By Isabel Ibarra


Disease Etiology:

       Blastomycosis, pronounced [blas-toh-mahy-koh-sis]is a granulomatous fungal infection caused by a fungus known as Blastomyces dermatitidis which is dimorphic.  Blastomycosis is also known by several names:  Chicago Disease, Gilchrist's disease, North American Blastomycosis.[1][4][12]   Blastomycosis is believed to be found in the midwestern, southeastern, and south central states of the United States, especially concentrated along the Mississippi and Ohio rivers.  “Microfoci are also found in Central and South America and parts of Africa.”[5]  This fungus is associated with areas that contain high moisture and high quantities of enriched organic or rotting wooded debris.  Persons most prone to the disease are those with exposure to endemic wooded areas, whether it is recreational or occupational.[4]


Disease Transmission:

       Blastomycosis outbreaks occur as a respiratory infection when the fungus is inhaled in its conidia form after having been disturbed in contaminated soil.  It can then spread into other organs such as the skin, and bones.  It can also manifest itself as subcutaneous nodules, genitourinary infections, joint infections, as well as other organ infections.[4][5]  Symptoms can manifest anywhere from 3 to 15 weeks from the time of inoculation, with 50% of the infected population being asymptomatic.[4][5]  To date, “it is not known to be transmitted from person to person”.[5]  Dogs can also be prone to the disease.  B. dermatitidis can range from an acute pulmonary infection to a fatal disease.[10]  And, usually manifests in immunocompromised individuals, such as those with organ transplants or HIV.[11]



      It has been found that moist decomposing soils serve as reservoirs for B. dermatitidis.  Once disturbed in the soil it becomes airborne and inhaled by humans or other animals.  Blastomycosis is self limiting to a single individual.  It has not been found to be contagious between humans.  The soils that have been found to contain the fungus are isolated to North America and South America, specifically Canada, the southeastern, south-central, and midwestern states of the United States as well as Africa.  Very few countries outside of the previously listed have reported such cases.[5]      


Specific Microbial Characteristics:

      B dermatitidis is a “thermal dimorphic fungus” occurring in mycelial form in nature.[10]  When present in infected tissue, such as the lungs, it takes on the form of yeast.  It grows as a fluffy white mold at 250 degrees in a Sabouraud agar.  When grown on a blood agar at body temperature, it forms a brown wrinkled colony. B. dermatitidis has a characteristic thick-wall in its yeast cell form and contains broad-based daughter cells.[10]

Specific Tests for Identification:

      Cultures of sputum, tracheal aspirates, broncho-alveolar lavage fluid, tissue biopsy specimens, cerebrospinal fluid, or urine are grown in brain-heart infusion and Sabouraud dextrose agar at room temperature.  In experienced hands the characteristic budding yeast that forms is easily and quickly diagnosed by visualization.  “Chemiluminescent DNA probes are available for identification of B dermatitidis.”  Other skin and serodiagnostic tests are poor indicators of B. dermatitidis.  Chest x-rays are abnormal in two-thirds of patients and “may reveal alveolar or mass like infiltrates, reticulonodular pattern, pleural effusion, and, rarely, cavitation”.  MRI and CT scans may also reveal some skeletal lesions or involvement.  Histological studies on skin biopsies can be a strong diagnostic tool.[10]


Signs and Symptoms:

       Fifty percent of infected individuals are asymptomatic.  Usually those with the infection isolated to the lungs show no symptoms.  Symptoms can appear from 3 to 15 weeks from time of inoculation.[4][5]  Individuals may complain of influenza like symptoms.  They may present with acute or chronic pneumonia. Symptoms range from skin or bone lesions to kidney, bladder, prostate, and testicular infections.  Some patients present with “chest pain, cough, unexplained fatigue, fever, malaise, joint pain and stiffness, muscle pain, rashes, shortness of breath, sweating, and unintentional weight loss”.  Symptoms may last 2 to 6 months.[10][6]


Historical Information:

       Thomas Casper Gilchrist was a doctor of dermatology and held positions at both The University of Maryland and Johns Hopkins.  He was the first to isolate Blastomyces dermatitidis.  He first described Blastomycosis in 1894 within the United States.  Today, the disease is sometimes called the Gilchrist’s disease.[9]


Virulence Factors:

       Infection begins with inhalation of fungal conidia.  The mold transforms into the yeast form as a result of heat related stress.  The yeast cells increase in number when there is a lack of host defense mechanisms.  Lymph nodes become involved and the disease process begins. It seems that 50% of infected individuals may have natural resistance since they never develop symptoms and the disease resolves itself.  “Cellular immune response mediated by antigen-specific T lymphocytes and lymphokine-derived macrophage's cell-mediated immunity plays a critical role in aborting fungal growth”.  The ulcerative skin lesions mimic some cancers and other disorders such as pyoderma gangrenosum which in turn make it challenging to correctly diagnose.[10]



       If the disease is isolated to the lungs, treatment may not be necessary, “unless it becomes severe”.  For treatment of severe cases or disease manifestation outside of the lungs the following antifungals may be prescribed:  Fluconazole, Itraconazole, Ketoconazole.  In severe cases, Amphotericin B is used.  Frequent follow up with your physician is recommended to make certain that the disease does not return.  [6]  “A successful outcome without relapse was noted in 86.5% of amphotericin B-treated patients and in 81.7% of ketoconazole-treated patients. The relapse rate for ketoconazole-treated patients was higher than for amphotericin B-treated patients (14% and 3.9% respectively).”[2]


Prevention/ Vaccines:

       Immunocompromised individuals living near or in blastomycosis-endemic areas should be counseled as to reducing their risk of acquiring the disease.  Logically, they are not able to completely avoid exposure but should avoid any occupational or recreational activities known to be at an increased risk of contamination.  Children with HIV can have “lifelong suppressive therapy with itraconazole” administered “after an acute episode of the disease”.[11]  And for the general public, avoid traveling to high risk areas.[6]  At the University of Wisconsin-Madison, mycologist Bruce Klein and colleagues have been working on a vaccine for B. dermatitidis.  They are performing further studies for the vaccine and hope to be able to use it in veterinary medicine with more common outbreaks occurring in dogs.[13]


Local cases/ outbreaks:

      Six hundred seventy cases of blastomycosis had been reported in Wisconsin to the DOH between 1986-1995.  This represented 1.4 people in 100,000.  Ninety five percent of these cases were confirmed.[7]  In 2006 between January and April, Lincoln County, Wisconsin had an outbreak of Blastomycosis.  In this 4 month period, there were 27 confirmed cases compared to the normal 8 cases per year.  After investigation, it was determined that the source was a pile of pine needles that had been relocated during a period in which “environmental and weather conditions deemed favorable for the growth of blastomycosis.[8]

Global cases/ outbreaks:

       Until 1989, blastomycosis was a reportable disease in Canada.  Ontario and Manitoba have reported the most cases in Canada.  THe most reported cases occur within the United States, 1 to 2 per 100,000; occurrences are less than this outside of the United States.[3] 




[1] "blastomycosis." The American Heritage® Stedman's Medical Dictionary. Houghton Mifflin Company. 28 Feb. 2010. <>. February 26, 2010


[2] Chapman SW, Lin AC, Hendricks KA, Nolan RL, Currier MM, Morris KR, Turner HR. “Endemic blastomycosis in Mississippi: epidemiological and clinical studies.” September 12, 1997.$=relatedarticles&logdbfrom=pubmed February 26, 2010


[3] Dermnet NZ.  “Blastomycosis”.  June 15, 2009.  February 26, 2010


[4]  Doctorfungus.  “Blastomycosis”.  doctorfungus.  1/27/2007.  February 27, 2010


[5] Division of Foodborne, Bacterial, and Mycotic diseases (DFBMD).  “Blastomycosis”.  March 27, 2008. February 26, 2010


[6] David C. Dugdale, III, MD, Jatin M. Vyas, PhD, MD, David Zieve, MD, MHA, Medical Director, A.D.A.M., Inc.  Blastomycosis.  January 25, 2010.  February 28, 2010


[7] MMWR. Blastomycosis -- Wisconsin, 1986-1995. July 19, 1996. February 26, 2010


[8] National Center for Zoonotic, Vector-Borne, and Enteric Diseases.  “Blastomycosis”.  July 17, 2009.  February 25, 2010


[9] ROBINSON, HARRY M. JR. MD. “The Birth and Development of Dermatology in Maryland”. November 1977. February 26, 2010


[10] Russell W Steele, MD, Avinash Shetty, MD.  “Blastomycosis”.  July 28, 2008. February 27, 2010

symptoms, mortality, causes, diagnosis,prevention


[11] Russell W Steele, MD, Avinash Shetty, MD.  “Blastomycosis”.  July 28, 2008. February 26, 2010


[12] Sheila Rodriguez Gonzalgo1, M.D., Samuel Ejadi1, M.D., and Colleen Christmas2, M.D. Clinical Fellow and 2Associate Professor, Johns Hopkins Geriatric Medicine.  The Johns Hopkins Arthritis Center. John Hopkins Medicine. February 27, 2010.


[13] U.S. Department of Health and Human Services NIH News National Institute of Health.  “Live Recombinant Vaccine Protects Against Fungal Disease”.  November 29,2000.  February 26, 2008