Blastomycosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

Blastomycosis is a fungal infection caused by the organism Blastomyces dermatitidis. It is endemic in portions of the Mississippi river and Ohio river basins and around the Great Lakes in North America, and causes clinical symptoms such as fever, productive cough and myalgia. The symptoms, develop between 3 to 15 weeks after exposure. Majority of the cases are self-limiting with out any progression. Antifungals are used to treat if symptoms persist for more than 4 weeks. Prognosis is good depending on the immune status of the individual.^[1][2]

Blastomycosis was first described in detail by Thomas Casper Gilchrist in 1894.

Infection occurs by inhalation of the conidia from its natural soil habitat. It has an average incubation period of 3 weeks to 3 months after exposure. Once inhaled, they multiply in lungs and initiate neutrophilic response with subsequent cell-mediated immune response leading to suppurative tissue destruction in lungs, and may disseminate through blood and lymphatics to other organs including skin, bone, genitourinary tract, and brain. The characteristic histopathological findings on sputum microscopy is the multi nucleated yeast form (budding).^[3][4][5]

Blastomycosis is a fungal infection caused by Blastomyces dermatitidis.^[6]

Blastomycosis presents as a mild flu-like illness and needs to be differentiated from other fungal disorders like coccidioidomycosis, histoplasmosis, aspergillosis, pneumocystis pneumoniasandporotrichosis.

Blastomycosis is endemic in the Mississippi river and Ohio river basins and around the Great Lakes in United States.The annual incidence is less than 1 case per 100,000 people in Mississippi, Louisiana, Kentucky, and Arkansas.^[7][8]

The risk factors are not well established for the acquisition of blastomycosis even in endemic areas. However, studies point out the role of moist soil rich in organic debris as a source of transmission.

According to the centers for disease control and prevention screening for blastomycosis is not recommended.

Blastomycosis is a granulomatous disease entity, that can produce a wide range of signs and symptoms, but in most cases, it is a mild illness. The symptoms include fever, productive cough, hemoptysis and weight loss. If left untreated, a significant proportion of these cases may further disseminate to other body parts, most commonly to skin, followed by bone and joint, genitourinary system and other sites in the body (Nervous systemlandymphatics). The route of spread is most commonly either hematogenous or lymphatic. Prognosis of the individual depends on the immune status of the individual and treatment, usually good in immunocompetent patients with treatment, on contrast prognosis is poor in patients even with treatment in immuno-compromised individuals. Complications that may develop with blastomycosis include cutaneous involvement can cause large sores with pus (abscesses), osteomyelitis from bone involvement, prostatitis and epididymo-orchitis in males and tubo-ovarian abscess in females have been reported, disease recurrence.

Symptoms of blastomycosis depends on the immune status of the individual, it presents as a flu-like illness with fever, chills, myalgia, headache, and a nonproductive cough which resolves within days in immunocompetent patients or as an acute illness resembling bacterial pneumonia, with symptoms of high fever, chills, a productive cough, and pleuritis in immunocompromised individuals. Blastomycosis can affect other organs through hematogenous spread or lymphatics which includes skin, bone, genitourinary tract and brain. Skin lesions, usually appear as ulcerated lesions and bone lesions can lead to osteomyelitis.

Blastomycosis is a primary disease of lung, but it may also affect other organs like skinbandone. Adetailed physical examination can guide towards the diagnosis. Lung examination findings include dullness to percussion, and creased fremitus. Signs of pleuritic involvement such as pleuritic chest pain and pleural rub may be found.

No radiographic findings are absolutely diagnostic of blastomycosis. Once suspected, the diagnosis of blastomycosis can usually be confirmed by demonstration of the characteristic broad-based budding organisms in sputum or tissues by KOH prep, cytology, or histology.

The findings on X-ray are not consistent or highly specific. Alveolar infiltrates may be present but are not localized to a particular lobe. Consolidations with or without cavitations, small pleural effusion‘s are relatively common. Sometimes, pulmonary nodules simulating tuberculosis or cancers may be present. Mediastinal lymph node enlargement is not a consistent finding but may be found occasionally.

The mainstay of treatment is antifungals. As per the current guidelines given by the Infectious Diseases Society of America, the appropriate regimen must be guided by the clinical form and severity of disease, as well as the immune status of patient and toxicity of antifungal agents. Only asymptomatic infections are left untreated, otherwise, all cases need therapy. Itraconazole given orally is the treatment of choice for most forms of the disease. Cure rates are high, and the treatment over a period of months is usually well tolerated. Amphotericin B is considerably more toxic, and is usually reserved for critically ill patients and those with central nervous system disease.^[9]

• Immuno-competent patient. (Non-Life threatening infection): Drug of choice in this cases is usually Itraconazole or Lipid Amphotericin B. Alternatively, daily fluconazole or ketaconazole may also be used.
• Immunocompetent patient. (Life-threatening infection): Pulmonary cases – These warrant treatment primarily with Lipid Amphotericin B or Deoxycholate Amphotericin B. Once the condition has been stabilized the patient may be switched to oral Itraconazole therapy. Disseminated cases – Drug of choice is same, however, patients nontolerant to Amphotericin B can be treated with fluconazole or Itraconazole.

• Immunocompromised patients: All patients warrant treatment with Lipid Amphotericin B as the drug of choice and Itraconazole once the disease has shown clinical improvement.

Avoiding travel to areas where the infection is known to occur may help prevent exposure to the fungus, but this may not always be possible.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: ; Vidit Bhargava, M.B.B.S [2]Aditya Ganti M.B.B.S. [3]

Blastomycosis is a fungal infection, which was first discovered by Philippe Edouard Léon Van Tieghem, a french biologist in 1876. Later in 1894, it was first described in detail by Thomas Casper Gilchrist and sometimes goes by the eponym Gilchrist’s disease. It is also sometimes referred to as Chicago Disease.^[1]

• In 1876, Philippe Edouard Léon Van Tieghem, a French botanist/biologist discovered blastomycosis for the first time.
• In 1894, Thomas Casper Gilchrist described blastomycosis in detail and thought it to be a dermatological disease. He named it B.dermatidis and it also goes by the eponym Gilchrist’s disease^[2]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]

Blastomycosis is fungal infection primarily involving lungs and the presentation is often confused with acute bacterial pneumonia. It can be classified into two categories based on the duration of symptoms and organ involvement as acute or chronic and pulmonary or extra-pulmonary blastomycosis.^[1][2]

• Acute: If the duration of symptoms is less than 4-6 weeks
• Chronic: If the symptoms persist for more than 6 weeks.

• Pulmonary Blastomycosis: Lungs are the most common site of primary infection in blastomycosis.
• Extra-pulmonary Blastomycosis: The most common extra pulmonary sites involved in blastomycosis are skin, bone, genitourinary and CNS.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: ; Vidit Bhargava, M.B.B.S [2]Aditya Ganti M.B.B.S. [3]

Blastomycosis is caused by a dimorphic fungi called Blastomyces dermatitidis. It has an average incubation period of 3 weeks to 3 months after exposure. The initial neutrophilic response and the subsequent cell-mediated immune response are manifested as a suppurative tissue destruction seen in lungs, skin, and other organs. The histopathological hallmark findings on sputum microscopy is the multinucleated yeast form (budding).

• Inhalation of the conidia from its natural soil habitat is considered the most significant route of transmission.^[1]
• Other less common route of transmission is by cutaneous inoculation through direct skin injury.^[2]

• The incubation period varies from 3 weeks to 3 months after exposure.

• Once inhaled in the lungs, the conidia are mostly destroyed due to their susceptibility to neutrophils, leukocytes and macrophages. ^[3]
• However, a few conidia escape this protective mechanism and evolve into yeast form, which being double walled structures are more resistant to destruction.
• This conversion releases a glycoprotien BAD-1, which induces cell mediated immunity. ^[4]
• This results in a pyogranulomatous response at the primary site of infection (lungs).
• Which eventually leads to the formation of a non-caseating granulomas.

• The fungi can disseminate through the blood and lymphatics to other organs, such as skin, bone, genitourinary tract and brain.^[1]

• Cyotoxic T cells are mainly responsible for persistence of infection and tissue damage.
• Ineffective type 4 delayed hypersensitivity reaction containing macrophages and sensitized T cells are mainly responsible for the cutaneous manifestations. ^[4]

There is no known genetic association for blastomycosis.

Classic appearance on modified Wright’s stain ^[1]

• Multinucleated yeast cell
• Single broad-based bud
• Round to oval in shape with 12 um diameter

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Blastomyces dermatitidis is the causal agent of blastomycosis, an invasive and often serious fungal infection found occasionally in humans and other animals in regions where the fungus is endemic.^[1] The causal organism is a fungus living in soil and wet, decaying wood, often in an area close to a waterway such as a lake, river or stream.^[1] Indoor growth may also occur, for example, in accumulated debris in damp sheds or shacks. The fungus is endemic to parts of eastern North America, particularly boreal northern Ontario, southeastern Manitoba, Quebec south of the St. Lawrence River, parts of the U.S. Appalachian mountains and interconnected eastern mountain chains, the west bank of Lake Michigan, the state of Wisconsin, and the entire Mississippi Valley including the valleys of some major tributaries such as the Ohio River. In addition, it occurs rarely in Africa both north and south of the Sahara desert, as well as in the Arabian Peninsula and the Indian subcontinent. Though it has never been directly observed growing in nature, it is thought to grow there as a cottony white mold, similar to the growth seen in artificial culture at 25 °C. In an infected human or animal, however, it converts in growth form and becomes a large-celled budding yeast.^[1] Blastomycosis is generally readily treatable with systemic antifungal drugs once it is correctly diagnosed; however, delayed diagnosis is very common except in highly endemic areas.

Blastomyces dermatitidis is the causal agent of blastomycosis, a potentially very serious disease that typically begins with a characteristically subtle pneumonia-like infection that may progress, after 1–6 months, to a disseminated phase that causes lesions to form in capillary beds throughout the body, most notably the skin, internal organs, central nervous system and bone marrow. Blastomyces dermatitidis is the name applied to the ascomycetous fungus, Ajellomyces dermatitidis. Recently an second species has been described in the genus Blastomyces, B. gilchristii, which subsumes certain strains previously assigned to B. dermatitidis.^[2] Despite widespread use, the genus Blastomyces is currently invalid under the International Code of Botanical Nomenclature.^[3] Along with two other important human-pathogenic fungi, Histoplasma capsulatum, Paracoccidioides brasiliensis and Polytolypa hystricis, species of Blastomyces belong to a recently recognized fungal family, the Ajellomycetaceae.^[4] The three principal pathogens in this family are all grouped physiologically as “dimorphic fungi”: fungi that switch from a mold-like (filamentous) growth form in the natural habitat to a yeast-like growth form in the warm-blooded animal host. Blastomyces dermatitidis itself is a sexual organism, occurring in nature as both a + mating type and a – mating type. This is epidemiologically important for two reasons: firstly, it implies that the organism will be genetically variable, potentially leading to variations in disease severity, treatment response and habitat preference; secondly, it implies that a suitable, stable habitat must exist for the complex process of sexual reproduction to take place. This habitat is as yet unknown. In its asexual form, the fungus grows as a typical colonial microfungus, comparable to Penicillium or Rhizopus mold forms commonly seen on mouldy bread.

In nature, the fungus forms a network of thread-like mycelium that penetrates the substratum on which it grows, and then after 3–5 days of growth begins to reproduce asexually with small (2–10 µm) conidia (asexual spores). These conidia are probably the main infectious particles produced by the fungus. They form on individual short stalks and readily become airborne when the colony is disturbed; their size places them well within the respirable size range for particles,^[5] meaning that they can deposit deeply in the lungs when inhaled. Sexual reproduction by the fungus requires the meeting of colonies of + and – mating type, probably a relatively rare event, and results in the production of small ascomata (sexual fruiting bodies) 200–350 µm, looking, to the naked eye, similar to a woollen fuzz ball, and in microscopic view consisting of a layer of spiralling, springy guard hairs surrounding a fertile core in which groups of 8 ascospores (sexual spores) are produced in small round reproductive sacs (asci). The ascospores, at 1.5–2.0 µm, are among the smallest reproductive particles produced by fungi, and are within the respirable size range.^[5] The budding yeast cells seen in infected tissues and bodily fluids are generally relatively large (ca. 8–15 µm) and characteristically bud through a broad base or neck, making them highly recognizable to the pathologist. A small (“nanic”) form is rarely seen with cells under 6 µm.

One of the unexplained regularities of nature is that there are several fungi of different phylogenetic ancestry that show a similar pattern of existence: dimorphism (conversion from a filamentous form in the environment to a yeast form in warm-blooded host tissues), virulent pathogenesis (ability to cause a significant infection in an animal host that is otherwise in good health), pulmonary infectivity (infection mainly via the lungs) and sharply delimited endemism (occurrence in only a limited geographic range.). Blastomyces dermatitidis is one of these fungi; the others are Histoplasma capsulatum, Paracoccidioides brasiliensis, Coccidioides immitis, C. posadasii and Penicillium marneffei.

The geographic range of B. dermatitidis is largely focused around the waterways of the St. Lawrence and Mississippi River systems of North America. There is a widely distributed and much republished, partially erroneous map that shows the U.S. portion of this range accurately, inclusive of occurrence in Minnesota, Wisconsin, Ohio, Kentucky, Arkansas, Tennessee, North and South Carolina, the Virginias, Mississippi, Louisiana, and a few regions of states adjacent to those named.^[6] The Canadian range of B. dermatitidis shows an abundance of blastomycosis in broad areas north and south of the St. Lawrence River in Quebec, as well as high endemicity along the north shore of Lake Erie and the low endemicity in southeastern corner of Manitoba. Though the Quebec distribution is reasonably accurate, the rest of Canada is strongly misrepresented. Blastomyces dermatitidis is absent or nearly so from the Lake Erie area, but occurs sporadically on the north shore of Lake Ontario, including metropolitan Toronto,^[7] and, most notably, has areas of high endemicity throughout northern Ontario.^[8]Remarkably high incidence is noted for some parts of the Kenora area and climatologically similar areas of northwestern Ontario^[9] To the west, the range of endemic blastomycosis extends across southern Manitoba and into adjacent Saskatchewan.^[10] A few cases have been reported from north central Alberta, e.g., the Edmonton area, though in these cases an atypical genetic group of the fungus may be involved.^[11]

In the rest of the world, B. dermatitidis occurs at low levels in various parts of Africa, from Algeria to South Africa, as well as in and near the Arabian Peninsula. The African isolates are divided into two biologically different antigen groups: isolates from north of the Sahara are similar to North American isolates in having A and K antigens, while southern African isolates lack the A antigen.^[12] Isolates from the middle east possess both antigens. The sub-Saharan African isolates differ in the laboratory from other isolates by being exceedingly difficult to convert to the yeast phase, and they also show some enzymatic distinctions.^[13]

Blastomyces dermatitidis is one of the most ecologically mysterious organisms causing human and animal disease. Prediction of disease risk and prevention of disease are both made extraordinarily difficult by our very poor understanding of where and how this organism normally grows in nature. Despite decades of attempts at isolating organisms from epidemiological foci, B. dermatitidis has only been isolated from the environment 21 times.^[14] Most of these isolations have been based on the arduous isolation techniques involving the suspension of soil or other environmental materials in aqueous medium with antibacterial antibiotics, and injection of mice with these materials, followed by sacrifice of the animals when they appear ill or at the end of six weeks.^[15] The internal organs of the mice are then checked microscopically for evidence of blastomycosis. Needless to say, the cost and complexity of performing such studies is imposing, especially as the ethical clearance procedures for work involving animals become ever more involved. More direct and economical mycological techniques for environmental isolation, such as dilution plating, have never yielded positive results for Blastomyces growth. Since B. dermatitidis will grow readily from clinical samples on common laboratory media, the lack of success in isolating it from environmental materials is generally ascribed to the inhibitory effects of co-occurring common molds and antibiotic-resistant bacteria.

In just one experiment, a single positive B. dermatitidis culture was gained via use of a novel enrichment broth technique.^[16] Recently, in an important breakthrough, a specific PCR technique was developed that was able to detect B. dermatitidis in three environmental samples from a dog kennel that had been experiencing problems with blastomycosis.^[14]

What has been learned from direct isolation and recent PCR studies is that B. dermatitidis tends to be associated with soils and wood debris in areas “characterized by an acidic pH, high organic content (due to rotting or decayed wood or vegetation and animal or bird droppings), abundant moisture, and proximity to waterways”.^[17] Recent PCR detections, for example, concerned a Kentucky dog kennel where 35 of 100 dogs had contracted blastomycosis.^[14] Previous isolations have been from comparable sites such as soil and wood debris from an abandoned Wisconsin beaver dam,^[18] and woody materials from a Wisconsin woodpile.^[16] Isolation of B. dermatitidis was also accomplished from an earthen floor indoors on one occasion.^[19]

There has been a long history of justifiable speculation that B. dermatitidis may associate in nature with one or more indigenous North American mammalian host species. To date, however, all the animal species that have been subjected to focused investigation have been exonerated of this specific connection. Unsubstantiated suspicion has particularly focused on the beaver,^[18][20][21] but the shrew,^[22] the bat^[23] and the prairie dog^[24] have also been focal points of interest, with no conclusive interspecies association being demonstrated to date. Interestingly, the closely related pathogenic fungus P. brasiliensis in South America has a well substantiated, though not well understood, ecological link with the nine-banded armadillo, Dasypus novemcinctus.^[25] This member of the mammalian order Edentata has no close relatives in the geographic range of B. dermatitidis.

Avoidance of exposure in endemic areas is the principal means of disease prevention. Because the agent is known to distribute in dusts, the minimization of dust-generating activities, such as digging, sweeping, etc., is key. Although a method of soil decontamination has been described and demonstrated to be effective, it uses hazardous chemicals and its use is best reserved for situations that cannot be managed otherwise.^[15]

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  Nodular skin lesions of blastomycosis, one of which is a bullous lesion on top of a nodule. From Public Health Image Library (PHIL). ^[26]
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  Histopathology of blastomycosis of skin. Budding cell of Blastomyces dermatitidis surrounded by neutrophils. From Public Health Image Library (PHIL). ^[26]
• 
  Histopathology of blastomycosis. Yeast cell of Blastomyces dermatitidis undergoing broad-base budding. From Public Health Image Library (PHIL). ^[26]
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  Note the histopathologic changes seen in blastomycosis due to Blastomyces dermatitidis using methenamine silver stain. From Public Health Image Library (PHIL). ^[26]
• 
  Note the histopathologic changes seen in blastomycosis due to Blastomyces dermatitidis using methenamine silver stain.From Public Health Image Library (PHIL). ^[26]
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  Direct FA stain revealing the histopathology of lung tissue blastomycosis due to the organism Blastomyces dermatitidis From Public Health Image Library (PHIL). ^[26]
• 
  Direct FA stain revealing the histopathology of lung tissue blastomycosis due to the organism Blastomyces dermatitidis. From Public Health Image Library (PHIL). ^[26]
• 
  This is a photomicrograph of Blastomyces dermatitidis using a cotton blue staining technique. From Public Health Image Library (PHIL). ^[26]
• 
  This micrograph shows histopathologic changes that reveal the presence of the fungal agent Blastomyces dermatitidis. From Public Health Image Library (PHIL). ^[26]
• 
  This micrograph shows histopathologic changes that reveal the presence of the fungal agent Blastomyces dermatitidis. From Public Health Image Library (PHIL). ^[26]
• 
  This photomicrograph depicts the fungal agent Blastomyces dermatitidis. From Public Health Image Library (PHIL). ^[26]
• 
  Histopathology of blastomycosis, lung of wolf. Yeast cells of Blastomyces dermatitidis. FA stain. From Public Health Image Library (PHIL). ^[26]
• 
  Ultrastructural histopathology in tissue specimen from a patient with a keloidean blastomycosis infection, which was caused by the fungus, Blastomyces dermatitidis. From Public Health Image Library (PHIL). ^[26]
• 
  Ultrastructural histopathology in a tissue specimen from a patient with a keloidean blastomycosis infection, which was caused by the fungus, Blastomyces dermatitidis. From Public Health Image Library (PHIL). ^[26]
• 
  Ultrastructural histopathology in a tissue specimen from a patient with a keloidean blastomycosis infection, which was caused by the fungus, Blastomyces dermatitidis. From Public Health Image Library (PHIL). ^[26]
• 
  H&E-stained photomicrograph reveals ultrastructural histopathology in an dermal skin tissue specimen in a patient with an intradermal keloidean blastomycosis infection, which was caused by the fungus, Blastomyces dermatitidis.From Public Health Image Library (PHIL). ^[26]
• 
  Morphologic changes that took place upon a patient’s arm, which included keloidal scarring brought on due to a case of cutaneous blastomycosis, caused by Blastomyces dermatitidis. From Public Health Image Library (PHIL). ^[26]
• 
  Morphologic changes that took place upon a patient’s arm, which included keloidal scarring brought on due to a case of cutaneous blastomycosis, caused by Blastomyces dermatitidis. From Public Health Image Library (PHIL). ^[26]
• 
  Ultrastructural histopathology in dermal skin tissue specimen in a patient with an intradermal keloidal blastomycosis infection. From Public Health Image Library (PHIL). ^[26]
• 
  Patient’s right knee revealed the keloidal scarring brought on due to a case of cutaneous blastomycosis, which was caused by Blastomyces dermatitidis. From Public Health Image Library (PHIL). ^[26]
• 
  Patient’s right knee revealed the keloidal scarring brought on due to a case of cutaneous blastomycosis, caused by Blastomyces dermatitidis. From Public Health Image Library (PHIL). ^[26]
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  Patient’s right ankle displayed keloidal scarring brought on due to a case of cutaneous blastomycosis, caused by Blastomyces dermatitidis. From Public Health Image Library (PHIL). ^[26]
• 
  Ultrastructural details of Blastomyces dermatitidis including the organism’s aerial hypha, developing sporangia. From Public Health Image Library (PHIL). ^[26]
• 
  “Digested”, and fluorescent antibody-stained photomicrograph reveals the presence of Blastomyces dermatitidis antigens in human lung tissue specimen (562x mag). From Public Health Image Library (PHIL). ^[26]
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  “Digested”, and fluorescent antibody-stained photomicrograph reveals the presence of Blastomyces dermatitidis antigens in human lung tissue specimen (562x mag). From Public Health Image Library (PHIL). ^[26]
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  “Undigested”, and fluorescent antibody-stained photomicrograph reveals presence of Blastomyces dermatitidis antigens in human lung tissue specimen (125x mag). From Public Health Image Library (PHIL). ^[26]
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  Gamori-stained photomicrograph of a canine liver tissue specimen, revealed the presence of budding Blastomyces dermatitidis fungal cells of various sizes (500x mag). From Public Health Image Library (PHIL). ^[26]

• Blastomyces at the US National Library of Medicine Medical Subject Headings (MeSH)
• http://www.mycology.adelaide.edu.au/Fungal_Descriptions/Dimorphic_Pathogens/Blastomyces/
• http://pathmicro.med.sc.edu/mycology/mycology-6.htm

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: ; Vidit Bhargava, M.B.B.S [2] Aditya Ganti M.B.B.S. [3]

Blastomycosis has overlapping signs & symptoms with that of other fungal and bacterial disorders. A detailed history, physical examination, and serological tests help us to pinpoint the diagnosis. All these disorders can be often misinterpreted as community acquired pneumonia as they all present with similar complaints such as fever, productive cough, chest pain and shortness of breath.

• Coccidioidomycosis
• Histoplasmosis
• Aspergillosis
• Pneumocystis pneumonia
• Sporotrichosis

The following table elaborates differentiating features between Blastomycosis from other fungal disorders:

• Anthrax
• Legionella
• Listeriosis
• Brucellosis
• Tuberculosis
• Scrub typhus
• Leptospirosis
• Cat scratch fever

• Chickenpox
• Herpes(Prodrome)
• Influenza
• Parainfluenza
• HIV -1/-2
• Coxsackie A virus
• Hepatits
• Cytomegalovirus
• Eastern equine encephalitis virus
• Venezuelan equine encephalitis
• Coronavirus
• California encephalitis virus

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: ; Vidit Bhargava, M.B.B.S [2] Aditya Ganti M.B.B.S. [3]

The annual incidence rates of blastomycosis is estimated approximately to be 1 to 2 cases per 100,000 population. Between 1993 and 2003, a total of 500 cases are reported, with the majority of cases coming from the northeastern part of United states. Most of the cases are reported in Wisconsin, Manitoba (Canada), and Ontario. The case fatality rate of blastomycosis is 0.21 per 1 million individuals when left untreated. Blastomycosis is also seen internationally, as cases are reported from Africa, India, Middle east, Mexico, Central and South America. Men and women are affected equally by blastomycosis. The prevalence of blastomycosis is not affected by age. All the individuals who are exposed to the fungi can develop the disease

• The annual incidence rates of blastomycosis is estimated approximately to be 1 to 2 cases per 100,000 population.
• Wisconsin has the highest incidence of blastomycosis of any state, with yearly rates ranging from 10 to 40 cases per 100,000 persons.^[1]

• During 1990-2010, the case fatality rate of blastomycosis is 0.21 per 1 million person.^[2]

The prevalence of blastomycosis is not effected by age. All the individuals who are exposed to the fungi can develop the disease.

• Men and women are affected equally by blastomycosis.

• There is no racial predilection to blastomycosis

• In the United States, blastomycosis is endemic in southern and southeastern states that border the Ohio River and Mississippi River valleys, as well as in Midwestern states and Canadian provinces that border the Great Lakes and the Saint Lawrence Riverway.
• Blastomycosis is reportable in Arkansas, Louisiana, Michigan, Minnesota, Illinois and Wisconsin.^[3]
• The disease is hyperendemic in north-central Wisconsin and the northern region of Ontario, Canada. ^[3]
• Blastomycosis is distributed internationally, cases are reported from Africa, India, Middle east, Mexico, Central and South America.^[4]

Map of eastern United States and Canada showing distribution of blastomycosis. From Public Health Image Library (PHIL). ^[5]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: ; Vidit Bhargava, M.B.B.S [2] Aditya Ganti M.B.B.S. [3]

The risk factors are not well established for the acquisition of blastomycosis in endemic areas. However, studies conducted over a period of several years, point out the role of moist soil rich in organic debris as a source of transmission.

• Woody areas especially in endemic areas
• People working outdoors in endemic areas including farmers, forest workers, hunters, campers are slightly more predisposed.^[1]
• Immunosuppression
• Collagen vascular disease
• Contact with a person having blastomycosis

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: ; Vidit Bhargava, M.B.B.S [2]Aditya Ganti M.B.B.S. [3]

Blastomycosis is a granulomatous disease entity, that can produce a wide array of signs and symptoms, but is usually a mild illness in many cases. The most common presentation is a mild acute pneumonia that is self-resolving, it can also cause chronic pneumonia and extra-pulmonary manifestations. The most common site of involvement is lungs, but it can often spread to other sites such as skin, bones and genitourinary systems. The route of spread is most commonly either hematogenous or lymphatic.

• Symptoms of acute blastomycosis include an influenza like illness with fever, cough, myalgia, arthralgia, and pleurisy developing 3-15 weeks after exposure.^[1]
• In most of the individuals the infection resolves spontaneously even without the treatment.
• But in some individuals with out treatment it may progress to a more chronic stage which confounds the diagnosis, mistaking it for tuberculosis, other fungal infections or even a malignancy.
• Patient may develop symptoms of high grade fever, productive cough, hemoptysis and weight loss.
• A significant proportion of these cases may further disseminate to other body parts, most commonly to skin, followed by bone and joint, genitourinary system and other sites in the body (nervous system and lymphatics).
• Leading to septicemia and finally death.

Complications that can develop as a result of Blastomycosis include :

• Pulmonary fibrosis
• Cutaneous abscesses
• Osteomyelitis ^[2]
• Prostatitis
• Epididymoorchitis
• tubo-ovarian abscess ^[3][4].
• Side effects from the treatment drugs such as Amphotericin B

Extra-pulmonary manifestations usually require a longer overall duration of treatment. The cases that do relapse after treatment, usually respond well to a second treatment course.
Mortality rate in treated cases is as follows:

• 0-2% in treated cases among immunocompetent patients
• 29% in immunocompromised patients
• 40% in the subgroup of patients with AIDS
• 68% in patients presenting as acute respiratory distress syndrome (ARDS)

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