Coccidioides posadasii: Difference between revisions

From MicrobeWiki, the student-edited microbiology resource
No edit summary
 
Line 1: Line 1:
{{Uncurated}}
{{Biorealm Genus}}
{{Biorealm Genus}}



Latest revision as of 03:16, 20 August 2010

This student page has not been curated.

A Microbial Biorealm page on the genus Coccidioides posadasii

Classification

Higher order taxa

Eukaryota; Fungi/Metazoa group; Fungi; Dikarya; Ascomycota; Pezizomycotina; Eurotiomycetes; Eurotiomycetidae; Onygenales; mitosporic Onygenales; Coccidioides [Others may be used. Use NCBI link to find]

Species

NCBI: Taxonomy

Coccidioides posadasii

Description and significance

Coccidioides posadasii is a pathogenic fungus found in the alkaline rich soil of arid/semiarid regions in Texas, Arizona, Mexico, and South America [12]. It was formally known as the non-California C. immitis because it was morphologically identical to this species and existed outside of California. But after comparison of RFLPs of 10 DNA loci from clinical isolates of C. immitis from California, Arizona, and Texas, a significant difference among the allele frequencies was found, thus, suggesting that C. immitis consisted of two different species: C. immitis and C. posadasii [6].

C. posadasii grows in the soil as infectious cells called arthroconidia which are dispersed into the air. And when inhaled by a host, the arthroconidia mature and divide into endospores 60 to >100 micrometers in size in the host lung [3] causing a respiratory disease called coccidioidomycosis.

The characterization of phenotypic differences in this pathogen is the key toward understanding its immune response and disease causing capabilities [6].

Genome structure

The genomic structure of C. posadasii has not been completely sequenced, but is still an ongoing project. Currently, C. posadasii is known to contain a linear DNA that is 7,870,074 base pairs long [8]. It is a haploid organism with a genome that is 29 Mb organized into 4 chromosomes [9].

Cell structure and metabolism

Coccidioides posadasii is a dimorphic fungus with a saprobic and pathogenic phase of development. In the saprobic phase, arthroconidia are formed by the division of hyphae and the differentiation of cellular compartments [12]. The saprobic phase is characterized by the up-regulated presence of Woronin body, a protein involved in sealing septal pores in response to cell damage [11]. During the pathogenic phase, arthroconidia mature and produce spherules that are internally septated to make endospores [14]. In this phase of growth, there is an increased expression of the enzymes nitrate reductase (nir), involved in ammonia fermentation and allows the fungi to grow under anaerobic conditions, and trehalose synthase and trehalose-6-phosphate phosphatase which are involved in the synthesis of trehalose, a molecule that protects the cell from environmental stresses [11].

Ecology

Coccidioides posadasii is a species of C. immitis that is present in Southwestern Unites States, Northern Mexico, and Central and South America. C. posadasii live in the soil forming filamentous saprobes. In the saprobic form, C. posadasii can withstand harsh conditions such as little rainfall, hot summers, low elevation, and alkaline rich soil with high salinity, and in its mycelial phase, it is capable of tolerating a pH range of pH 2 to 12 [5].

C. posadasii is an airborne mold that is a respiratory pathogen to humans and animals [5].

Pathology

Coccidioides posadasii causes the fungal disease coccidioidomycosis in both animal and human hosts [10]. Infection occurs by the inhalation of soil containing arthroconidia formed during the mycelial phase. Once inside the lung, the parasitic phase begins and arthroconidia divide into multinucleate spherules that mature and reproduce to form endospores [14 and 5]. Upon endosporulation, enzymatically active urease, the virulence factor, gets released and attaches to the host lung causing an inflammatory response [5].

Infection results in a wide variety of symptoms. The majority of exposures to the pathogen result in asymptomatic infection while others experience a primary or benign pulmonary infection (known as “Valley Fever”) marked by flu like symptoms: fever, cough, chest pains, fatigue, shortness of breath, chills, sputum production, night sweats, and headaches [1]; or a severe/fatal case of progressive pulmonary or extrapulmonary disease affecting the skin, bones (and/or joints), the central nervous system, and other organs.

The disease in not contagious and lifelong immunity is observed with patients who have recovered from primary infection [10].

Application to Biotechnology

The observation that recovery from coccidioidomycosis leads to immunity has prompted researchers to search for a vaccine. Such studies are aimed at determining enzymes encoding cell wall proteins in C. posadasii and using these molecules as possible candidates for a human vaccine.

One candidate that has been proposed is a family of structurally and functionally related β-1,3-glucanosyltransferases expressed in C. posadasii. β-1,3-glucanosyltransferases are believed to be vital for mold and yeast development [4].

Current Research

1. In the article, “Evolution of the Mating Type Locus: Insights Gained from the Dimorphic Primary Fungal Pathogens Histoplasma capsulatum, Coccidioides immitis, and Coccidioides posadasii,” genomic analysis, dirt sequencing, and bioinformatics was used to determine that the mating type (MAT) locus of the three species named. It was found that the MAT loci of H. capsulatum, C. immitis, and C. posadasii contained alleles that encoded either an α-box protein or an HMG domain protein which is in accordance to a heterothallic sexual cycle. These MAT sequences also led to the creation of a PCR test that allowed mating type to be determined rapidly [7].

2. In the study, “Detection of Coccidioides Species in Clinical Specimens by Real-time PCR,” researchers developed a real-time PCR assay able to rapidly and safely diagnose coccidioidomycosis from clinical specimens. The ITS2 region of Coccidioides was selected as the target for PCR assay, and after the testing of various specimens and comparison of results was completed, it was determined that the real-time PCR assay was an effective method for diagnosing coccidioidomycosis, but lacked the ability to distinguish between the two species of Coccidioides: C. immitis and C. posadasii [2].

3. Due to the infectious dangers that C. immitis possesses, the Public Health Security and Bioterrorism Preparedness Response Act of 2002 has imposed requirements over its transfer, use, and possession. Such requirements has resulted in various difficulties for laboratories carrying the pathogen as a control in identifying isolates of C. immitis; thus, the paper “Use of the Coccidioides posadasii ∆chs5 Strain for Quality Control in the ACCUPROBE Culture Identification Test for Coccidioides immitis” sought to determine an alternative strain of Coccidioides that could be used as the quality control isolate. The alternative chosen was C. posadasii ∆chs5 because it was excluded from the select agents list compiled by the Department of Health and Human Services and the U.S. Department of Agriculture, was modified to be nonvirulent, and passed the ACCUPROBE culture identification test for C. immitis [13].

References

1. Arsura, E. L. and Hospenthal, D. R. “Coccidioidomycosis (Infectious Diseases).” 2005. www.emedicine.com/med/topic539.htm

2. Binnicker, M. J., Buckwalter, S. P., Eisberner, J. J., Stewart, R. A., McCullough, A. E., Wohlfiel, S. L., and Wengenack, N. L. “Detection of Coccidioides Species in Clinical Specimens by Real-Time PCR.” Journal of Clinical Microbiology. 2007. Vol. 45(1). p. 173-178.

3. Cole, G. T., Seshan, K. R., Franco, M., Bukownik, E., Sun, S. H., and Hearn, V. M. “Isolation and Morphology of an Immunoreactive Outer Wall Fraction Produced by Spherule of Coccidioides immitis.” Infection and Immunity. 1988. p. 2686-2694.

4. Delgado, N., Xue, J., Yu, J.-J., Hung, C.-Y., and Cole, G. T. “A Recombinant β-1,3-Glucanosyltransferase Homolog of Coccidioides posadasii Protects Mice against Coccidioidomycosis.” Infection and Immunity. 2003. Vol. 71(6). p. 3010-3019.

5. Donovan, F. M., Schaller, R., Hung, C.-Y., Xue, J., Reichard, U., and Cole, G. T. “Urease Produced by Coccidioides posadasii Contributes to the Virulence of This Respiratory Pathogen.” Infection and Immunity. 2006. Vol. 74(1). p. 504-515.

6. Fisher, M. C., Koenig, G. L., White, T. J., Taylor, J. W. “Molecular and phenotypic description of Coccidioides posadasii sp. nov., previously recognized as the non-Californian population of Coccidioides immitis.” Mycologia. 2002. 94(1). p. 73-84.

7. Fraser, J. A., Stajich, J. E., Tarcha, E. J., Cole, G. T., Inglis, D. O., Sil, A., and Heitman, J. “Evolution of the Mating Type Locus: Insights Gained from the Dimorphic Prim ary Fungal Pathogens Histoplasma capsulatum, Coccidioides immitis, and Coccidioides posadasii.” Eukaryotic Cell. 2007. Vol. 6(4). p. 622-629.

8. Genome of Coccidioides posadasii (NCBI Sequence Viewer)

9. Genome Project for Coccidioides posadasii (NCBI)

10. Hector, R. F. and Laborin, R. L. “Coccidioidomycosis – A Fungal Disease of the Americas.” PLoS Medicine. 2005. 2(1):e2.

11. Johannesson, H., Kasuga, T., Schaller, R. A., Good, B., Gardner, M. J., Townsend, J. P., Cole, G. T., and Taylor, J. W. “Phase-specific gene expression underlying morphological adaptations of the dimorphic human pathogenic fungus, Coccidioides posadasii.” Fungal Genetics and Biology. 2006. Vol. 43. p. 545-559.

12. Kellner, E. M., Orsborn, K. I., Siegel, E. M., Mandel, M. A., Orbach, M. J., and Galgiani, J. N. “Coccidioides posadasii Contains a Single 1,3-β-Glucan Synthase Gene That Appears To Be Essential for Growth.” Eukaryotic Cell. 2005. Vol. 4. p. 111-120.

13. McGinnis, M. R., Smith, M. B., and Hinson, E. “Use of the Coccidioides posadasii ∆chs5 Strain for Quality Control in the ACCUPROBE Culture Identification Test for Coccidioides immitis.” Journal of Clinical Microbiology. 2006. Vol. 44(11). p. 4250-4251.

14. Viriyakosol, S., Fierer, J., Brown, G. D., Kirkland, T. N. “Innate Immunity to the Pathogenic Fungus Coccidioides posadasii Is Dependent on Toll-Like Receptor 2 and Dectin-1.” Infection and Immunity. 2005. Vol. 73. p. 1553-1560.

15. Yu, J. J., Kirkland, T. N., Hall, L. K., Wopschall, J., Smith, R. C., Hung, C. Y., Chen, X., Tarcha, E., Thomas, P. W., and Cole, G. T. “Characterization of a Serodiagnostic Complement Fixation Antigen of Coccidioides posadasii Expressed in the Nonpathogenic Fungus Uncinocarpus reesii.” Journal of Clinical Microbiology. 2005. 43(1). p. 5462-5469.

Edited by Stephanie Dela Cruz student of Rachel Larsen