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Journal of Clinical Microbiology, June 1998, p. 1772-1776, Vol. 36, No. 6
0095-1137/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
Invasive Infection with Fusarium
chlamydosporum in a Patient with Aplastic Anemia
Brahm H.
Segal,1,*
Thomas J.
Walsh,2
Johnson M.
Liu,3
Jon D.
Wilson,4 and
Kyung J.
Kwon-Chung5
Laboratory of Host
Defenses1 and
Molecular Biology Section,
Laboratory of Clinical Investigation,5
National Institute of Allergy and Infectious Diseases,
Immunocompromised Host Section, Pediatric
Branch,2 and
Laboratory of
Pathology,4 National Cancer Institute, and
Hematology Branch, National Heart, Lung, and Blood
Institute,3 National Institutes of Health,
Bethesda, Maryland
Received 13 January 1998/Returned for modification 11 February
1998/Accepted 9 March 1998
 |
ABSTRACT |
We report the first case of invasive disease caused by
Fusarium chlamydosporum. The patient had aplastic
anemia with prolonged neutropenia and was treated with
immunosuppressive therapy. While she was receiving empirical
amphotericin B, a dark crusted lesion developed on her nasal turbinate.
Histologic analysis revealed invasive hyaline hyphae and some darkly
pigmented structures that resembled conidia of dematiaceous molds. Only
after the mold was grown in culture were characteristic colonial
morphology, phialides, conidia, and chlamydospores
evident, thus permitting the identification of F. chlamydosporum. This case illustrates the ever-increasing spectrum of pathogenic Fusarium spp. in immunocompromised
patients and emphasizes the potential pitfalls in histologic diagnosis, which may have important treatment implications.
| |
TEXT |
Fusarium species have
emerged as a major cause of invasive disease and mortality among
neutropenic patients (1-5, 8, 17, 19, 21, 23, 28).
Fusarium spp. are common soil saprophytes and plant
pathogens which, in humans, are mostly associated with superficial mycoses and keratitis. However, with the widespread use of intensive antineoplastic chemotherapy and bone marrow
transplantation, more than 100 cases of invasive and disseminated
infection caused by Fusarium spp. have been reported
most
within the past 10 years.
Most cases of invasive fusariosis are caused by Fusarium
solani, Fusarium oxysporum, and Fusarium
moniliforme, but in about one-third the species is not identified
(8, 17). Disseminated fusariosis commonly manifests with
cutaneous lesions, pulmonary infiltrates, and, less often, sinusitis
and involvement of the nasal cavity (17). In about one-half
of cases of dissemination, Fusarium spp. are isolated from
blood culture (5, 17). To our knowledge, the only reported
case of human infection by Fusarium chlamydosporum was
catheter-related fungemia in a patient with lymphoma (10).
Here, we report the first case of invasive tissue disease caused by
F. chlamydosporum. The patient was severely
immunocompromised due to aplastic anemia with prolonged neutropenia and
was treated with immunosuppressive therapy. While she was receiving
empirical amphotericin B for prolonged neutropenic fever, a lesion
excised from her nasal turbinate showed invasive hyaline and darkly
pigmented hyphal structures. This finding raised the suspicion of a
dematiaceous mold, prompting the addition of itraconazole to the
therapy. Subsequent evaluation of the mold grown in culture and
correlation of the culture results with the histopathology confirmed
the identification of F. chlamydosporum.
Case report.
The patient was a 40-year-old female with
aplastic anemia who was treated with combination antithymocyte
globulin (ATG) and cyclosporin A (CSA) at the National Heart,
Lung, and Blood Institute at the Warren-Grant Magnuson Clinical
Center, National Institutes of Health (NIH). Prior to transfer to the
NIH, she had had fulminant hepatitis of unknown etiology, as well as
prolonged neutropenic fever treated with broad-spectrum
antibiotics. Approximately 3 weeks after the ATG-CSA protocol was
started and while she was receiving empirical amphotericin B (0.5 mg/kg
of body weight/day) for persistent neutropenic fever, a raised dark
crusted lesion developed on her left middle nasal turbinate. Surgical
excision was performed, and material was sent for histologic analysis. Biopsy material was inadvertently not sent for culture. The procedure was complicated by epistaxis requiring packing of the nasal cavity. The gauze used for packing was subsequently sent for culture. Histologic evaluation of the lesion revealed an invasive mold with
hyaline as well as darkly pigmented hyphal structures. The appearance
was nonspecific and did not permit diagnosis of the genus. The presence
of pigment on routine hematoxylin and eosin preparations and
Masson-Fontana silver stained materials raised the possibility of
phaeohyphomycosis. The dosage of amphotericin B was increased to 1.0 mg/kg/day, and itraconazole (600 mg/day) was added to the schedule.
Because of progressive azotemia, amphotericin B lipid complex (5 mg/kg/day) was substituted for amphotericin B. Approximately 2 weeks
elapsed before the definitive diagnosis of F. chlamydosporum
was made from culture (see below). Once the diagnosis was made,
itraconazole was discontinued because of the known resistance of
Fusarium spp. to this triazole.
An isolated sputum culture yielded F. chlamydosporum
shortly after excision of the nasal lesion. There was no evidence
of pulmonary disease on multiple chest radiographs or on a chest computed tomography scan. This isolate therefore most likely colonized the patient's airway and was not a pulmonary pathogen. Serial computed
tomography scans of the sinuses showed opacification of the maxillary,
ethmoid, and sphenoid sinuses. However, no bone involvement or
progression of disease was detected over the next several weeks.
Otolaryngologic examinations showed no recurrence of disease in the
nasal cavity. Multiple routine and fungal blood cultures were negative
for Fusarium species. Thus, the fusariosis in this patient
was considered to be localized and likely to have been cured by
surgical excision.
The bone marrow failure did not improve with ATG-CSA treatment, and the
patient underwent transplantation with T-cell-replete stem cells.
Despite successful engraftment, the patient died of multiorgan failure
5 weeks after transplantation, with no evidence of residual fusariosis.
Mycological methods and diagnosis.
Material from the gauze
packing in the nasal cavity was cultured on various mycological agar
media. Within 48 h of incubation at 30°C, fluffy colonies of the
same fungus grew on all media. The fungus was subcultured on Sabouraud
agar and potato dextrose agar. Within 1 week, the isolate produced
intensely pinkish red, floccose colonies 6 to 7 cm in diameter. It also
grew well at 37°C, reaching a diameter of 4.5 cm in 7 days on potato
dextrose agar. On a cornmeal agar slide culture, the isolate produced
numerous one- to two-celled, clavate, oblong to fusiform microconidia
(2.5 to 4 µm by 8 to 12 µm) directly on short and narrow phialides (denticles) on sympodially proliferating conidiophores (Fig.
1A). Canoe-shaped macroconidia of four or
more cells, characteristic of the genus Fusarium, measuring
3 by 30 µm were observed only rarely on the cornmeal agar slide
culture (Fig. 1B) and were not observed on the other culture media.
Intercalary, smooth or slightly rough, brown-walled chlamydospores
(Fig. 1C) were abundantly produced on all cultures in 7 to 10 days. The
chlamydospores were mostly globose (6 to 15 µm in diameter) and
formed in short chains, but some produced cross septae and became
muriform (Fig. 1D). The colony reverse was faintly brown in the
beginning but became dark brown as the culture aged due to the
increasingly abundant, darkly pigmented chlamydospores.
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FIG. 1.
F. chlamydosporum grown on cornmeal agar
(magnification, ×1,200). (A) Conidiophores with sympodially
proliferating phialides and microconidia; (B) a fusiform macroconidium
with four cells and a microconidium with two cells; (C and D)
chlamydospores.
|
|
Although such chlamydospore morphology was also seen in
histopathological sections of the biopsy specimen (Fig.
2A and
B),
the histologic appearance was not
specific enough for the identification
of the etiologic agent. The
morphology of the invasive hyphal
structures in the submucosa was
consistent with that of a
Fusarium species (Fig.
2C), but
the presence of darkly pigmented thick-walled
chlamydospores in
hematoxylin and eosin-stained materials raised
the possibility of a
dematiaceous mold. This possibility was strengthened
by the results of
Masson-Fontana staining. Not only the thick-walled
chlamydospores but
also portions of many hyphae morphologically
consistent with a
Fusarium species growing toward the periphery
of tissue
sections were positive for this staining (data not shown).
Only with
evaluation of the cultured mold and comparison with
the histologic
specimens was the diagnosis of invasive fusariosis
established.
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FIG. 2.
In vivo morphology of F. chlamydosporum
(magnification, ×1,200). (A) Dark-walled chlamydospores seen in the
hematoxylin and eosin-stained section; (B) muriform chlamydospore
(Gomori methenamine-silver stained); (C) septate hyphae (Gomori
methenamine-silver stained).
|
|
Thus, the isolate was identified as
F. chlamydosporum on the
basis of intensely pinkish red colonies, sympodially proliferating
polyphialidic conidiophores, clavate to fusiform microconidia
borne
directly on the short and pointed phialides (denticles),
numerous
intercalary brown-walled chlamydospores, and rarity of
macroconidial
formation on agar media.
MICs were determined by broth macrodilution methods, as previously
described (
6). Briefly, a suspension was adjusted with
a
spectrophotometer to 68 to 71% transmission at a wavelength
of
530 nm and diluted 100-fold to yield an inoculum of 1 × 10
4 to 5 × 10
4 CFU/ml. Amphotericin B
and itraconazole were tested in 0.165
M morpholinepropanesulfonic acid
(MOPS)-buffered RPMI 1640 (Bio-Whittaker,
Walkersville, Md.) at a pH of
7.0. A 100-µl volume of concentrated
antifungal compound was diluted
10-fold with 900 µl of inoculum
suspension and incubated at 35°C
for 24 and 48 h. The final concentration
ranges for
amphotericin B (Bristol-Myers Squibb, Princeton, N.J.)
and itraconazole
(Janssen Pharmaceutica, Piscataway, N.J.) were
0.03 to 16.0 µg/ml.
The MIC was graded on a scale of 0 to 4+,
with 0 being optically clear,
1+ being slightly hazy, 2+ being
a 50% reduction of growth, 3+ being a
25% reduction of growth,
and 4+ being equal to MIC for the growth
control tube. The MIC
was defined as the lowest concentration of
antifungal compound
which rendered no growth (0) for amphotericin B and
a 50% reduction
of growth (2+) for itraconazole. The minimum lethal
concentration
(MLC) was determined by dispensing and streaking 100 µl
of broth
from the first four tubes containing drug concentrations above
the MIC exhibiting no growth onto Sabouraud glucose agar (NIH
Media
Department, Bethesda, Md.) and incubating it at 35°C. A
concentration
yielding growth of three or fewer colonies was considered
fungicidal.
The MLC was defined as the lowest concentration of
antifungal compound
yielding growth of three or fewer colonies.
The MIC and MLC of
amphotericin B were 0.5 and 1.0 µg/ml, respectively.
The MIC of
itraconazole was 1.0 µg/ml.
Discussion.
This is the first reported case of F. chlamydosporum causing invasive tissue disease. More commonly
known pathogenic Fusarium species, such as F. solani and F. oxysporum, also produce chlamydospores in
vitro, but these structures have not been seen in vivo. The production
by F. chlamydosporum of pigmented chlamydospores in tissue
in our case is likely an infection site-associated phenomenon rather than a species characteristic. Fungi may produce
species-specific structures in tissue exposed to air, such as in the
nasal cavity. For example, Aspergillus species produce
conidiophores and cleistothecia only in tissue exposed to ambient air
(12).
The histologic appearance of
Fusarium spp. is variable and
can mimic those of several other molds. Therefore, identification
of
Fusarium spp. requires culture and cannot rely solely on
histologic
morphology (
19). However, as in our case, a
significant amount
of time may elapse before culture results are
available. Thus,
therapy under these circumstances must be empirical
until a definitive
diagnosis is made.
The clinical manifestations and histological appearance of
Fusarium spp. may be indistinguishable from those of
organisms
causing invasive aspergillosis. Both genera infect profoundly
immunocompromised patients, and both are associated with vascular
invasion, tissue infarction, and hemorrhage. Recently, Liu et
al.
(
14) reviewed biopsy and cytology specimens from
culture-confirmed
hyalohyphomycosis caused by
Fusarium,
Paecilomyces, or
Acremonium species to identify
histologic features that distinguish these
molds from
Aspergillus species. Sporadic phialide- and
phialoconidium-like
structures were present in 16 of 19 cases,
including 7 of 10 cases
of infection by a
Fusarium species
(
14). Phialoconium-like structures
seen in tissue were
either spherical, oval, curved, or elliptical.
These specialized
structures may be helpful in alerting the pathologist
to the
possibility of a non-
Aspergillus species but are not readily
detected unless inspected with a 100× oil immersion lens
(
14).
The authors point out that the presumptive histologic
diagnosis
should be confirmed by culture whenever possible
(
14). In the
absence of definitive identification by
culturing, the likelihood
of infection with a
Fusarium
species is substantially increased
if either widespread cutaneous
dissemination or the isolation
of the mold from a blood culture occurs
(
5).
The identification of a
Fusarium species in a culture is
difficult if macroconidia are not present (
8). In these
instances
confusion with other genera, such as
Acremonium,
Cylindrocarpon,
or
Verticillium, may occur
(
8). Rarely, infection of the nasopharynx
and sinuses by a
Fusarium species may resemble rhinocerebral zygomycosis
(
27). Usually the distinction between these two molds can be
made histologically because the hyphae of zygomycetes are wider,
branch
at right angles, and demonstrate a paucity of septations
(
27).
Typically,
Fusarium spp. are not confused with dematiaceous
molds. In our case, the presence of pigmented chlamydospores in
histologic specimens stained with hematoxylin and eosin raised
the
suspicion of phaeohyphomycosis. The considerable number of
dark-walled
hyphae seen after Masson-Fontana staining further
supported this
presumptive, but incorrect, diagnosis.
Masson-Fontana staining for fungal cells was introduced by Kwon-Chung
et al. (
13) in an attempt to discern melanin formation
by
Cryptococcus neoformans in brain tissue. They observed that
though Masson-Fontana staining was not specific for melanin, it
was
useful in differentiating cryptococcal cells from other yeast-like
pathogens. The Masson-Fontana reagent stains any phenolic compound,
including melanin. Since then, the staining has been frequently
used
for fungal histopathology to detect melanin-like pigment
when the
pathogen is suspected to be a dematiaceous mold that
fails to produce
brown-walled hyphae in tissue (
4,
16,
29).
It must be
emphasized that Masson-Fontana staining is not specific
for melanin and
that hyphae without melanin can produce positive
results as long as
phenol compounds are present.
In patients with severe and prolonged neutropenia, early diagnosis of
infection by a
Fusarium species is important because
of the
high risk of dissemination. Disseminated fusariosis in
this population
is associated with a high mortality, and survival
is dependent on the
rapid recovery of the neutrophil count (
17).
As in our
patient, localized disease may be cured with excision
alone; however,
we believe that in neutropenic patients, systemic
antifungal therapy is
warranted because of the high risk of clinically
inapparent
disseminated disease (
20).
In a review of nasopharyngeal and sinus infection caused by
Fusarium spp., Lopes et al. (
15) reported that of
19 patients,
14 had a hematologic malignancy, 1 had aplastic anemia, 1 had
diabetes, and 3 had no risk factors. Disseminated fusariosis
occurred
in all patients with a hematologic malignancy as well as the
patient
with aplastic anemia; 10 (67%) of these 15 patients died.
In contrast,
among the immunocompetent patients,
Fusarium
disease was localized
and surgery, with or without systemic antifungal
therapy, was
curative (
11).
Our patient developed invasive fusariosis while receiving empirical
amphotericin B (0.5 mg/kg/day). This is not an unusual
occurrence.
Infection by
Fusarium spp. in neutropenic hosts typically
does not respond to conventional dosages of amphotericin B. Even
at
high dosages (1 to 2 mg/kg/day), the response is generally
poor without
the rapid recovery from neutropenia (
17).
The optimal selection of antifungal therapy for fusariosis is not well
defined in the literature. Despite the poor response,
high-dose
amphotericin B (1 to 2 mg/kg/day) or a lipid formulation
of
amphotericin is considered standard therapy. Numerous case
studies and
small-scale studies have investigated various combinations
of
antifungal regimens (
8,
18,
21) and the use of cytokine
therapy and granulocyte transfusions (
26) in neutropenic
patients
with infection by
Fusarium spp. In a retrospective
study of 43
patients with hematologic malignancy and fusariosis treated
at
the M.D. Anderson Cancer Center, use of transfusions with
granulocyte
colony-stimulating factor-elicited granulocytes appeared to
be
associated with a positive response (
5). However, the
responders
in this study also tended to be in remission from the
underlying
malignancy, to have already recovered their neutrophil
counts,
and to have localized fusariosis; thus, the independent
contribution
of the granulocyte transfusions was uncertain
(
5). No controlled
studies of treatment of fusariosis have
been published.
Likewise, published data on in vitro susceptibility of
Fusarium spp. were generally derived from case studies. Even
when the
clinical isolates have been susceptible to amphotericin B, the
correlation with the clinical response has been poor. Information
about
the methodology used has not been consistently provided,
and there have
been significant methodological differences between
laboratories in
medium composition, pH, inoculum size, incubation
time, and temperature
(
22). With these caveats made, only amphotericin
B,
natamycin, and miconazole have shown in vitro activity against
some
Fusarium isolates (
22). There is agreement among
several
published reports that
Fusarium spp. are resistant
to rifampin,
the triazoles, and flucytosine (
8,
22,
25).
The number of patients with fusariosis is likely to increase in the
future as more patients receive intensive immunosuppressive
therapy.
Our purposes here are to report the first known case
of tissue disease
caused by
F. chlamydosporum and to alert the
clinician and
pathologist to the varied histologic appearance
of
Fusarium
spp. Rapid diagnostic methods for mold identification
from histologic
specimens would increase our diagnostic precision.
To this end,
immunohistologic techniques which can rapidly identify
a number of
medically important fungal genera, including
Fusarium,
have been introduced in a few specialized laboratories
(
7,
9,
24). Moreover, given the dismal prognosis of
fusariosis
in neutropenic patients, more effective antifungal therapy
and
reliable fungal susceptibility testing methods are urgently needed.
| |
FOOTNOTES |
*
Corresponding author. Mailing address: Laboratory of
Host Defenses, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Building 10, Room 11N103, Bethesda, MD
20892. Phone: (301) 480-1705. Fax: (301) 402-4369. E-mail: bsegal{at}atlas.niaid.nih.gov.
| |
REFERENCES |
| 1.
|
Anaissie, E.,
G. P. Bodey,
H. Kantarjian,
J. Ro,
S. E. Vartivarian,
R. Hopfer,
J. Hoy, and K. Rolston.
1989.
New spectrum of fungal infections in patients with cancer.
Rev. Infect. Dis.
11:369-378[Medline].
|
| 2.
|
Anaissie, E.,
H. Kantarjian,
P. Jones,
B. Barlogie,
M. Luna,
G. Lopez-Berestein, and G. P. Bodey.
1986.
Fusarium: a newly recognized fungal pathogen in immunosuppressed patients.
Cancer
57:2141-2145[Medline].
|
| 3.
|
Anaissie, E.,
H. Kantarjian,
J. Ro,
R. Hopfer,
K. Rolston,
V. Fainstein, and G. Bodey.
1988.
The emerging role of Fusarium infections in patients with cancer.
Medicine
67:77-83[Medline].
|
| 4.
|
Anaissie, E. J.,
G. P. Bodey, and M. G. Rinaldi.
1989.
Emerging fungal infections.
Eur. J. Clin. Microbiol. Infect. Dis.
8:323-330[Medline].
|
| 5.
|
Boutati, E. I., and E. J. Anaissie.
1997.
Fusarium, a significant emerging pathogen in patients with hematologic malignancy: ten years' experience at a cancer center and implications for management.
Blood
90:999-1008[Abstract/Free Full Text].
|
| 6.
|
Espinel-Ingroff, A.,
K. Dawson,
M. Pfaller,
E. Anaissie,
B. Breslin,
D. Dixon,
A. Fothergill,
V. Paetznick,
J. Peter,
M. Rinaldi, and T. Walsh.
1995.
Comparative and collaborative evaluation of standardization of antifungal susceptibility testing for filamentous fungi.
Antimicrob. Agents Chemother.
39:314-319[Abstract/Free Full Text].
|
| 7.
|
Fukuzawa, M.,
H. Inaba,
M. Hayama,
N. Sakaguchi,
K. Sano,
M. Ito, and M. Hotchi.
1995.
Improved detection of medically important fungi by immunoperoxidase staining with polyclonal antibodies.
Virchows Arch.
427:407-414[Medline].
|
| 8.
|
Guarro, J., and J. Gené.
1995.
Opportunistic fusarial infections in humans.
Eur. J. Clin. Microbiol. Infect. Dis.
14:741-754[Medline].
|
| 9.
|
Kaufman, L.,
P. G. Standard,
M. Jalbert, and D. E. Kraft.
1997.
Immunohistologic identification of Aspergillus spp. and other hyaline fungi by using polyclonal fluorescent antibodies.
J. Clin. Microbiol.
35:2206-2209[Abstract].
|
| 10.
|
Kiehn, T. E.,
P. E. Nelson,
E. M. Bernard,
F. F. Edwards,
B. Koziner, and D. Armstrong.
1985.
Catheter-associated fungemia caused by Fusarium chlamydosporum in a patient with lymphocytic lymphoma.
J. Clin. Microbiol.
21:501-504[Abstract/Free Full Text].
|
| 11.
|
Kurien, M.,
V. Anandi,
R. Raman, and K. N. Brahmadathan.
1992.
Maxillary sinus fusariosis in immunocompetent hosts.
J. Laryngol. Otol.
106:733-736[Medline].
|
| 12.
|
Kwon-Chung, K. J., and J. E. Bennett.
1992.
Medical mycology, p. 201-247.
Lea & Febiger, Malvern, Pa.
|
| 13.
|
Kwon-Chung, K. J.,
W. B. Hill, and J. E. Bennett.
1981.
New, special stain for histopathologic diagnosis of cryptococcosis.
J. Clin. Microbiol.
13:383-387[Abstract/Free Full Text].
|
| 14.
|
Liu, K.,
D. N. Howell,
J. R. Perfect, and W. A. Schell.
1998.
Morphologic criteria for the preliminary identification of Fusarium, Paecilomyces, and Acremonium species by histopathology.
Am. J. Clin. Pathol.
109:45-54[Medline].
|
| 15.
|
Lopes, J. O.,
E. S. de Mello, and C. Klock.
1995.
Mixed intranasal infection caused by Fusarium solani and a zygomycete in a leukaemic patient.
Mycoses
38:281-284[Medline].
|
| 16.
|
Magnon, K. C.,
M. Jalbert, and A. A. Padhye.
1993.
Osteolytic phaeohyphomycosis caused by Phialemonium obovatum.
Arch. Pathol. Lab. Med.
117:841-843[Medline].
|
| 17.
| Martino, P., R. Gastaldi, R. Raccah, and C. Girmenia. 1994. Clinical patterns of Fusarium
infections in immunocompromised patients. J. Infect.
128(Suppl. 1):7-15.
|
| 18.
|
Merz, W. G.,
J. E. Karp,
M. Hoagland,
M. Jett-Goheen,
J. M. Junknis, and A. F. Hood.
1988.
Diagnosis and successful treatment of fusariosis in the compromised host.
J. Infect. Dis.
158:1046-1055[Medline].
|
| 19.
|
Nelson, P. E.,
M. C. Dignani, and E. J. Anaissie.
1994.
Taxonomy, biology, and clinical aspects of Fusarium species.
Clin. Microbiol. Rev.
7:479-504[Abstract/Free Full Text].
|
| 20.
|
Nucci, M.,
N. Spector,
S. Lucena,
P. C. Bacha,
W. Pulcheri,
A. Lamosa,
A. Derossi,
M. J. Caiuby,
J. Macieira, and H. O. Oliveira.
1992.
Three cases of infection with Fusarium species in neutropenic patients.
Eur. J. Clin. Microbiol. Infect. Dis.
11:1160-1162[Medline].
|
| 21.
|
Rabodonirina, M.,
M. A. Piens,
M. F. Monier,
E. Guého,
D. Fière, and M. Mojon.
1994.
Fusarium infections in immunocompromised patients: case reports and literature review.
Eur. J. Clin. Microbiol. Infect. Dis.
13:152-161[Medline].
|
| 22.
|
Reuben, A.,
E. Anaissie,
P. E. Nelson,
R. Hashem,
C. Legrand,
D. H. Ho, and G. P. Bodey.
1989.
Antifungal susceptibility of 44 clinical isolates of Fusarium species determined by using a broth microdilution method.
Antimicrob. Agents Chemother.
33:1647-1649[Abstract/Free Full Text].
|
| 23.
|
Richardson, S. E.,
R. M. Bannatyne,
R. C. Summerbell,
J. Milliken,
R. Gold, and S. S. Weitzman.
1988.
Disseminated fusarial infection in the immunocompromised host.
Rev. Infect. Dis.
10:1171-1181[Medline].
|
| 24.
|
Sekhon, A. S.,
L. Kaufman,
N. Moledina,
R. C. Summerbell,
A. A. Padhye,
E. A. Ambroisie, and T. Panter.
1995.
An exoantigen test for the rapid identification of medically significant Fusarium species.
J. Med. Vet. Mycol.
33:287-289[Medline].
|
| 25.
|
Sekhon, A. S.,
A. A. Padhye,
A. K. Garg,
H. Ahmad, and N. Moledina.
1994.
In vitro sensitivity of medically significant Fusarium species to various antimycotics.
Chemotherapy (Basel)
40:239-244.
|
| 26.
|
Spielberger, R. T.,
M. J. Falleroni,
A. J. Coene, and R. A. Larson.
1993.
Concomitant amphotericin B therapy, granulocyte transfusions, and GM-CSF administration for disseminated infection with Fusarium in a granulocytopenic patient.
Clin. Infect. Dis.
16:528-530[Medline].
|
| 27.
|
Valenstein, P., and W. A. Schell.
1986.
Primary intranasal Fusarium infection: potential for confusion with rhinocerebral zygomycosis.
Arch. Pathol. Lab. Med.
110:751-754[Medline].
|
| 28.
| Vartivarian, S. E., E. J. Anaissie, and
G. P. Bodey. 1993. Emerging fungal pathogens in
immunocompromised patients: classification, diagnosis, and management.
Clin. Infect. Dis. 17(Suppl. 2):S487-S491.
|
| 29.
|
Zaatari, G. S.,
R. Reed, and R. Morewessel.
1984.
Subcutaneous hyphomycosis caused by Scytalidium hyalinum.
Am. J. Clin. Pathol.
82:252-256[Medline].
|
Journal of Clinical Microbiology, June 1998, p. 1772-1776, Vol. 36, No. 6
0095-1137/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
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