JOURNAL OF CLINICAL MICROBIOLOGY, May 1989, p.

927-931

Vol. 27, No. 5

0095-1137/89/050927-05$02.00/0
Copyright (O 1989, American Society for Microbiology

Clinical, Microbiological, and Experimental Animal Studies of

Candida lipolytica
THOMAS J. WALSH 1.2.3* IRA F. SALKIN,4 DENNIS M. DIXON,4 AND NANCY J. HURD4
Infectious Diseases Section, National Cancer Institute, Bethesda, Maryland 208921*; Baltimore Veterans Administration
Medical Center, Baltimore, Maryland 212182; Department of Medicine, University of Maryland School of Medicine,
Baltimore, Maryland 212013; and Wadsworth Center for Laboratories and Research, New York State
Department of Health, Albany, New York 122014
Received 28 July 1988/Accepted 28 December 1988

Candida lipolytica (Harrison) Diddens et Lodder has

seldom been identified as a cause of infection. When
fungemia caused by C. lipolytica developed in one of our
patients, we found that there was no single study which
examined the clinical manifestations, microbiological features, and in vivo characteristics of this fungus. C. lipolytica
was not included in several large case series as a cause of
fungemia (3, 7, 8, 13). Only one well-described case of
fungemia (18) and three cases of traumatic ocular infection
(11) caused by C. lipolytica have been reported previously.
While the morphological and physiological properties of C.
lipolytica have been described in standard monographs (2,
10), little is known about the characteristics of C. lipolytica
in the new rapid diagnostic systems for yeasts. There are
virtually no studies of the in vitro susceptibility of C.
lipolytica to antifungal agents. Finally, with the exception of
one study in which a strain from a nonclinical source was
used (6), there were no reported in vivo studies in which the
virulence of C. lipolytica has been evaluated.
Since relatively little was known about C. lipolytica, we
studied the clinical features of six cases of infection or
colonization involving C. lipolytica, investigated the morphological characteristics and biochemical properties of 26
isolates, and evaluated the antifungal susceptibilities of 9
isolates of this yeastlike fungus. We particularly examined
the properties of these isolates of C. lipolytica in a new rapid
yeast identification systems. We also studied the virulence of
the isolate that caused clinical fungemia in experimental
animals. Since clinical isolates of C. lipolytica were misidentified as Candida ingens van der Walt et van Kerken, we also
studied the clinical microbiological features of this saprobic
fungus in comparison with those of C. lipolytica.

Center, Baltimore, Md.; University of Maryland Medical

Systems, Baltimore; or the Clinical Center of the National
Institutes of Health, Bethesda, Md. Cases of infection were
classified as fungemia, localized infection, or colonization.
(i) Fungemia. Fungemia and suppurative thrombophlebitis
developed in a 54-year-old male with a history of alcohol
abuse who underwent cholecystectomy for cholelithiasis and
cholecystitis. After cholecystectomy and placement of a T
tube in the common bile duct, he received six different
antibacterial agents in different combinations over 26 days
for cholangitis. Blood cultures obtained on day 27 of hospitalization for a fever of 39.2C grew a pure culture of a germ
tube-negative Candida sp. in a bottle (6 A) of a radiometric
blood culture system (BACTEC 460; Becton-Dickinson Diagnostic Instrument Systems, Towson, Md.) after 24 h of
incubation at 35C. Although the isolate was identified
initially as C. ingens, further studies with the API 20C
system (Analytab Products, Plainview, N.Y.) confirmed its
identification as C. lipolytica (5697-82). Several colonies that
were sampled yielded consistent results indicating that they
were C. lipolytica. Antifungal therapy was not administered
at this time or later in the hospitalization.
An intravenous catheter-associated thrombophlebitis of
the right forearm was found on day 28 of hospitalization. The
catheter was removed, and a Trypticase soy broth (BBL
Microbiology Systems, Cockeysville, Md.) culture inoculated with a purulent discharge from the venipuncture site
yielded C. lipolytica. Fever persisted and another set of
blood cultures obtained on day 32 of hospitalization grew C.
lipolytica in the BACTEC system. No other organisms were
cultured.
Daily physical examinations performed from the time of
detection of fungemia revealed no chorioretinal or cutaneous
lesions, no cardiac murmurs, and no hemodynamic instability. There was no azotemia, and urine cultures showed no C.
lipolytica. Although the erythema, swelling, and tenderness
of the peripheral thrombophlebitis decreased, fever persisted and a third set of blood cultures obtained on day 39
yielded C. lipolytica. Thrombophlebitis and fever resolved

MATERIALS AND METHODS

Cases. The six clinical cases of C. lipolytica infection were

identified between 1980 and 1987 at one of the following
institutions: Baltimore Veterans Administration Medical
*

Corresponding author.
927

Downloaded from http://jcm.asm.org/ on September 30, 2015 by guest

Candida lipolytica was recovered from six patients in three different clinical centers. The index isolate caused
persistent fungemia with catheter-associated Candida thrombophlebitis, the second isolate was from a
polymicrobial sinusitis, and the remaining four isolates were involved in tissue colonization. These and 20 other
isolates were consistent in their morphological and physiological characteristics. Ail formed true hyphae and
blastoconidia on cornmeal-Tween 80 agar and all assimilated glucose, glycerol, and erythritol. In a murine
model of disseminated candidiasis, the index isolate that caused clinical fungemia caused no mortality and
produced only two lesions on a kidney, as determined at necropsy. The nine isolates selected for in vitro
antifungal susceptibility studies had interniediate susceptibilities to amphotericin B but were susceptible to
ketoconazole. We conclude that C. lipolytica is a weakly virulent pathogen which may require an intravascular
foreign body to cause fungemia.
a

928

WALSH ET AL.

and two more sets of blood cultures were negative. The

patient was discharged, and no evidence of recurrent or
disseminated infection was found during 7 months of followup care.

TABLE 1. Codes and sources of isolates of C. lipolytica

and C. ingens

Organism and

Site

code no.

C. lipolytica
2029-79
2751-82
605-84
565-84
NYS 98A
NYS 103
1250-85
1542-85
16-86
1034-86
84M27
84M28
84M29
84M245
85MR89
YB423

YB423-3
5697-82
7755-83
118-88
119-88
120-88
121-88
122-88
123-88
124-88

Unknown

Sputum
Left leg
Sputum
Unknown
Unknown
Skin rash scrapings
Unknownb

Sputum

Bronchial washing
Unknown'
Unknown'

Unknownc
Unknown'

Unknownc
Corn processing plant
Unknown
Blood

Sputum
Sinus aspirate

Oropharynx
Stool

Oropharynx
Unknown
Unknown
Unknown

Source"

NYSDH
NYSDH
NYSDH
NYSDH
NYSDH
NYSDH
NYSDH
NYSDH
NYSDH
NYSDH
API 20C
API 20C
API 20C
API 20C
API 20C
NRRL and ATCC

(ATCC 18942)
(Yarrowia lipolytica;
type culture)
NRRL and ATCC 18943
BVAMC
BVAMC
NYSDH
NYSDH
NYSDH
NYSDH
NYSDH
NYSDH
NYSDH

C. ingens

Y6053
Y7796
Y7797
Y7930
Y10939

Unknown
Unknown
Unknown

Piggery waste
Kamaboko (minced fish)

NRRL
NRRL
NRRL
NRRL
NRRL

" NYSDH, New York State Department of Health; API 20C, Analytab
Products; NRRL, Northern Regional Research Laboratory (now designated
the Agricultural Research Service), U.S. Department of Agriculture; ATCC,
American Type Culture Collection, Rockville, Md.; BVAMC, Baltimore
Veterans Administration Medical Center.
'Proficiency test isolate; New York State Department of Health.
Isolates used as standards in API 20C kit (Analytab Products).

The susceptibilities of the same C. lipolytica isolates to

ketoconazole (Nizoral; Janssen Pharmaceutica, Piscataway,
N.J.) were assessed with an agar dilution series (4, 5). A
yeast cell suspension was prepared as described above, and
the concentration was adjusted to 85% transmission at 530
nm with a spectrophotometer; this corresponded to 3.4 x 106
cells per ml. A portion of the suspension was added to the
surface of nutrient agar plates containing a twofold serial
dilution series of ketoconazole ranging from 40 to 2 x 1i-O
p.g/ml. Kluyveromyces marxianus var. marxianus (Hansen)
van der Walt (NYS 110A) served as a control for all studies.
The assays for amphotericin B and ketoconazole were
developed as separate assays (4, 5) in which different inoculum preparation methods were used. Although the wavelengths and percent transmission for the preparation of
inocula were different for amphotericin B and ketoconazole,
the final concentrations of cells measured with a hemacytometer were similar.
The virulence of the fungemia isolate (isolate 5697-82) was
studied in a murine model of experimental disseminated

Downloaded from http://jcm.asm.org/ on September 30, 2015 by guest

(i) Localized infection. A 46-year-old female presented

with an acute exacerbation of chronic sinusitis. Radiographs
of the paranasal sinuses revealed opacifications of the left
maxillary sinus. A Gram stain of the specimen revealed
inflammatory cells, bacteria, and occasional budding yeasts
and hyphae. Cultures inoculated with the sinus aspirate
material on several media, including 5% sheep blood-Trypticase soy agar, Sabouraud glucose agar with chloramphenicol and gentamicin, and brain heart infusion broth with
chloramphenicol and gentamicin yielded Staphylococcus
aureus Rosenbach, Pseudomonas aeruginosa (Schroeter)
Migula, and C. lipolytica (118-88). Since postnasal discharge
continued despite antibacterial therapy, ketoconazole (200
mg orally) was initiated to treat the fungal component of the
infection. The patient reported improvement of symptoms
within 1 month after ketoconazole therapy was started. C.
lipolytica was not recovered again after the completion of
the course of ketoconazole.
(iii) Colonization. Stool (120-88), oropharyngeal swab
(119-88, 121-88), and sputum (7755-83) specimens from four
patients with no evidence of invasive candidiasis yielded C.
lipolytica.
Test organisms. Twenty isolates of C. lipolytica from
various sources were provided from collections of the Maryland State Health Laboratories; the University of Maryland
School of Medical Technology; and the Laboratories for
Mycology, Wadsworth Center for Laboratories and Research, New York State Department of Health. Cletus
Kurtzman of the Northern Regional Research Center, U.S.
Department of Agriculture, provided five isolates of C.
ingens (Table 1). These and a single isolate from each of the
patients discussed above were maintained at 4C on Sabouraud glucose agar and serially transferred at monthly
intervals to fresh nutrient medium.
Microbiological studies. For all microbiological studies, a
portion of growth from a stock culture of each isolate was
transferred aseptically to fresh Sabouraud glucose agar and
incubated for 72 h at 27C. The morphological features of all
isolates were studied by inoculating a portion of each 72h-old culture onto cornmeal-Tween 80 agar in 100-mmdiameter petri plates. Their assimilation and enzyme profiles
were investigated with the API 20C and Yeast-Ident yeast
identification kits (Analytab Products). The commercial
products were inoculated with colonies from a 72-h-old
culture, and the tests were conducted as directed by the
manufacturer. In addition, conventional methods were used
to study the following characteristics of the isolates: urease
activity; glucose fermentation; and assimilation of erythritol,
galactose, and growth in vitamin-free medium (15).
The in vitro susceptibilities on nine isolates to amphotericin B (Fungizone IV; E. R. Squibb & Sons, Princeton, N.J.)
were evaluated by a tube dilution procedure (4). A suspension of yeast cells of each isolate was prepared by flooding a
72-h-old Sabouraud glucose agar slant with sterile distilled
water and adjusting the final concentration to 50% transmission at 650 nm with a spectrophotometer (Beckman Instruments, Inc., Fullerton, Calif.); this corresponded to 1.8 x
107 cells per ml, as determined with a hemacytometer. A
portion of the suspension was then added to each tube of a
twofold serial dilution series of amphotericin B ranging from
4.0 to 1.9 x 10-3 ,ug/ml. Candida albicans (Robin) Berkhout
(Squibb 1539) served as a control for ahl studies.

J. CLIN. MICROBIOL.

CANDIDA LIPOL YTICA

VOL. 27, 1989

RESULTS
Morphological and physiological studies. C. lipolytica
formed distinctive cerebriform, convoluted, white, firm colonies on Sabouraud glucose agar (Fig. 1). All C. lipolytica
isolates formed narrow, multibranched, true hyphae on
cornmeal-Tween 80 agar. Blastoconidia, which generally
developed only after several days of incubation, were found
at the apices and less commonly along the length of the
hyphae. In contrast, isolates of C. ingens on the same
medium formed chains of budding yeast cells and broad
pseudohyphae without blastoconidia. No true hyphae were
observed in the cultures of C. ingens on cornmeal-Tween 80
agar.
As a group, the isolates of C. lipolytica were physiologically consistent. Ail were urease positive and none fermented glucose. In conventional Wickerham assimilation
tests, all isolates assimilated glucose, glycerol, and erythritol. None utilized galactose, with the exception of one
isolate (isolate 121-88), which was weakly positive for galactose assimilation. Growth was negative or weakly positive in
vitamin-free medium for all isolates with the exception of
one isolate (isolate 120-88), which was positive. Maximum
growth temperatures fared between 35 and 37C, with the
exception of that for one isolate, which did not grow at 30C.
The isolate that caused fungemia grew at 37C during three
trials and at 35C during a fourth trial. Isolates gave either a
6-002-100 code or a 6-000-100 code when grown in the API
20C system. Both of the API 20C codes indicated that there
was a good likelihood that C. lipolytica was the organism.
All isolates were identified with the Yeast-Ident kit as C.
lipolytica with biocodes of 2-067-573 (good likelihood; C.
lipolytica most probable), 2-067-173 (good likelihood; C.

FIG. 1. Typical colony of C. lipolytica derived from point inoculation and incubated for 6 days at 270C on Sabouraud glucose agar
supplemented with penicillin and streptomycin.

lipolytica

most

probable), 2-167-573 (good identification for

lipolytica), and 2-167-173 (acceptable identification for C.

lipolytica).
Isolates of C. ingens were physiologically more variable
than those of C. lipolytica. Three of five isolates were urease

C.

positive. None fermented glucose and none assimilated

erythritol, as determined by the conventional Wickerham
assimilation test. Two isolates (isolates Y-7796 and Y-7797)
assimilated galactose within 72 h of inoculation in the
Wickerham test, but the remaining three isolates (isolates
Y-7930, Y-6053, and Y-10939) only began to utilize this
carbohydrate source after 7 to 10 days of inoculation in the
Wickerham test. While two isolates (isolates Y-7796 and
Y-7797) could not develop in a vitamin-free broth, the other
three isolates developed rapidly in this medium. A code of
6-040-000 was found with four isolates in the API 20C kit and
a code of 6-000-000 was noted with the remaining isolate.
Since C. ingens was not included in the API 20C data base,
these codes merely indicated variations in the assimilation
capabilities of the test isolates. Similar differences were
observed with the Yeast-Ident system, in which C. ingens
also was not included in the data base. Two isolates (isolates
Y-6053 and Y-10939) were identified by the Yeast-Ident kit
as Candida tropicalis (Castellani) Berkhout, and one (isolate
Y-7797), was identified as Candida guillermondi (Castellani)
Langeron et Guerra. No corresponding codes could be found
for the two remaining isolates (isolates Y-7930 and Y-7796).
In vitro antifungal susceptibility. The mean MIC of amphotericin B after 24 h of incubation of the nine test isolates of
C. lipolytica was 0.660 ,ug/ml (range, 0.313 to 1.25 ,ug/ml).
All test isolates were susceptible to ketoconazole, which had
a mean MIC of 0.22 ,ug/ml (range, 0.078 to 0.313 ,ug/ml). The
MICs for each isolate are presented in Table 2.
Virulence. All mice receiving C. albicans died of disseminated candidiasis within the 2-week experimental period.
Autopsy revealed multiple abscesses caused by C. albicans
in brain, liver, spleen, and kidneys. In contrast, all mice

Downloaded from http://jcm.asm.org/ on September 30, 2015 by guest

candidiasis. This isolate was preserved (after one subculture) in sterile distilled water at 4C. A clinical isolate (UM
83-7700) of C. albicans (Robin) Berkhout served as the
virulence control. A portion of growth of each test isolate
was aseptically streaked over the surface of a Sabouraud
glucose agar plate and grown overnight at 37C. A single
isolated colony was removed with a sterile loop and aseptically transferred to 50 ml of glucose-peptone-yeast extract
broth contained in a 250-ml Erlenmeyer flask and grown in a
gyrarotary shaker at 120 rpm for 2 h at 37C. Five milliliters
of broth from the flask was then aseptically removed with a
pipette, transferred to each of four similarly prepared Erlenmeyer flasks, and grown overnight at 37C. The entire broth
volume of each Erlenmeyer flask was centrifuged at 9,200 x
g for 15 min at 4C. The pellets were suspended and washed
three times in sterile normal saline. The concentration of
cells was adjusted with a hemacytometer to an inoculum
10-fold dilution series of 104 to 108 CFU. The concentrations
were confirmed by quantitative colony counts on Sabouraud
glucose agar plates inoculated with 10-fold serial dilutions of
each inoculum concentration.
Groups of two male CD-1 mice (Charles River, Breeding
Laboratories, Inc., Wilmington, Mass.) each received 0.1 ml
of one of the five 10-fold dilution series of each inoculum of
each fungus via the lateral tail vein. All mice were housed,
maintained, and treated as described in the Guide for the
Care and Use of Laboratory Animals (Publication 85-23,
National Institutes of Health, Bethesda, Md.). Mice were
euthanized when they were moribund; the remaining mice
were euthanized at 14 days after inoculation. Brain, liver,
spleen, and kidneys were examined postmortem and cultured quantitatively.

929

930

J. CLIN. MICROBIOL.

WALSH ET AL.

TABLE 2. In vitro susceptibility of C. lipolytica to

amphotericin B and ketoconazole
MIC (,ug/mlj

Accession no.

118-88
119-88

120-88
121-88
122-88
123-88
124-88
5697-82
7755-83

Amphotericin B

Ketoconazole

0.313
0.313
1.25

0.078
0.313
0.156
0.156
0.313
0.156
0.078
0.313
0.313

0.625
0.625
0.625
0.313
0.625
1.25

DISCUSSION
C. lipolytica is a weak pathogen that is associated most
clearly with vascular catheter-related fungemia. The 26
isolates of C. lipolytica examined in this study demonstrated
consistent morphological and physiological characteristics.
The C. lipolytica isolates could be differentiated easily from
the more physiologically variable isolates of C. ingens by
colonial morphology, formation of true hyphae on cornmealTween 80 agar, and an inability to assimilate galactose as the
sole carbon source. To our knowledge, C. ingens has not
been described as a human pathogen.
The absence of clinically overt deep visceral infection in
the index patient with persistent fungemia and the favorable
outcome without the use of antifungal therapy suggests that
C. lipolytica is a weakly virulent pathogen. This observation
is further substantiated by the report of Wherspann and
Fullbrandt (18), who described another case of fungemia
caused by C. lipolytica. That patient also had fungemia
without evidence of deep visceral infection, such as endophthalmitis, osteomyelitis, arthritis, or hepatic infection. Moreover, the absence of mortality and development of only two
lesions on one of many visceral organs sampled from mice
inoculated with C. lipolytica indicates that this species is
weakly virulent.
The index case reported here and the other documented
case (18) of C. lipolytica fungemia were associated with
intravenous catheter infections. These two cases suggest
that a vascular catheter may be required for the introduction
of C. lipolytica into the bloodstream. Although the infected
venous catheter was removed from the index patient,
fungemia persisted. This persistent fungemia was likely
caused by an infected catheter-associated mural thrombus
(14, 16, 17). Segmental peripheral venous resection often is
effective in eliminating Candida thrombophlebitis as a
source of candidemia.
In our opinion, most cases of vascular catheter-associated
candidemia should be treated with a course of amphotericin
B and, when possible, the vascular catheter should be
removed because of the risks of subsequent hematogenous

lipolytica infections.
The results of this investigation of C. lipolytica indicate
that (i) C. lipolytica is a weakly virulent pathogen associated
with vascular catheter infections, (i) C. lipolytica is less
virulent in experimental animals than is C. albicans, (iii)
isolates of C. lipolytica, are susceptible in vitro to amphotericin B as well as to ketoconazole, and (iv) isolates of C.
lipolytica demonstrate generally consistent morphological
and physiological characteristics.
ACKNOWLEDGMENTS
We thank Ed Lapa for assistance in conducting the in vitro
antifungal susceptibility studies. We thank Sharon Hansen, Marcia
Moody, Frank Witebsky, Cletus Kurtzman, Nancy Hooper, Sherril
Ross, and Lynn Still for identifying and providing isolates of C.

Downloaded from http://jcm.asm.org/ on September 30, 2015 by guest

inoculated with C. lipolytica survived the experimental

period. Two abscesses were found postmortem in the left
kidney of a mouse that received the highest inoculum (108
CFU). Cultures inoculated with portions of the kidney tissue
yielded C. lipolytica. No fungus was revealed in quantitative
cultures of tissue from other organs of this mouse or from
any of the other mice inoculated with C. lipolytica. Since the
infected kidney specimen was processed for quantitative
cultures, histopathological studies were not performed.

Candida endophthamitis and othr complications of untreated candidemia. However, to our knowledge C. lipolytica has not been associated with deep visceral infections,
such as hematogenous endophthalmitis or hepatosplenic
candidiasis.
Given the low virulence of C. lipolytica, one must question whether removal of a vascular catheter without the
concomitant administration of amphotericin B would be
appropriate management of catheter-associated candidemia
caused by this organism. Infections in both our patient and
the previously reported patient with C. lipolytica fungemia
(18) were associated with vascular catheters and neither was
apparently complicated by a deep visceral infection. Nevertheless, until more experience is acquired in managing this
infection, we suggest that catheter-associated C. lipolytica
fungemia be managed in a similar manner as that of other
Candida spp. fungemias: a course of systemic antifungal
therapy and removal of potentially infected vascular catheters.
Amphotericin B is the cornerstone of treatment of candidemia caused by susceptible Candida spp. The dosage and
duration of amphotericin B therapy for candidemia depend
on the extent of infection and the type of host. The nine C.
lipolytica isolates that we tested were found to be susceptible to achievable concentrations of amphotericin B in serum
(0.313 to 1.25 ,ug/ml). These concentrations are usually
achieved when amphotericin B is administered intravenously at 0.5 mg/kg per day (1, 9). If fungemia persists
despite amphotericin B therapy, consideration should be
given to resection of any potentially infected catheter-associated peripheral venous thrombus.
An antifungal azole, however, may be considered in
selected patients as a possible alternative for the treatment
of C. lipolytica infections. All isolates tested in this study
were susceptible to ketoconazole. The patient reported by
Wherspann and Fullbrandt (18) responded successfully to
removal of the infected venous catheter and administration
of ketoconazole; the patient with sinusitis had an apparent
improvement from ketoconazole therapy. Perhaps localized
mucosal infections caused by C. lipolytica may be amenable
to ketoconazole therapy. However, since the correlation
between in vitro and in vivo effects of ketoconazole are often
variable (12) and since therapeutic experience with C. lipolytica is limited, such patients treated with ketoconazole
require careful selection and follow-up. Investigational antifungal triazoles, such as fluconazole and itraconazole, also
may be active against isolates of C. lipolytica and may be
more active than ketoconazole. We suggest that antifungal
azoles be considered as a possible alternative to amphotericin B in the management of selected patients with C.

VOL. 27, 1989

lipolytica for this study. We also thank Philip A. Pizzo and Mark
Miller for reviewing the manuscript.

crobiol. 26:1874-1877.
6. Holzschu, D. L., F. W. Chandler, L. Ajello, and D. G. Ahearn.
1979. Evaluation of industrial yeasts for pathogenicity. Sabouraudia 17:71-78.
7. Hopfer, R. L., A. Orengo, S. Chesnut, and M. Wenglar. 1980.
Radiometric detection of yeasts in blood cultures of cancer
patients. J. Clin. Microbiol. 12:329-331.
8. Horn, R., B. Wong, T. E. Kiehn, and D. Armstrong. 1985.
Fungemia in a cancer hospital: changing frequency, earlier
onset, and results of therapy. Rev. Infect. Dis. 7:646-655.
9. Koren, G., A. Lau, J. Klein, C. Golas, M. Bologa-Campenau, S.
Soldin, S. M. MacLeod, and C. Prober. 1988. Pharmacokinetics
and adverse effects of amphotericin B in infants and children. J.
Pediatr. 113:559-563.
10. Kreger-van Rij, N. J. W. 1984. Genus 24. Saccharomycopsis

931

Schionning, p. 406-408. In N. J. W. Kreger-van Rij (ed.), The

yeasts. A taxonomic study, 3rd ed. Elsevier Science Publications, Amsterdam.
11. Nitzulescu, V., and M. Niculescu. 1976. Three cases of ocular
candidiasis caused by Candida lipolytica. Arch. Roum. Pathol.

Exp. Microbiol. 35:269-272.

12. Polak, A., and D. M. Dixon. 1987. In vitrolin vivo correlation of
antifungal susceptibility testing using 5-fluorocytosine and ketoconazole as examples of two extremes, p. 45-59. In R. A.
Fromtling (ed.), Recent trends in the discovery, development
and evaluation of antifungal agents. J. R. Prous Science Pub-

lishers, Barcelona, Spain.

13. Prevost, E., and E. Bannister. 1981. Detection of yeast septicemia by biphasic and radiometric methods. J. Clin. Microbiol.
13:655-660.
14. Strinden, W. D., R. B. Helgersen, and D. G. Maki. 1985.
Candida septic thrombosis of the great central veins associated
with central catheters: clinical features and management. Ann.
Surg. 202:653-658.
15. van der Walt, J. P., and D. Yarrow. 1984. Methods for the
isolation, maintenance, classification, and identification of
yeasts, p. 45-104. In N. J. W. Kreger-van Rij (ed.), The yeasts.
A taxonomic study, 3rd ed. Elsevier Science Publications,
Amsterdam.
16. Walsh, T. J., C. I. Bustamente, D. Vlahov, and H. C. Standiford.
1986. Candidal suppurative thrombophlebitis: recognition, prevention and management: Infect. Control 7:16-22.
17. Walsh, T. J., and G. M. Hutchins. 1980. Postoperative Candida
infections of the heart in children. J. Pediatr. Surg. 15:325-331.
18. Wherspann, P., and U. Fullbrandt. 1985. Yarrowia lipolytica
(Wickerham et al) van der Walt and von Arx isolated from a
blood culture. Mykosen 28:217-222.

Downloaded from http://jcm.asm.org/ on September 30, 2015 by guest

LITERATURE CITED
1. Atkinson, A. J., Jr., and J. E. Bennett. 1978. Amphotericin B
pharmacokinetics in humans. Antimicrob. Agents Chemother.
13:271-276.
2. Barnett, J. A., R. W. Payne, and D. Yarrow. 1983. Yeasts.
Characteristics and identification, p. 461. Cambridge`University
Press, New York.
3. Bille, J., L. Stockman, and G. D. Roberts. 1982. Detection of
yeasts and filamentous fungi in blood cultures during a ten-year
period (1972 to 1981). J. Clin. Microbiol. 16:968-970.
4. Gordon, M. A. 1984. Paecilomyces lilacinus (Thom) Samson
from systemic infection in an armadillo (Dasypus novemcinctus). Sabouraudia 22:109-116.
5. Gordon, M. A., E. W. Lapa, and P. G. Passero. 1988. Improved
method for azole antifungal susceptibility testing. J. Clin. Mi-

CANDIDA LIPOLYTICA