Help! Please Register

  The Fungi

  Introduction
  Descriptions
  Synonyms
  Image Bank
  Lecture Bank
  Video Bank


  Mycoses

  Introduction
  Human
  Veterinary
  Environmental
   Industrial
  Agricultural
  MSG


  Drugs

  Introduction
  Medical
  Veterinary
  Environmental
   Industrial
  Agricultural


  Laboratory

  Introduction
  Susceptibility
  MIC Database
  Procedures
  Histopathology


  Education &
  Tools

  Introduction
  Abbreviations
  Links
  CME
  Conference
   Highlights
  Bibliography
  Glossary
  Good Books
  Events Calendar


  About Us

  Introduction
  Our Mission
  Editorial Board
  Editorial Staff
  Supporters
  Contributors
  Legal Stuff
  Privacy Policy
  Kudos


  The Fungi

  Introduction
  Descriptions
  Synonyms
  Image Bank
  Lecture Bank
  Video Bank



This page updated:
1/27/2007 9:23:00 AM


DoctorFungus - All Rights Reserved © 2007 Copyright
& Privacy Policy


Site built and designed for doctorfungus by Webillustrated



You are here: The Fungi > Descriptions >


Coccidioides sp.
(described by Rixford and Gilchrist in 1896)

Say Me

Taxonomic Classification

Kingdom: Fungi
Phylum: Ascomycota
Class: Euascomycetes
Order: Onygenales
Family: Onygenaceae
Genus: Coccidioides

Description and Natural Habitats

Coccidioides immitis and C. posadasii are thermally dimorphic fungi found in soil particularly at warm and dry areas with low rain fall, high summer temperatures, and low altitude. The two species are morphologically identical but genetically and epidemiologically distinct [738, 739]. C. immitis is geographically limited to California's San Joaquin valley region, whereas C. posadasii is found in the desert southwest of the United States, Mexico, and South America. The two species appear to co-exist in the desert southwest and Mexico.

Although it was recognized for some years that C. immitis contained two genetic subgroups, their description as separate species did not occur until 2002 [739]. Prior to this, the two groups were simply known as the California and non-California variants of C. immitis. Thus, essentially all prior literature treats them as a single species. As the two species can be distinguished only by genetic analysis and different rates of growth in the presence of high salt concentrations (C. posadasii grows more slowly), little is known as yet about differences in pathogenicity. Thus, the remainder of this discussion will simply refer to the pair of species as C. immitis/posadasii.

C. immitis/posadasii specifically inhabits alkaline soil. It is isolated in rodent burrows at desert-like areas of southwest United States. It has no known teleomorph [531, 1295, 2202].

Coccidioides immitis/posadasii is a pathogenic fungus and is among the causative agents of true systemic (endemic) mycoses. It is endemic at southwest United States, Northern Mexico, and certain areas in Central and South America. Imported cases may be observed following travel to endemic areas [86, 360].

Species

Coccidioides immitis and C. posadasii are the only species included in the genus Coccidioides. See the summary of synonyms for Coccidioides immitis.

Pathogenicity and Clinical Significance

Coccidioides immitis/posadasii is the causative agent of coccidioidomycosis in humans. Coccidioidomycosis is one of the true systemic (endemic) mycoses [794]. It is acquired by inhalation and initially presents with a pulmonary infection which may later disseminate to other organs and systems. Airway coccidioidomycosis involving the endotracheal and endobronchial tissues may develop [1821]. Inhalation of the dry arthroconidia of Coccidioides immitis/posadasii, which are carried by dust storms, initiates the infection. Afterwards, hematogenous spread of the organism results in infection of skin, bones, joints, lymph nodes, adrenal glands, and central nervous system [60, 208, 255]. The clinical picture has a remarkably wide spectrum. The infection remains as an acute and self-limited respiratory infection in most exposed hosts, but it progresses to a chronic and sometimes fatal disease in others. Spontaneous healing is observed in as high as 95% of the otherwise healthy hosts. Dissemination may occur particularly during pregnany and carries a high risk of mortality [1837].

Although coccidioidomycosis basically effects otherwise healthy immunocompetent hosts due to the true pathogenic nature of the fungus, it may also develop in immunocompromised patients, such as patients with AIDS and organ transplant recipients [255, 1504]. Activities and professions related to tillage of the soil, such as agricultural work, telephone post digging, archeology, or simply playing with soil appear to be associated with development of coccidioidomycosis [531].

Coccidioidomycosis has also been described in warm-blooded water animals such as bottlenose dolphins [1888] and horses [2497].

Macroscopic Features

Coccidioides immitis/posadasii colonies grow rapidly. The macroscopic morphology may be very variable. At 25 or 37°C and on Sabouraud dextrose agar, the colonies are moist, glabrous, membranous, and grayish initially, later producing white and cottony aerial mycelium. With age, colonies become tan to brown in color.

Microscopic Features

Microscopic appearance of the fungus depends on the temperature of isolation [531, 1295, 2202]:

1. At 25°C
Hyphae and arthroconidia are produced. Hyphae are hyaline, septate and thin. Racquet hyphae may occasionally be observed on slides prepared from young cultures. Arthroconidia are thick-walled, barrel-shaped, and 2-4 x 3-6 µm in size. Typically, these arthroconidia alternate with empty disjunctor cells. On the released arthroconidia, annular frills that are the remnants of the disjunctor cells are observed.

2. At 37°C
Large, round, thick-walled spherules (10-80 µm in diameter) filled with endospores (2-5 µm in diameter) are observed. Production of spherules in vitro requires inoculation into a special synthetic medium, such as converse liquid medium, an incubation temperature of 37-40°C and presence of CO2 at a concentration as high as 20%.

Coccidioides immitis/posadasii continues to grow as a mould and does not produce spherules at any temperature unless special growth medium is provided in vitro. This finding indicates that temperature is not the only variable that controls the spherule formation. Thus, some authorities prefer not to classify this fungus as thermally dimorphic. Nevertheless, Coccidioides immitis/posadasii is commonly classified among the thermally dimorphic fungi.

The definitive identification of an isolated Coccidioides immitis/posadasii strain requires demonstration of spherule production in vitro, use of DNA probes, application of exoantigen tests, or demonstration of spherule production in vivo by animal experiments [1295, 1350]. Molecular typing studies have also been initiated and appear useful in identification [1484].

Histopathologic Features

Spherules containing endospores are the typical structures formed in infected tissues [1173]. The transition form of C. immitis/posadasii producing septate hyphae that develop into arthroconidia may be observed in necrotic nodules and misdiagnosed as one of the fungi in hyphomycetes group, particularly if the spherules are not yet evident [462, 1174]. Hyphal forms may also be observed in brain tissue or cerebrospinal fluid in the presence of plastic devices. These devices presumably trigger the morphological reversion to the saprophytic form [964].

See our histopathology page for histopathologic staining methods.

Compare to

Blastomyces dermatitidis
Malbranchea

Immature nonendosporulationg cells are produced by Coccidioides immitis/posadasii at early growth phases. These cells may resemble nonbudding forms of Blastomyces dermatitidis and may cause diffulty in differentiation of the two fungi [1174, 1295].

Due to the existence of arthroconidia and the disjunctor cells, the two genera Malbranchea and Coccidioides are similar microscopically. However, Malbranchea differs from Coccidioides immitis/posadasii by its failure to produce spherules containing endospores and by not reacting with Coccidiodies immitis/posadasii specific reagents in the exoantigen test or the DNA test probe. In addition, the fertile hyphae of Malbranchea are curved whereas those of Coccidioides are straight [531, 2202].

Laboratory Precautions

The arthroconidia of Coccidioides immitis/posadasii are very infectious. All manipulations should be done in a biological safety cabinet.

Susceptibility

Amphotericin B [1338], itraconazole [1338], and voriconazole [1152, 1338] appear active in vitro against Coccidioides immitis/posadasii. However, amphotericin B is less active against some of the isolates for which it fails to exert fungicidal activity. Itraconazole and voriconazole, on the other hand, do not have any fungicidal activity at all against Coccidioides immitis/posadasii [1338]. Nikkomycins are additive to synergistic in vitro with fluconazole or itraconazole against Coccidioides immitis/posadasii [1339].

For MICs of various antifungal drugs for Coccidioides immitis/posadasii, see our susceptibility database.

Patients with self-limited disease or relatively localized acute pulmonary infections usually do not require antifungal therapy. Antifungal therapy should be given to patients who have disseminated disease or are under risk of complications due to their underlying immunosuppression and other factors. Amphotericin B [624] and azoles, such as fluconazole, itraconazole, and ketoconazole are used for treatment of coccidioidomycosis [255, 795, 1504]. However, clinical failure during antifungal therapy is not uncommon [624]. Azoles, particularly fluconazole, is preferred for treatment of cases with meningitis. Available data suggest that the azole therapy should be continued life long in cases with meningitis to prevent relapses [583]. Amphotericin B, if used for treatment of meningitis, should be given via intrathecal route and for a prolonged duration [624].

Animal experiments suggest that caspofungin [868], sordarins [145, 452, 1673], and nikkomycins [1015] are also promising in treatment of coccidioidomycosis.

Concomitant surgical interventions may be required for some patients with pulmonary coccidioidomycosis [468] as well as cases with bone and joint involvement [624].

Prophylaxis for Coccidioidomycosis

Research that focuses on vaccine development for prevention of coccidioidomycosis is in progress [601, 1122, 1711, 1749, 2498].

Search

PubMed

Nucleotides

GenBank



Coccidioides immitis arthroconidia
Arthroconidia of C. immitis



References

60. Ampel, N. M., K. J. Ryan, P. J. Carry, M. A. Wieden, and R. B. Schifman. 1986. Fungemia due to Coccidioides immitis. Medicine. 65:312-321.

86. Anonymous. 2000. Coccidioidomycosis in travelers returning from Mexico--Pennsylvania, 2000 [In Process Citation]. MMWR Morb Mortal Wkly Rep. 49:1004-6.

145. Aviles, P., A. Pateman, R. S. Roman, M. J. Guillen, F. G. De las Heras, and D. Gargallo-Viola. 2001. Animal pharmacokinetics and interspecies scaling of sordarin derivatives following intravenous administration. Antimicrob. Agents Chemother. 45:2787-2792.

208. Bayer, A. S., and L. B. Guze. 1979. Fungal arthritis. II. Coccidioidal synovitis: clinical, diagnostic, therapeutic, and prognostic considerations. Seminars in Arthritis & Rheumatism. 8:200-11.

255. Blair, J. E., and J. L. Logan. 2001. Coccidioidomycosis in solid organ transplantation. Clin Infect Dis. 33:1536-1544.

360. Cairns, L., D. Blythe, A. Kao, D. Pappagianis, L. Kaufman, J. Kobayashi, and R. Hajjeh. 2000. Outbreak of coccidioidomycosis in Washington State residents returning from Mexico. Clin Infect Dis. 30:61-64.

452. Clemons, K. V., and D. A. Stevens. 2000. Efficacies of sordarin derivatives GM193663, GM211676, and GM237354 in a murine model of systemic coccidioidomycosis. Antimicrob. Agents Chemother. 44:1874-1877.

462. Collier, L., A. Balows, and M. Sussman. 1998. Topley & Wilson's Microbiology and Microbial Infections, 9th ed, vol. 4. Arnold, London, Sydney, Auckland, New York.

468. Connelly, M. B., and J. T. Zerella. 2000. Surgical management of coccidioidomycosis in children [In Process Citation]. J Pediatr Surg. 35:1633-4.

531. de Hoog, G. S., J. Guarro, J. Gene, and M. J. Figueras. 2000. Atlas of Clinical Fungi, 2nd ed, vol. 1. Centraalbureau voor Schimmelcultures, Utrecht, The Netherlands.

583. Dewsnup, D. H., J. N. Galgiani, J. R. Graybill, M. Diaz, A. Rendon, G. A. Cloud, and D. A. Stevens. 1996. Is it ever safe to stop azole therapy for Coccidioides immitis meningitis? Ann. Intern. Med. 124:305-10.

601. Dixon, D. M., A. Casadevall, B. Klein, L. Mendoza, L. Travassos, and G. S. Deepe. 1998. Development of vaccines and their use in the prevention of fungal infections. Med Mycol. 36:57-67.

624. Drutz, D. J. 1983. Amphotericin B in the treatment of coccidioidomycosis. Drugs. 26:337-46.

738. Fisher, M. C., G. L. Koenig, T. J. White, G. San-Blas, R. Negroni, I. G. Alvarez, B. Wanke, and J. W. Taylor. 2001. Biogeographic range expansion into South America by Coccidioides immitis mirrors New World patterns of human migration. Proc Natl Acad Sci U S A. 98:4558-62.

739. Fisher, M. C., G. L. Koenig, T. J. White, and J. W. Taylor. 2002. Molecular and phenotypic description of Coccidioides posadasii sp. nov., previously recognized as the non-California population of Coccidioides immitis. Mycologia. 94:73-84.

794. Galgiani, J. N. 1999. Coccidioidomycosis: A regional disease of national importance - Rethinking approaches for control. Ann. Intern. Med. 130:293-300.

795. Galgiani, J. N., N. M. Ampel, A. Catanzaro, R. H. Johnson, D. A. Stevens, and P. L. Williams. 2000. Practice guidelines for the treatment of coccidioidomycosis. Clin. Infect. Dis. 30:658-661.

868. Gonzalez, G. M., R. Tijerina, L. K. Najvar, R. Bocanegra, M. Luther, M. G. Rinaldi, and J. R. Graybill. 2001. Correlation between antifungal susceptibilities of Coccidioides immitis in vitro and antifungal treatment with caspofungin in a mouse model. Antimicrob. Agents Chemother. 45:1854-1859.

964. Hagman, H. M., E. G. Madnick, A. N. D'Agostino, P. L. Williams, S. Shatsky, L. F. Mirels, R. M. Tucker, M. G. Rinaldi, D. A. Stevens, and R. E. Bryant. 2000. Hyphal forms in the central nervous system of patients with coccidioidomycosis. Clin Infect Dis. 30:349-355.

1015. Hector, R. F., B. L. Zimmer, and D. Pappagianis. 1990. Evaluation of nikkomycins X and Z in murine models of coccidioidomycosis, histoplasmosis, and blastomycosis. Antimicrob. Agents Chemother. 34:587-93.

1122. Jiang, C., D. M. Magee, T. N. Quitugua, and R. A. Cox. 1999. Genetic vaccination against Coccidioides immitis: Comparison of vaccine efficacy of recombinant antigen 2 and antigen 2 cDNA. Infec Immunity. 67:630-635.

1152. Kappe, R. 1999. Antifungal activity of the new azole UK-109, 496 (voriconazole). Mycoses. 42:83-86.

1173. Kaufman, L. 1992. Immunohistologic diagnosis of systemic mycoses: an update. Eur J Epidemiol. 8:377-82.

1174. Kaufman, L., G. Valero, and A. A. Padhye. 1998. Misleading manifestations of Coccidioides immitis in vivo. J Clin Microbiol. 36:3721-3723.

1295. Larone, D. H. 1995. Medically Important Fungi - A Guide to Identification, 3rd ed. ASM Press, Washington, D.C.

1338. Li, R. K., M. A. Ciblak, N. Nordoff, L. Pasarell, D. W. Warnock, and M. R. McGinnis. 2000. In vitro activities of voriconazole, itraconazole, and amphotericin B against Blastomyces dermatitidis, Coccidioides immitis and Histoplasma capsulatum. Antimicrob. Agents Chemother. 44:1734-1736.

1339. Li, R. K., and M. G. Rinaldi. 1999. In vitro antifungal activity of nikkomycin Z in combination with fluconazole or itraconazole. Antimicrob. Agents Chemother. 43:1401-1405.

1350. Lindsley, M. D., S. F. Hurst, N. J. Iqbal, and C. J. Morrison. 2001. Rapid identification of dimorphic and yeast-like fungal pathogens using specific DNA probes. J Clin Microbiol. 39:3505-3511.

1484. McEwen, J. G., J. W. Taylor, D. Carter, J. Xu, M. S. S. Felipe, R. Vilgalys, T. G. Mitchell, T. Kasuga, T. White, T. Bui, and C. M. A. Soares. 2000. Molecular typing of pathogenic fungi. Med Mycol. 38:189-197.

1504. Medoff, G., W. E. Dismukes, D. Pappagianis, R. Diamond, H. A. Gallis, and D. Drutz. 1992. Evaluation of new antifungal drugs for the treatment of systemic fungal infections. Infectious Diseases Society of America and the Food and Drug Administration. Clin Infect Dis. 15 Suppl 1:S274-81.

1673. Odds, F. C. 2001. Sordarin antifungal agents. Expert Opin Ther Patents. 11:283-294.

1711. Pappagianis, D. 1993. Evaluation of the protective efficacy of the killed Coccidioides immitis spherule vaccine in humans. The Valley Fever Vaccine Study Group. Am Rev Respir Dis. 148:656-60.

1749. Peng, T., K. I. Orsborn, M. J. Orbach, and J. N. Galgiani. 1999. Proline-rich vaccine candidate antigen of Coccidioides immitis: Conservation among isolates and differential expression with spherule maturation. J Infec Dis. 179:518-521.

1821. Polesky, A., C. M. Kirsch, L. S. Snyder, P. LoBue, F. T. Kagawa, B. J. Dykstra, J. H. Wehner, A. Catanzaro, N. M. Ampel, and D. A. Stevens. 1999. Airway coccidioidomycosis - Report of cases and review. Clin Infect Dis. 28:1273-1280.

1837. Powell, B. L., D. J. Drutz, M. Huppert, and S. H. Sun. 1983. Relationship of progesterone- and estradiol-binding proteins in Coccidioides immitis to coccidioidal dissemination in pregnancy. Infect Immun. 40:478-485.

1888. Reidarson, T. H., L. A. Griner, D. Pappagiansis, and J. McBain. 1998. Coccidioidomycosis in a bottlenose dolphin. J Wildlife Dis. 34:629-631.

2202. Sutton, D. A., A. W. Fothergill, and M. G. Rinaldi (ed.). 1998. Guide to Clinically Significant Fungi, 1st ed. Williams & Wilkins, Baltimore.

2497. Ziemer, E. L., D. Pappagianis, J. E. Madigan, R. A. Mansmann, and K. D. Hoffman. 1992. Coccidioidomycosis in horses: 15 cases (1975-1984). J Am Vet Med Assoc. 201:910-6.

2498. Zimmermann, C. R., S. M. Johnson, G. W. Martens, A. G. White, B. L. Zimmer, and D. Pappagianis. 1998. Protection against lethal murine coccidioidomycosis by a soluble vaccine from spherules. Infec Immunity. 66:2342-2345.



  Home | Image Bank | Lecture Bank | Knowledgebase | Site Map | Contact Us |
The Fungi | Mycoses | Drugs |
Laboratory | Education & Tools | About Us

  bttm_banner_indv2_02[1].gif