This is an interesting report on molds that was posted on the Centers for Disease Control (CDC) website titled, “Mold Prevention Strategies and Possible Health Effects in the Aftermath of Hurricanes and Major Floods.”
The report was originated by the National Center for Environmental Health, Agency for Toxic Substances Disease Registry, Howard Franklin, MD, Director, and the Division of Environmental Hazards and Health Effects, Michael A. McGeehin, PhD, Director.
The report is interesting because it details the serious health effects that wet buildings and mold can cause to humans.
Various diseases, infections, and illnesses such as asthma, an immune-mediated disease known as hypersensitivity pneumoniti, and long-term ingestion of aflatoxins (produced by Aspergillus species) which has been associated with hepatocellular cancer.
Below you will find the main points of the CDC report that detail the MANY health effects.
How Persons Are Exposed to Mold
Mold exposure can produce disease in several ways. Inhalation is usually presumed to be the most important mechanism of exposure to viable (live) or nonviable (dead) fungi, fungal fragments or components, and other dampness-related microbial agents in indoor environments.
The majority of fungal spores have aerodynamic diameters of 2–10 µm, which are in the size range that allow particles to be deposited in the upper and lower respiratory tract (5).
Inhalation exposure to a fungal spore requires that the spore be initially aerosolized at the site of growth. Aerosolization can happen in many ways, ranging from disturbance of contaminated materials by human activity to dispersal of fungi from contaminated surfaces in heating, ventilating, and air-conditioning (HVAC) systems.
Fungal spores also can be transported indoors from outdoors. Overall, the process of fungal-spore aerosolization and related issues (e.g., transport, deposition, resuspension, and tracking of fungi to other areas) are poorly understood.
Persons can be exposed to mold through skin contact, inhalation, or ingestion. Because of the ubiquity of mold in the environment, some level of exposure is inevitable.
Persons can be exposed to mold through contact with airborne spores or through contact with mycelial fragments. Exposure to high airborne concentrations of mold spores could occur when persons come into contact with a large mass of mold, such as might occur in a building that has been flooded for a long time.
Exposure to mycelia fragments could occur when a person encounters a nutrient source for mold that has become disrupted, such as would occur during removal of mold-contaminated building material. Skin contact or exposure by inhalation to either spores or mycelial fragments also could occur in a dusty environment, if the components of dust include these fungal elements.
For the majority of adverse health outcomes related to mold exposure, a higher level of exposure to living molds or a higher concentration of allergens on spores and mycelia results in a greater likelihood of illness. However, no standardized method exists to measure the magnitude of exposure to molds.
In addition, data are limited about the relation between the level of exposure to mold and how that causes adverse health effects and how this relation is affected by the interaction between molds and other microorganisms and chemicals in the environment.
For this reason, it is not possible to sample an environment, measure the mold level in that sample, and make a determination as to whether the level is low enough to be safe or high enough to be associated with adverse health effects.
Persons affected by major hurricanes or floods probably will have exposure to a wide variety of hazardous substances distributed by or contained within the floodwater. This report does not provide a comprehensive discussion of all such potential hazards; such situations will of necessity require case by case evaluation and assessment.
Guidance has been provided by CDC for such issues in a number of documents, including NIOSH Hazard Based Interim Guidelines: Protective Equipment for Workers in Hurricane Flood Response (9) and the CDC guidance: Protect Yourself From Chemicals Released During a Natural Disaster (10).
Factors That Cause Disease from Mold
Numerous species of mold cause infection through respiratory exposure. In general, persons who are immunosuppressed are at increased risk for infection from mold (11). Immunosuppression can result from immunosuppressive medication, from medical conditions and diseases that cause immunosuppression, or from therapy for cancer that causes transient immunosuppression.
Although certain species of mold cause infection (5,8,11), many mold species do not cause infection. Infections from mold might be localized to a specific organ or disseminated throughout the body.
Many of the major noninfectious health effects of mold exposure have an immunologic (i.e., allergic) basis (6). Exposure to mold can sensitize persons, who then might experience symptoms when re-exposed to the same mold species. For sensitized persons, hay fever symptoms and asthma exacerbations are prominent manifestations of mold allergy (6).
Although different mold species might have different propensities to cause allergy, available data do not permit a relative ranking of species by risk for creating or exacerbating allergy. In addition, exposure to beta glucans might have an inflammatory effect in the respiratory system (12).
Prolonged exposure to high levels of mold (and some bacterial species) can produce an immune-mediated disease known as hypersensitivity pneumonitis (13). Clinically, hypersensitivity pneumonitis is known by the variety of exposures that can cause this disorder (e.g., farmer’s lung, woodworker’s lung, and malt worker’s lung).
Ingesting toxins that molds produce can cause disease. Longterm ingestion of aflatoxins (produced by Aspergillus species) has been associated with hepatocellular cancer (14). In addition, ingestion of high doses of aflatoxin in contaminated food causes aflatoxicosis and can result in hepatic failure (11).
Whether concentrations of airborne mold toxins are high enough to cause human disease through inhalation is unknown, and no health effects from airborne exposure to mold-related toxins are proven.
For the Public Unable to Use PPE or at High Health Risk from Exposure to Mold
The effect of exposure to mold varies widely. Persons who might be affected to a greater extent than the majority of healthy adults include (5,6,9):
- persons with respiratory conditions (e.g., asthma) or allergies, and
- persons with weakened immune systems (e.g., patients receiving chemotherapy, organ or bone marrow transplant recipients, or persons with human immunodeficiency virus infection or autoimmune diseases).
Persons with special health concerns should consult their health-care provider if they are concerned about mold exposure. Symptoms that might seem related to mold exposure might have other causes, such as bacterial or viral infections or other allergies.
The level of risk associated with exposure activities and the potential benefit of recommended PPE are unknown for pregnant women, persons aged >65 years, and children aged <12 years; exposure-reducing behavior and respiratory protection might be difficult for children aged <12 years.
Using respirators or other PPE might increase health risks for persons with underlying health conditions. Persons who have trouble breathing while using a respirator should stop working and contact a doctor or other medical provider (1).
For persons at potentially increased health risks from exposure to mold, persons of unknown or uncertain risk, or persons unable to use respirators, caution is recommended when entering heavily mold contaminated environments, particularly when mold clean-up is occurring. Persons in these categories should avoid such situations if possible.
Potential Health Effects of Fungal Contamination
In recent years, the health effects of exposure to mold in built environments have been a subject of intense public concern. These concerns and how they are approached will have important implications for the reconstruction and rehabilitation of cities in states affected by major hurricanes or floods.
Many clinical conditions could be caused by the fungal contamination associated with flooding after major hurricanes or floods. Predicting what might occur is speculative. However, many of these conditions are uncommon and will be recognized only if there is a high clinical index of suspicion (Table 2).
Anticipating what medical problems could be associated with post-flood fungal contamination might help in preventing them by identifying susceptible populations and making recommendations for reducing potentially harmful exposures.
Although this report focuses on potential health effects of fungal contamination, other exposures are also of concern. For example, dampness favors proliferation of dust mites and microorganisms such as bacteria (44,45) and nontuberculous mycobacteria (46).
Endotoxins (components of the cell walls of Gram-negative bacteria) have strong inflammatory properties (6,44,45,47–49). Moisture also can release chemical constituents from building materials (6).
Standing water supports rodent and cockroach infestations (15,44,45) and proliferation of mosquitoes (30). Fecal contamination of the environment raises concerns about protozoal and helminthic parasites (50).
Fungi are not the sole potential cause of many conditions discussed in this report, and these conditions are only a subset of the conditions of concern to clinicians and public health professionals dealing with the aftermath of major hurricanes or floods (51).
Overview of Fungal-Induced Diseases
Fungi can cause a variety of infectious (52–58) and noninfectious conditions (6,44,45,47,59,60). Several basic mechanisms can underlie these conditions, including immunologic (e.g., IgE-mediated allergic), infectious, and toxic (6). Several of these mechanisms contribute to pathogenesis of a fungal-induced disease.
The types and severity of symptoms and diseases related to mold exposure depend in part on the extent of the mold present, the extent of the person’s exposure, and the susceptibility of the person (e.g., persons who have allergic conditions or who are immunosuppressed are more susceptible than those without such conditions).
Molds produce a variety of volatile organic compounds (6,7,60), the most common being ethanol (61), which are responsible for the musty odors associated with fungal growth. Exposure to moldy indoor environments is also associated with a variety of upper and lower respiratory tract symptoms (6).
Institute of Medicine Report on Damp Indoor Spaces and Health
In recent years, the issue of how damp indoor spaces and mold contamination affect human health has been highly controversial. In response, CDC commissioned the Institute of Medicine (IOM) to perform a comprehensive review of the scientific literature in this area. The resulting report (6) was published in 2004 and remains the most current and authoritative source of information on this subject. The IOM categorized its findings into four categories:
- sufficient evidence of a causal relation,
- sufficient evidence of an association,
- limited or suggestive evidence of an association, and
- inadequate or insufficient evidence to determine whether an association exists.
“Inadequate or insufficient evidence to determine whether an association exists” does not rule out the possibility of an association. Rather, it indicates that no studies examined the relation or that published study results were of insufficient quality, consistency, or statistical power to permit a conclusion about an association.
No conditions exists for which the IOM found sufficient evidence of a causal relation with mold or with damp indoor spaces. Several of the conditions are of particular interest to those engaged in the response to major hurricanes or floods (Table 3).
Sufficient evidence links upper respiratory tract symptoms (e.g., nasal congestion, sneezing, runny or itchy nose, and throat irritation) to damp indoor environments and mold (with exposure to mold often determined by self-report).
Similarly, sufficient evidence exists for a link with the lower respiratory tract symptoms of cough and wheeze. Sufficient evidence also was found for a link between damp indoor environments, mold, and asthma symptoms in sensitized persons with asthma.
Evidence also is sufficient for an association between mold exposure and hypersensitivity pneumonitis in a small proportion of susceptible persons, invasive respiratory and other fungal infections in severely immunocompromised persons, and fungal colonization of the respiratory tract or infection in persons with chronic pulmonary disorders.
IgE-Mediated Diseases Caused by Fungi
IgE-mediated, or allergic, responses underlie the most common types of diseases associated with exposure to fungi (6,45,47,48,49). Atopy, or the genetic predisposition to form IgE responses to aeroallergens, is an important risk factor (45,47,48,49). Clinical conditions associated with allergies include allergic rhinitis and asthma (6,45,47,48,49). Allergic rhinitis is often associated with allergic conjunctivitis and sinusitis (45,47,49).
Symptoms of allergic rhinitis include sneezing; itching of the nose, eyes, mouth, or throat; nasal stuffiness; clear rhinorrhea; and, if associated with allergic conjunctivitis, red, itchy eyes. If associated with sinusitis, persons also might complain of sinus fullness or postnasal drip, often purulent (47–49).
Signs on physical examination include pale, boggy nasal mucosa; nasal obstruction; and conjunctival redness. Examination of nasal scrapings or secretions indicates eosinophilic inflammation (47–49).
If appropriate allergy prick skin testing reagents or in vitro tests for serum specific IgE are conducted, they demonstrate specific IgE-sensitization to causative allergens (45,47–49). Skin testing reagents and blood tests documenting IgE-sensitization to molds are, with few exceptions, poorly standardized and of unclear sensitivity and specificity (45).
The conventional hierarchy of treatment is avoidance of exposure to inciting agents; pharmacotherapy with antihistamines, decongestants, or anti-inflammatory agents (e.g., nasal steroid sprays); or, as a last resort, allergen immunotherapy (47–49). Immunotherapy with fungal allergenic extracts is, with a few exceptions, of unknown efficacy (47).
Asthma is a disease characterized by episodic, reversible airways obstruction and eosinophilic airways inflammation (45,47–49,62,63). Over time, chronic asthma can lead to airways remodeling and irreversible airways obstruction (45,47–49,62,63).
Persons with asthma often have symptoms such as chest tightness, wheezing, dyspnea, or cough (45,47–49,62,63). Physical examination during active asthma might indicate wheezing, but results of examinations between attacks are most often normal (62,63).
If performed during an active asthma attack, spirometry most often indicates obstruction that reverses with inhalation of a bronchodilator (62,63). Persons with asthma generally exhibit bronchial hyperreactivity to methacholine challenge (45,47–49,62).
However, a small proportion of persons without asthma and a substantial proportion of persons with airway disorders, including chronic obstructive pulmonary disease (COPD), also might exhibit hyperreactivity to inhaled methacholine (49); therefore, test results must be considered together with other clinical information (47–49,62,63).
Approaches to demonstrating specific IgE sensitization to molds and limitations of available methods are as described for allergic rhinitis (45,47–49). Asthma is associated with airways inflammation that can be demonstrated by examining induced sputum for eosinophils or measuring exhaled nitric oxide (47), but these tests are often not performed in clinical settings.
Comprehensive guidelines for the staging and treatment of asthma are provided by the National Institutes of Health (62,63). Identifying and avoiding triggers, including occupational triggers, is a critical element of treatment. It is important to identify persons with asthma triggered by materials in flood-damaged areas so avoidance measures can be taken.
Drug treatment of asthma consists of symptom controllers such as bronchodilators and anti-inflammatory agents (e.g., corticosteroids or leukotriene antagonists) (47–49,62,63). The role of allergen immunotherapy with most fungal agents in treatment of asthma is unclear (48).
Therapy with monoclonal anti-IgE is a recently developed treatment option that can be used in carefully selected patients when other, less expensive modalities fail to reduce dependence on systemic corticosteroids (63).
The exacerbation of symptoms of asthma is consistently associated with damp buildings (6). If persons with asthma must engage in activities within damp or mold contaminated buildings, their asthma should be well controlled before entering these buildings, and those around them should be aware of the signs of asthma symptoms. The onset of symptoms while in damp moldy environments, especially while wearing PPE, should be an indication to leave the area and to seek appropriate medical care.
Allergic Diseases Associated With Airways Colonization
Allergic bronchopulmonary aspergillosis (ABPA) is a disease that can occur when the airways of persons with obstructive pulmonary diseases (e.g., asthma or cystic fibrosis) become colonized with Aspergillus fumigatus or other Aspergillus species (6,17,45,47–49). Inflammatory responses lead to additional airways damage.
Marked worsening of existing asthma is a typical presentation of ABPA. Symptoms include recurrent episodes of bronchial obstruction, fever, malaise, expectoration of brownish plugs, peripheral blood eosinophilia, hemoptysis, and sometimes asymptomatic pulmonary consolidation.
Other features include immediate skin test reactivity to Aspergillus spp. antigens, precipitating serum antibodies to A. fumigatus, markedly elevated serum total IgE, fleeting lung infiltrates, and central bronchiectasis (45,47–49). Criteria for diagnosis have been published (45,47–49).
Airways colonization with other fungal species can result in a similar clinical picture. Although no known relation exists between levels of exposure to Aspergillus spp. and development of ABPA, clinicians should suspect and evaluate for the condition when appropriate.
Allergic fungal sinusitis (AFS) is typically noninvasive and occurs in allergic, immunocompetent patients (6,45,47–49): most have asthma, and 85% have nasal polyps (47). Invasive fungal sinusitis can occur in patients who are immunocompromised with illnesses such as diabetes, hematologic malignancies or immunosuppressive treatments or chronic steroid therapy (6,47).
Fungal colonization is associated with a characteristic allergic mucin containing high levels of eosinophils (6,45,47–49). The mere presence of fungi in the nasal passages is not indicative of an active infection.
Hypersensitivity pneumonitis (HP), also known as extrinsic allergic alveolitis, is a granulomatous interstitial lung disease (6,17,45,47–49). A wide range of materials, including fungi, can be inhaled and thus sensitize susceptible persons by inducing both antibody and cell-mediated immune responses (6,17,45,47–49). Re-exposure of sensitized persons leads to lung inflammation and disease (6,17,45,47–49).
Building-related HP caused by fungi and bacteria has been well documented (6,17). Usually, only a small fraction of those with a given exposure develop HP; therefore, poorly understood host factors play an important role in disease pathogenesis (6,47–49).
The presentation of HP is complex and can be either acute, subacute, or chronic (6,47,48). The acute form is often associated with heavy exposures and characterized by chills, fever, malaise, cough, and dyspnea appearing 4–8 hours after exposure (6,47,48) and is often confused with pneumonia. The chronic form is thought to be induced by continuous low-level exposure.
Onset generally occurs without chills, fever, or malaise and is characterized by progressive shortness of breath with weight loss (47,48). Chronic HP can be confused with idiopathic pulmonary fibrosis or other forms of interstitial lung disease (47,48).
The diagnosis of HP, especially the chronic form or when presentation is mild, is often missed early in the course of the disease. If it does occur in the aftermath of major hurricanes or floods, a high degree of clinical suspicion is required for detection.
In general, when HP is suspected, a clinical and exposure history should be performed. Patients should be asked about their possible exposure to damp and water-damaged areas, farms, birds, hot tubs, and other environments that might cause HP.
Environmental sampling for the presence of microorganisms known to cause HP and serologic testing for circulating precipitins can help to establish causative exposures (47–49). Chest imaging using chest radiographs or high-resolution computed tomography scanning of the thorax, lung-function tests, broncholaveolar lavage, and lung biopsy all have roles in diagnosis (47–49).
Although established criteria exist for the diagnosis of hypersensitivity pneumonitis (64,65), in the setting of a documented post-disaster HP outbreak, a noninvasive approach to identifying cases could be more appropriate and cost-effective than requiring conventional diagnostic testing.
A recent, large multicenter study indicated that under conditions of low or high prevalence, six predictors could be used in combination for noninvasive diagnosis of HP (66):
- exposure to a known offending antigen,
- positive precipitating antibodies to the offending antigen,
- recurrent episodes of symptoms,
- inspiratory crackles on physical examination,
- symptoms occurring 4–8 hours after exposure, and
- weight loss.
Optimal treatment is elimination of causative exposures. The IOM report (6) provides information about management of building-related HP that is relevant to reoccupation of structures contaminated by fungi after major hurricanes or floods.
Such management includes giving standard medical therapy (e.g., systemic corticosteroids and removing sources of fungal contamination from the environment). In some cases, if efforts to remove mold from a building are unsuccessful in relieving symptoms, the patient might need to move to another home or office.
Inhalation fever is a general name given to a variety of influenza-like, self-limited syndromes that might be caused by a variety of stimuli. Two types of inhalation fevers are of potential concern after major hurricanes or floods.
Humidifier fever is characterized by fever, respiratory symptoms, and fatigue with onset within hours after exposure to contaminated humidification systems (6,17,45,47). Obtaining a supportive history is critical to diagnosis. Thermophilic actinomycetes; other bacteria, including species of Legionella and Pseudomonas; and protozoa have been associated with humidifier fever (17).
Aerosolized endotoxin derived from Gram-negative bacteria has an important role in this condition (17,47). Although humidifier fever can be confused with acute HP, it is a short-term ailment and removal from exposure is effective treatment (17,47). Humidifier fever is thought to represent a nonspecific inflammatory response to exposure (17,47).
Organic dust toxic syndrome (ODTS) has been reported among workers in a variety of agricultural and industrial settings and is thought to involve inhalation exposure to materials with heavy microbial contamination (67–69). Etiologic exposures that cause ODTS are often a poorly defined mixture of substances, including fungi, bacteria, and microbial constituents such as endotoxin (67–69).
ODTS is characterized by fever and influenza-like symptoms, including general weakness, headache, chills, body aches, and cough occurring 4–12 hours after heavy exposure to organic dust (67–69). Dyspnea also is sometimes present.
Results of chest auscultation and chest radiographs are usually normal (67,68). The peripheral white blood count is often elevated during attacks. Accurate patient history is critical for making a correct diagnosis. Although the symptoms resemble those of acute HP, they are not caused by response of the immune system to a specific antigen in the environment (67,68).
ODTS poses a risk for workers performing renovation work on building materials and is a realistic concern for workers handling heavily contaminated materials in the aftermath of major hurricanes or floods. ODTS is best prevented by minimizing exposure through engineering controls, administrative controls, and respirators (69).
For agricultural workers handling organic dusts, CDC recommends using the most practical respirator with the highest assigned protection factor.
Toxic Effects of Fungi
Certain common molds can produce metabolites with a wide range of toxic activities such as antibiotic (e.g., penicillium), immune-suppressive (e.g., cyclosporine), carcinogenic (e.g., aflatoxins), emetic, and hallucinogenic (e.g., ergot alkaloids) (6,11,17,59). Mycotoxins are fungal metabolites that poison humans and animals.
Although ingestion is the most common route of exposure, inhalation and dermal contact also are exposures of concern (6,11,17,59). Mycotoxin production is dependent not only on species and strain of mold, but also on environmental conditions (e.g., temperature, water activity, light) and growth substrate (11,17). Thus, the presence of toxin-producing mold species does not necessarily indicate whether mycotoxins are present.
Mycotoxins were prematurely proposed as the cause of a disease outbreak of eight cases of acute pulmonary hemorrhage/hemosiderosis in infants in Cleveland, Ohio, in 1993 and 1994 (70). The cluster was attributed to exposure to mycotoxins produced by Stachybotrys chartarum. Subsequent reviews of the evidence concluded that insufficient information existed and no such association was proven (71).
Almost all of the known effects of mycotoxin exposures are attributable to ingestion of contaminated food (72). Health effects from inhalational exposures to toxins are not well documented. IOM found inadequate or insufficient evidence for a link between exposure to damp indoor environments and molds with a variety of conditions that have been attributed to toxicity (6) (Table 3).
Certain case studies of agricultural and remediation workers have described adverse health effects such as skin irritation, skin necrosis, cough, rhinitis, and bloody nasal exudate after inhaling or touching materials with heavy fungal contamination (73–76).
Whether these effects resulted from exposure to mycotoxins or from a general overload of organic material is unknown. No commercial clinical diagnostic tools are available to determine whether a person’s health effect is related to exposure to mycotoxins.
Because of the lack of information about noningestion mycotoxin exposure and adverse health effects in humans, precautions should be taken when handling heavily contaminated building materials.
No reports of increased fungal infections related to floods in the United States exist. However, anecdotal case reports of fungal infection after floods include Apophysomyces elegans wound infection in a man who sustained traumatic injuries after the southeast Asian tsunami in December 2004 (77).
A. elegans belongs to the Zygomycetes class of fungi. Infections are most commonly seen in immunocompromised and diabetic patients, and rarely in immunocompetent persons. The cause of infection in immunocompetent persons is usually cutaneous trauma with direct implantation of fungal organisms into the wound from soil contamination (78).
Theoretically, infection with fungal species that contaminate buildings, building constituents, and the environment after major hurricanes or floods is a potential concern. In general, persons with impaired host defenses (especially if impaired because of cell-mediated immunity or neutropenia) suffer the most severe types of fungal infections (6,52,53) (Table 4).
However, invasive fungal infections also can occur in persons with normal host defenses and, in certain situations, can be life threatening (52,53) (Table 5). Persons at greatest risk for invasive fungal infection from heavy fungal contamination after major hurricanes or floods are those with impaired host defenses (6,52,53) (Table 4).
Any impairment in cell-mediated immunity or neutropenia (e.g., human immunodeficiency virus [HIV] infection, leukemia, lymphoma, and diabetes mellitus) increases risk for many types of invasive fungal infections (52,53).
Severely immunosuppressed persons, such as solid-organ or stem-cell transplant recipients or those receiving cancer chemotherapy agents, corticosteroids, or other agents inhibiting immune function, are at much higher risk for locally invasive infections of the lungs, sinuses, or skin and systemic infections (52,53). Aspergillus spp., zygomycetes, and Fusarium spp. are particularly important problems (52,53,56). These serious infections are often fatal, even with aggressive antifungal therapy (52,53,56).
Protective measures, such as HEPA filtration, implemented during periods of extreme susceptibility to invasive fungal infections are well established and effective in hospitals (79). However, preventive measures outside the hospital are less well established.
Current guidelines emphasize the importance of avoiding areas of high dust (e.g., excavation sites, building construction or renovation sites, chicken coops, and caves) and factors associated with fungal infections (e.g., foods that increase a person’s risk for fungal exposure) (80).
Obstructive pulmonary diseases such as asthma, cystic fibrosis, and COPD, might predispose persons to airway colonization with Aspergillus spp. (6,17,45,47–49).
Inflammatory host responses to colonization can lead to ABPA (6,17,45,47–49,52). Aspergillus spp. also can cause invasive or semi-invasive infection in persons with COPD, especially in those being treated with corticosteroids. Chronic necrotizing pulmonary aspergillosis is an indolent condition observed in persons with underlying lung disease (53).
Colonization of lung cavities (e.g., tuberculosis cavities or emphysematous blebs) by Aspergillus spp. can cause pulmonary aspergillomas (fungus balls) (6,52), which are conglomerations of Aspergillus spp. hyphae matted together with fibrin, mucus, and cellular debris.
These often do not cause symptoms, but they can be associated with hemoptysis (52,53). An exposure-response relation has never been established linking levels of exposure to Aspergillus spp. with development of any of these conditions.
Therefore, to what degree exposure to fungal contamination after major hurricanes or floods would increase any risk is unclear. However, despite unknown benefit, persons with clinically significant obstructive pulmonary diseases (e.g., asthma, cystic fibrosis, COPD), and persons with cavitary lung disease from conditions such as tuberculosis should avoid airborne exposure to materials that have become heavily contaminated with fungal growth in the wake of major hurricanes or floods.
Persons with normal host defenses also are subject to fungal infections (52,53) (Table 5), and persons with impaired host defenses can acquire any of these, often with greater severity. Ocular, skin, and superficial infections occur in those with normal host defenses and range from the relatively common (e.g., ringworm, athlete’s foot) to the relatively rare (e.g., sporotrichosis) (52,53).
Of particular relevance in areas with fungal contamination after major hurricanes or floods are organisms that cause localized skin and superficial infections following traumatic inoculation with soil and plant saprophytes, which are found in air, soil, and plant materials. For example, Scedosporium apiospermum (Pseudallescheria boydii) can be recovered from polluted water, sewage, swamps, and poultry or cattle manure (52,53,55,58).
Although rare in the United States, this organism can cause a soft tissue infection called Madura foot, a mycetoma in which the draining sinuses show white grains containing fungal elements. This organism also can produce septic arthritis or osteomyelitis after penetrating trauma.
Sporothrix schenckii is a dimorphic fungus that produces soft tissue infections after traumatic inoculation from a contaminated environmental source (52,53), such as sphagnum moss, roses, plant seedlings, and other vegetation.
Lymphocutaneous lesions are the hallmark of sporotrichosis, as the organisms spread through the local lymphatics after primary inoculation. A high degree of clinical suspicion is needed to diagnose the less common, locally invasive fungal infections. Diagnosis is made by histopathology and culture after biopsy of the affected lesion.
Histopathology must be performed to verify that a recovered isolate is the cause of disease and not an environmental contaminant. Culture must be performed to identify the agent correctly. Fungal isolates are identified in a clinical mycology laboratory.
Exposures that result in invasive pulmonary mycoses in persons with normal host defenses are generally thought to occur outdoors where active disturbance of a reservoir has occurred (52,53). The mode of transmission is inhalation of fungal spores.
Person-to-person transmission of pulmonary mycoses does not occur (53). Diseases relevant to flood prone areas such as the Gulf Coast states include histoplasmosis and blastomycosis.
Histoplasmosis is unlikely to be increased as a result of fungal contamination after major hurricanes or floods. The condition is caused by Histoplasma capsulatum, a dimorphic fungus found in soil enriched with the droppings of birds and bats (52,53).
Areas with endemic disease in the United States include the Mississippi and Ohio River valleys, but cases have occurred in other parts of the United States. Many persons develop no symptoms when exposed to H. capsulatum in an endemic setting.
Blastomycosis is a potential problem after major hurricanes or floods in areas with endemic disease because it can cause serious disease even in those with normal host defenses (52,53). Blastomycosis is caused by the dimorphic fungus Blastomyces dermatitidis (52,53).
The organism is found in moist soil, frequently along streams or rivers enriched with decaying vegetation. In the United States, the organism is most commonly found in states surrounding the Mississippi and Ohio rivers (52,53).
An area in Louisiana about 70 miles from New Orleans has endemic blastomycosis (81). In Louisiana, cases occur at an incidence of about 1–10 per year, mostly in the area of Washington Parish where the condition is endemic (81).
Outbreaks have been associated with manipulation of decaying vegetation or recreational activity near lakes or rivers (53). The incubation period is not certain but, on the basis of data from outbreaks, appears to be about 45 days (82), ranging from weeks to months.
The clinical spectrum of blastomycosis includes asymptomatic infection, acute or chronic pneumonia, and disseminated disease (52,53). Pulmonary infection can mimic acute bacterial pneumonia or tuberculosis with progression to acute respiratory distress syndrome.
Alveolar infiltrates, mass lesions that mimic bronchogenic carcinoma, and fibronodular interstitial infiltrates are the most common radiographic findings (52,53). Disseminated blastomycosis often appears as ulcerative skin lesions with multiple necrotic bone lesions in the vertebrae, skull, or long bones (52,53).
Culture of lesions or histopathologic evidence from infected tissue is required for diagnosis of blastomycosis (52,53). Direct microscopy of pus, scrapings from skin lesions, or sputum showing thick-walled broad-based budding yeast cells 5–15 µm in diameter supports a presumptive diagnosis of blastomycosis and might, in the appropriate clinical setting, prompt the initiation of antifungal therapy (52,53). Serologic tests can be performed on serum from patients showing signs of suspected pulmonary blastomycosis or with suggestive skin lesions.
A positive immunodiffusion (ID) test, showing a precipitin band with the Blastomyces A antigen, is highly specific for the disease and does not require paired serum samples (52,53). However, the sensitivity is poor (33%–88%), so a negative ID test does not rule out the disease (52,53).
For cases with negative results, the test should be repeated in 3–4 weeks after the initial sampling. The complement fixation (CF) test for blastomycosis has poor sensitivity and specificity.
Fungal brain abscesses are uncommon in healthy persons (52,53,57). The primary infection results from inhalation of infectious conidia from the environment; the route of infection appears to be hematogenous dissemination from the lungs (52,53,57).
Of particular interest after major hurricanes or floods is S. apiospermum (P. boydii) (52,53,57). Many case reports document patients with focal neurologic defects caused by multiple brain abscesses weeks or months after nearly drowning.
The organism apparently spreads hematogenously after initial aspiration of sewage-laden water (from floods, lagoons, or bayous) into the lungs. Near drowning presumptively results in a massive inoculation of mold into the lungs.
SOURCE: CDC – Mold Prevention Strategies and Possible Health Effects in the Aftermath of Hurricanes and Major Floods
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