Histoplasmosis: Causes, Symptoms, Diagnosis & Treatment

Histoplasmosis is an infection caused by breathing in tiny fungal spores from Histoplasma capsulatum, a fungus that grows in soil containing bird or bat droppings. The disease occurs worldwide, including in the Americas, Africa, and Asia, but is especially common in the Ohio and Mississippi River valleys of the United States. Studies show that 60–90% of people living in these high-risk areas have been exposed to the fungus at some point.

Most people who breathe in the spores do not develop any symptoms, meaning the infection is usually asymptomatic. A small percentage, historically estimated at about 1% of typical, everyday exposures, develop a flu-like illness. Symptoms may include fever, cough, headache, chest pain, chills, and muscle aches, and they usually appear 3 to 17 days after exposure.

In rare situations, especially when someone breathes in a large number of spores or has a weakened immune system, the infection can spread from the lungs to other organs. This more dangerous form is called disseminated histoplasmosis and can be life-threatening without treatment.

Because many countries do not require reporting of histoplasmosis cases, global data on how common it is remain unclear. Older estimates suggest there may be up to 500,000 new infections each year in the United States. Worldwide, the severe disseminated form is estimated to affect about 100,000 people annually, mostly those with weakened immune defenses.

Treatment varies based on severity. Mild cases usually clear on their own without medication. More serious, long-lasting, or disseminated infections require antifungal drugs, commonly itraconazole or amphotericin B. The type and duration of treatment depend on how severe the illness is and which organs are affected.

Prevention focuses on limiting exposure to contaminated soil. This includes avoiding areas with bird or bat droppings and using protective equipment, such as appropriate masks, during activities that disturb soil, including construction, demolition, cleanup work, or cave exploration.

Classification of Histoplasmosis

Histoplasma capsulatum is the fungus that causes histoplasmosis. It is a dimorphic fungus, meaning it lives in two different forms depending on the environment. In soil or dust (especially where bird or bat droppings enrich the soil), it exists as a mold. When its spores are inhaled into a warm-blooded host (such as a human), the fungus transforms into a yeast.

This ability to switch forms helps the fungus survive and multiply inside human cells, enabling infection.

Histoplasmosis can present in several clinical forms:

Acute pulmonary histoplasmosis — a short-term lung infection.
Chronic pulmonary histoplasmosis — a long-lasting lung disease, sometimes lasting months or years, often resembling other lung diseases.
Disseminated histoplasmosis — a severe form where the fungus spreads beyond the lungs to affect other organs.

Also, there are two main variants (or species) of the fungus associated with human disease:

H. capsulatum var. capsulatum — has a nearly worldwide distribution and is responsible for the classical form of histoplasmosis.
Histoplasma duboisii (previously called H. capsulatum var. duboisii) — mainly found in Africa and associated more often with skin, subcutaneous tissue, or bone infections (rather than just lungs).

Epidemiology

Histoplasmosis occurs worldwide. However, it is particularly common (endemic) in certain geographic regions, notably:

The valleys of the Ohio River Valley and Mississippi River Valley in the central and eastern United States.
Many parts of Central and South America.
Regions in Africa (especially where H. duboisii circulates), as well as parts of Asia and Australia.

In the historically endemic U.S. river-valley areas, studies have found that 60–90% of people show signs of exposure to the fungus at some point in their lives (serologic evidence of past infection).

In those same regions, the incidence of reported disease is lower. For example, a recent study from 2013 to 2023 found that the nationwide incidence of diagnosed histoplasmosis rose from about 2.9 cases per 100,000 person-years to 6.5 cases per 100,000 person-years.

Incidence varies by region. For instance, in some U.S. states outside the traditional river valleys, rates have exceeded 20 cases per 100,000 person-years in recent years.

Worldwide, prevalence estimates vary, depending on local conditions and how frequently people are exposed to contaminated soil or droppings. In some parts of Latin America, skin-test surveys (which show prior exposure) have found up to 93% positivity in certain locales — indicating very high exposure history.

Because many infections are mild or asymptomatic, and because healthcare systems in many countries lack advanced fungal-disease diagnostics, the true global burden of histoplasmosis is likely under-recognized.

Causative Organism

Histoplasmosis is caused by Histoplasma capsulatum, a thermally dimorphic fungus, meaning it changes its form depending on the surrounding temperature. This ability is central to its survival and pathogenicity. In the environment—usually at 25–30°C—the fungus exists in a mold form, producing two key types of spores: microconidia and macroconidia. The microconidia are small and light enough to become airborne, making them the primary infectious particles. When these microscopic spores are inhaled and reach the warmer temperature of the human lungs (around 37°C), the organism transforms into its yeast form, which is adapted for survival inside the body.

A critical feature of Histoplasma is its ability to survive and replicate inside macrophages, the very immune cells designed to destroy pathogens. Once inside these cells, the yeast form uses sophisticated mechanisms to evade killing, including altering the pH of the phagolysosome and resisting oxidative stress. This intracellular lifestyle gives the fungus the ability to spread (disseminate) from the lungs to other parts of the body through the bloodstream and lymphatic system.

Two major varieties of Histoplasma capsulatum exist:

H. capsulatum var. capsulatum – Found worldwide, responsible for the majority of classical histoplasmosis cases.
H. capsulatum var. duboisii – Predominantly found in Africa, associated more with skin, bone, and lymph node disease (often called “African histoplasmosis”).

Transmission and Risk Factors

Histoplasmosis spreads through specific environmental sources and affects certain populations more severely.

Modes of Transmission

Histoplasmosis is caused by the dimorphic fungus Histoplasma capsulatum, which exists in the soil as a mold that produces infectious microconidia (spores). The primary route of transmission is the inhalation of these airborne spores. When contaminated soil or organic material is disturbed, the microscopic spores become aerosolized and can be inhaled deep into the lungs. Because the spores are so small, they often bypass the upper respiratory defenses and lodge in the alveoli, where they begin to convert into their yeast form and multiply.

Activities that involve digging, renovation, demolition, agriculture, excavation, or spelunking increase the likelihood of disturbing contaminated sites. Even simple actions like sweeping dusty floors of old barns or cleaning chicken coops can release large numbers of spores. Natural forces such as strong winds, storms, or erosion can also mobilize spores into the air.

Importantly, histoplasmosis is not contagious. It does not spread through direct human-to-human contact, shared air, or respiratory droplets in the way that common viral infections do. Even living with or caring for someone with histoplasmosis does not pose a transmission risk. The infection can only occur when a person inhales spores directly from an environmental source. This makes prevention primarily dependent on environmental awareness rather than isolation of patients.

Rarely, histoplasmosis may be transmitted through organ transplantation, where donor organs contain latent fungal infection.

High-Risk Populations

Although anyone exposed to airborne spores can become infected, most healthy individuals either remain asymptomatic or develop mild, self-limiting disease. However, several groups face markedly increased risk for severe or disseminated histoplasmosis.

1. People with weakened immune systems are the most vulnerable. This includes:

Individuals with HIV/AIDS, particularly those with low CD4 counts
Cancer patients undergoing chemotherapy
Organ transplant recipients taking immunosuppressive therapy
Patients on long-term corticosteroids or TNF-alpha inhibitors used for autoimmune diseases. The weakened immune response in these groups makes it difficult to contain fungal growth once spores reach the lungs, increasing the risk of widespread infection.

2. Certain jobs involve frequent contact with environments where spores are likely present. These include:

Construction and demolition workers
Farmers and agricultural laborers
Spelunkers or cave explorers
Pest control workers
Poultry farm employees
Archaeologists or geologists working in excavation sites. These occupations often involve soil disturbance, handling animals or droppings, or working in confined, humid spaces like caves, conditions highly conducive to fungal release.

3. Individuals with COPD, emphysema, asthma, or previous tuberculosis scars may experience more severe respiratory symptoms, as the fungus exploits already compromised lung structures.

4. Infants, young children, and older adults may have less robust immune responses, making them more susceptible to severe forms of the disease.

5. Communities living near river valleys, bat colonies, or areas with heavy bird populations may encounter higher baseline exposure, even without direct occupational risk.

Environmental Reservoirs

The environmental niche of Histoplasma capsulatum strongly influences where cases of histoplasmosis occur. The fungus grows best in moist, nitrogen-rich soils, particularly those enriched with bird or bat droppings. These droppings provide an ideal nutrient supply for fungal growth and sporulation.

Common environmental reservoirs include:

Old chicken coops and poultry farms
Abandoned buildings, attics, and barns where birds roost
Caves, especially those inhabited by bats
Hollow tree trunks with bat colonies
Riverbanks and floodplain areas with moist soil
Construction or excavation sites in contaminated zones

One of the most well-documented endemic areas is the Ohio and Mississippi River valleys in the United States, where the fungus thrives due to the humid, temperate climate and favorable soil composition. Similar ecological niches exist in parts of Africa, Central and South America, and portions of Southeast Asia.

Environmental conditions that promote fungal survival include:

High humidity
Moderate temperatures
Soil with decaying organic matter
Frequent moisture from rainfall or flooding

When these conditions align, large quantities of spores can accumulate unseen in the soil. Once the soil is disturbed, especially during dry periods, spores easily become airborne.

Pathogenesis and Life Cycle

Histoplasma capsulatum exists in distinct forms depending on its environment and interaction with hosts.

Fungal Life Cycle

Histoplasma capsulatum is a thermally dimorphic fungus, meaning it changes its form depending on the temperature and environment. In its natural habitat, cool, moist soil enriched with bird or bat droppings, it exists as a mold with a complex mycelial network. In this environmental phase, the organism produces two major types of asexual reproductive spores:

Microconidia – small, smooth-walled spores (2–5 µm) that are readily aerosolized and most likely to be inhaled.
Macroconidia – larger, thick-walled spores (7–15 µm) with characteristic tuberculate (spiny) projections. These are less frequently inhaled but serve as diagnostic markers in laboratory identification.

These spores accumulate in the soil and become airborne when disturbed. Because microconidia are small enough to bypass the upper respiratory filtration system, they reach the alveolar spaces when inhaled.

Once inside the host lungs and exposed to body temperature (37°C), microconidia rapidly convert into the yeast phase, which is better adapted for intracellular survival. This transformation is critical to pathogenesis; without it, Histoplasma cannot establish infection.

Inside the lungs, the yeast forms are engulfed by alveolar macrophages. However, instead of being destroyed, the yeast thrives within the phagolysosome, using several survival strategies:

Inhibition of phagolysosomal acidification: The yeast modulates the internal pH, preventing the macrophage’s digestive enzymes from functioning optimally.
Production of antioxidant enzymes such as catalase and superoxide dismutase, which neutralize reactive oxygen species meant to kill pathogens.
Expression of heat shock proteins, particularly Hsp60, which facilitate attachment to macrophage receptors and protect the yeast from stress.
Acquisition of nutrients, especially iron and calcium, through specialized transport systems, allowing proliferation inside the macrophage.

Replicating intracellular yeast cells can travel through macrophages to regional lymph nodes, and from there, spread through the bloodstream or lymphatic system, potentially reaching the liver, spleen, bone marrow, and other organs. This dissemination is more likely when the host’s immune response is weak or delayed.

Although the fungus primarily exists as a yeast inside the host, it can remain dormant in granulomas for years. Reactivation is possible if the host becomes immunocompromised, mirroring the behavior of Mycobacterium tuberculosis.

Host Response to Infection

The host’s immune system responds to Histoplasma capsulatum in a staged manner, involving both the innate and adaptive immune systems. The outcome of infection, resolution, latency, or dissemination, depends largely on the balance and effectiveness of these responses.

Innate Immune Response

Within minutes of inhalation, alveolar macrophages recognize and engulf the invading yeast cells. However, because the yeast form is adapted to survive intracellularly, macrophages alone are insufficient to clear the infection.

Several innate mechanisms begin to respond:

Release of pro-inflammatory cytokines, particularly TNF-α, IL-12, and IL-18, which recruit additional immune cells.
Dendritic cells process Histoplasma antigens and migrate to lymph nodes, initiating T-cell activation.
Neutrophils may provide early fungal containment, although they are less effective than macrophages in killing the yeast.

A hallmark response to Histoplasma infection is the formation of granulomas—organized clusters of immune cells designed to wall off the pathogen. Granuloma formation helps contain the yeast, preventing further spread.

Adaptive Immune Response

Resolution of histoplasmosis heavily depends on a strong T-helper 1 (Th1) response.

Key elements include:

Th1 T cells produce interferon-gamma (IFN-γ), a crucial cytokine that activates macrophages.
Activated macrophages enhance their ability to kill intracellular yeast through: Increased production of reactive oxygen and nitrogen species, Improved phagolysosome maturation
TNF-α is essential for maintaining granuloma structure. Patients on TNF-α inhibitors (for conditions like rheumatoid arthritis) are at high risk for severe histoplasmosis.

When the immune system succeeds, infection may resolve completely or become latent, with yeast cells trapped within stable granulomas.

In Immunocompromised Individuals

In individuals with weakened immunity, such as those with HIV/AIDS, on chemotherapy, or taking immunosuppressive drugs, the immune response is insufficient to contain the fungus:

Macrophages remain unable to effectively kill yeast cells.
Granulomas may not form adequately or may break down.
Uncontrolled yeast proliferation leads to disseminated histoplasmosis, affecting multiple organs.

Clinical Manifestations

Histoplasmosis presents with a variety of clinical patterns depending on host immunity and exposure intensity. Manifestations range from mild respiratory symptoms to severe systemic illness involving multiple organs.

Acute Pulmonary Histoplasmosis

This form typically occurs after inhaling a large number of Histoplasma spores. Symptoms generally appear 3 to 17 days post-exposure and include fever, cough, chest pain, and fatigue.

Radiographic findings often show patchy infiltrates or mediastinal lymphadenopathy. Most cases are self-limiting but can cause significant morbidity in healthy individuals with intense exposure.

Chronic Pulmonary Histoplasmosis

Chronic pulmonary histoplasmosis affects individuals with underlying lung disease, such as emphysema. It progresses slowly with symptoms like productive cough, weight loss, and night sweats.

Imaging usually reveals upper lobe cavitary lesions resembling tuberculosis. The condition can cause progressive lung damage if untreated, requiring prolonged antifungal therapy.

Disseminated Histoplasmosis

Disseminated disease occurs when Histoplasma spreads beyond the lungs to organs like the liver, spleen, bone marrow, and central nervous system. It mainly affects immunocompromised patients.

Clinical features include fever, hepatosplenomegaly, lymphadenopathy, anemia, and sometimes ulcers of the mucous membranes. This form is life-threatening without prompt antifungal treatment.

Other Forms

Less common presentations include mediastinal granuloma and mediastinal fibrosis. The granuloma can cause airway compression or obstruction, whereas fibrosis leads to chronic mediastinal scarring.

Rarely, histoplasmosis involves the skin or adrenal glands, typically in disseminated cases. These manifestations require specific therapies and careful clinical monitoring.

Diagnosis of Histoplasmosis

Diagnosing histoplasmosis involves a combination of clinical assessment, laboratory tests, and imaging studies. Each component provides critical data to confirm infection, evaluate severity, and guide treatment.

Clinical Evaluation

Clinical evaluation begins with a detailed history, including exposure to environments with bird or bat droppings, such as caves or old buildings. Symptoms vary but often include fever, cough, chest pain, and fatigue. In acute cases, symptoms resemble mild pneumonia; chronic cases may present with progressive respiratory issues.

Physical examination may reveal signs such as hepatosplenomegaly or lymphadenopathy, especially in disseminated disease. Immunocompromised individuals often show more severe symptoms. Clinical suspicion is essential for prompt diagnostic testing, particularly in endemic areas.

Laboratory Testing

Laboratory diagnosis relies heavily on antigen detection, culture, and serology. Urine and serum antigen tests are sensitive, especially for disseminated histoplasmosis, and provide rapid results.

Culture of respiratory specimens, blood, or bone marrow can confirm diagnosis but often requires 2-6 weeks. Serologic tests detect antibodies but may be less reliable early in infection or in immunosuppressed patients. Polymerase chain reaction (PCR) assays are emerging tools but not yet standard.

Imaging Findings

Chest radiographs often show patchy infiltrates, mediastinal lymphadenopathy, or granulomas, depending on disease stage. In acute histoplasmosis, diffuse reticulonodular patterns are common.

Computed tomography (CT) scans provide detailed visualization of lung nodules, fibrosis, or mediastinal masses. Imaging assists in differentiating histoplasmosis from other pulmonary infections or malignancies and helps monitor treatment response.

Treatment and Management

While many infections remain mild or asymptomatic, moderate, severe, chronic, or disseminated forms require timely antifungal therapy to prevent progression and organ damage.

Antifungal Therapy

The antifungal agents used for histoplasmosis target the fungal cell membrane or intracellular processes, impairing fungal viability. The primary drug classes used include azoles and polyenes, with the choice guided by disease severity.

1. Mild or Acute Pulmonary Histoplasmosis

In healthy individuals with low-level exposure, acute infection often resolves naturally within a few weeks. Symptoms may mimic influenza, fever, cough, fatigue, and subside without pharmacological treatment.

However, treatment becomes necessary if:

Symptoms persist longer than one month
The patient has underlying chronic lung disease
There is significant functional impairment
The patient belongs to a high-risk group (e.g., immunosuppressed individuals)

2. Itraconazole: First-Line Therapy for Most Cases

Itraconazole, an azole antifungal, is the drug of choice for mild-to-moderate histoplasmosis and many chronic forms of the disease.

Key characteristics:

Mechanism of action: Inhibits ergosterol synthesis, disrupting fungal cell membrane integrity.
Administration: Oral capsules, solution, or tablets. The oral solution has better absorption but may be less tolerable.
Duration: Typically 6 to 12 weeks, though chronic or cavitary pulmonary histoplasmosis may require 12 to 24 months of therapy.

Itraconazole therapy requires careful monitoring because:

It can cause hepatotoxicity, necessitating routine liver function tests.
It interacts with numerous drugs, including some antiretrovirals, anticonvulsants, and immunosuppressants.
Gastric acidity influences absorption; acid-suppressing medications can reduce its effectiveness.

Patients must be monitored to ensure therapeutic blood levels (usually checked after 2 weeks of therapy). Subtherapeutic levels increase the risk of treatment failure.

3. Amphotericin B: Treatment for Severe or Disseminated Disease

For severe acute pulmonary histoplasmosis, chronic complicated disease, or disseminated infection, amphotericin B is the preferred initial therapy, particularly in immunocompromised patients.

Mechanism of action: Binds to ergosterol in fungal membranes, creating pores that cause cell death.
Formulations: Liposomal amphotericin B is preferred over the conventional deoxycholate formulation because it has significantly lower kidney toxicity.

Typical treatment plan:

1 to 2 weeks of intravenous amphotericin B until clinical stabilization
Followed by oral itraconazole for 12 weeks to 1 year, depending on disease extent

Longer maintenance therapy (sometimes lifelong) may be required for patients with advanced HIV/AIDS or those who cannot correct underlying immune deficits.

Side effects and monitoring:

Renal toxicity, electrolyte imbalances (especially potassium and magnesium), anemia, and infusion-related reactions
Regular monitoring of kidney function and electrolytes is essential
Pre-hydration and slow infusion rates reduce toxicity

4. Special Situations

CNS histoplasmosis: Requires high-dose liposomal amphotericin B for 4–6 weeks, followed by itraconazole for at least 12 months.
Pregnancy: Amphotericin B is preferred; azoles are avoided due to teratogenicity.
In patients on TNF-α inhibitors: These drugs must be paused, and antifungal therapy initiated promptly.

Management of Complications

Complications can include respiratory failure, mediastinal fibrosis, or dissemination to organs such as the central nervous system.

For respiratory issues, supportive oxygen or mechanical ventilation may be necessary. Surgical intervention can be required for fibrosing mediastinitis causing vascular or airway obstruction. Disseminated histoplasmosis, especially in immunocompromised individuals, requires aggressive antifungal therapy and management of underlying immunosuppressive conditions.

Prevention and Control

Effective prevention of histoplasmosis relies on minimizing exposure to environments that harbor the fungus and protecting individuals most susceptible to infection.

Environmental Control Measures

Effective prevention of histoplasmosis hinges on reducing human exposure to Histoplasma capsulatum spores, which are primarily found in soil enriched with bird or bat droppings. Because the fungus thrives in moist, nitrogen-rich environments, such as old chicken coops, abandoned buildings, barns, caves, and roosting sites environmental control begins with identifying and managing these high-risk areas.

One of the most practical environmental strategies is the safe removal of bird nests, accumulated bat guano, and other organic debris that support fungal growth. This should be carried out using appropriate protective equipment, especially respiratory protection, to prevent aerosolization and inhalation of spores. Before disturbing contaminated materials, applying disinfectants or water to the site helps suppress dust and significantly lowers the risk of airborne spore release.

Construction activities, excavation, demolition, and agricultural operations represent common triggers for outbreaks due to soil disruption. In endemic regions, especially the Ohio and Mississippi River Valleys, these activities should be carefully planned and supervised. Using wetting agents during excavation prevents dust from becoming airborne, while trained workers should always wear approved respirators. Large-scale projects may also require environmental assessments to determine levels of Histoplasma contamination in the soil.

Routine soil testing in areas like poultry farms, warehouses, abandoned structures, and public parks can be an essential surveillance tool. Although soil testing is not always routinely practiced in many locations, incorporating it into environmental health programs can help identify hotspots and guide public health responses. Furthermore, establishing buffer zones or restricting access to heavily contaminated sites can prevent unnecessary contact with infectious spores.

Protective Strategies for At-Risk Groups

Individuals with weakened immune systems require special precautions because they are far more vulnerable to developing severe or disseminated forms of histoplasmosis. This includes people living with HIV/AIDS, organ transplant recipients, individuals on long-term corticosteroid therapy, and cancer patients undergoing chemotherapy. For these groups, strict avoidance of environments known to harbor Histoplasma spores is the most effective preventive measure. Even short-term exposure can lead to significant health complications due to their reduced ability to fight infections.

Healthcare providers caring for immunocompromised individuals should educate them about areas they should avoid, such as caves, old barns, construction zones, or sites with heavy bird or bat presence. In some cases, especially for individuals living in highly endemic regions, prophylactic antifungal medication may be considered based on clinical guidelines, although this decision must be individualized and medically supervised.

For the general public, proper use of personal protective equipment (PPE) remains a simple yet powerful line of defense. N95 respirators or higher-grade masks are recommended during activities that may disturb contaminated soil or droppings. Workers in high-risk occupations, such as poultry farmers, wildlife handlers, pest control workers, demolition crews, and agricultural laborers, should receive routine training on safe work practices to prevent exposure.

Employers have a responsibility to enforce strict occupational safety protocols. This includes providing PPE, ensuring that employees are trained in its correct use, and implementing engineering controls, such as ventilation systems, dust suppression mechanisms, or enclosed equipment, to reduce airborne particles in the work environment. Regular workplace assessments can identify potential hazards early and prevent accidental exposure during routine tasks.

In addition to occupational safety, community-level interventions such as warning signs at caves, abandoned properties, and areas with heavy guano accumulation can help protect both residents and tourists. Clear messaging about when and how to use protective equipment.

Prognosis and Long-Term Outcomes

The prognosis of histoplasmosis varies depending on the severity of infection and the immune status of the individual. Most immunocompetent patients with mild to moderate disease recover fully with appropriate antifungal treatment.

In cases of disseminated histoplasmosis or infections occurring in immunocompromised patients, the prognosis is more guarded. These patients often require prolonged therapy and close monitoring due to the risk of relapse.

Long-term outcomes may include residual lung damage, especially if there was extensive pulmonary involvement. Pulmonary fibrosis or calcified granulomas can persist but often remain asymptomatic.

Outcome	Risk Factors	Notes
Full recovery	Mild infection, healthy immunity	Typical with timely treatment
Chronic pulmonary symptoms	Severe initial disease	May experience ongoing cough or fatigue
Relapse or persistent infection	Immunosuppression, incomplete treatment	Requires second course of therapy

Some patients develop chronic pulmonary histoplasmosis, characterized by progressive lung damage. This is more common in those with underlying lung conditions such as COPD.

Regular follow-up is recommended for patients with severe or chronic disease to assess lung function and ensure eradication of the fungus.

Histoplasmosis in Special Populations

Certain groups face increased risks and complications from histoplasmosis due to their immune status or age. Understanding these differences helps tailor diagnosis and treatment effectively.

Immunocompromised Individuals

Patients with weakened immune systems, such as those with HIV/AIDS, organ transplant recipients, or on immunosuppressive therapies, are at higher risk for severe and disseminated histoplasmosis.

In these individuals, the infection can rapidly spread beyond the lungs to multiple organs, causing systemic illness. Symptoms often include fever, weight loss, and respiratory difficulties.

Diagnosis may require blood cultures, antigen detection, and biopsy due to atypical presentations. Treatment usually involves longer courses of antifungal medications like amphotericin B or itraconazole, with careful monitoring to prevent relapse.

Children and Elderly

Children and elderly patients are more vulnerable to both infection and complications from histoplasmosis due to immature or declining immune function.

In children, the disease may resemble common respiratory infections but can progress quickly to severe lung involvement or disseminated forms if untreated.

In elderly persons, symptoms might be subtle or mistaken for other chronic lung diseases, delaying diagnosis. Comorbidities increase the risk of complications.

Treatment regimens are adjusted according to age and overall health, often requiring close observation to manage side effects and optimize outcomes.