1887

Chapter 17 : Mixed Mycotic Infections

MyBook is a cheap paperback edition of the original book and will be sold at uniform, low price.

Ebook: Choose a downloadable PDF or ePub file. Chapter is a downloadable PDF file. File must be downloaded within 48 hours of purchase

Buy this Chapter
Digital (?) $15.00

Preview this chapter:
Zoom in
Zoomout

Mixed Mycotic Infections, Page 1 of 2

| /docserver/preview/fulltext/10.1128/9781555817947/9781555812447_Chap17-1.gif /docserver/preview/fulltext/10.1128/9781555817947/9781555812447_Chap17-2.gif

Abstract:

In considering the question of mixed mycotic infections, one is faced with a number of issues related to the specific pathogenic strategies that have developed in different species and related to the phylogenetic levels of unrelatedness. First, one must consider, where relevant, the issues of commensalism, opportunism, and infection. Second, one must consider exactly what is meant by mixed colonization, or mixed infection, as it relates to genetic relatedness. Mixing can occur between kingdoms (e.g., bacteria and fungi), between genera within a kingdom (e.g., . And spp.), between species within a genus (e.g., and ), between strains within a species, and between substrains within a strain, a result of microevolution. Each of these combinations is relevant since each involves combinations of genetically distinct organisms with potentially different phenotypes, even at the substrain level. In this context, colonizing populations can also contain mixed phenotypes that are quite stable but which may be the result of high-frequency phenotypic switching systems that involve epigenetic mechanisms rather than genetic change at the level of DNA sequence. The intention of this chapter is to consider all of the levels of genetic and phenotypic mixing.

Citation: Soll D. 2002. Mixed Mycotic Infections, p 335-356. In Brogden K, Guthmiller J (ed), Polymicrobial Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817947.ch17

Key Concept Ranking

Restriction Fragment Length Polymorphism
0.4841767
Random Amplified Polymorphic DNA
0.4804234
Candida albicans
0.40046299
0.4841767
Highlighted Text: Show | Hide
Loading full text...

Full text loading...

Figures

Image of FIGURE 1
FIGURE 1

The levels of genetic relatedness (or unrelatedness) basic to mixed infections. In the scheme, mixing based on genetic differences (upper triangle) is separated from mixing due to epigenetic switching (lower triangle).

Citation: Soll D. 2002. Mixed Mycotic Infections, p 335-356. In Brogden K, Guthmiller J (ed), Polymicrobial Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817947.ch17
Permissions and Reprints Request Permissions
Download as Powerpoint
Image of FIGURE 2
FIGURE 2

Primary culture from the vaginal canal in which the bacterial colony (B) alters the morphology of closely associated colonies by inducing hypha and pseudohypha formation. Altered portions of colonies (arrowheads) and an entirely altered colony (arrow) are indicated. The changes are not hereditary (Soll and Lockhart, unpublished observation).

Citation: Soll D. 2002. Mixed Mycotic Infections, p 335-356. In Brogden K, Guthmiller J (ed), Polymicrobial Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817947.ch17
Permissions and Reprints Request Permissions
Download as Powerpoint
Image of FIGURE 3
FIGURE 3

Dendrogram generated from the s computed for every pair in a set of test isolates that included identical, highly related, and unrelated isolates, originally analyzed by Pujol et al. ( ). This set of isolates has been separated into three clusters and outliers (strains not in clusters). The unrelated and highly related ranges of s are arbitrarily set between 0.57 and 0.80 and between 0.90 and 0.99, respectively ( ). Strains were fingerprinted by Southern blot analysis with the complex probe Ca3.

Citation: Soll D. 2002. Mixed Mycotic Infections, p 335-356. In Brogden K, Guthmiller J (ed), Polymicrobial Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817947.ch17
Permissions and Reprints Request Permissions
Download as Powerpoint
Image of FIGURE 4
FIGURE 4

Collections of clonal isolates, each from a primary sample from two patients (P2 and P3), were DNA fingerprinted with the complex probe Ca3 and incorporated into a mixed dendrogram that includes a more general collection of unrelated isolates. Note how the P2 and P3 collections cluster at very high s and exhibit microevolution in each case.

Citation: Soll D. 2002. Mixed Mycotic Infections, p 335-356. In Brogden K, Guthmiller J (ed), Polymicrobial Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817947.ch17
Permissions and Reprints Request Permissions
Download as Powerpoint
Image of FIGURE 5
FIGURE 5

Surveillance of yeast colonization and drug regimen of a bone marrow transplant patient infected with two strains of in the blood and a variety of yeasts in other body locations. The origins of samples are indicated as follows: ur, urine; bl, blood; sk-b, skin blister; th, throat; st, stool. The major colony phenotypes were the following: sw, smooth white; ie, irregular edge; F, fuzzy; bh, bumpy halo. The names of the yeast colonies before identification and DNA fingerprinting are presented under “Major Colony Phenotype and Strain” (in parentheses) and with the identified species and strains. The identified species and strain, for example, C.alb-1, refer to species and strain number in order of isolation. Low-dosage (hatched bar) and maximum-dosage (solid bars) drug regimens are indicated. 5-FC, flucytosine. Modified from reference .

Citation: Soll D. 2002. Mixed Mycotic Infections, p 335-356. In Brogden K, Guthmiller J (ed), Polymicrobial Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817947.ch17
Permissions and Reprints Request Permissions
Download as Powerpoint
Image of FIGURE 6
FIGURE 6

The basic bud-hypha transition in (A) A budding cell in which the mother and daughter cell have in turn budded and are separating; (B) a cell forming a germ tube. Note the bud scars on the mother cell.

Citation: Soll D. 2002. Mixed Mycotic Infections, p 335-356. In Brogden K, Guthmiller J (ed), Polymicrobial Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817947.ch17
Permissions and Reprints Request Permissions
Download as Powerpoint
Image of FIGURE 7
FIGURE 7

Colony morphologies in the switching system in 3153A. (A) Original smooth; (B) star; (C) ring; (D) wrinkle; (E) mottled; (F) hat; (G) fuzzy; (H) revertant smooth. Reprinted from reference with permission.

Citation: Soll D. 2002. Mixed Mycotic Infections, p 335-356. In Brogden K, Guthmiller J (ed), Polymicrobial Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817947.ch17
Permissions and Reprints Request Permissions
Download as Powerpoint
Image of FIGURE 8
FIGURE 8

Isolates from sequential episodes of recurrent vaginal candidiasis caused by a single strain. (A) The original large-colony phenotype in episode 1. (B) The small- and medium-sized-colony phenotype in episode 2. DNA fingerprinting with probe Ca3 demonstrated that all colonies represented the same strain. Plating experiments demonstrated that smalland medium-sized-colony phenotype cells switched back to the large- colony phenotype. Reprinted from reference .

Citation: Soll D. 2002. Mixed Mycotic Infections, p 335-356. In Brogden K, Guthmiller J (ed), Polymicrobial Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817947.ch17
Permissions and Reprints Request Permissions
Download as Powerpoint

References

/content/book/10.1128/9781555817947.chap17
1. Anderson, J.,, L. Cundiff,, B. Schnars,, M. Gao,, I. Mackenzie,, and D. R. Soll. 1989. Hypha formation in the white-opaque transition of Candida albicans. Infect. Immun. 57:458467.
2. Anderson, J.,, R. Mihalik,, and D. R. Soll. 1990. Ultrastructure and antigenicity of the unique cell wall pimple of the Candida opaque phenotype. J. Bacteriol. 172:224235.
3. Anderson, J. M.,, T. Srikantha,, B. Morrow,, S. H. Miyasaki,, T. C. White,, N. Agabian,, J. Schmid,, and D. R. Soll. 1993. Characterization and partial nucleotide sequence of the DNA fingerprinting probe Ca3 of Candida albicans. J. Clin. Microbiol. 31:14721480.
4. Bayle, E.,, B. Pelle,, J. P. Halgrain,, K. Tran- Ky,, and K. Moussalier. 1979. Perforation duodenal a Candida albicans. Nouv. Presse Med. 8:3674.
5. Bernal, S.,, E. Martin Mazuelos,, M. Chavez,, J. Coronilla,, and A. Valverde. 1998. Evaluation of the new API Candida system for identification of the most clinically important yeast species. Diagn. Microbiol. Infect. Dis. 32:217221.
6. Boyce, J. M. H. 1975. A case of prosthetic valve endocarditis caused by Corynebacterium hogmanni and Candida albicans. Br. Heart J. 37:11951197.
7. Calderone, R. (ed.). 2002. Candida and Candidiasis. ASM Press, Washington, D.C.
8.Case Records of the Massachusetts General Hospital. 1975. Case 30-1975. N. Engl. J. Med. 293:247253.
9. de Doncker, P. R.,, R. K. Scher,, R. L. Baran,, J. Decroix,, H. J. Degreef,, D. I. Roseeuw,, V. Havu,, T. Rosen,, A. K. Gupta,, and G. E. Pierard. 1997. Itraconazole therapy is effective for pedal onychomycosis caused by some nondermatophyte molds and in mixed infection with dermatophytes and molds: a multicenter study with 36 patients. J. Am. Acad. Dermatol. 36:173177.
10. Ellner, K. M.,, M. E. McBride,, D. C. Kalter,, J. A. Tschen,, and J. E. Wolf, Jr. 1990. White piedra: evidence for a synergistic infection. Br. J. Dermatol. 123:355363.
11. Enger, L.,, S. Joly,, C. Pujol,, P. Simonson,, M. A. Pfaller,, and D. R. Soll. 2001. Cloning and characterization of a complex DNA fingerprinting probe for Candida parapsilosis. J. Clin. Microbiol. 39:658669.
12. Freund, U.,, Z. Gimmon,, and S. Katz. 1979. Candida infected ascites caused by perforated ulcer. Mycopathologia 66:191192.
13. Fries, B. C.,, D. C. Goldman,, R. Cherniak,, R. Ju,, and A. Casadevall. 1999. Phenotypic switching in Cryptococcus neoformans results in changes in the cellular morphology and glucuronoxyomannan structure. Infect. Immun. 67:60766083.
14. Galask, R. P.,, and M. J. Ohm. 1978. Bacterial flora and mycotic infections of the vagina and cervix in post-hysterectomy patients. Mykosen 1(Suppl. 1):236245.
15. Girardin, H.,, J.-P. Latge,, T. Srikantha,, B. Morrow,, and D. R. Soll. 1993. Development of DNA probes for fingerprinting Aspergillus fumigatus. J. Clin. Microbiol. 31:15471554.
16. Goldman, D.,, B. Fries,, S. Franzot,, L. Montella,, and A. Casadevall. 1998. Phenotypic switching in the human pathogenic fungus Cryptococcus neoformans is associated with changes in virulence and pulmonary inflammatory response in rodents. Proc. Natl. Acad. Sci. USA 95:1496714972.
17. Gonzalez-Lavin, L.,, E. Scappatura,, M. Lise,, and D. N. Ross. 1970. Mycotic aneurysms of the aortic root. Ann. Thorac. Surg. 9:551561.
18. Gow, N. A. 1997. Germ tube growth of Candida albicans. Curr. Top. Med. Mycol. 8:4355.
19. Gugnani, H. C.,, B. C. Okafor,, F. Nzelibe,, and A. N. Njoku-Obi. 1989. Etiological agents of otomycosis in Nigeria. Mycoses 32:224229.
20. Hairston, P.,, and W. H. Lee, Jr. 1970. Management of infected prosthetic heart valves. Ann. Thorac. Surg. 9:229237.
21. Hazen, K. C. 1995. New and emerging yeast pathogens. Clin. Microbiol. Rev. 8:462478.
22. Hellstein, J.,, H. Vawter-Hugart,, P. Fotos,, J. Schmid,, and D. R. Soll. 1993. Genetic similarity and phenotypic diversity of commensal and pathogenic strains of Candida albicans isolated from the oral cavity. J. Clin. Microbiol. 31:31903199.
23. Henderson, J.,, and J. F. Nickerson. 1964. Bacterial endocarditis with Candida albicans superinfection. Can. Med. Assoc. J. 90:452458.
24. Hitchcock, C. A.,, G. Pye,, P. F. Troke,, E. M. Johnson,, and D. W. Warnock. 1993. Fluconazole resistance in Candida glabrata. Antimicrob. Agents Chemother. 37:19621965.
25. Hube, B.,, M. Monod,, D. A. Schofield,, A. J. Brown,, and N. A. Gow. 1994. Expression of seven members of the gene family encoding secretory aspartyl proteinases in Candida albicans. Med. Microbiol. 14:8799.
26. Jabra-Rizk, M. A.,, W. A. Falker,, W. G. Merz,, A. A. Bagui,, J. I. Kelley,, and T. F. Meiller. 2000. Retrospective identification and characterization of Candida dubliniensis isolates among Candida albicans clinical laboratory isolates from human immunodeficiency virus (HIV)-infected and non-HIV-infected individuals. J. Clin. Microbiol. 38:24232426.
27. Johnson, D. E.,, M. M. Conroy,, J. E. Foker,, P. Ferrieri,, and T. R. Thompson. 1980. Candida peritonitis in the newborn infant. J. Pediatr. 97:298300.
28. Joly, S.,, C. Pujol,, M. Rysz,, K. Vargas,, and D. R. Soll. 1999. Development and characterization of complex DNA fingerprinting probes for the infectious agent Candida dubliniensis. J. Clin. Microbiol. 37:10351044.
29. Joly, S.,, C. Pujol,, K. Schroppel,, and D. R. Soll. 1996. Development and verification of two species fingerprinting probes for Candida tropicalis amenable to computer analysis. J. Clin. Microbiol. 34:30633071.
30. Jones, S.,, G. White,, and P. R. Hunter. 1994. Increased phenotypic switching in strains of Candida albicans associated with invasive infections. J. Clin. Microbiol. 32:28692870.
31. Kennedy, M. J. 1981. Inhibition of Candida albicans by the anaerobic oral flora of mice in vitro. Sabouraudia 19:205208.
32. Kennedy, M. J.,, A. L. Rogers,, L. R. Hanselman,, D. R. Soll,, and R. J. Yancey. 1988. Variation in adhesion and cell surface hydrophobicity in Candida albicans white and opaque phenotypes. Mycopathologia 102:149156.
33. Kennedy, M. J.,, and P. A. Volz. 1985. Effect of various antibiotics on gastrointestinal colonization and dissemination by Candida albicans. Sabouraudia J. Med. Vet. Mycol. 23:265273.
34. Kennedy, M. J.,, and P. A. Volz. 1985. Ecology of Candida albicans gut colonization: inhibition of Candida adhesion, colonization, and dissemination from the gastrointestinal tract by bacterial antagonism. Infect. Immun. 49:654663.
35. Kimura, M.,, H. Takahashi,, T. Satou,, and S. Hashimoto. 1989. An autopsy case of disseminated trichosporonosis with candidiasis of the urinary bladder. Virchows Arch. A Pathol. Anat. Histopathol. 416:159162.
36. Klar, A.,, T. Srikantha,, and D. R. Soll. 2001. A histone deacetylation inhibitor and mutant promote colony-type switching of the human pathogen Candida albicans. Genetics 158:919924.
37. Kleinegger, C.,, S. T. Lockhart,, K. Vargas,, and D. R. Soll. 1996. Frequency, intensity, species, and strains of oral yeast vary as a function of host age. J. Clin. Microbiol. 34:22462254.
38. Kolotila, M. P.,, and R. D. Diamond. 1990. Effects of neutrophils and in vitro oxidants on survival and phenotypic switching of Candida albicans WO-1. Infect. Immun. 58:11741179.
39. Kvaal, C.,, S. Lachke,, T. Srikantha,, K. Daniels,, J. McCoy,, and D. R. Soll. 1999. Misexpression of the opaque phase-specific gene PEP1 (SAP1) in the white phase of Candida albicans confers increased virulence in a mouse model of cutaneous infection. Infect. Immun. 67:66526662.
40. Kvaal, C. A.,, T. Srikantha,, and D. R. Soll. 1997. Misexpression of the white phase-specific gene WH11 in the opaque phase of Candida albicans affects switching and virulence. Infect. Immun. 65:44684475.
41. Lachke, S.,, T. Srikantha,, L. Tsai,, K. Daniels,, and D. R. Soll. 2000. Phenotypic switching in Candida glabrata involves phase-specific regulation of the metallothionein gene MT-II and the newly discovered hemolysin gene HLP. Infect. Immun. 68:884895.
42. Latgé, J. P. 1999. Aspergillus fumigatus and aspergillosis. Clin. Microbiol. Rev. 12:310350.
43. Lisiak, M.,, C. Klyszejko,, Z. Marcinkowski,, and Z. Gwiezdzinski. 2000. Yeast species identification in vulvovaginal candidiasis: susceptibility to nystatin. Ginekol. Pol. 71:959963.
44. Lockhart, S.,, J. J. Fritch,, A. S. Meier,, K. Schroppel,, T. Srikantha,, R. Galask,, and D. R. Soll. 1995. Colonizing populations of Candida albicans are clonal in origin but undergo microevolution through C1 fragment reorganization as demonstrated by DNA fingerprinting and C1 sequencing. J. Clin. Microbiol. 33:15011509.
45. Lockhart, S. R.,, S. Joly,, C. Pujol,, J. D. Sobel,, M. A. Waller,, and D. R. Soll. 1997. Development and verification of fingerprinting probes for Candida glabrata. Microbiology 143:37333746.
46. Lockhart, S. R.,, S. Joly,, K. Vargas,, J. Swails-Wenger,, L. Enger,, and D. R. Soll. 1999. Natural defenses against Candida colonization breakdown in the oral cavities of the elderly. J. Dent. Res. 78:857868.
47. Lockhart, S. R.,, B. D. Reed,, C. L. Pierson,, and D. R. Soll. 1996. Most frequent scenario for recurrent Candida vaginitis is strain maintenance with “substrain shuffling”: demonstration by sequential DNA fingerprinting with probes Ca3, C1, and CARE2. J. Clin. Microbiol. 34:767777.
48. Lott, T. J.,, D. A. Logan,, B. P. Holloway,, R. Fundyga,, and J. Arnold. 1999. Towards understanding the evolution of the human commensal yeast, Candida albicans. Microbiology 145:11371143.
49. Mehta, A. B.,, H. R. Mahajam,, D. D. Vora,, A. C. Shah,, and A. B. Agarwala. 1970. Comparative evaluation of antifungal agents in the prevention of tetracycline-induced candidiasis of gastrointestinal tract. J. Assoc. Physicians India 18:621626.
50. Meyers, J. D. 1990. Fungal infections in bone marrow transplant patients. Semin. Oncol. 17:1013.
51. Mohapatra, L. N.,, K. Ramachandran,, J. C. M. Shastry,, and B. M. Tandon. 1969. Prophylactic use of amphotericin B for Candida infection amongst patients on broad-spectrum antibiotic treatment. Indian J. Med. Res. 57:128132.
52. Morrow, B.,, T. Srikantha,, and D. R. Soll. 1992. Transcription of the gene for a pepsinogen, PEP1, is regulated by white-opaque switching in Candida albicans. Mol. Cell. Biol. 12:29973005.
53. Mullins, J.,, P. Hutchinson,, and R. G. Slavin. 1984. Aspergillus fumigatus spore concentrations in outside air: Cardiff and St. Louis compared. Clin. Allergy 14:251254.
54. Neuveglise, C.,, J. Sarfati,, J. P. Debeaupuis,, H. Vu Thien,, J. Just,, G. Tournier,, and J. P. Latge. 1997. Longitudinal study of Aspergillus fumigatus strains isolated from cystic fibrosis patients. Eur. J. Clin. Microbiol. Infect. Dis. 16:747750.
55. Niebel, J.,, U. Farack,, and V. Mursic. 1984. Bacterial-mycotic liver abscess in nonimmunocompromised host. Infection 12:256257.
56. Odds, F. C. 1988. Candida and Candidosis: a Review and Bibliography. Bailliere Tindall, London, United Kingdom.
57. Odds, F. C. 1997. Switch of phenotype as an escape mechanism of the intruder. Mycoses 40:S9S12.
58. Odds, F. C.,, and R. Bernaerts. 1994. CHROMagar Candida, a new differential isolation medium for presumptive identification of clinically important Candida species. J. Clin. Microbiol. 32:19231929.
59. Ohm, M. J.,, and R. P. Galask. 1975. Bacterial flora of the cervix from 100 prehysterectomy patients. Am. J. Obstet. Gynecol. 122:683687.
60. Perez-Martin, J.,, J. A. Uria,, and A. D. Johnson. 1999. Phenotypic switching in Candida albicans is controlled by a SIR2 gene. EMBO J. 18:25802592.
61. Perrenoud, J. J.,, and G. Lanitis. 1976. La septicemie a levures en chirurgie. Rev. Med. Suisse Romande 96:923930.
62. Pfaller, M. A.,, A. Houston,, and S. Coffmann. 1996. Application of CHROMagar Candida for rapid screening of clinical specimens for Candida albicans, Candida tropicalis, and Candida (Torulopsis) glabrata. J. Clin. Microbiol. 34:5861.
63. Pfaller, M. A.,, R. N. Jones,, S. A. Messer,, M. B. Edmond,, R. P. Wenzel,, and S. P. Group. 1988. National surveillance of nosocomial blood stream infection due to species of Candida albicans: frequency of occurrence and antifungal susceptibility in the SCOPE Program. Diagn. Microbiol. Infect. Dis. 30:121129.
64. Pomes, R.,, C. Gil,, and C. Nombela. 1985. Genetic analysis of Candida albicans morphological mutants. J. Gen. Microbiol. 131:21072113.
65. Pujol, C.,, S. Joly,, S. Lockhart,, S. Noel,, M. Tibayrenc,, and D. R. Soll. 1997. Parity of MLEE, RAPD, and Ca3 hybridization as fingerprinting methods for Candida albicans. J. Clin. Microbiol. 35:23482358.
66. Pujol, C.,, S. Joly,, B. Nolan,, T. Srikantha,, S. Lockhart,, and D. R. Soll. 1999. Microevolutionary changes in Candida albicans identified by the complex Ca3 probe involve insertions and deletions of RPS units at specific genomic sites. Microbiology 145:26352646.
67. Redondo-Lopez, V.,, C. Meriwether,, C. Schmitt,, M. Opitz,, R. Cook,, and J. D. Sobel. 1990. Vulvovaginal candidiasis complicating recurrent bacterial vagnosis. Sex Transm. Dis. 17:5153.
68. Sadhu, C.,, M. J. McEachern,, E. P. Rustchenko-Bulgac,, J. Schmid,, D. R. Soll,, and J. Hicks. 1991. Telomeric and dispersed repeat sequences in Candida yeasts and their use in strain identification. J. Bacteriol. 173:842850.
69. San-Milian, R.,, L. Ribacoba,, J. Ponton,, and G. Quindos. 1996. Evaluation of a commercial medium for identification of Candida species. J. Clin. Microbiol. Infect. Dis. 15:153158.
70. Schmid, J.,, E. Voss,, and D. R. Soll. 1990. Computer-assisted methods for assessing strain relatedness in Candida albicans by fingerprinting with the moderately repetitive sequence Ca3. J. Clin. Microbiol. 28:12361243.
71. Shastry, J. C.,, K. Ramachandran,, L. N. Mohapatra,, and B. N. Tandon. 1969. A study of Candida in throat swabs and gastrointestinal tract of the patients on broad-spectrum antibiotic or steroid treatment. Indian J. Med. Res. 57:133140.
72. Slutsky, B.,, J. Buffo,, and D. R. Soll. 1985. High frequency switching of colony morphology in Candida albicans. Science 230:666669.
73. Slutsky, B.,, M. Staebell,, J. Anderson,, L. Risen,, M. Pfaller,, and D. R. Soll. 1987. “White-opaque transition”: a second high-frequency switching system in Candida albicans. J. Bacteriol. 169:189197.
74. Sobel, J. D.,, and W. Chaim. 1997. Treatment of Torulopsis glabrata vaginitis: retrospective review of boric acid therapy. Clin. Infect. Dis. 24:649652.
75. Soll, D. R. 1986. The regulation of cellular differentiation in the dimorphic yeast Candida albicans. Bioessays 5:511.
76. Soll, D. R. 1992. High frequency switching in Candida albicans. Clin. Microbiol. Rev. 5:188203.
77. Soll, D. R., 1992. Switching and its possible role in Candida pathogenesis, p. 156172. In J. E. Bennett,, R. J. Hay,, and P. K. Peterson (ed.), New Fungal Strategies. Churchill Livingstone, Edinburgh, Scotland.
78. Soll, D. R. 2000. The ins and outs of DNA fingerprinting the infectious fungi. Clin. Microbiol. Rev. 13:332370.
79. Soll, D. R., 2001. The molecular biology of switching in Candida, p. 161182. In R. A. Calderone, and R. L. Cihlar (ed.), Fungal Pathogenesis: Principles and Clinical Application. Marcel Dekker, New York, N.Y.
80. Soll, D. R., 2002. Phenotypic switching, p. 123142. In R. Calderone (ed.), Candida and Candidiasis. ASM Press, Washington, D.C.
81. Soll, D. R.,, J. Anderson,, and M. Bergen,. 1991. The developmental biology of the whiteopaque transition in Candida albicans, p. 2045. In R. Prasad (ed.), Candida albicans: Cellular and Molecular Biology. Springer-Verlag KG, Berlin, Germany.
82. Soll, D. R.,, R. Galask,, S. Isley,, T. V. G. Rao,, D. Stone,, J. Hicks,, J. Schmid,, K. Mac,, and C. Hanna. 1989. “Switching” of Candida albicans during successive episodes of recurrent vaginitis. J. Clin. Microbiol. 27:681690.
83. Soll, D. R.,, R. Galask,, J. Schmid,, C. Hanna,, K. Mac,, and B. Morrow. 1991. Genetic dissimilarity of commensal strains of Candida spp. carried in different anatomical locations of the same healthy women. J. Clin. Microbiol. 29:17021710.
84. Soll, D. R.,, C. J. Langtimm,, J. McDowell,, J. Hicks,, and R. Galask. 1987. High-frequency switching in Candida strains isolated from vaginitis patients. J. Clin. Microbiol. 25:16111622.
85. Soll, D. R.,, S. R. Lockhart,, and C. Pujol,. Laboratory procedures for the epidemiological analysis of microorganisms. In P. R. Murray,, E. J. Baron,, M. A. Pfaller,, F. C. Tenover,, and R. H. Yolken (ed.), Manual of Clinical Microbiology, 8th ed., in press. American Society for Microbiology, Washington, D.C.
86. Soll, D. R.,, M. Staebell,, C. J. Langtimm,, M. Pfaller,, J. Hicks,, and T. V. G. Rao. 1988. Multiple Candida strains in the course of a single systemic infection. J. Clin. Microbiol. 26:14481459.
87. Spinillo, A.,, A. M. Bernuzzi,, C. Cevini,, R. Gulminetti,, S. Luzi,, and A. De Santalo. 1997. The relationship of bacterial vaginosis, Candida and Trichomonas infection to symptomatic vaginitis in postmenopausal women attending a vaginitis clinic. Maturitas 27:253260.
88. Srakaki, F. M.,, M. Higa,, M. Tateyama,, Y. Yamozato,, T. Ishimine,, M. Toyama,, T. Miyara,, M. Koide,, and A. Saito. 1999. Concurrent infection with Legionella pneumophila and Pneumocystis carinii in a patient with T cell leukemia. Intern. Med. 38:160163.
89. Srikantha, T.,, L. K. Tsai,, A. Klar,, and D. R. Soll. 2001. The histone deacetylases HDA1 and RPD3 play distinct roles in the regulation of highfrequency phenotypic switching in Candida albicans. J. Bacteriol. 183:46144625.
90. Steelig, M. S. 1996. Mechanisms by which antibiotics increase the incidence and severity of candidiasis and alter the immunological defenses. Bacteriol. Rev. 30:442459.
91. Vajpayee, R. B.,, N. Sharma,, M. Chand,, G. C. Tabin,, M. Vajpayee,, and J. R. Anand. 1998. Corneal superinfection in acute hemorrhagic conjunctivitis. Cornea 17:614617.
92. Valenti, S.,, C. Vignolo,, E. Benevolo,, and F. Braido. 1996. Mixed infection by Staphylococcus and Candida, and Wigener’s granulomatosis. Mon. Arch. Chest Dis. 51:387390.
93. Vargas, K. 1998. Molecular epidemiology of Candida albicans in patients with AIDS. Ph.D. thesis. University of Iowa, Iowa City.
94. Vargas, K. G.,, S. A. Messer,, M. A. Pfaller,, S. R. Lockhart,, J. T. Stapleton,, J. Hellstein,, and D. R. Soll. 2000. Elevated phenotypic switching and drug resistance of Candida albicans from human immunodeficiency virus-positive individuals prior to first thrush episode. J. Clin. Microbiol. 38:35953607.
95. Vargas, K.,, P. W. Wertz,, D. Drake,, B. Morrow,, and D. R. Soll. 1994. Differences in adhesion of Candida albicans 3153A cells exhibiting switch phenotypes to buccal epithelium and stratum corneum. Infect. Immun. 62:13281335.
96. White, T. C.,, K. A. Marr,, and R. A. Bowden. 1998. Clinical, cellular, and molecular factors that contribute to antifungal drug resistance. Clin. Microbiol. Rev. 11:382402.
97. White, T. C.,, S. H. Miysaki,, and N. Agabian. 1993. Three distinct secreted aspartyl proteinases in Candida albicans. J. Bacteriol. 175:61266133.
98. White, T. C.,, M. A. Pfaller,, M. G. Rinaldi,, J. Smith,, and S. W. Bedding. 1997. Stable azole drug resistance associated with a substrain of Candida albicans from an HIV-infected patient. Oral Dis. 3:S102S109.
99. Willinger, B.,, and M. Manafi. 1999. Evaluation of CHROMagar Candida for rapid screening of clinical specimens for Candida species. Mycoses 42:6165.
100. Winner, H. I.,, and R. Hurley. 1964. Candida albicans. Churchill, London, United Kingdom.
101. Xu, J.,, C. M. Boyd,, E. Livingston,, W. Meyer,, J. F. Mudden,, and T. G. Mitchell. 1999. Species and genotypic diversity and similarities of pathogenic yeasts colonizing women. J. Clin. Microbiol. 37:38353843.

Tables

Generic image for table
TABLE 1

Summary of carriage of spp. in 17 body locations of 52 healthy young women

Citation: Soll D. 2002. Mixed Mycotic Infections, p 335-356. In Brogden K, Guthmiller J (ed), Polymicrobial Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817947.ch17
Generic image for table
TABLE 2

Proportions of posthysterectomy patients carrying bacteria and yeast

Citation: Soll D. 2002. Mixed Mycotic Infections, p 335-356. In Brogden K, Guthmiller J (ed), Polymicrobial Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817947.ch17
Generic image for table
TABLE 3

Species and intensities of carriage in healthy individuals over 70 years of age

Citation: Soll D. 2002. Mixed Mycotic Infections, p 335-356. In Brogden K, Guthmiller J (ed), Polymicrobial Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817947.ch17
Generic image for table
TABLE 4

Microevolution in commensal and pathogenic populations revealed by C1 fingerprinting of

Citation: Soll D. 2002. Mixed Mycotic Infections, p 335-356. In Brogden K, Guthmiller J (ed), Polymicrobial Diseases. ASM Press, Washington, DC. doi: 10.1128/9781555817947.ch17

This is a required field
Please enter a valid email address
Please check the format of the address you have entered.
Approval was a Success
Invalid data
An Error Occurred
Approval was partially successful, following selected items could not be processed due to error