Despite increasing reports of life-threatening Fusarium infections, little is known about its pathogenesis and management. To evaluate the epidemiology, clinicopathologic features, and outcome of invasive fusariosis in patients with hematologic cancer, we conducted a retrospective study of invasive fusarial infections in patients with hematologic malignancy treated at a referral cancer center over a 10-year period (1986 to 1995), as well as a literature review. Forty patients with disseminated and three patients with invasive lung infection were included in the analysis. All patients were immunocompromised. The infection occurred in three patients postengraftment following bone marrow transplantation. All patients were diagnosed antemortem. Thirteen patients responded to therapy, but the infection relapsed in two of them. Response was associated with granulocyte transfusions, amphotericin B lipid formulations (four patients each), and an investigational triazole (two patients). Resolution of infection was only seen in patients who ultimately recovered from myelosuppression. Portal of entry was the skin (33%), the sinopulmonary tree (30%), and unknown (37%). Fusarium causes serious morbidity and mortality, and may mimic aspergillosis. The infection seems to respond to newer therapeutic approaches, but only in patients with ultimate recovery from myelosuppression, and it may relapse if neutropenia recurs.

DISSEMINATED FUNGAL infections constitute one of the most difficult challenges for clinicians caring for patients with hematologic cancer.1-8 Although the incidence of hematogenous candidiasis has been significantly reduced with the introduction of fluconazole prophylaxis, the opportunistic molds have become the leading cause of infectious mortality in this patient population.9-15 Aspergillosis remains clearly the most common mold infection in patients with hematologic cancer.16-18 However, new opportunistic pathogens have now emerged as a cause of life-threatening infection worldwide. The most frequent of these pathogens is Fusarium, which has been reported to cause disseminated infections in 42 reports from different institutions treating patients with hematologic malignancies worldwide.19-60 Infection with Fusarium is associated with a high mortality and may respond to novel therapies.55-62 Since infection with this organism may mimic aspergillosis, patients are usually treated with amphotericin B, an agent with poor activity against fusariosis.20,27 63-65 Hence, early diagnosis of fusariosis is of paramount importance. Yet despite increasing reports of fatal infections with this organism, little is known about the pathogenesis, clinical characteristics, and management of these infections. In this report, we describe 43 patients with hematologic cancer who developed invasive Fusarium infection during the course of the disease. We also review the worldwide literature (54 patients) and present novel concepts regarding the pathogenesis, prevention, and treatment of Fusarium infection.

The medical records of patients with positive cultures for Fusarium species treated at The University of Texas M.D. Anderson Cancer Center between January 1986 and December 1995 were reviewed to determine the pathogenesis, clinical characteristics, and management of patients with invasive Fusarium infection.

Invasive organ infection was documented by both culture and histopathologic examination of the involved organ. Disseminated infection was defined as involvement of at least two noncontiguous organs by Fusarium species in association with more than one positive culture. Patients with fungemia alone or infection at a single extrapulmonary site and patients with an underlying disease other than hematologic cancer were excluded even if they had evidence of multiorgan involvement. Laboratory identification of Fusarium species was conducted as previously reported.20 A literature search based on MEDLINE and CANCERLIT was conducted for the period 1976 to 1995, and only patients with hematologic cancer and invasive infections were analyzed. Findings from the literature search were then compared with those obtained from our series.

Thirty-eight patients with invasive or disseminated Fusarium infection were identified during the study period. Four cases of disseminated and one case of invasive Fusarium infection previously reported from our institution were also added.19 20 The baseline patient characteristics are shown in Table 1. Thirty patients had acute leukemia, mostly acute nonlymphocytic, and only five patients were in remission from the underlying disease at the time of infection diagnosis. Twelve patients had undergone bone marrow transplantation (allogeneic in nine), and the remaining patients had received cytotoxic chemotherapy alone. Two of nine patients who underwent allogeneic transplantation developed the infection before engraftment (days 13 and 30), and the remaining seven had postengraftment fusariosis (days 43, 44, 48, 59, 73, 82, and 151). Except for seven patients who had an adequate neutrophil count, all patients were neutropenic at presentation. Of nine allogeneic transplant recipients, four had grade 2 or higher graft-versus-host disease (GVHD). Fourteen patients were receiving adrenal corticosteroids. Most patients had concomitant bacterial or fungal infections; seven patients had a history of invasive fungal infection (disseminated candidiasis in four and aspergillosis in three).

Table 1.

Characteristics of Patients With Hematologic Cancer and Invasive or Disseminated Fusarial Infection: Comparison Between the M.D. Anderson Cancer Center Experience and the Published Literature

CharacteristicM.D. AndersonLiterature
No.%No.%
Patients 43  54  
Age (yr) 
Median 43 
  31 
    
Range 14-78 
  2-71 
    
Sex (male/female) 24/19 
  35/19 
    
Underlying disease 
Acute nonlymphocytic leukemia 23 53 26 48 
Acute lymphocytic leukemia 16 20 37 
Lymphoproliferative disorders 13 31 15 
Neutropenia at diagnosis 
ANC < 1,000/μL 36 84 54 100 
ANC < 100/μL 28 65 22 41* 
BMT 12 28 16 30 
Autologous 25 33 
Allogeneic 75 12 67 
Culture-documented sites of involvement 
Skin 39 91ρ 39 72 
Bloodstream 18 42 30 56 
Eye 
Bone 
Radiologic evidence in lung 36 84 16 70 
Nonspecific infiltrates 29 81 12 52 
Nodular lesions 14 13 
Cavitary lesions 
Radiologic evidence of sinus involvement 24 71 11 79 
Outcome 
Resolution of infection1-155 13 30 26 48 
Death with disseminated infection1-154 30 70 28 52 
CharacteristicM.D. AndersonLiterature
No.%No.%
Patients 43  54  
Age (yr) 
Median 43 
  31 
    
Range 14-78 
  2-71 
    
Sex (male/female) 24/19 
  35/19 
    
Underlying disease 
Acute nonlymphocytic leukemia 23 53 26 48 
Acute lymphocytic leukemia 16 20 37 
Lymphoproliferative disorders 13 31 15 
Neutropenia at diagnosis 
ANC < 1,000/μL 36 84 54 100 
ANC < 100/μL 28 65 22 41* 
BMT 12 28 16 30 
Autologous 25 33 
Allogeneic 75 12 67 
Culture-documented sites of involvement 
Skin 39 91ρ 39 72 
Bloodstream 18 42 30 56 
Eye 
Bone 
Radiologic evidence in lung 36 84 16 70 
Nonspecific infiltrates 29 81 12 52 
Nodular lesions 14 13 
Cavitary lesions 
Radiologic evidence of sinus involvement 24 71 11 79 
Outcome 
Resolution of infection1-155 13 30 26 48 
Death with disseminated infection1-154 30 70 28 52 

Abbreviations: ANC, absolute neutrophil count; BMT, bone marrow transplantation.

*

The exact ANC was not mentioned in 31 patients reported in the literature.

Chest x-ray findings were not discussed in 31 cases reported in the literature; in 7 cases (30%), they were normal. Radiologic evaluation was available for all of our patients: in 7 patients (16%), radiologic evaluation of the lungs was normal.

Thirty-four and 14 patients, respectively, had radiologic examination of the sinuses.

ρ Skin not involved in 4 of 43 patients; in 4 patients, description of skin lesions was not available.

F1-155

Resolution of infection occurred only in patients who recovered from myelosuppression.

F1-154

Autopsy documentation was obtained in 41% of our patients who died with disseminated infection and 17% of cases, respectively. Two of our patients died with disseminated infection at a subsequent recurrent episode of Fusarium infection after having cleared a first episode of disseminated fusariosis.

Thirty patients were receiving antifungal prophylaxis for a median of 13 days (range, 2 to 100). Prophylaxis consisted of fluconazole (22 patients), intravenous amphotericin B (five patients), itraconazole (two patients), or ketoconazole (one patient).

The most common presentation of the infection was persistent fever refractory to antibacterial and antifungal therapy (35 patients). Other findings at presentation included sinusitis (11 patients), painful skin lesions (six patients), and pneumonia (six patients). Myalgias were part of the clinical presentation in three patients, and one patient each presented with hemoptysis and altered mental status.

Infection documentation was obtained from the bloodstream of 18 patients and from the nails of five patients with onychomycoses and concomitant toe or finger cellulitis. The infection was documented from a bone and a deep-tissue ocular specimen in three patients each. Brain involvement was presumed in four patients. Pulmonary involvement was presumed in 36 patients (84%), either as nonspecific infiltrates in 29 (bilateral in 18) or as nodular lesions in five (bilateral in all five); two patients had a cavitary lung lesion. Twenty-four of 34 patients (71%) in whom radiologic evaluation of the sinuses was obtained had positive findings. These findings were limited to the maxillary or ethmoid sinuses in 19 and four patients, respectively. Abnormal findings in at least two sinuses were noted in the remaining patients. Radiologic findings consisted mainly of mucosal thickening or opacification of the sinuses.

Fig. 1.

Primary fusarial skin lesions: Cellulitis at the site of a wound (A) or at the site of a pre-existing onychomycosis (B-E) with surrounding cellulitis.

Fig. 1.

Primary fusarial skin lesions: Cellulitis at the site of a wound (A) or at the site of a pre-existing onychomycosis (B-E) with surrounding cellulitis.

Close modal
Fig. 2.

Metastatic fusarial skin lesions tend to evolve from a subcutaneous nodule (A), to a necrotic lesion with a central ulcer and surrounding cellulitis (B), rarely surrounded by a thin rim of erythema (ie, a target lesion) (C). At times, lesions of different ages coexist in the same patient (D).

Fig. 2.

Metastatic fusarial skin lesions tend to evolve from a subcutaneous nodule (A), to a necrotic lesion with a central ulcer and surrounding cellulitis (B), rarely surrounded by a thin rim of erythema (ie, a target lesion) (C). At times, lesions of different ages coexist in the same patient (D).

Close modal

Thirty-nine patients (91%) presented with skin lesions, either metastatic (34 patients) or primary (five patients). All 18 patients who had positive blood cultures had metastatic skin lesions. The primary skin lesions consisted of cellulitis at the site of onychomycosis or at a wound site (Fig 1), or facial and periorbital cellulitis in patients with fusarial sinusitis. Metastatic skin lesions included subcutaneous nodular lesions (hemorrhagic in one) and ecthyma gangrenosum–like lesions. Some patients had lesions of different ages that evolved from subcutaneous nodules, usually painful, to erythematous lesions followed by central necrosis (ecthyma gangrenosum–like lesions) (Fig 2). In one of these patients, this latter lesion was surrounded by a thin rim of erythema. Among 12 patients who had undergone bone marrow transplantation, infection occurred before engraftment in three. Of interest, nine bone marrow transplant recipients developed infection after engraftment when they had adequate neutrophil counts. The incidence of fusarial infection was 1.2% among 750 patients who underwent an allogeneic transplant, compared with 0.2% among 1,537 autograft recipients.

Infections tended to occur predominantly during the rainy season in Houston (May through September), although scattered cases occurred throughout the year (Fig 3). Fusaria were subjected to species analysis in 22 patients: the most common isolated species were solani (12 cases), moniliforme (four cases), and oxysporum (two cases), and proliferatum, dimerum, semitecum, and equiseti were identified in one case each.

Fig. 3.

Monthly distribution of fusarial infection for the years 1986 to 1995 at M.D. Anderson Cancer Center.

Fig. 3.

Monthly distribution of fusarial infection for the years 1986 to 1995 at M.D. Anderson Cancer Center.

Close modal

Diagnosis was made antemortem in all 43 patients. All 43 patients received antifungal therapy consisting of regular or lipid formulations of amphotericin B, or an investigational triazole, SCH 39304 (Schering-Plough, Kenilworth, NJ). Granulocyte- (G-CSF) or granulocyte-macrophage (GM-CSF) colony-stimulating factor were part of the therapeutic regimen in 17 patients. Fifteen patients received granulocyte transfusion, seven after donor stimulation with G-CSF. Disseminated or invasive fusarial infection was documented at autopsy in 12 of 14 patients who underwent autopsy examination.

Thirteen patients responded to therapy (30%). Thirty patients died with disseminated infection, including two who initially responded but relapsed after subsequent episodes of neutropenia. Resolution of myelosuppression coincided with a favorable outcome in all 13 responders. Analysis of our cases shows significant differences among the 13 responders and the nonresponders (Table 2). Responders tended to be in remission from the underlying disease (100% v 10%) and to have an adequate number of circulating neutrophils (100% v 0%) and no significant (≥grade II) GVHD (0% v 66%). More responders had infection limited to the skin, sinuses, or lungs (15%) than nonresponders (3%), and had received G-CSF–stimulated white blood cell transfusions (24% v 13%).

Table 2.

Characteristics of Patients With Hematologic Cancer and Fusariosis: Comparison Between Responders and Nonresponders

CharacteristicRespondersNonresponders
(n = 13)(n = 30)
Age (year) 
Median 52 42 
Range 22-75 14-71 
Sex (males/females) 7/6 19/11 
Underlying disease (n) 
Acute nonlymphocytic leukemia 17 
Acute lymphocytic leukemia 
Other hematologic disorders 10 
Active underlying disease at start of infection (n) 10 28 
Active underlying disease at end of infection (n) 27 
Patients with neutropenia at start of infection (n) 27 
Patients with neutropenia at end of infection (n) 30 
Duration of neutropenia (d) 
Median 23 26 
Range 0-55 5-65 
Type of transplant (12 patients) (n) 
Autologous 
Allogeneic 
Patients with GVDH at start of infection* (n) 
Prior history of invasive fungal infection (n) 
Cumulative dose of AmB (mg) 
Median 1,380 775 
Range 720-2,740 120-4,295 
Cumulative dose of liposomal preparations of AmB (mg) 
Median 7,100 5,325 
Range 4,215-31,525 1,700-28,995 
Patients receiving growth factors (n) 10 
Start of infection after BMT (d) 
Median 30 46 
Range 13-73 7-151 
Patients receiving WBC transfusions (G-CSF–elicited) (n) 
Extent of infection (n) 
Disseminated 11 29 
Limited 
CharacteristicRespondersNonresponders
(n = 13)(n = 30)
Age (year) 
Median 52 42 
Range 22-75 14-71 
Sex (males/females) 7/6 19/11 
Underlying disease (n) 
Acute nonlymphocytic leukemia 17 
Acute lymphocytic leukemia 
Other hematologic disorders 10 
Active underlying disease at start of infection (n) 10 28 
Active underlying disease at end of infection (n) 27 
Patients with neutropenia at start of infection (n) 27 
Patients with neutropenia at end of infection (n) 30 
Duration of neutropenia (d) 
Median 23 26 
Range 0-55 5-65 
Type of transplant (12 patients) (n) 
Autologous 
Allogeneic 
Patients with GVDH at start of infection* (n) 
Prior history of invasive fungal infection (n) 
Cumulative dose of AmB (mg) 
Median 1,380 775 
Range 720-2,740 120-4,295 
Cumulative dose of liposomal preparations of AmB (mg) 
Median 7,100 5,325 
Range 4,215-31,525 1,700-28,995 
Patients receiving growth factors (n) 10 
Start of infection after BMT (d) 
Median 30 46 
Range 13-73 7-151 
Patients receiving WBC transfusions (G-CSF–elicited) (n) 
Extent of infection (n) 
Disseminated 11 29 
Limited 
*

Grade II or greater acute GVHD of extensive chronic GVHD.

Primary skin, sinus, lung.

We attempted to define the primary source of infection based on clinical and laboratory findings. The two most common sites of infection were the skin (14 patients) or the sinopulmonary tree (13 patients). Skin breakdown was secondary to trauma (eight patients), onychomycosis with associated cellulitis (four patients), and a spider bite (two patients). In 16 patients, the primary source of infection could not be determined, although the sinopulmonary tree was possibly the primary source of infection in four patients.

The literature search yielded 42 reports with a total of 54 cases of invasive or disseminated fusarial infection in patients with hematologic cancer.19-60 Infections caused by Fusarium have been reported from different institutions treating patients with cancer from four continents, America (40 reports), Europe (30 reports), Asia (seven reports), and Australia (one report).19-99 Not all of these reports were included in our comparison, because they did not fulfill the criteria for disseminated or invasive fusariosis and some of them occurred in patients without hematologic malignancy. Clinicopathologic features were compared in 54 reported patients with an underlying hematologic malignancy and invasive or disseminated fusarial infection versus patients treated at our Center (Table 1).

Fusarium solani was the predominantly isolated species both in the literature and in our series, followed by F moniliforme, F oxysporum, and F proliferatum. There was only one report of infection caused by F napiforme,49  whereas we isolated F semitecum, F dimerum, and F equiseti in one case each of our current series.

Patient characteristics were comparable in both series regarding sex, underlying disease (mostly acute nonlymphocytic leukemia with active disease), therapy (cytotoxic chemotherapy with or without bone marrow transplantation), and neutropenia, although patients from our center were older.

A specific portal of entry of Fusarium infection was discussed in only a few reports, and was presumed to be the respiratory tract in five reports.28,35,44,54,73 Onychomycosis was reported as the potential primary source of the infection in only three reports,28,77,81 whereas the infection was considered secondary to wound contamination in four case reports.25,28,39,73 In two reports, the infection was thought to originate in the gastrointestinal tract.32,67 A catheter was considered the origin of disseminated infection by two studies,24,64 and fungemia by two others.87 88 By contrast, a potential source of entry (skin or respiratory tract) was identified in the majority of our patients.

The clinical presentation of invasive fusarial infection in our patients was similar to that of the reported patients. Fever refractory to antibacterial antibiotics was frequently observed, followed by sinusitis and/or pneumonia. Skin lesions both primary and metastatic were common in both series and consisted mainly of subcutaneous nodules, at times vesicular, and of ecthyma gangrenosum–like lesions with a black necrotic center. Similar to the findings of our series, infection documentation was achieved mainly through cultures of the bloodstream (56%) or the primary or metastatic skin lesions (72%).

Fig. 4.

Comparison of the clinicopathologic features of aspergillosis and fusariosis. BMT, bone marrow transplant.

Fig. 4.

Comparison of the clinicopathologic features of aspergillosis and fusariosis. BMT, bone marrow transplant.

Close modal

Resolution of infection was reported in a higher proportion of patients (26 of 54, 48%) than in our series (13 of 43, 30%). As expected, recovery from the infection occurred only in patients with resolving myelosuppression, whereas relapse was observed exclusively among patients who received additional myeloablative therapy after an apparent resolution of the initial fusarial infection.

This study constitutes the largest series of invasive fusarial infection in a well-defined population of patients with hematologic cancer treated at a single institution. Although our results are in agreement with findings reported by our group and others in smaller series and case reports,19-60 new findings have emerged, possibly due to the larger sample size of our current study and inclusion of consecutive patients: (1) The significant role of the skin as a portal of entry for the infection. Although this has been previously reported by us and others, the importance of this finding had been underestimated, with the majority of the reports focusing on the respiratory route of infection. The incidence observed in our larger series is therefore a better reflection of the role of the skin as a primary source; (2) The response of these infections to novel therapeutic modalities, particularly cytokine-stimulated granulocyte transfusions; (3) The high risk of recurrence following subsequent myelosuppression; (4) The bimodal distribution (before and after engraftment) in bone marrow transplant recipients; (5) The description of the spectrum and evolution of metastatic fusarial skin lesions from subcutaneous lesions, usually painful, to erythematous indurations, followed by ecthyma gangrenosum–like necrotic lesions, which may be surrounded in the occasional patient by a thin rim of erythema. We have coined the term “target lesion” for this finding, which we believe is only seen with fusarial infection; (6) The characterization of the pulmonary radiologic findings, from nonspecific infiltrates to nodular and/or cavitary lesions. However, of note is the fact that not all pulmonary radiologic findings were histopathologically proven to be secondary to fusariosis, and they could have been caused by other pathogens that were not recovered. Confirmation of our radiologic findings by others is needed.

The clinical implications of these new findings are many. Since the skin is frequently the primary source of these life-threatening infections, every attempt to prevent these infections from occurring and/or spreading should be made. Hence, we recommend that patients with hematologic cancer and onychomycosis and/or a significant break in the integrity of skin surfaces who are about to undergo cytotoxic chemotherapy and/or bone marrow transplantation be evaluated by a dermatologist to ascertain the nature of the onychomycosis or skin breakdown and rule out the presence of fusarial infection. These patients are likely to benefit from local therapy including surgical debridement of the infected area and topical application of the antifungal natamycin, known to have adequate antifusarial activity.63 In the presence of cellulitis, a bone scan should be obtained to rule out osteomyelitis, and consideration should be given to resection of all infected tissues. In addition, primary skin lesions following a trauma or a bite, such as a spider bite, should be considered in these high-risk patients as potentially infected by Fusarium species, hence requiring biopsy and culture and surgical debridement if fusarial origin is confirmed. Although amphotericin B and itraconazole have limited activity against fusarial infections, administration of either of these agents (or of the lipid formulations of amphotericin B) in patients with primary fusarial skin lesions who are about to undergo cytotoxic chemotherapy or bone marrow transplantation should be seriously considered.

Because of the high rate of relapse and death in patients with a prior history of invasive fusarial infection, clinicians should consider either postponing cytotoxic therapy or using prophylactic G-CSF– or GM-CSF–stimulated granulocyte transfusion if a delay in treating the underlying cancer is not a viable option.100 Since CSF-elicited granulocyte transfusions do not represent the standard of care, this approach should be evaluated in the setting of a research protocol. We believe that this novel therapy modality should also be considered as early as possible in patients with invasive fusarial infection who are likely to have spontaneous recovery from myelosuppression. This recommendation is based on the high mortality rate for disseminated fusariosis in the setting of persistent profound neutropenia101 and the favorable responses seen in patients who received white blood cell transfusions and subsequently had resolution of the myelosuppression.100 The granulocyte transfusions may thus “buy time” until spontaneous recovery occurs. Additional data are needed before granulocyte transfusions can be readily recommended as a standard of care for these patients. The antifungal triazole SCH 39304 is no longer available, but a closely related drug is currently under investigation and may prove useful in this setting.102 Amphotericin B lipid complex is now available in the United States and has been associated with good responses in some patients.103 

Our findings with regard to the type of metastatic skin lesions should raise the index of suspicion of fusarial infection and prompt skin biopsy and culture and initiation of appropriate therapy. Since both nodular and cavitary lesions can be observed with fusarial infection, Fusarium should be added to Aspergillus and other pathogens in the differential diagnosis of pulmonary lesions in febrile neutropenic patients with hematologic cancer. Fusarium should also be considered in the differential diagnosis of invasive mold infections following engraftment in bone marrow transplant recipients, since fusarial infections may mimic aspergillosis, which is known to occur postengraftment in bone marrow transplant recipients (Fig 4).

Our findings also confirm those reported by our group and others including the ability to culture Fusarium from the bloodstream with regularity, the high frequency of metastatic skin lesions, the high mortality rate associated with this infection, the poor antifungal activity of amphotericin B, and the importance of the sinopulmonary tree as a potential portal of entry.101 Appropriate infection-control measures should be taken in cancer wards where fusarial infections have occurred, and an aggressive search for a potential source should be conducted. Our findings also confirm the potential of this infection to cause osteomyelitis,85,104-107 deep infections of the eye with potential of loss of vision,35,108-111 and catheter-related infections,101 hence requiring prompt diagnosis and treatment, including surgical debridement of the infected organ and removal of the venous catheter in patients with catheter-related fungemia.

Fig. 5.

Algorithm for the diagnosis and management of Fusarial infection. G-CSF, granulocyte colony-stimulating factor.

Fig. 5.

Algorithm for the diagnosis and management of Fusarial infection. G-CSF, granulocyte colony-stimulating factor.

Close modal

The lower response rate observed in our series as compared with the literature could be best explained by the referral pattern at our institution, a tertiary cancer center where heavily pretreated patients with refractory disease are frequently referred, and the higher percentage of patients with disseminated infection in our series. Unfortunately, complete data on most patients reported in the literature were not available, including information such as the status of the underlying disease, the extent of the infection, and the length and duration of neutropenia. In addition, the literature reflects a series of case reports, as opposed to our series of consecutive patients. In general, patients with a successful outcome are more likely to be reported in single case reports than patients who failed to respond to therapy.

Giving the high fatality rate of this infection, every effort at early diagnosis should be made. In Fig 5, we have outlined clues that should raise the index of suspicion for the presence of fusarial infection in this patient population, and practical guidelines for the clinical evaluation and management of this infection are given.

The number of patients included in our study was substantial, but we must point out some of the limitations of our study that stemmed from its retrospective nature. For example, we did not prospectively evaluate the evolution of the skin lesions, the onychomycosis, the radiologic findings, or the rate of bloodstream infection, nor did we conduct a therapeutic trial focused on this serious infection. In addition, not all of our cases of pulmonary infection were histopathologically documented.

In conclusion, invasive fusarial infections represent an increasing cause of infectious morbidity and mortality in patients with hematologic cancer. These infections are either airborne or inoculated through breakdown of the skin barrier. Once established, these infections are refractory to standard antifungal therapy and appear to respond to novel therapeutic modalities such as investigational or newly released lipid-associated amphotericin B or CSF-stimulated granulocyte transfusions. Every attempt should be made to prevent these infections from occurring.

Address reprint requests to Elias J. Anaissie, MD, Professor of Medicine, The University of Arkansas for Medical Sciences, 4301 W Markham, MS 508, Little Rock, AR 72205.

1
Uzun
 
O
Anaissie
 
EJ
Antifungal prophylaxis in patients with hematological malignancies: A reappraisal.
Blood
86
1995
2063
2
Meyers JD: Infection in recipients of bone marrow transplants, in Remington JS, Swartz MN (eds): Current Topics in Infectious Diseases. New York, NY, McGraw-Hill, 1985, p 262
3
Meyers JD: Infection in bone marrow transplant recipients. Am J Med 81:27, 1986 (suppl 1A)
4
Allan
 
BT
Patton
 
D
Ramsey
 
NK
Day
 
DL
Pulmonary fungal infections after bone marrow transplantation.
Pediatr Radiol
18
1988
118
5
Stein DK, Sugar AM: Fungal infections in the immunocompromised host. Diagn Microbiol Infect Dis 12:221S, 1989 (suppl 4)
6
Pizzo
 
PA
Walsh
 
TJ
Fungal infections in the pediatric cancer patient.
Semin Oncol
17
1990
6
7
Meyers
 
JD
Fungal infections in bone marrow transplant patients.
Semin Oncol
17
1990
10
8
Brown
 
AE
Overview of fungal infections in cancer patients.
Semin Oncol
17
1990
2
9
Horn
 
R
Wong
 
B
Kiehn
 
TE
Armstrong
 
D
Fungemia in a cancer hospital: Changing frequency, earlier onset, and results of therapy.
Rev Infect Dis
7
1985
646
10
Denning DW: Epidemiology and pathogenesis of systemic fungal infections in the immunocompromised host. J Antimicrob Chemother 28:1, 1991 (suppl B)
11
Koll BS, Brown AE: The changing epidemiology of infections at cancer hospitals. Clin Infect Dis 17:S322, 1993 (suppl 2)
12
EORTC Invasive Fugal Infections Cooperative Group: Epidemiology of invasive fungal infections in bone marrow transplantation. Bone Marrow Transplant 14:S1, 1994 (suppl 5)
13
Goodman
 
JL
Winston
 
DJ
Greenfield
 
RA
Chandrasekar
 
PH
Fox
 
P
Kaizer
 
H
Shadduck
 
RK
Shea
 
TC
Stiff
 
P
Friedman
 
DJ
Powderly
 
WG
Silber
 
JL
Horowitz
 
H
Lichtin
 
A
Wolff
 
SN
Mangan
 
KF
Silver
 
SM
Weisdorf
 
D
Ho
 
WG
Gilbert
 
G
Buell
 
D
A controlled trial of fluconazole to prevent fungal infections in patients undergoing bone marrow transplantation.
N Engl J Med
326
1992
845
14
Anaissie
 
EJ
Bodey
 
GP
Rinaldi
 
MG
Emerging fungal pathogens.
Eur J Clin Microbiol Infect Dis
8
1989
323
15
Anaissie EJ: Opportunistic mycoses in the immunocompromised host: Experience at a cancer center and review. Clin Infect Dis 14:S43, 1992 (suppl)
16
Morrison
 
VA
Haake
 
RJ
Weisdorf
 
DJ
The spectrum of non-Candida fungal infections following bone marrow transplantation.
Medicine
72
1993
78
17
Morrison
 
VA
Haake
 
RJ
Weisdorf
 
DJ
Non-Candida fungal infections after bone marrow transplantation: Risk factors and outcome.
Am J Med
96
1994
497
18
Pfaller
 
M
Wenzel
 
R
Impact of the changing epidemiology of fungal infections in the 1990s.
Eur J Clin Microbiol Infect Dis
11
1992
287
19
Anaissie
 
E
Kantarjian
 
H
Jones
 
P
Barlogie
 
B
Luna
 
M
Lopez-Berestein
 
G
Bodey
 
GP
Fusarium, a newly recognized fungal pathogen in immunosuppressed patients.
Cancer
57
1986
2141
20
Anaissie
 
E
Kantarjian
 
H
Ro
 
J
Hopfer
 
R
Rolston
 
K
Fainstein
 
V
Bodey
 
G
The emerging role of Fusarium infections in patients with cancer.
Medicine
67
1988
77
21
Cho
 
CT
Vats
 
TS
Lowman
 
JT
Brandsberg
 
JW
Tosh
 
FE
Fusarium solani infection during treatment for acute leukemia.
J Pediatr
83
1973
1028
22
Young
 
NA
Kwong-Chung
 
KJ
Kubota
 
TT
Jennings
 
AE
Fischer
 
RI
Disseminated infection by Fusarium moniliforme during treatment for malignant lymphoma.
J Clin Microbiol
7
1978
589
23
Perez-Villaroya JC, Fernandez-Guerrero ML, Moran V, Ponte MC, Soriano F, Barat A, de Villalobos E: Fusarium oxysporum infection. J Infect 5:307, 1982 (letter)
24
Blazar
 
BR
Hurd
 
DD
Snover
 
DC
Alexander
 
JW
McGlave
 
PB
Invasive Fusarium infections in bone marrow transplant recipients.
Am J Med
77
1984
645
25
Chaulk
 
CP
Smith
 
PW
Feagler
 
JR
Verdirame
 
J
Commers
 
JR
Fungemia due to Fusarium solani in an immunocompromised child.
Pediatr Infect Dis
5
1986
363
26
June
 
CH
Beatty
 
PG
Shulman
 
HM
Rinaldi
 
MG
Disseminated Fusarium moniliforme infection after allogeneic marrow transplantation.
South Med J
41
1986
47
27
Veglia
 
KS
Marks
 
VJ
Fusarium as pathogen; a case of Fusarium sepsis and review of the literature.
J Am Acad Dermatol
16
1987
260
28
Datry
 
A
Leblond
 
V
Feger
 
C
Gabarre
 
J
Gueho
 
E
Lesco
 
G
Danis
 
M
Binet
 
JL
Gentilini
 
M
A propos de trois cas de mycose à Fusarium sp.
Bull Soc Fr Mycol Med
17
1988
137
29
Merz
 
WG
Karp
 
JE
Hoagland
 
M
Jett-Goheen
 
M
Junkins
 
JM
Hood
 
AF
Diagnosis and successful treatment of fusariosis in the compromised host.
J Infect Dis
158
1988
1046
30
Mowbray
 
DN
Paller
 
AS
Nelson
 
PE
Kaplan
 
RL
Disseminated Fusarium solani infection with cutaneous nodules in a bone marrow transplant patient.
Int J Dermatol
27
1988
698
31
Nati
 
R
Dreyfus
 
F
Lanore
 
JJ
Brunet
 
F
Robin
 
P
Bordier
 
C
Dupouy-Camet
 
J
Localization cutanées d' une septicémie à Fusarium oxysporum survenant chez un patient en aplasie médullaire.
Ann Dermatol Venereol
115
1988
337
32
Richardson
 
SE
Bannatyne
 
RM
Summerbell
 
RC
Milliken
 
J
Gold
 
R
Weitzman
 
SS
Disseminated fusarial infection in the immunocompromised host.
Rev Infect Dis
10
1988
1171
33
Rippon
 
JW
Larson
 
RA
Rosenthal
 
DM
Clayman
 
J
Disseminated cutaneous and peritoneal hyalohyphomycosis caused by Fusarium species: Three cases and review of the literature.
Mycopathologia
101
1988
105
34
Summerbell
 
RC
Richardson
 
SE
Kane
 
J
Fusarium proliferatum as an agent of disseminated infection in an immunosuppressed patient.
J Clin Microbiol
26
1988
82
35
Venditti
 
M
Micozzi
 
A
Gentille
 
G
Polonelli
 
L
Morace
 
G
Bianco
 
P
Avvisati
 
G
Papa
 
G
Martino
 
P
Invasive Fusarium solani infections in patients with acute leukemia.
Rev Infect Dis
10
1988
653
36
Minor
 
RL
Pfaller
 
MA
Gingrich
 
RD
Burns
 
LJ
Disseminated Fusarium infections in patients following bone marrow transplantation.
Bone Marrow Transplant
4
1989
653
37
Helm
 
TN
Longworth
 
DL
Hall
 
GS
Bolwell
 
BJ
Fernandez
 
B
Tomecki
 
KJ
Case report and review of resolved fusariosis.
J Am Acad Dermatol
23
1990
393
38
Lupinetti
 
FM
Giller
 
RH
Trigg
 
ME
Operative treatment of Fusarium fungal infection of the lung.
Ann Thorac Surg
49
1990
991
39
Schneller
 
FRG
Gulati
 
SC
Cunningham
 
IB
O'Reilly
 
RJ
Schmitt
 
HJ
Clarkson
 
BD
Fusarium infections in patients with hematologic malignancies.
Leuk Res
14
1990
961
40
Agamanolis
 
DP
Kalwinsky
 
DK
Krill
 
CE
Dasu
 
S
Halasa
 
B
Galloway
 
PG
Fusarium meningoencephalitis in a child with acute leukemia.
Neuropediatrics
22
1991
110
41
Gamis
 
AS
Gudnason
 
GS
Giebink
 
GS
Ramsay
 
NKC
Disseminated infection with Fusarium in recipients of bone marrow transplants.
Rev Infect Dis
13
1991
1077
42
Robertson
 
MJ
Socinski
 
MA
Soiffer
 
RJ
Finberg
 
RW
Wilson
 
C
Anderson
 
KC
Bosserman
 
L
Sang
 
DN
Salkin
 
IF
Ritz
 
J
Successful treatment of disseminated Fusarium infection after autologous bone marrow transplantation for acute myeloid leukemia.
Bone Marrow Transplant
8
1991
143
43
Alvarez-Franco
 
M
Reyes-Mugica
 
M
Paller
 
AS
Cutaneous Fusarium infection in an adolescent with acute leukemia.
Pediatr Dermatol
9
1992
62
44
Brint
 
JM
Flynn
 
PM
Pearson
 
TA
Pui
 
CH
Disseminated fusariosis involving bone in an adolescent with leukemia.
Pediatr Infect Dis J
11
1992
965
45
Nucci
 
M
Spector
 
N
Lucena
 
S
Bacha
 
PC
Pulcheri
 
W
Lamosa
 
A
Derossi
 
A
Caiuby
 
MJ
Macieira
 
J
Oliveira
 
HP
Three cases of infections with Fusarium species in neutropenic patients.
Eur J Clin Microbiol Infect Dis
11
1992
1160
46
Patoux-Pibouin
 
M
Couatarmanach
 
A
Le Gall
 
F
Bergeron
 
C
De Bièvre
 
C
Guiguen
 
C
Chevrant-Breton
 
J
Fusariose à Fusarium solani chez un adolescent leucémique.
Ann Dermatol Venereol
119
1992
377
47
Caux
 
F
Aractingi
 
S
Baurmann
 
H
Reygagne
 
P
Dombret
 
H
Romand
 
S
Dubertret
 
L
Fusarium solani cutaneous infection in a neutropenic patient.
Dermatology
186
1993
232
48
Drakos
 
PE
Nagler
 
A
Or
 
R
Naparstek
 
E
Kapelushnik
 
J
Engelhard
 
D
Rahav
 
G
Ne'emean
 
D
Slavin
 
S
Invasive fungal sinusitis in patients undergoing bone marrow transplantation.
Bone Marrow Transplant
12
1993
203
49
Melcher
 
GP
McGough
 
DA
Fothergill
 
AW
Norris
 
C
Rinaldi
 
MG
Disseminated hyalohyphomycosis caused by a novel human pathogen, Fusarium napiforme.
J Clin Microbiol
31
1993
1461
50
Martino P, Gastaldi R, Raccah R, Girmenia C: Clinical patterns of Fusarium infections in immunocompromised patients. J Infect 28:7, 1994 (suppl 1)
51
Rabodonirina
 
M
Piens
 
MA
Monier
 
MF
Guého
 
E
Fière
 
D
Mojon
 
M
Fusarium infections in immunocompromised patients: Case reports and literature review.
Eur J Clin Microbiol Infect Dis
13
1994
152
52
Sunshine
 
JL
Gentili
 
A
Imaging of disseminated infection by a rare fungal pathogen, Fusarium.
Clin Nucl Med
19
1994
435
53
Bushelman
 
SJ
Callen
 
JP
Roth
 
DN
Cohen
 
LM
Disseminated Fusarium solani infection.
J Am Acad Dermatol
32
1995
346
54
Freidank
 
H
Hyalohyphomycosis due to Fusarium sp. Two case reports and review of the literature.
Mycoses
38
1995
69
55
Barrios
 
NJ
Kirkpatrick
 
DV
Murciano
 
A
Stine
 
K
Van Dyke
 
RB
Humbert
 
JR
Successful treatment of disseminated Fusarium infection in an immunocompromised child.
Am J Pediatr Hematol Oncol
12
1990
319
56
Viviani
 
AM
Cofrancesco
 
E
Boschetti
 
C
Tortorano
 
AM
Cortellaro
 
M
Eradication of Fusarium infection in a leukopenic patient treated with liposomal amphotericin B.
Mycoses
34
1991
255
57
Cofrancesco
 
E
Boschetti
 
C
Viviani
 
MA
Bargiggia
 
C
Tortorano
 
AM
Cortellaro
 
M
Zanussi
 
C
Efficacy of liposomal amphotericin B (AmBisome) in the eradication of Fusarium infection in a leukaemic patient.
Haematologica
77
1992
280
58
Spielberger
 
RT
Falleroni
 
MJ
Coene
 
AJ
Larson
 
RA
Concomitant amphotericin B therapy, granulocyte transfusions, and GM-CSF administration for disseminated infection with Fusarium in a granulocytopenic patient.
Clin Infect Dis
16
1993
528
59
Hennequin
 
C
Benkerrou
 
M
Gaillard
 
JL
Blanche
 
S
Fraitag
 
S
Role of granulocyte colony-stimulating factor in the management of infection with Fusarium oxysporum in a neutropenic child.
Clin Infect Dis
18
1994
490
60
Engelhard
 
D
Eldor
 
A
Polacheck
 
I
Hardan
 
I
Ben-Yehuda
 
D
Amselem
 
S
Salkin
 
IF
Lopez-Berestein
 
G
Sacks
 
T
Rachmilewitz
 
EA
Barenholz
 
Y
Disseminated visceral fusariosis treated with amphotericin B–phospholipid complex.
Leuk Lymphoma
9
1993
385
61
Ellis
 
ME
Clink
 
H
Younge
 
D
Hainau
 
B
Successful combined surgical and medical treatment of Fusarium infection after bone marrow transplantation.
Scand J Infect Dis
26
1994
225
62
Hay RJ: Liposomal amphotericin B, Ambisome. J Infect 28:35, 1994 (suppl 1)
63
Reuben
 
A
Anaissie
 
EJ
Nelson
 
PE
Hashem
 
R
Legrand
 
C
Ho
 
DH
Bodey
 
GP
Antifungal susceptibility of 44 isolates of Fusarium species determined by using a broth microdilution method.
Antimicrob Agents Chemother
33
1989
1647
64
Anaissie
 
EJ
Hashem
 
R
Legrand
 
C
Legenne
 
P
Nelson
 
P
Bodey
 
GP
Lack of activity of amphotericin B in systemic murine fusarial infection.
J Infect Dis
165
1992
1155
65
Kiehn
 
TE
Nelson
 
PE
Bernard
 
EM
Edwards
 
FF
Koziner
 
B
Armstrong
 
D
Catheter-associated fungemia caused by F. chlamydosporum in a patient with lymphocytic lymphoma.
J Clin Microbiol
21
1985
501
66
Gutmann
 
L
Chou
 
SM
Pore
 
RS
Fusariosis, myasthenic syndrome and aplastic anemia.
Neurology
25
1975
922
67
Krick
 
JA
Remington
 
JS
Opportunistic invasive fungal infections in patients with leukemia and lymphoma.
Clin Haematol
5
1976
249
68
Mutton
 
KJ
Lucas
 
TJ
Harkness
 
JL
Disseminated Fusarium infection.
Med J Aust
2
1980
624
69
Raicu
 
MD
Infectie diseminata cu Fusarium sp.
Rev Ig Bacteriol Virusol Parazitol Epidemiol
28
1984
69
70
Ohnishi
 
M
Koyama
 
S
Kishi
 
K
Moriyama
 
Y
Shinada
 
S
Hattori
 
A
Shibata
 
A
Fusarium infection during the first remission induction therapy in a patient with acute lymphocytic leukemia.
Rinsho Ketsueki
26
1985
442
71
Dreizen
 
S
McCredie
 
KB
Bodey
 
GP
Keating
 
MJ
Unusual mucocutaneous infections in immunosuppressed patients with leukemia — Expansion of an earlier study.
Postgrad Med
79
1986
287
72
Matsuda
 
T
Matsumoto
 
T
Disseminated hyalohyphomycosis in a leukemic patient.
Arch Dermatol
122
1986
1171
73
Okuda
 
C
Ito
 
M
Sato
 
Y
Oka
 
K
Hotchi
 
M
Disseminated cutaneous Fusarium infection with vascular invasion in a leukemic patient.
J Med Vet Mycol
25
1987
177
74
Lacroix
 
C
Jacquemin
 
JL
Mycoses profondes dues à Acremonium et à Fusarium.
Bull Soc Fr Mycol Med
17
1988
351
75
Dermoumi H, Petrasch S, Quabeck K: Systemische fusariosen bei immundefizienten patienten. Med Klin 85:166, 1990 (suppl 1)
76
El-Ani
 
AS
Disseminated infection caused by Fusarium solani in a patient with aplastic anemia.
NY State J Med
90
1990
609
77
Lozano M, Ribera JM, Puig J, Rives A, Sierra J, Granena A, Rozman C: Fusarium solani bronchopneumonia in a patient with acute myeloblastic leukemia. Enferm Infecc Microbiol Clin 8:124, 1990 (letter)
78
Nadler JP: Disseminated fusarial infection. Rev Infect 12:162, 1990 (letter)
79
Rutten
 
A
Hantschke
 
D
Goos
 
M
Kutane manifestation einer pilzepsis.
Hautarzt
41
1990
392
80
Viscoli
 
C
Castagnola
 
CE
Moroni
 
C
Garaventa
 
A
Manno
 
G
Savioli
 
C
Infection with Fusarium species in two children with neuroblastoma.
Eur J Microbiol Infect Dis
9
1990
773
81
Alvarez-Franco
 
M
Reyes-Mugica
 
M
Paller
 
AS
Cutaneous Fusarium infection in an adolescent with acute leukemia.
Pediatr Dermatol
9
1992
62
82
Girmenia C, Arcese W, Micozzi A, Martino P, Bianco P, Morace G: Onychomycosis as a possible origin of disseminated Fusarium solani infection in a patient with severe aplastic anemia. Clin Infect Dis 14:1167, 1992 (letter)
83
Herbrecht
 
R
Waller
 
J
Dufour
 
P
Koening
 
H
Lioure
 
B
Marcellin
 
L
Oberling
 
F
Rare opportunistic fungal diseases in patients with organ or bone marrow transplantation.
Agressologie
33
1992
77
84
Madhavan
 
M
Ratnakar
 
C
Veliath
 
AJ
Kanungo
 
R
Robinson
 
Smile S
Bhat
 
S
Primary disseminated fusarial infection.
Postgrad Med J
68
1992
143
85
Mascar'o J, Vadillo M, Ferrer JE, Carratal'a J: Post-traumatic osteomyelitis caused by Fusarium solani. Enferm Infecc Microbiol Clin 10:508, 1992 (letter)
86
Neumeister
 
B
Bartmann
 
P
Gaedicke
 
G
Marre
 
R
A fatal infection due to Fusarium oxysporum in a child with Wilms' tumor. Case report and review of the literature.
Mycoses
35
1992
115
87
Nucci
 
M
Pulcheri
 
W
Spector
 
N
Maiolino
 
A
Caiuby
 
MJ
Cutaneous involvement of systemic fungal infections in neutropenic patients.
Haematologica
77
1992
522
88
Ammari
 
LK
Puck
 
JM
McGowan
 
KL
Catheter-related Fusarium solani fungemia and pulmonary infection in a patient with leukemia in remission.
Clin Infect Dis
16
1993
148
89
Castagnola
 
E
Garaventa
 
A
Conte
 
M
Barretta
 
A
Faggi
 
E
Viscoli
 
C
Survival after fungemia due to Fusarium moniliforme in a child with neuroblastoma.
Eur J Clin Microbiol Infect Dis
12
1993
308
90
Drakos
 
PE
Nagler
 
A
Or
 
R
Naparstek
 
E
Kapelushnik
 
J
Engelhard
 
D
Rahav
 
G
Ne'emean
 
D
Slavin
 
S
Invasive fungal sinusitis in patients undergoing bone marrow transplantation.
Bone Marrow Transplant
12
1993
203
91
Krcmery
 
V Jr
Fuchsberger
 
P
Trupl
 
J
Blabova
 
M
Danisovicova
 
A
Svek
 
J
Drgona
 
L
Fungal pathogens in etiology of septic shock in neutropenic patients with cancer.
Int J Med Microbiol Virol Parasitol Infect Dis
278
1993
562
92
Mardiak J, Danisovicova A, Trupl J, Sloboda J, Jesenska Z, Krcmery V Jr: Three cases of fatal infection due to Fusarium solani in patients with cancer. Clin Infect Dis 17:930, 1993 (letter)
93
Jesenka
 
Z
Fusarium and fusariosis.
Epidemiol Mikrobiol Imunol
43
1994
142
94
Smith
 
AG
Bustamante
 
CI
Wood
 
C
Disseminated cutaneous and vascular invasion by Fusarium moniliforme in a fatal case of acute lymphocytic leukemia.
Mycopathologia
122
1993
15
95
Louie
 
T
el Baba
 
F
Shulman
 
M
Jimenez-Lucho
 
V
Endogenous endophthalmitis due to Fusarium: Case report and review.
Clin Infect Dis
18
1994
585
96
Patel
 
AS
Hemady
 
RK
Rodrigues
 
M
Rajagopalan
 
S
Elman
 
MJ
Endogenous Fusarium endophthalmitis in a patient with acute lymphocytic leukemia.
Am J Ophthalmol
117
1994
363
97
Perez MC, Campos-Herrero MI, Mataix R, Elcuaz R, Gomez-Casares T, Pena JM, Campo C: Fusarium sp. disseminated infection in an allogeneic bone marrow transplantation recipient. Enferm Infecc Microbiol Clin 12:358, 1994 (letter)
98
Schell
 
WA
New aspects of emerging fungal pathogens. A multifaceted challenge.
Clin Lab Med
15
1995
365
99
Myoken
 
Y
Sugata
 
T
Kyo
 
T
Fujihara
 
M
Oral Fusarium infection in a granulocytopenic patient with acute myelogenous leukemia: A case report.
J Oral Pathol Med
24
1995
237
100
Fleming R, Anaissie EJ, O'Brien S, Kantarjian H, Estey E, Lichtiger B, Jendiroba B, Freireich E: Treatment of neutropenia-related fungal infections with G-CSF mobilized granulocytes transfusions. Proceedings of the 38th Annual Meeting of the American Society of Hematology, Orlando, FL, December 6-10, 1996
101
Nelson
 
PE
Dignani
 
CM
Anaissie
 
EJ
Taxonomy, biology, and clinical aspects of Fusarium species.
Clin Microbiol Rev
7
1994
479
102
Anaissie
 
EJ
Kontoyiannis
 
DP
Kantarjian
 
HM
Vartivarian
 
S
O'Brien
 
Giralt SA
Anderson
 
BS
Karl
 
S
Champlin
 
RE
Bodey
 
GP
Effectiveness of an oral triazole for opportunistic mold infections in patients with cancer: Experience with SCH 39304.
Clin Infect Dis
17
1993
1022
103
Anaissie EJ, Ramphal R, Horwith G: Efficacy and safety of amphotericin B lipid complex injection in the treatment of patients with fusariosis. Proceedings of the 38th Annual Meeting of the American Society of Hematology, Orlando, FL, December 6-10, 1996
104
Bourguinion
 
RL
Walsh
 
AF
Flynn
 
JC
Baro
 
C
Spinos
 
E
Fusarium species osteomyelitis.
J Bone Joint Surg Am
58
1976
722
105
Page
 
JC
Friedlander
 
C
Dockery
 
GL
Postoperative Fusarium osteomyelitis.
J Foot Surg
21
1982
174
106
Jakle
 
C
Leek
 
J
Olson
 
D
Robbins
 
DL
Septic arthritis due to Fusarium solani.
J Rheumatol
10
1983
151
107
Gradon J, Lerman A, Lutwick L: Septic arthritis due to Fusarium moniliforme. Rev Infect Dis 12:716, 1990 (letter)
108
Lieberman
 
TW
Ferry
 
AP
Bottone
 
EJ
Fusarium solani endophthalmitis without primary corneal involvement.
Am J Ophthalmol
88
1979
764
109
Pflugfelder
 
SC
Flynn
 
HW
Zwickey
 
TA
Forster
 
RK
Tsiligianni
 
A
Culberston
 
WW
Mandelbaum
 
S
Exogenous fungal endophthalmitis.
Ophthalmology
95
1988
19
110
Brod RD, Clarkson JG, Flynn HW Jr, Green WR: Endogenous fungal endophthalmitis, in Duane TD (ed): Clinical Ophthalmology, vol 3. Philadelphia, PA, Lippincott, 1990
111
Comhaire-Poutchinian
 
Y
Berthe-Bonnet
 
S
Grek
 
V
Cremer
 
V
Endophthalmie à Fusarium: Une étiologie exceptionnelle.
Bull Soc Belge Ophthalmol
239
1990
75
Sign in via your Institution