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Fungal pericarditis: Causes, Symptoms, Diagnosis, and Treatment Pathways

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Fungal pericarditis is an uncommon but serious infection of the sac around the heart. The pericardium—the heart’s thin protective lining—normally lets the heart move smoothly as it beats. When fungi invade this space, inflammation and fluid can build up quickly, sometimes over hours to days. That pressure can limit how well the heart fills, leading to sudden shortness of breath, low blood pressure, and collapse. Because the early symptoms can resemble more common illnesses, people may not realize how urgent it is—especially if they recently had surgery, have a weakened immune system, or have a long-term catheter. The good news is that outcomes improve when clinicians recognize the pattern early, drain infected fluid promptly, and start the right antifungal therapy with careful monitoring.

Table of Contents

What it is and why it can turn dangerous

The pericardium is a two-layered sac that wraps the heart. A small amount of fluid between those layers acts like lubrication. In fungal pericarditis, fungi trigger inflammation and can infect that fluid, the pericardial layers, or both. The problem is not only the infection itself—it is also what the infection does to heart function.

There are three ways fungal pericarditis can become dangerous:

  • Rapid fluid buildup (pericardial effusion): Inflammation can cause fluid to accumulate faster than the pericardium can stretch. Even a “moderate” amount of fluid can be life-threatening if it appears quickly.
  • Cardiac tamponade: This is when pressure around the heart prevents it from filling normally. The result can be sudden low blood pressure, fainting, shock, and organ injury.
  • Longer-term scarring: Ongoing inflammation can leave the pericardium thick and stiff, a condition called constrictive pericarditis. When that happens, the heart struggles to fill even after the infection is controlled, leading to fatigue, swelling, and shortness of breath.

Fungal pericarditis is different from “typical” viral or idiopathic pericarditis. It is more likely to occur in people with a weakened immune system, after cardiothoracic surgery, or in the setting of invasive fungal infection elsewhere in the body. It also tends to require more than anti-inflammatory medication—source control (draining infected fluid) and prolonged antifungal therapy are central.

A practical way to think about it: fungal pericarditis is less about “treating chest pain” and more about preventing pressure on the heart, stopping the fungus from spreading, and avoiding relapse. That is why clinicians often treat it as an urgent infection until proven otherwise.

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How fungi reach the pericardium

Fungi do not usually live in the pericardial space. When they get there, it is typically because the body’s defenses are compromised or because there is a direct route for invasion. Understanding the pathways helps explain why treatment often includes both drainage and antifungal medication.

Common routes include:

  • Hematogenous spread (through the bloodstream): This is a major pathway for Candida species. A bloodstream infection can seed the pericardium, especially when a person has a central venous catheter, is receiving total parenteral nutrition, or is critically ill.
  • Direct extension from nearby infection: Lung infections, mediastinal infections, or surgical site infections can spread into the pericardium. This pathway is often considered with molds such as Aspergillus, particularly in people with severe immune suppression.
  • Iatrogenic inoculation (introduced during procedures): Cardiac surgery, device implantation, and repeated invasive procedures can rarely introduce organisms, especially if wound healing is impaired or there is prolonged hospitalization.
  • Fistulas and perforations: Abnormal connections between the gastrointestinal tract and pericardium—after surgery, cancer, ulcers, or injury—can allow fungi to enter the pericardial space. These situations can be especially severe because they create ongoing contamination until the source is repaired.

The fungi involved vary by exposure and immune status. Yeasts (especially Candida) are common in hospital-associated cases and bloodstream spread. Molds (such as Aspergillus) are more often linked to profound immune suppression and can be harder to diagnose because blood cultures are frequently negative. In certain regions, endemic fungi (for example, Histoplasma or Coccidioides) can involve the pericardium as part of disseminated disease.

One reason fungal pericarditis is challenging is that symptoms may start before anyone suspects an invasive fungal infection. Fever may be mild or absent in some immunosuppressed patients. Meanwhile, inflammation can progress and fluid can accumulate silently. This is why clinicians often move quickly to imaging and pericardial fluid testing when risk factors and symptoms line up.

The key takeaway: fungal pericarditis is rarely a “standalone” problem. It often reflects a larger vulnerability—immune suppression, invasive lines, recent surgery, or infection elsewhere—and successful care usually addresses both the pericardium and the underlying pathway that allowed fungi to get there.

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Who is at risk

Most people with pericarditis do not have a fungal cause. When fungi are involved, there is usually a clear reason the body could not keep the organisms contained. Risk is best understood in layers: immune defenses, medical exposures, and background health.

Higher-risk groups include:

  • People with weakened immune systems
  • Hematologic cancers (like leukemia or lymphoma), especially during chemotherapy
  • Stem cell or solid-organ transplant recipients
  • Advanced HIV infection or other causes of severe immune dysfunction
  • Long-term or high-dose corticosteroid use and other immunosuppressive drugs
  • People with major recent medical or surgical exposures
  • Recent cardiothoracic surgery (valve surgery, bypass surgery, pericardial procedures)
  • Prolonged intensive care stay, especially with multiple antibiotics
  • Central venous catheters, hemodialysis access, or long-term intravenous therapy
  • Total parenteral nutrition
  • People with serious underlying illness
  • Poorly controlled diabetes
  • Chronic kidney disease, especially with dialysis
  • Severe malnutrition or frailty
  • Chronic lung disease when combined with immune suppression

Certain situations should raise suspicion even more:

  • Persistent fever despite broad antibiotics in a high-risk patient
  • Known candidemia (Candida bloodstream infection) with new chest symptoms or an enlarging pericardial effusion
  • Neutropenia (very low white blood cell count) with respiratory symptoms plus signs of pericardial involvement
  • Post-surgical complications, such as wound infection, mediastinitis, or unexplained fluid collections
  • Unusual sources, like esophageal injury or gastrointestinal surgery complicated by fistula formation

It can also help to think about why these risks matter. Fungi often exploit breaks in barriers (like lines and surgery) and gaps in immune surveillance (like low neutrophils). Broad-spectrum antibiotics can also shift normal microbial balance, making yeast overgrowth more likely. The result is not just “more infections,” but a different type of infection—one that may be harder to culture, slower to clear, and more prone to relapse if therapy is stopped too soon.

If you are a patient or caregiver, a practical risk checklist is: recent major surgery, a central line, immune-suppressing medication, cancer therapy, transplant history, or unexplained persistent fever. Having one factor does not mean you have fungal pericarditis—but it does mean that chest symptoms and breathlessness should be assessed promptly, not watched at home for days.

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Symptoms and red flags

Fungal pericarditis can look like other conditions at first. Some people develop classic pericarditis symptoms; others mainly show signs of fluid buildup or systemic infection. Paying attention to the pattern—and how quickly it changes—matters.

Common symptoms include:

  • Chest pain, often sharp or stabbing, sometimes worse with deep breaths or lying flat
  • Shortness of breath, especially when lying down or with mild activity
  • Fever or chills, though fever may be absent in severely immunosuppressed patients
  • Fatigue and weakness
  • Cough or discomfort that overlaps with lung symptoms

Signs that suggest a growing pericardial effusion include:

  • Increasing breathlessness over hours to days
  • A feeling of chest heaviness or tightness rather than sharp pain
  • New swelling in the legs or abdomen (more likely with slower, chronic buildup)
  • Lightheadedness when standing

Red flags that suggest cardiac tamponade (an emergency) include:

  • Fainting, near-fainting, or sudden severe weakness
  • Confusion, gray or clammy skin, or extreme anxiety with breathlessness
  • Very low blood pressure or a rapid pulse
  • Marked shortness of breath at rest
  • Symptoms that escalate quickly over minutes to hours

Because fungal pericarditis often occurs in medically complex situations, symptoms can be “masked” by other problems. For example, a patient recovering from surgery may assume breathlessness is due to pain or deconditioning. A person on chemotherapy may assume fatigue is expected. The danger is missing a turning point when fluid pressure around the heart becomes the main driver.

Complications to be aware of include:

  • Septic shock when infection spreads or the body’s response becomes overwhelming
  • Arrhythmias (irregular heartbeats), sometimes due to inflammation involving the heart muscle
  • Constrictive pericarditis, which can appear weeks to months after infection
  • Recurrence, especially if the source (like an infected line or fistula) is not removed or repaired

A helpful rule: chest pain alone is concerning; chest pain plus worsening breathlessness is more concerning; breathlessness plus fainting or low blood pressure is an emergency. If fungal pericarditis is a possibility because of immune suppression or recent surgery, it is safer to seek urgent evaluation rather than “wait and see.”

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How doctors confirm the diagnosis

Diagnosis usually happens in two phases: confirming pericardial inflammation or effusion, and then identifying the cause—specifically whether fungi are involved. Because delays can be dangerous, clinicians often start evaluation and stabilization in parallel.

Typical steps include:

1) Bedside assessment and basic tests

Clinicians check blood pressure, oxygen levels, heart rate, and signs of poor circulation. They may listen for muffled heart sounds and look for neck vein distension, though these signs are not always present. Common early tests include:

  • Electrocardiogram (ECG): May show changes consistent with pericarditis, but findings can be non-specific.
  • Blood work: Inflammatory markers, complete blood count, kidney and liver function, and blood cultures. In high-risk patients, clinicians may add fungal markers or antigen tests to support suspicion.

2) Imaging to assess fluid and heart function

  • Echocardiography is the key first-line test because it can detect pericardial fluid and show whether the heart is being compressed. It also guides urgent drainage when tamponade is suspected.
  • CT or cardiac MRI may be used when the anatomy is complex, effusions are loculated, or clinicians need a detailed view of pericardial thickening or adjacent infection.

3) Pericardial fluid sampling (often decisive)

If there is enough fluid to drain safely, clinicians may perform pericardiocentesis (needle drainage) or create a pericardial window (surgical drainage). The fluid is tested for:

  • Cell count and chemistry
  • Bacterial and fungal cultures
  • Microscopy and stains for fungi
  • Molecular tests (when available) that can detect fungal DNA
  • Cytology if malignancy is also a concern

A key point: blood cultures can be negative even when fungal pericarditis is present, especially with mold infections. That makes direct sampling of pericardial fluid (and sometimes pericardial tissue) especially important.

4) Looking for the source

Clinicians also search for where the fungus came from: an infected catheter, recent surgical site infection, lung infection, bloodstream infection, or gastrointestinal fistula. This part changes management. For example, treating Candida without removing an infected line increases the chance of relapse. Treating a fistula-related infection without repairing the fistula can make cure impossible.

Because fungal pericarditis is rare, diagnosis often relies on combining clues: risk factors, imaging, pericardial fluid testing, and the patient’s overall clinical course. When suspicion is high, clinicians may start antifungal therapy before all tests return—especially if the patient is unstable.

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Treatment: what happens in the hospital

Fungal pericarditis is typically managed in the hospital because patients can deteriorate quickly and because therapy often needs procedures, intravenous medications, and close monitoring. Treatment has three pillars: stabilize the patient, remove infected fluid or tissue, and give targeted antifungal therapy long enough to prevent relapse.

1) Stabilization and urgent decisions

If tamponade is suspected, clinicians focus on maintaining blood pressure and oxygenation while preparing for drainage. The most effective “medicine” for tamponade is often removing the pressure by draining the pericardial space. Supportive care may include intravenous fluids, vasopressors, oxygen, and treatment of shock.

2) Drainage and source control

Drainage choices depend on the situation:

  • Pericardiocentesis: Often used for urgent decompression and diagnostic sampling.
  • Pericardial window: A surgical approach that allows ongoing drainage and may be preferred when fluid is thick, infected, or likely to reaccumulate.
  • Pericardiectomy: Partial or complete removal of the pericardium may be considered when infection is persistent, loculated collections cannot be drained adequately, or constriction develops.

Source control usually extends beyond the pericardium:

  • Remove or exchange infected catheters when suspected.
  • Treat adjacent infections (lungs, mediastinum, surgical sites).
  • Repair fistulas or perforations when present.

3) Antifungal therapy tailored to the organism

Clinicians aim to identify the fungus and test susceptibility, then choose therapy based on the organism and the patient’s kidney and liver function.

Common approaches (general patterns, individualized by specialists) include:

  • Candida pericarditis: Often starts with an intravenous echinocandin or liposomal amphotericin B, then may transition to an oral azole (such as fluconazole) if the species is susceptible and the patient is improving.
  • Aspergillus pericarditis: Often treated with a mold-active azole (commonly voriconazole) or another mold-active regimen, sometimes in combination in severe cases, guided by specialist input.
  • Endemic fungi or Cryptococcus: Regimens vary and may include amphotericin-based induction followed by a longer oral phase, depending on disease extent.

Duration is typically weeks to months, not days. Many patients require at least 6 weeks of effective antifungal therapy, and longer courses are common when there is disseminated infection, immune suppression, or difficulty achieving complete source control.

4) Monitoring for safety and response

Antifungal drugs can interact with many medications and may affect the liver, kidneys, or heart rhythm. Monitoring often includes:

  • Kidney and liver blood tests at regular intervals
  • Drug levels for certain azoles when needed
  • Repeat echocardiograms to ensure fluid is resolving
  • Clinical monitoring for recurrent fever, breathlessness, or new chest pain

In short, treatment is not just “take an antifungal.” It is a coordinated plan: drain the problem, stop the fungus, fix the route of infection, and watch closely for recurrence or scarring.

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Recovery, follow-up, and prevention

Recovery after fungal pericarditis depends on how early the condition was treated, how well source control was achieved, and whether the immune system can rebound. Some people recover fully; others need prolonged therapy and monitoring for months.

What recovery often looks like

Many patients feel better soon after effective drainage—breathing improves and pressure symptoms ease. Fatigue can linger, especially after critical illness or surgery. Clinicians typically arrange follow-up to confirm:

  • The pericardial effusion has resolved or is steadily shrinking
  • There are no signs of recurrent infection
  • Heart function is stable
  • Medication side effects are being avoided or managed

Repeat echocardiography is common, especially if the original effusion was large, loculated, or associated with tamponade. If symptoms return—new shortness of breath, chest discomfort, fever, or fainting—patients are usually advised to seek urgent reassessment rather than waiting for the next clinic visit.

Watching for constrictive pericarditis

Constrictive pericarditis can develop after significant inflammation or infection. It may show up as:

  • Persistent or progressive shortness of breath
  • Swelling in the legs or abdomen
  • Early fullness with meals or abdominal discomfort
  • Reduced exercise tolerance that does not improve as expected

When clinicians suspect constriction, they may use echocardiography and advanced imaging, and they may adjust therapy. In some cases, surgery is needed, but decisions are individualized and often involve experienced centers.

Prevention and risk reduction

Not all cases are preventable, but risk can be lowered by addressing common entry points:

  • Catheter care: Meticulous line care, prompt removal of unnecessary catheters, and rapid evaluation of suspected line infections.
  • Surgical aftercare: Early attention to wound changes, fevers, or unexpected breathlessness after cardiothoracic surgery.
  • Antibiotic stewardship: Avoiding unnecessarily prolonged broad-spectrum antibiotics when alternatives exist, since they can increase fungal overgrowth risk in some settings.
  • Immune support planning: For people on chemotherapy, transplant medications, or high-dose steroids, clinicians may use antifungal prophylaxis in selected high-risk scenarios and emphasize rapid evaluation of fevers.

When to seek urgent care

Seek emergency evaluation for any of the following, especially if you are immunosuppressed or recently had heart or chest surgery:

  • Sudden or severe shortness of breath
  • Fainting, near-fainting, or confusion
  • Chest pain with weakness, sweating, or low blood pressure
  • Rapidly worsening symptoms over hours
  • Fever with chest symptoms in a high-risk patient

Living through fungal pericarditis can be unsettling. A helpful approach is to keep a simple plan: know your warning signs, keep follow-up appointments, take antifungals exactly as prescribed, and report side effects early so therapy can be adjusted without losing momentum against the infection.

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References

Disclaimer

This article is for general educational purposes and does not replace individualized medical advice, diagnosis, or treatment. Fungal pericarditis can become a medical emergency, especially when fluid around the heart builds quickly or when the immune system is weakened. If you have chest pain, worsening shortness of breath, fainting, or signs of shock, seek emergency care immediately. Treatment decisions—such as drainage procedures, antifungal selection, and therapy duration—must be tailored by qualified clinicians using your medical history, test results, and medication profile.

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