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Aspergillosis illnesses & Aspergillus mold in buildings:
This article provides basic descriptions of Aspergillus-related illnesses and discusses valid versus in-valid inspection and testing techniques used to detect mold contamination in buildings, including Aspergillus sp. molds.
At page top: an Aspergillus sp. conidiophores under the microscope at about 1200x.
Aspergillus related illnesses & Aspergillus Contamination Testing in Buildings
Watch out: people who are concerned about possible mold-related illness should consult their primary care physician and with that doctor's advice decide if referral to a pulmonologist with expertise in mold related illness is appropriate. We also issue this trigger warning: reading this material can cause an anxiety-induced asthma attach, though most likely if you read with care you'll see that for most people anxiety is merited.
Greenberger (2002) discusses allergic bronchopulmonary aspergillosis (ABPA) as an illness complicating asthma and cystic fibrosis, noting that The survival factors in Aspergillus fumigatus that support saprophytic growth in bronchial mucus are not understood.
At left: Aspergillus fumigatus conidiophore showing characteristic long spore chains - lab photo, Daniel Friedman.
[Click to enlarge any image]
Beyond asthmatics and people with cystic fibrosis, and focusing on immunie-impaired patients, Cornet (2002) notes that invasive aspergillosis is the most prevalent mould infection, and Soubani (2002) offers this recap of the importance of recognizing and treating pulmonary aspergillosis, particularly for people with a compromised immune system but as well for patients suffering from asthma:
Aspergillus is a ubiquitous fungus that causes a variety of clinical syndromes in the lung, ranging from aspergilloma in patients with lung cavities, to chronic necrotizing aspergillosis in those who are mildly immunocompromised or have chronic lung disease. Invasive pulmonary aspergillosis (IPA) is a severe and commonly fatal disease that is seen in immunocompromised patients, while allergic bronchopulmonary aspergillosis is a hypersensitivity reaction to Aspergillus antigens that mainly affects patients with asthma.
In light of the increasing risk factors leading to IPA, such as organ transplantation and immunosuppressive therapy, and recent advances in the diagnosis and treatment of Aspergillus-related lung diseases, it is essential for clinicians to be familiar with the clinical presentation, diagnostic methods, and approach to management of the spectrum of pulmonary aspergillosis.
Patterson (2000) as well as virtually all authors writing in this field emphasize the importance of early diagnosis and treatment in the successful outcome for people with invasive aspergillosis while also noting that rapid diagnosis of invasive aspergillosis - a more serious illness - is difficult as most facilities lack the tools for definite diagnosis, making clinical detection of central importance.
By 2007 Greene described the use of computed tomography (CT) and the "halo sign" in diagnosing invasive pulmonary aspergillosis (IPA), concluding
Initiation of antifungal treatment on the basis of the identification of a halo sign by chest CT is associated with a significantly better response to treatment and improved survival.
Reader Question: what kind of home tests make sense for someone testing positive for Aspergillus fumigatus?
15 September 2015 Caroline said:
My father tested positive for Aspergillus fumigatus. I called some mold testing people to come out & all of them said they would do an air test in his room ( which is in the basement) and in the basement. I read how you said an air quality test is not always accurate because of the changes in the room, so I was wondering what kind of testing you would recommend. Also, I do have a compost heap outside. So I wondered if I got rid of it, would it take care of the situation?
You can find my email at the page bottom CONTACT link and by email I can offer a number for pro-bono consulting in this matter.
There is a place for air testing and properly done it can be informative. But considering the orders of magnitude variation in measurements of the level of airborne particles just in response to very small changes (waving a notebook in the air for example), a "negative" air test result cannot be trusted, and even a "positive" air test for mold that produces a high mold count cannot for a moment be presumed to actually describe the level of exposure of the building occupants to mold.
Recommended Buiding Inspection & Test Procedures for Mold Contamination
And no “test for mold” alone is going to tell us where the problem is nor what needs to be done about it. It’s instead a profitable “indicator test” that might find evidence of a problem that’s really there - or it might miss a real problem. The physician needs to be included in the process.
An effective mold contamination investigation, to be useful, must be accurate and it must be prescriptive.
A thorough client interview, case history, complaints, relationship of complaints to building, other occupants' experiences. If the client or person of concern has not yet done so she or he should see their doctor promptly. If you and your doctor need to look further for a specialist in environmental medicine
See MOLD DOCTORS - ENVIRONMENTAL MEDICINE
Collection of a few intelligently-selected samples of settled building dust to be screened for unusual levels of harmful molds or even at very low levels, for clues suggesting a nearby Aspergillus contamination source (mold reservoir) such as the observation of Aspergillus spores in spore chains.
See MOLD TEST KIT INSTRUCTIONS - note: do not send mold samples to InspectApedia; select a qualified mold lab.
Air tests as a screen for mold: Optionally, I don't mind air testing as well, with the caveats I've already given. A negative air test result, taken alone, cannot be trusted.
See AIR TEST FOR MOLD: ACCURACY
See MOLD TEST PROCEDURES
Watch out: opportunists of all levels of education and training have leapt enthusiastically into the "mold business"; but only a few do the real job. It is far too tempting, too profitable, and easier and faster to just stop by and "collect an air sample. Even if the sample’s lab result says “yes there is a problem here” that alone is not diagnostic nor prescriptive. It doesn't tell us where the problem is (or where they are), what cleanup is needed, what corrections are needed to prevent future problems.
Photographs of Aspergillus sp. mold spores under the microscope (above left) and Aspergillus niger culture (above right). Because their airborne spores look similar, also see Penicillium culture [image file], and also see these Penicillium spores [image file].
Aspergillus and Penicillium spores are difficult to
differentiate when they are found in air that you may see them reported in
test results as "Pen/Asp".
Watch out: Most Pen/Asp spores are round, hyaline (colorless) and small and lack surface features to aid in their precise identification by microscope when the spores are found alone, or in air samples (and if not in spore chains). In that case the spores may not even be identified as (potentially harmful) molds and may just be called amerospores in the lab report. But when these spores appear in spore chains (as that's how they are born) they should not be labeled as amerospores, and at least some of these airborne spores in the Aspergillus/Penicillium group can be identified
from the spore alone (such as Aspergillus niger).
Above at left we're examining an Aspergillus fumigatus conidiophore from a top-down view. The Aspergillus fumigatus conidiophore is the spore-producing structure and as you can see spores are produced in dense profusion and in long chains.
Above at right we illustrate a quite dense building-surface growth of Aspergillus niger and Aspergillus fumigatus side by side, in the same surface sample, but not quite intermixed. These spores were collected by a tape lift sample. The colorless spores in the open area may be another species of Aspergillus or of Penicillium.
Allergic Bronchiopulmonary Aspergillosis (ABPA) - worsening of underlying asthma or cystic fibrosis,
coughing up blood, weight loss, fever, wheezing, mucous plugs produced by coughing - uncommon, occurs in persons with asthma and those with cystic fibrosis (CF).
Aspergilloma (fungal growth in lung), cough, cough, fever, weight loss. Uncommon. May be asymptomatic but show up in a lung X-ray in some patients who have a pre-existing lung cavity (e.g. due to T.B.), occurs in patients suffering HIV + pneumonia; coughing up blood is a serious and life threatening condition.
Aspergillosis, Chronic necrotizing Aspergillus pneumonia, or Chronic necrotizing pulmonary aspergillosis (CNPA) occurs in patients with an underlying disease such as COPD or alcoholism, symptoms include sub acute pneu7monia, fever, cough, night sweats, weight loss.
Aspergillosis, Invasive, occurs in patients who suffer from immunosuppression or prolonged neutropenia, leukemia, and others; symptoms include fever, cough, chest pain, difficulty breathing (dyspena), rapid breathing (tachypnea).
Everyone breathes in some Aspergillus spores every day, including Aspergillus fumigatus that is itself quite common in the air. In healthy people breathing in mold spores does not cause a health problem as they are breathed out, coughed-out, or handled by the individual's immune system. In people with a suppressed immune system there are however health risks from breathing in such spores.
I don’t know what test your Dad had performed nor whether or not the test that was performed distinguishes between the presence
of Aspergillus spores (they can be hard to speciate) and the existence of Aspergillosis disease.
Many people have Aspergillus spores in their lungs. I do. I have exampled coughed up flem for, and found, significant levels of Aspergillus spores.
That alone does not mean that a person has Aspergillosis.
Aspergillosis is detected by a variety of means including a combination of imaging and sometimes biopsy or even surgical procedures. Under the microscope
we’d see not just spores but living, branching fungal hyphae (think “roots” or “branches” that ultimately produce as well conidiophores or spore-producing structures).
Denning (1998) notes that invasive aspergillosis was first identified as an opportunistic infection in 1958 and adds that the diagnosis of Aspergillosis has since then increased significantly. He cites four reasons for an increase in the number of poeple at risk of developing invasive aspergillosis:
The spread of AIDS
Increased use of chemotherapy for treatment of solid tumors, lymphoma, leukemia and myeloma
Increase occurrence of organ transplants
Increased use of immunosuppressive treaments for other illnesses such as lupus and erythematosus.
For those of us including myself who can be frightened by reading about Aspergillosis it is significant to note that while there are fungal diseases that can affect healthy people, those whose immune system is impaired or suppressed are at the greatest risk. Having some Aspergillus spores in your spit doesn't mean you've got Aspergillosis.
Fisher (1981) noted that:
In one year, only 9 percent of the patients with Aspergillus species isolated from the sputum had an invasive infection.
Yu (1986) points out:
One hundred and eight consecutive patients were evaluated in whom Aspergillus species were isolated from respiratory secretions. Invasive aspergillosis was not demonstrated in non-immunosuppressed patients or in patients with solid tumors in the absence of neutropenia. Lung tissue was examined in 17 patients with leukemia and/or neutropenia [few neutrophils in the blood, leading to increased susceptibility to infection. It is an undesirable side effect of some cancer treatments - Ed.]; all had invasive aspergillosis. Tissue examination was not performed in 20 neutropenic patients; of 17 not receiving antifungal therapy, 16 died.
Aspergillosis is usually a quite serious medical problem deserving expert medical care (often treated with anti-fungal medicines, steroids, sometimes surgery).
Un-treated it can be fatal.
A common species of Aspergillus found in people suffering from Aspergillosis is Aspergillus fumigatus - shown below in photos from our laboratory.
Your dad will want to discuss his medical condition with his doctor immediately and if they agree, to be referred to a pulmonologist who is a specialist in the area of fungal diseases.
I add that Aspergillosis usually affects seriously people who suffer from immune system impairment for any of a variety of reasons. In healthy people the Aspergillus spores that we inhale do not cause a medical problem.
Aspergillosis related diseases can occur in anyone (at least some of of the Aspergillus-related diseases) but affect particularly seriously people who suffer from immune system impairment for any of a variety of reasons. In healthy people the Aspergillus spores that we inhale do not normally cause a medical problem.
Why are Aspergillus and Penicillium of Particular Health Concern Inside Buildings?
Well they are and they aren't. Certainly there are other mold genera/species that can be quite harmful, pathogenic, toxic, or allergenic to humans.
But these two mold groups, in my opinion, particularly Aspergillus sp., grow happily on an enormous variety of materials that are found on or in building interiors. So do some other molds such as Stachybotrys chartarum that has taken a beating in the public media and that is often a mycotoxin-rich mold spore. Here's an important difference:
Stachybotrys chartarum is a comparatively huge spore, maybe 10 x 20 microns, and it's sticky. It evolved to be spread by sticking to a cow's foot as the cow rambled around in damp or wet straw. Bit spores are not easily airborne unless you kick them around and they tend not to be airborne in huge numbers unless you're doing a maniacal demolition of moldy drywall without dust control. Big mold spores want to get stuck in the nose of the inhaler.
Aspergillus and Penicillium spores can be as small as 1u, that's 1 micron. These teensy spores pass easily through small openings, remain airborne for a long time, are easily carried on indoor convection currents, and can be inhaled deeply into the lung.
During a building investigation for problematic levels of mold contamination (more than 30 sq. ft. deserves professional remediation) we need to look not just at the external visible surfaces but we need to be alert for the possibility of a large but hidden mold reservoir in a building ceiling or wall cavity or even in building insulation.
How do those Aspergillus spores get out to become inhaled? Building pressure changes can indeed cause air to move in and out of walls or ceilings enough that if there is a significant mold reservoir we may find it in the indoor environment even though it's not visible. And surprisingly (to those of us who are not mycologists), changes in temperature, humidity, and sometimes even barometric pressure can cause a veritable explosion of production of mold spores.
In a college library in New York and inspecting and testing both before and after a building dry-out project began, I could both measure and actually see a tremendous increase in the airborne Aspergillus sp. level in the building after a mold "remediation" company installed fans and dehumidifiers.
The drop in humidity converted a large mold reservoir on some books to a large airborne mold cloud. When the humidity level plummeted I could actually see little clouds of green Aspergillus spores swirl into the air as I walked past moldy books on shelves. The Aspergillus had been there for a while, in a damp environment. Things dried out and the Aspergillus conidiophore mommas said to their spore-babies: Hey you kids, you're outa-here! Everybody into the air, now!
Should We Cut Holes to Inspect for Mold in Ceilings or Walls?
I don't suggest running through the house with an axe, but it is worth a careful inspection for humidity or moisture traps as well as possibly hidden leaks. If I can identify one or more high risk locations in a building I'd make a small test cut to look inside the cavity.
If I cannot find any high risk locations AND if there are not building-related IAQ complaints AND if I do not find abnormal occurrences of problematic mold spores in tape samples of representative settled dust, then I have to conclude there's not sufficient evidence of an indoor resevoir to cut or dig further.
Aspergillosis Research & References
Aspergillosis, a write-up by Eloise M. Harman and other experts and posted at emedicine.medscape.com provides a thorough review of the types of Aspergillus-related illnesses, their detection, treatment, and related information. - retrieved 15 Sept 2015, original source: http://emedicine.medscape.com/article/296052-overview
Cornet, M., L. Fleury, C. Maslo, J-F. Bernard, G. Brücker, and Invasive Aspergillosis Surveillance Network of the Assistance Publique-Hopitaux de Paris. "Epidemiology of invasive aspergillosis in France: a six-year multicentric survey in the Greater Paris area." Journal of Hospital Infection 51, no. 4 (2002): 288-296.
Invasive aspergillosis is the most prevalent mould infection. An epidemiological surveillance network was set up in 18 teaching hospitals in Paris and the Greater Paris area. Prospective surveillance was conducted between 1994 and 1999. Between 1994 and 1997 cases were categorized as proven or probable aspergillosis and then the European Organization for Research and Treatment of Cancer/Mycoses Study Group criteria were used. The authors analysed 621 cases (115 proven, 506 probable). No seasonal variation was found. Haematological disorders (73%) including stem-cell transplantation (36%), solid-organ transplantations (10%) and AIDS (9%) were the main underlying conditions. The crude mortality was 63%. Incidence of IA was 8% (CI95: 6.5–9.5) in acute myelocytic leukaemia and 6.3% (CI95: 4.3–8.3) in acute lymphocytic leukaemia. Incidence was 12.8% (CI95: 10.8–14.8) following allogeneic stem-cell transplantation and 1.1% (CI95: 0.7–1.5) following autologous stem-cell transplantation. In solid-organ recipients incidence ranged from 11% following heart–lung transplantation and small bowel to 0.4% following kidney transplantation. Incidence in HIV infected patients ranged from 0.02 to 0.13% per annum. This large series confirmed that patients with haematologic disorders and transplantations are the most at risk for IA.
Denning, David W. "Invasive aspergillosis." Clinical infectious diseases (1998): 781-803.
Denning, David W., Jeanette Y. Lee, John S. Hostetler, Peter Pappas, Carol A. Kauffman, Daniel H. Dewsnup, John N. Galgiani et al. "NIAID Mycoses Study Group multicenter trial of oral itraconazole therapy for invasive aspergillosis." The American journal of medicine 97, no. 2 (1994): 135-144. Abstract
Background: Invasive aspergillosis is the most common invasive mould infection and a major cause of mortality in immunocompromised patients. Response to amphotericin B, the only antifungal agent licensed in the United States for the treatment of aspergillosis, is suboptimal. Methods: A multicenter open study with strict entry criteria for invasive aspergillosis evaluated oral itraconazole (600 mg/d for 4 days followed by 400 mg/d) in patients with various underlying conditions. Response was based on clinical and radiologic criteria plus microbiology, histopathology, and autopsy data. Responses were categorized as complete, partial, or stable. Failure was categorized as an itraconazole failure or overall failure.
Results: Our study population consisted of 76 evaluable patients. Therapy duration varied from 0.3 to 97 weeks (median 46). At the end of treatment, 30 (39%) patients had a complete or partial response, and 3 (4%) had a stable response, and in 20 patients (26%), the protocol therapy was discontinued early (at 0.6 to 54.3 weeks) because of a worsening clinical course or death due to aspergillosis (itraconazole failure). Twenty-three (30%) patients withdrew for other reasons including possible toxicity (7%) and death due to another cause but without resolution of aspergillosis (20%). Itraconazole failure rates varied widely according to site of disease and underlying disease group: 14% for pulmonary and tracheobronchial disease, 50% for sinus disease, 63% for central nervous system disease, and 44% for other sites; 7% in solid organ transplant, 29% in allogeneic bone marrow transplant patients, and 14% in those with prolonged granulocytopenia (median 19 days), 44% in AIDS patients, and 32% in other host groups. The relapse rates among those who completed therapy and those who discontinued early for possible toxicity were 12% and 40%, respectively; all were still immunosuppressed. Conclusion: Oral itraconazole is a useful alternative therapy for invasive aspergillosis with response rates apparently comparable to amphotericin B. Relapse in immunocompromised patients may be a problem. Controlled trials are necessary to fully assess the role of itraconazole in the treatment of invasive aspergillosis.
Fisher, Bruce D., Donald Armstrong, Bessie Yu, and Jonathan WM Gold. "Invasive aspergillosis: progress in early diagnosis and treatment." The American journal of medicine 71, no. 4 (1981): 571-577.
Ninety-one patients with documented invasive infections due to an Aspergillus species were identified at Memorial Sloan-Kettering Cancer Center from July 1, 1971, through December 31, 1976. Of the 29 patients in whom the diagnosis was made during life, 10 had successful treatment and survived the Aspergillus infection by two to 17 months. An immunodiffusion test was useful in the early diagnosis of invasive aspergillosis, and in 11 patients in whom the diagnosis was supported by seroconversion and who underwent treatment, the survival rate was 64 percent. Cultures of respiratory secretions were not reliable because they often reflected only colonization. In one year, only 9 percent of the patients with Aspergillus species isolated from the sputum had an invasive infection. The lung was the commonest site of involvement, 91 percent of the patients having pulmonary lesions. The most frequently affected extrapulmonary organ was the brain (18.3 percent). Eight patients had nonpulmonary aspergillosis as the only manifestation of this infection. Most of the 91 patients had hematologic neoplasms as the underlying disease, and neutropenia and antibacterial therapy preceded the diagnosis of aspergillosis in the majority of cases.
Greene, Reginald E., Haran T. Schlamm, Jörg-W. Oestmann, Paul Stark, Christine Durand, Olivier Lortholary, John R. Wingard et al. "Imaging findings in acute invasive pulmonary aspergillosis: clinical significance of the halo sign." Clinical Infectious Diseases 44, no. 3 (2007): 373-379.
Abstract Background. Computed tomography (CT) of the chest may be used to identify the halo sign, a macronodule surrounded by a perimeter of ground-glass opacity, which is an early sign of invasive pulmonary aspergillosis (IPA). This study analyzed chest CT findings at presentation from a large series of patients with IPA, to assess the prevalence of these imaging findings and to evaluate the clinical utility of the halo sign for early identification of this potentially life-threatening infection.
Methods. Baseline chest CT imaging findings from 235 patients with IPA who participated in a previously published study were systematically analyzed. To evaluate the clinical utility of the halo sign for the early identification and treatment of IPA, we compared response to treatment and survival after 12 weeks of treatment in 143 patients who presented with a halo sign and in 79 patients with other imaging findings.
Results. At presentation, most patients (94%) had ⩾1 macronodules, and many (61%) also had halo signs. Other imaging findings at presentation, including consolidations (30%), infarct-shaped nodules (27%), cavitary lesions (20%), and air-crescent signs (10%), were less common. Patients presenting with a halo sign had significantly better responses to treatment (52% vs. 29%; P < .001) and greater survival to 84 days (71% vs. 53%; P < .01) than did patients who presented with other imaging findings.
Conclusions. Most patients presented with a halo sign and/or a macronodule in this large imaging study of IPA. Initiation of antifungal treatment on the basis of the identification of a halo sign by chest CT is associated with a significantly better response to treatment and improved survival.
Greenberger, Paul A. "Allergic bronchopulmonary aspergillosis." Journal of Allergy and Clinical Immunology 110, no. 5 (2002): 685-692.
Allergic bronchopulmonary aspergillosis (ABPA) complicates asthma and cystic fibrosis. The survival factors in Aspergillus fumigatus that support saprophytic growth in bronchial mucus are not understood. Prednisone remains the most definitive treatment but need not be administered indefinitely. MHC II –restricted CD4+ T H2 clones have been derived from patients with ABPA. The total serum IgE concentration is elevated sharply but is “nonspecific. ” IgE serum isotypic antibodies to A fumigatus are useful in diagnosis; this is in contrast to the situation for patients with asthma without ABPA. High-resolution computed tomography of the chest demonstrates multiple areas of bronchiectasis in most patients with ABPA and is a useful radiologic tool. Some asthma control patients might have a few bronchiectatic airways, but not to the extent seen in or of the same character as those in ABPA. This review discusses clinical, radiologic, investigational, pathogenetic, and treatment issues of ABPA. (J Allergy Clin Immunol 2002;110:685-92.)
Herbrecht, Raoul, David W. Denning, Thomas F. Patterson, John E. Bennett, Reginald E. Greene, Jörg-W. Oestmann, Winfried V. Kern et al. "Voriconazole versus amphotericin B for primary therapy of invasive aspergillosis." New England Journal of Medicine 347, no. 6 (2002): 408-415.
Latgé, Jean-Paul. "Aspergillus fumigatus and aspergillosis." Clinical microbiology reviews 12, no. 2 (1999): 310-350.
Abstract: Aspergillus fumigatus is one of the most ubiquitous of the airborne saprophytic fungi. Humans and animals constantly inhale numerous conidia of this fungus. The conidia are normally eliminated in the immunocompetent host by innate immune mechanisms, and aspergilloma and allergic bronchopulmonary aspergillosis, uncommon clinical syndromes, are the only infections observed in such hosts. Thus, A. fumigatus was considered for years to be a weak pathogen. With increases in the number of immunosuppressed patients, however, there has been a dramatic increase in severe and usually fatal invasive aspergillosis, now the most common mold infection worldwide. In this review, the focus is on the biology of A. fumigatus and the diseases it causes. Included are discussions of (i) genomic and molecular characterization of the organism, (ii) clinical and laboratory methods available for the diagnosis of aspergillosis in immunocompetent and immunocompromised hosts, (iii) identification of host and fungal factors that play a role in the establishment of the fungus in vivo, and (iv) problems associated with antifungal therapy.
Lin, Swu-Jane, Jennifer Schranz, and Steven M. Teutsch. "Aspergillosis case-fatality rate: systematic review of the literature." Clinical Infectious Diseases 32, no. 3 (2001): 358-366. Abstract: To update the case-fatality rate (CFR) associated with invasive aspergillosis according to underlying conditions, site of infection, and antifungal therapy, data were systematically reviewed and pooled from clinical trials, cohort or case-control studies, and case series of ⩾10 patients with definite or probable aspergillosis. Subjects were 1941 patients described in studies published after 1995 that provided sufficient outcome data; cases included were identified by MEDLINE and EMBASE searches. The main outcome measure was the CFR. Fifty of 222 studies met the inclusion criteria. The overall CFR was 58%, and the CFR was highest for bone marrow transplant recipients (86.7%) and for patients with central nervous system or disseminated aspergillosis (88.1%). Amphotericin B deoxycholate and lipid formulations of amphotericin B failed to prevent death in one-half to two-thirds of patients. Mortality is high despite improvements in diagnosis and despite the advent of newer formulations of amphotericin B. Underlying patient conditions and the site of infection remain important prognostic factors.
Marr, Kieren A., Michael Boeckh, Rachel A. Carter, Hyung Woo Kim, and Lawrence Corey. "Combination antifungal therapy for invasive aspergillosis." Clinical infectious diseases 39, no. 6 (2004): 797-802.
Meyer, Richard D., Lowell S. Young, Donald Armstrong, and Bessie Yu. "Aspergillosis complicating neoplastic disease." The American journal of medicine 54, no. 1 (1973): 6-15. Abstract From 1964 to June 1971, 93 cases of aspergillosis were encountered at Memorial Sloan-Kettering Cancer Center. The 29 cases diagnosed in 1969–1970 and the 15 cases diagnosed in the first half of 1971 represented, respectively, a doubling and a quadrupling since 1964–1965. The incidence of aspergillosis in patients with leukemia was seven times greater than in patients with Hodgkin's disease or lymphoma (p < 0.0005). By the first half of 1971, 41 per cent of the patients who died with acute leukemia had evidence of aspergillosis. Fourteen patients with solid tumors resembled patients with leukemia or lymphoma in that they had at least two of the following in common: corticosteroid treatment, cytotoxic therapy and leukopenia (less than 4,000 cells/mm3). Pulmonary involvement was present in 90 of 93 cases, disseminated disease in 23. The commonest clinical pattern was unremitting fever and development of pulmonary infiltrates despite broad-spectrurh antibiotic therapy. In an increasing number of cases aspergillosis followed Pseudomonas aeruginosa infections. When present, serum aspergillus precipitins correlated well with invasive disease, but a negative test result was far less reliable. In one case of acute myelogenous leukemia the patient recovered from pulmonary aspergillosis after surgical excision of the lesion and remission of her leukemia.
The incidence of aspergillosis is increasing and should be considered in the setting of progressive pulmonary infiltrates in leukemic and other heavily immunosuppressed patients who respond poorly to antibacterial therapy. Earlier diagnosis may lead to more effective therapy.
Pfeiffer, Christopher D., Jason P. Fine, and Nasia Safdar. "Diagnosis of invasive aspergillosis using a galactomannan assay: a meta-analysis." Clinical Infectious Diseases 42, no. 10 (2006): 1417-1727.
Soubani, Ayman O., and Pranatharthi H. Chandrasekar. "The clinical spectrum of pulmonary aspergillosis." Chest Journal 121, no. 6 (2002): 1988-1999.
Abstract: Aspergillus is a ubiquitous fungus that causes a variety of clinical syndromes in the lung, ranging from aspergilloma in patients with lung cavities, to chronic necrotizing aspergillosis in those who are mildly immunocompromised or have chronic lung disease. Invasive pulmonary aspergillosis (IPA) is a severe and commonly fatal disease that is seen in immunocompromised patients, while allergic bronchopulmonary aspergillosis is a hypersensitivity reaction to Aspergillus antigens that mainly affects patients with asthma. In light of the increasing risk factors leading to IPA, such as organ transplantation and immunosuppressive therapy, and recent advances in the diagnosis and treatment of Aspergillus-related lung diseases, it is essential for clinicians to be familiar with the clinical presentation, diagnostic methods, and approach to management of the spectrum of pulmonary aspergillosis.
Victor, L. Yu, Robert R. Muder, and Abbas Poorsattar. "Significance of isolation of Aspergillus from the respiratory tract in diagnosis of invasive pulmonary aspergillosis. Results from a three-year prospective study." The American journal of medicine 81, no. 2 (1986): 249-254.
Abstract The isolation of Aspergillus species from respiratory secretions has been regarded as being of limited usefulness in the antemortem diagnosis of invasive pulmonary aspergillosis. One hundred and eight consecutive patients were evaluated in whom Aspergillus species were isolated from respiratory secretions. Invasive aspergillosis was not demonstrated in non-immunosuppressed patients or in patients with solid tumors in the absence of neutropenia. Lung tissue was examined in 17 patients with leukemia and/or neutropenia; all had invasive aspergillosis. Tissue examination was not performed in 20 neutropenic patients; of 17 not receiving antifungal therapy, 16 died. Multivariate statistical analysis showed that neutropenia and absence of cigarette smoking were significant predictors of invasive aspergillosis in patients with respiratory tract cultures yielding Aspergillus. All cases of invasive aspergillosis were associated with A. fumigatus or A. flavus. The isolation of A. fumigatus or A. flavus from the respiratory tract of a patient with leukemia and/or neutropenia is highly predictive of invasive infection. Empiric amphotericin B therapy, without the necessity for tissue diagnosis, should be considered in this patient subgroup.
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