more common than you might think. Gardeners pricked by thorns, farmers cut by plant material, and anyone who sustains an injury outdoors can introduce fungal organisms beneath the skin’s protective barrier. Sporotrichosis, sometimes called “rose gardener’s disease,” follows this exact pattern: the Sporothrix fungus enters through a thorn prick or scratch and causes nodules that spread along the lymphatic channels of the arm.

Eye injuries are another example. A case report described a patient who developed a rare fungal keratitis (corneal infection) after being injured by a thorn, with the infection progressing over months before it was correctly identified.¹⁹ Agricultural workers and contact lens wearers are at elevated risk for fungal eye infections, the former because of trauma from plant material and the latter because of microabrasions on the corneal surface. The key difference between traumatic inoculation and other routes is that it physically bypasses your skin barrier, so even fungi that would normally be unable to invade intact skin can establish an infection.

Catching Fungal Infections From Animals

Pets and livestock can be a direct source of fungal infection, especially for dermatophytes. While fungal infections from animal contact are relatively uncommon compared to all fungal infections, they represent a meaningful proportion of skin-related cases.²⁰ Cats are particularly important carriers. Microsporum canis, a dermatophyte that naturally colonizes cat fur, is one of the main zoonotic fungal agents worldwide and has a strong public health impact.²¹ Kittens and stray cats are the usual culprits, and children who handle them are the usual victims, often developing circular patches of ringworm on the arms, face, or scalp.

Sporothrix brasiliensis, the organism behind sporotrichosis in South America, has also gained attention as a zoonotic threat spreading primarily through contact with infected cats, including through scratches and bites. Unlike the classic “rose gardener” transmission of other Sporothrix species, this cat-associated strain has caused large outbreaks in Brazil. If you adopt a stray cat or kitten, particularly one with skin lesions or patchy fur, having it evaluated by a veterinarian is a reasonable precaution.

Genetic Vulnerability

Most discussions of fungal infection risk focus on acquired factors like medications, diabetes, or HIV. But some people are genetically predisposed to recurrent or severe fungal disease, even when the rest of their immune system works normally. One well-characterized example involves mutations in a gene called CARD9, which plays a role in how immune cells recognize and respond to fungi. People with CARD9 deficiency appear immunocompetent by conventional testing but are highly susceptible to severe infections from Candida, dermatophytes, and certain other fungal groups.²²

Defects in the IL-17 pathway, as mentioned earlier, are another genetic cause of chronic mucocutaneous candidiasis, a condition where Candida infections of the mouth, nails, and skin recur throughout life.⁹ These genetic conditions are rare, but they are worth knowing about because they explain the occasional patient who gets devastating fungal disease with no obvious risk factors. If you or someone in your family has had unusually severe or recurrent fungal infections without an apparent cause, immunogenetic testing is something a specialist might consider.

Climate Change and Expanding Fungal Threats

The geography of fungal disease is shifting. Valley fever was once considered a problem confined to parts of Arizona, California, and Nevada. Climate modeling based on temperature and precipitation trends projects that the area suitable for Valley fever will more than double by 2100 under a high-warming scenario, potentially expanding into states like Idaho, Montana, Wyoming, and the Dakotas. The number of cases could increase by about 50%.²³

The broader concern is not limited to one disease. Fungi have a remarkable ability to adapt to rising temperatures, pollution, and changing ecosystems. They can spread via air, water, and even wildfire smoke, and their genetic plasticity allows them to evolve thermotolerance, meaning they can grow at higher temperatures than their ancestors could.²⁴ The thermal barrier that protects mammals from most fungi depends on a temperature gap between your body and the environment. As the environment warms, fungal species have more opportunity to evolve the heat tolerance needed to survive inside a human host. This is a slow-moving threat, but one that infectious disease researchers are watching closely.⁷

When Fungal Infections Pretend to Be Something Else

One of the less-discussed risks associated with fungal infections is misdiagnosis. Fungal lung infections can produce masses and nodules on imaging that look remarkably like lung cancer. Distinguishing between a fungal granuloma and a malignant tumor remains challenging, and misdiagnosis can significantly delay appropriate treatment in both directions: patients with fungal infections may undergo unnecessary biopsies or even surgery for suspected cancer, while patients with actual cancer may receive antifungal therapy instead of chemotherapy.²⁵

This issue is especially relevant in areas where endemic fungi are common. A person living in the Ohio River Valley who develops a lung nodule may have histoplasmosis rather than cancer, but a radiologist unfamiliar with endemic fungal patterns could easily miss the possibility. If you live in or have traveled through an area where fungal infections are common and a scan turns up a suspicious lung lesion, it is worth making sure your medical team considers fungal disease in the differential diagnosis. A simple blood test or urine antigen test can sometimes clarify things without an invasive procedure.

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