Coccidioides posadasii

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Coccidioides posadasii
Scientific classification OOjs UI icon edit-ltr.svg
Domain: Eukaryota
Kingdom: Fungi
Division: Ascomycota
Class: Eurotiomycetes
Order: Onygenales
Family: Onygenaceae
Genus: Coccidioides
Species:
C. posadasii
Binomial name
Coccidioides posadasii
M.C.Fisher, G.L.Koenig, T.J.White & J.W.Taylor

Coccidioides posadasii is a pathogenic fungus that, along with Coccidioides immitis , is the causative agent of coccidioidomycosis, [1] or valley fever in humans. It resides in the soil in certain parts of the Southwestern United States, northern Mexico, and some other areas in the Americas, but its evolution was connected to its animal hosts. [2]

Contents

Coccidioides posadasii and C. immitis are morphologically identical, but genetically and epidemiologically distinct. [3] C. posadasii was identified as a separate species other than C. immitis in 2002 after a phylogenetic analysis. [4] The two species can be distinguished by DNA polymorphisms and different rates of growth in the presence of high salt concentrations: C. posadasii grows more slowly. It also differs epidemiologically, since it is found outside the San Joaquin Valley. Unlike C. immitis, which is geographically largely limited to California, C. posadasii can also be found in northern Mexico and South America.

Early history

As an intern in Buenos Aires in 1892, Alejandro Posadas described an Argentine soldier that had a dermatological problem since 1889. Posadas had seen the patient while a medical student in 1891 and skin biopsies revealed organisms resembling the protozoan Coccidia. The patient died in 1898 but during the interim Posadas successfully transmitted the infection to a dog, a cat, and a monkey, by inoculating them with material from his patient.

In 1899 a 40 year old manual laborer from the San Joaquin Valley, a native of the Azores, entered a San Francisco hospital with fungating lesions similar to those of Posadas' patient. Dr. Emmet Rixford, [5] a surgeon at San Francisco's Cooper Medical College, in attempts to determine the cause, concluded it was not from inadvertent self-inoculation. Further research produced a chronic ulcer in a rabbit and a lesion in a dog both excreting pus with the same organisms. Rixford issued a report, co-authored by Dr. Thomas Caspar Gilchrist (1862-1927), [6] that was printed in 1896, one year after the patient died. A pathologist at Johns Hopkins Medical School and Gilchrist studied the material and determined the microbe was not a fungus but a protozoan resembling Coccidia. With the help of parasitologist C.W. Stiles, the organism was named Coccidioides (“resembling Coccidia”) immitis (“not mild”). Four years later William Ophüls and Herbert C. Moffitt proved that C. immitis was not a protozoan but was a fungus that existed in 2 forms. In 1905 Ophüls called the infections "coccidioidal granuloma" and that it could develop from inhalation of the organism. Also in 1905 Samuel Darling studied a case and, referring to the misnamed organism a protozoan, named it Histoplasma capsulatum, meaning three major endemic fungi in the United States were all initially misidentified as protozoa.

Studies by Cooke on the immunology of the disease, and in 1927 a filtrate of culture specimens, later named coccidioidin, began to be used in skin testing to delineate the epidemiology of infection. In 1929 a second-year medical student, Harold Chope, was studying C. immitis in the laboratory of Ernest Dickson at Stanford University Medical School, and breathed in spores becoming infected but he later recovered. In 1934 Myrnie Gifford, a physician at San Francisco General Hospital, joined the Health Department of Kern County, California. [7] She had observed that San Joaquin Valley Fever patients often suffered from erythema nodosum, and all tested positive for coccidioidomycosis. [8] She met Ernest County when he visited her in Kern County, California, and together they presented evidence to the California Medical Association. [7] The two determined that San Joaquin fever represented C. immitis infection. The Kern County Health Department began obtaining epidemiologic histories and skin testing all cases involving Valley Fever. The investigations revealed, among other things, that a majority of the cases described a history of dust exposure, that coccidioidomycosis was common in the area, and that racial differences determined the host's response to the fungus.

Chope left Stanford Medical School and Dickson recruited a classmate, Charles E. Smith, to replace him. Smith began an extensive 17-month study of coccidioidomycosis in Kern and Tulare County, that also began a lifelong professional focus of study of C. immitis and coccidioidomycosis, even after he became Dean of the School of Public Health at the University of California at Berkeley in 1951, until his death in 1967. Research by Smith resulted in more than a few discoveries that included serologic testing, that chlamydospores of the fungus c. immitis could be wind-blown dispersing the spores when the hot weather converted the soil to dust, scientific results of military personnel testing in the southern San Joaquin Valley before and during WWII, as well as people of Japanese descent (many US citizens) interned in camps, prisoners of war, and agricultural workers. Diagnoses of active disease and skin testing, showed that it was also found in southern Nevada and Utah, western Texas, as well as Arizona, where the southern and central areas appeared to impose the highest risk of infection in the United States. An important Smith's research added to the fundamental discoveries of microbiology, epidemiology, clinical findings, and diagnosis that had emerged since Posadas' initial case report in 1892. [9]

Later history

Progress in studies from 1997 to 2007, including genomic restriction fragment length polymorphism (RFLP) concluded that there were two separate species. Earlier the two were referred to as types I and II, and later as Non-California and California distributions, determined as clades through microsatellite analyses. Genealogical Concordance Phylogenetic Species Recognition (GCPSR) criteria were met, so the two entities were proposed and generally recognized as two separate species: Coccidioides immitis, and the novel species Coccidioides posadasii. [10]

Related Research Articles

<span class="mw-page-title-main">Coccidioidomycosis</span> Fungal infection

Coccidioidomycosis, commonly known as cocci, Valley fever, as well as California fever, desert rheumatism, or San Joaquin Valley fever, is a mammalian fungal disease caused by Coccidioides immitis or Coccidioides posadasii. Coccidioidomycosis is endemic in certain parts of the United States in Arizona, California, Nevada, New Mexico, Texas, Utah, and northern Mexico.

<span class="mw-page-title-main">Histoplasmosis</span> Human disease

Histoplasmosis is a fungal infection caused by Histoplasma capsulatum. Symptoms of this infection vary greatly, but the disease affects primarily the lungs. Occasionally, other organs are affected; called disseminated histoplasmosis, it can be fatal if left untreated.

<i>Talaromyces marneffei</i> Species of fungus

Talaromyces marneffei, formerly called Penicillium marneffei, was identified in 1956. The organism is endemic to southeast Asia where it is an important cause of opportunistic infections in those with HIV/AIDS-related immunodeficiency. Incidence of T. marneffei infections has increased due to a rise in HIV infection rates in the region.

<i>Coccidioides immitis</i> Species of fungus

Coccidioides immitis is a pathogenic fungus that resides in the soil in certain parts of the southwestern United States, northern Mexico, and a few other areas in the Western Hemisphere.

<span class="mw-page-title-main">Coccidia</span> Subclass of protists

Coccidia (Coccidiasina) are a subclass of microscopic, spore-forming, single-celled obligate intracellular parasites belonging to the apicomplexan class Conoidasida. As obligate intracellular parasites, they must live and reproduce within an animal cell. Coccidian parasites infect the intestinal tracts of animals, and are the largest group of apicomplexan protozoa.

<span class="mw-page-title-main">Opportunistic infection</span> Infection caused by pathogens that take advantage of an opportunity not normally available

An opportunistic infection is an infection caused by pathogens that take advantage of an opportunity not normally available. These opportunities can stem from a variety of sources, such as a weakened immune system, an altered microbiome, or breached integumentary barriers. Many of these pathogens do not necessarily cause disease in a healthy host that has a non-compromised immune system, and can, in some cases, act as commensals until the balance of the immune system is disrupted. Opportunistic infections can also be attributed to pathogens which cause mild illness in healthy individuals but lead to more serious illness when given the opportunity to take advantage of an immunocompromised host.

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<span class="mw-page-title-main">Arthroconidium</span>

Arthroconidia are a type of fungal spore typically produced by segmentation of pre-existing fungal hyphae.

<i>Coccidioides</i> Genus of fungi

Coccidioides is a genus of dimorphic ascomycetes in the family Onygenaceae. Member species are the cause of coccidioidomycosis, also known as San Joaquin Valley fever, an infectious fungal disease largely confined to the Western Hemisphere and endemic in the Southwestern United States. The host acquires the disease by respiratory inhalation of spores disseminated in their natural habitat. The causative agents of coccidioidomycosis are Coccidioides immitis and Coccidioides posadasii. Both C. immitis and C. posadasii are indistinguishable during laboratory testing and commonly referred in literature as Coccidioides.

<span class="mw-page-title-main">San Joaquin (soil)</span>

San Joaquin is an officially designated state insignia, the state soil of the U.S. state of California.

<i>Blastomyces dermatitidis</i> Species of fungus

Blastomyces dermatitidis is a dimorphic fungus that causes blastomycosis, an invasive and often serious fungal infection found occasionally in humans and other animals. It lives in soil and wet, decaying wood, often in an area close to a waterway such as a lake, river or stream. 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 (77 °F). In an infected human or animal, however, it converts in growth form and becomes a large-celled budding yeast. 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.

<span class="mw-page-title-main">Dimorphic fungus</span> Fungi that can exist as mold or yeast

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Lorraine Friedman was an American medical mycologist who was recruited to Tulane University to create a center for medical mycology. She was a faculty member at Tulane University from 1955-1981 where she extensively researched Tinea capitis, “Ringworm of the hair.” She was instrumental in creating the Medical Mycological Society of the Americas and served as the President in 1975.

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References

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  2. Sharpton, T. J.; Stajich, J. E.; Rounsley, S. D.; et al. (October 2009). "Comparative Genomic Analyses of the Human Fungal Pathogens Coccidioides and Their Relatives". Genome Research. 19 (10): 1722–31. doi:10.1101/gr.087551.108. PMC   2765278 . PMID   19717792. Archived from the original on 2014-11-03. Retrieved 2013-07-18.
  3. Miranda, Elizabeth (2011). "Coccidioides posadasii". The Encyclopedia of Life (EOL). eol.org. Retrieved 17 July 2013.
  4. Fisher, M. C.; Koenig, G. L.; White, T. J. & Taylor, J. W. (2002). "Molecular and phenotypic description of Coccidioides posadasii sp. nov., previously recognized as the non-California population of Coccidioides immitis" (PDF). Mycologia. 94 (1): 73–84. doi:10.2307/3761847. hdl:10044/1/4213. JSTOR   3761847. PMID   21156479.
  5. Dr. Emmet Rixford died 1938-01-02- Retrieved 2017-01-22
  6. coccidioidal protozoan infection- Retrieved 2017-01-22
  7. 1 2 Baker, Roger Denio; Angulo, O. A.; Barroso-Tobila, C.; Carbonell, L. M.; Cespedes, R.; Chick, E. W.; Clark, B. M.; Duque, O.; Edington, G. M. (2012-12-06). The Pathologic Anatomy of Mycoses: Human Infection with Fungi, Actinomycetes and Algae. Springer Science & Business Media. ISBN   9783642805707.
  8. MD, Kevin Glynn (2017-08-03). Gasping for Air: How Breathing Is Killing Us and What We Can Do about It. Rowman & Littlefield. ISBN   9781442246249.
  9. The Early History of Coccidioidomycosis: 1892–1945: Oxford journals, Retrieved 2017-01-22
  10. Taxonomic and diagnostic markers for identification of Coccidioides immitis and Coccidioides posadasii: From Medical Mycology August 2007, 45, 385-393- Retrieved 2017-01-22