Authors: Marcio Nucci, M.D.Elias Anaissie, M.D.


Fusarium is a plant and human pathogen widely distributed in soil, subterranean and aerial plant parts, plant debris and other organic substrates (44). In addition,Fusarium species are present in the water worldwide, as part of water biofilms (21). More than 50 species of Fusarium have been identified, including plant pathogens, but a few cause infections in humans. Fusarium solani is the most frequent species, accounting for about 50% of all infections, followed by Fusarium oxysporum (~20%), Fusarium verticillioidis and Fusarium moniliforme. Other species include Fusarium dimerum, Fusarium proliferatum, Fusarium chlamidosporum, Fusarium sacchari, Fusarium nygamai, Fusarium napiforme, Fusarium antophilum and Fusarium vasinfectum.

Fusarium species grow easily and rapidly in most media without cycloheximide. On potato dextrose agar, the colonies have a velvety or cottony surface, and are white, yellow, pink, purple salmon or gray on the surface, with a pale, red, violet, brown or sometimes blue reverse. Although the genus Fusarium can be identified by the production of hyaline, banana-shaped, multicellular macroconidia with a foot cell at the base, species identification is difficult and may require molecular methods. Recently, a commercially available PCR-based method (DiversiLab System) showed agreement with species sequence identification in 26 isolates of Fusarium species (31). In tissue, the hyphae are hyaline and septate filaments that typically dichotomize in acute and right angles. This pattern is typical of the agents of hyalohyphomycosis, and similar to that produced by Aspergillus species. In the absence of microbial growth, the differential diagnosis between fusariosis and other hyalohyphomycoses is difficult, and requires the use of in-situ hybridization in paraffin-embedded tissue specimens (30).


Fusarium species cause a broad spectrum of infections in humans, including allergic disease (sinusitis and bronchopulmonary disease), superficial, locally invasive, and disseminated infection (Table 1). The clinical form of fusariosis depends largely on the immune status of the host and the portal of entry if the infection. The most common infections in immunocompetent individuals are keratitis and onychomycosis. Less frequently, the infection may occur as a result of skin breakdown, such as burns and wounds (45), or the presence of foreign bodies, such as keratitis in contact lens wearers (16), peritonitis in patients receiving continuous ambulatory peritoneal dialysis (23), and catheter-associated fungemia (61). Other infections in immunocompetent patients include sinusitis (38), pneumonia (57), thrombophlebitis (42), fungemia with or without organ involvement (45), endophtalmitis (24), septic arthritis (36), and osteomyelitis (10).

Immunocompromised patients at high risk for fusariosis are those with prolonged neutropenia and T-cell immunodeficiency (11). Unlike infection in the normal host, fusariosis in the immunocompromised population is typically invasive and disseminated. In a review of 259 cases of fusariosis, including both immunocompromised and immunocompetent patients, 79 percent had a diagnosis of cancer (45). In a study of 84 patients with hematologic diseases, the infection occurred more frequently in patients with acute leukemia (56%), and most patients (83%) were neutropenic at diagnosis (46). On the other hand, HSCT recipients may develop late fusariosis, weeks or months after neutrophil recovery. In the allogeneic HSCT population, the infection has a trimodal pattern of occurrence: first peak in the early post-transplant period (during neutropenia), a second peak at a median of 70 days after transplant (patients with graft versus host disease [GvHD] receiving corticosteroids), and a later peak more than one year after transplant, usually in the setting of treatment of chronic extensive GvHD. Severe T-cell immunodeficiency and not neutropenia is the major risk factor for fusariosis in these patients (47).

The overall incidence of fusariosis per 1,000 HSCT recipients is 5.97 cases, and is lowest (1.4 – 2.0/1,000) among autologous HSCT, intermediate (2.28 – 5.0/1000) in matched-related and matched unrelated allogeneic HSCT, and highest (20.19/1000) among mismatched-related donor allogeneic HSCT (47).

The principal portal of entry for Fusarium spp. is the airways, followed by the skin at site of tissue breakdown, and possibly the mucosal membranes. A recent outbreak of fusarial keratitis resulted from contaminated solutions in contact lens wearers (1). Airborne fusariosis is thought to be acquired by the inhalation airborne conidia. Given the ubiquity of Fusarium species in the environment, fusariosis may be acquired both in the community and in the hospital, though most commonly during hospitalization, when the immune system of the host is severely impaired. Hospital water systems may be a reservoir for Fusarium spp. (6). Showering appears to be an efficient mechanism for the dispersion of airborne fusarial conidia and transmission to the immunosuppressed host, and molecular studies showed close relatedness between hospital water and patients’ isolates (6).

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Keratitis and Endophthalmitis

Fusarium is a frequent cause of fungal keratitis, with an incidence ranging from a low of 8% in India to a high of 75% in Tanzania (16). These differences may be related to climate characteristics, with the highest rates observed in tropical and sub-tropical areas compared to areas with temperate weather. The most frequent predisposing factor for fungal keratitis is corneal trauma by plants, animal matter, dusts and soil. The presence of an underlying corneal disease and/or the concomitant use of topical corticosteroids, antibiotics and contaminated contact lens or its paraphernalia also appear to increase the risk of fusarial keratitis. The clinical manifestations of fusarial keratitis are non-specific. In immunocompetent individuals, endophthalmitis caused by Fusarium spp. may occur as a complication of advanced keratitis (19) or ocular surgery, such as cataract extraction (22). By contrast, fusarial endophthalmitis in the immunosuppressed host results from hematogenous seeding, in the setting of disseminated infection (54).


Disease related to Fusarium spp. may manifest as allergic (63) and chronic non-invasive sinusitis in the immunocompetent host (59), and invasive sinusitis in both immunocompetent (38) and immunocompromised hosts (58). In the latter setting, sinusitis can serve as the port for disseminated fusariosis (4). Sinusitis occurred in 54 (18%) of 294 cases of fusariosis reported in the literature, and was more frequently seen in the setting of immunosuppression (52/262, 20%) than among immunocompetent hosts (2/32, 6%, p=0.06). Among immunocompromised patients, fusarial sinusitis is more common among patients with acute myeloid leukemia, and in those with profound neutropenia. Sinusitis occurs typically in the context of disseminated fusariosis (~70% of cases). The clinical manifestations of fusarial sinusitis are indistinguishable from those caused byAspergillus: nasal discharge and obstruction. Necrosis of the mucosa is a hallmark, and is a consequence of the angioinvasive nature of these mycoses. Periorbital and paranasal cellulitis may be present.


Lung involvement is common in invasive fusariosis. In a series of 84 patients with fusariosis and an underlying hematologic disease, lung infiltrates were present in 54% of patients and like in aspergillosis, consisted of non-specific alveolar or interstitial infiltrates, nodules and cavities. The clinical presentation is non-specific, with some presenting with a clinical picture similar to that of invasive aspergillosis, with dry cough, pleuritic chest pain and shortness of breath (46). Among 294 reported cases of fusariosis, lung involvement was present in 114 (39%), and was more common among immunocompromised patients. Risk factors for fusarial pneumonia include a diagnosis of acute leukemia, prolonged neutropenia and HSCT. Similar to allergic bronchopulmonary aspergillosis, Fusarium may also be associated with allergic bronchopulmonary disease (8).

Skin Involvement

A common feature of infection by Fusarium is the development of skin lesions, which are frequently the only source of diagnostic material. In a review of 259 published cases of fusariosis (232 immunocompromised and 27 immunocompetent) (45), skin involvement by fusariosis was present in 181 patients (70%). Lesions were localized in 13 of the 14 immunocompetent patients, and followed a recent history of skin breakdown at the site of the fusarial infection in 10 patients, either as a result of trauma (7 patients with cellulitis and necrosis) or of a preexisting onychomycosis (3 patients). Three additional patients presented with ulcerated lesions resembling chromoblastomycosis. The single case of disseminated metastatic skin lesion occurred in a child with no apparent underlying disease, who developed fever, pulmonary infiltrates, multiple erythematous papules and nodules, and several blood cultures yielding Fusarium sp.. Two cases of mycetoma caused by Fusarium spp. have been recently reported (60,64).

In immunocompromised patients, disseminated skin lesions predominate (45). These patients typically have multiple erythematous papular or nodular and painful lesions, frequently with central necrosis giving the lesions an ecthyma gangrenosum-like appearance. Target lesions (a thin rim of erythema of 1-3 cm in diameter surrounding the above-mentioned papular or nodular lesions) and bullae and vesicles may also appear. Fusarial skin lesions involve practically any site, with predominance for the extremities and evolve rapidly, usually over a few days. Lesions at different stages of evolution (papules, nodules and necrotic lesions) are frequent, and concomitant myalgias (suggesting muscle involvement) have also been described. Localized lesions in immunocompromised patients include primary cellulitis following skin breakdown (most commonly at the site of preexisting onychomycosis), periorbital cellulitis in patients with sinusitis, and primary ulcerative lesions.


A striking characteristic of fusariosis, as opposed to aspergillosis and most other invasive mould infections is the high frequency of positive blood cultures, usually in the context of disseminated disease. Among 294 reported cases, blood cultures yielded the organism in 119 (40.5%). Fungemia as the only manifestation of fusariosis occurred in 28 patients (9.5%): 1 of 32 immunocompetent patients (3%) and 27 of 262 immunocompromised patients (10%). In the latter population fungemia was more frequent in the absence of neutropenia (10/52, 19% vs. 17/210 in neutropenic patients, 8%, p=0.02). The mortality rate of patients with fungemia was lower than among those without (12/28, 43% vs. 167/266, 63%, p=0.04), probably because of the significant proportion of isolated fungemia among the former group, some of which with venous catheter-related infection. Ten cases of catheter-related fusarial infection were reported (3,1220,37,43,52,61), all with a favorable outcome following antifungal treatment and catheter removal.

Disseminated Infection

Disseminated disease is the most frequent clinical form of fusariosis in immunocompromised patients, and was reported in 79% of 84 patients with hematologic diseases (46), 75% of 61 HSCT recipients (47), and in 64% of all 294 published cases. Except for one patient, who did not have an underlying disease (45), all cases of disseminated fusariosis occurred in the setting of immunosuppression, usually among patients with acute leukemia (124/155, 80% vs. 64/139, 46%, p<0.001), HSCT recipients (53/67, 79% vs. 135/227, 59.5%, p=0.003), and those with profound neutropenia (168/210, 80% vs. 20/84, 24%, p<0.001). As expected, the death rate is higher among patients with disseminated disease (141/188, 75% vs. 38/106, 36%, p<0.001), and this association remained statistically significant even after controlling for the presence of neutropenia, HSCT, underlying disease and organ involvement. The most frequent pattern of disseminated disease is a combination of metastatic cutaneous lesions and positive blood cultures, with or without lung or sinus involvement. The typical clinical presentation is that of a patient with prolonged (>10 days) and profound (<100/mm3) neutropenia who is persistently febrile, and develops disseminated and characteristic skin lesions, with a positive blood culture for a mould.

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The diagnosis of fusariosis depends on the clinical form of the disease. The clinical picture is not of help in the diagnosis of keratitis, since the clinical manifestations are similar regardless of etiology (bacteria, fungi). Culture of corneal scraping (most frequent) or tissue biopsy is usually required for a definitive diagnosis. In invasive fusariosis, confirmatory diagnosis requires culture of the involved tissue and histopathology showing tissue invasion by the fungus. The typical histopathologic pattern is of tissue invasion by acute-branching, septate hyaline hyphae, a pattern common to all agents of hyalohyphomycosis, including Aspergillus species, Acremonium species,Scedosporium apiospermum and others. In the absence of microbial growth, the differential diagnosis between fusariosis and other hyalohyphomycoses is difficult, and requires the use of in-situ hybridization in paraffin-embedded tissue specimens (30).

The interpretation of the growth of Fusarium species from different biological materials depends on the clinical context. The clinician and the microbiologist must be cautious, because Fusarium species may contaminate laboratory specimens, and pseudo outbreaks of fusariosis have been reported (27). The isolation of several colonies from the same specimen or the same fungus from different specimens is highly suggestive of a true growth, whereas the isolation of a single colony from only one biological sample should raise the index of suspicion for contamination. A positive direct examination of the biological material in addition to the isolation of Fusarium species in culture suggests a true infection.

Although histopathology is considered important for the diagnosis, culture of sinus aspirate or respiratory secretions are virtually diagnostic of sinus and lung fusariosis, respectively, in the severely immunocompromised host. Among 54 reported cases of fusarial sinusitis, the sinuses were the main source of diagnosis in 11% of cases, usually by means of sinus biopsy or aspirate. Among 114 cases of fusariosis with pulmonary infiltrates, confirmation of lung involvement was obtained in 60 cases (53%). The most frequent pulmonary material that contributed to the diagnosis was lung tissue obtained from autopsy (63%), followed by sputum (17%), bronchial aspirate (8%), lung biopsy (7%) and bronchoalveolar lavage (5%).

Skin lesions are the single source of diagnosis of fusarial infection in a large proportion of patients (55%) of 181 reported patients with skin lesions. Diagnosis was based on culture (32 patients) and both culture and histopathology (68 patients) (45). In a series of 84 cases of fusariosis in patients with hematologic malignancies, skin lesions were present in 77% of cases and 55% had positive blood cultures. These two sites contributed to the diagnosis in 87% of cases (46). While there are no specific recommendations for the collection and processing of blood cultures for the diagnosis of fusariosis, a study compared the performance of aerobic and fungal medium of Bactec. The median time to positive blood culture was 5 days with both media, but fungal growth was detected earlier with the fungal media: 10 h for Fusarium dimerum, 14 hours forFusarium solani, and 35 hours for Fusarium verticillioides (33).

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Experimental Infections

Oral inoculation of Fusarium spp. in 24-day-old healthy chicks did not result in disseminated infection. Intranasal inoculation of Fusarium spp. caused disseminated infection to brain, liver, and air sacs. However, no mortality was observed (2). A murine model of lethal disseminated fusarial infection has been developed (39). F. solani conidia were injected intravenously into healthy and immunosuppressed CF1 mice, leading to 100% mortality. Survival was correlated with inoculum size, as mice injected with the higher inocula had shorter survival times. Neutropenia was also associated with shorter survival, absence of tissue inflammatory cellular reaction, and persistent disseminated infection. Histopathologic findings were similar in many respects to those seen in human infections: presence of necrotizing abscesses, acute branching septate hyphae, and neutrophil and macrophage infiltration. Endovascular invasion and thrombosis were also found. This reproducible murine model is currently used to study the pathogenesis of murine fusarial infections.

An interesting feature of Fusarium spp. is their ability to disseminate into the bloodstream, resulting in a high rate of isolation from blood culture specimens. The rate of isolation for most opportunistic molds, particularly Aspergillus spp., is very low (26). To understand the pathogenesis of this finding, a reproducible rabbit model that would allow frequent sampling of adequate volumes of blood was developed (5). Rabbits were pretreated with daily doses of triamcinolone and repeated intravenous doses of cyclophosphamide. Intravenous inoculation of F. solani conidia resulted in disseminated infection that was repeatedly documented by its isolation from blood cultures.

Determinants of Virulence of Fusarium Species

While the particular susceptibility of the host is a major determining factor in the establishment of infection by Fusariumspecies, it is also clear that the fungus possess several cellular and molecular attributes that, together, may confer different degrees of inherent virulence on these organisms. The combination of these virulence factors and the immunocompromised status of the host contribute to the development of invasive fusarial infections. Toxins, enzyme production, and adherence to prosthetic materials have all been postulated as virulence factors for Fusarium spp.

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Single Drugs

The typical antifungal susceptibility profile of Fusarium species is that of relative resistance to most antifungal agents. However, in vitro susceptibility may vary among different species, with Fusarium solani exhibiting higher MICs than Fusarium oxysporum (14). The MIC range for amphotericin B is high, usually 1-2 μg/ml, with MIC50 and MIC90 of 1 and 2 μg/ml, respectively. High MICs are also exhibited by other antifungal agents: itraconazole (MIC range 1-16 μg/ml, MIC50 >8 μg/ml, MIC90 >8 μg/ml), voriconazole (MIC range 0.25-16 μg/ml, MIC50 8 μg/ml, MIC90 >8 μg/ml), posaconazole (MIC range 0.5-8 μg/ml, MIC50 >8 μg/ml, MIC90 >8 μg/ml), and caspofungin (MIC range >8 μg/ml, MIC50 >8 μg/ml, MIC90 >8 μg/ml) (50). The echinocandins have no activity against Fusarium species (65).

Combination Drugs

The in vitro activity of voriconazole and micafungin was tested in one isolate of Fusarium solani. The MIC values of voriconazole before and after the addition of micafungin were 2 and 1 μg/ml, respectively, while the MIC values of micafungin before and after the addition of voriconazole were 64 and 0.03 μg/ml, respectively (34). In another study, the combination of anidulafungin with itraconazole, voriconazole or amphotericin B against 5 isolates of Fusarium solani and 2 isolates of Fusarium oxysporumshowed indifference (51).

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Drug of Choice 

Antifungal agents with some activity against Fusarium species include amphotericin Bvoriconazole and posaconazole. The optimal treatment strategy for patients with severe fusarial infection remains unclear because of the lack of controlled trial, and because the outcome is largely influenced by the immune status of the host. However, based on clinical experience and a few reported series, a lipid formulation of amphotericin B given at high doses (>3 mg/kg/d) seems to be a reasonable choice. In a retrospective analysis of 84 patients with hematologic diseases and invasive fusariosis, 69 patients received deoxycholate amphotericin B and 13 received a lipid formulation of amphotericin B. The overall response rate was 32%, but only 18 patients (21%) were alive 90 days after diagnosis. The response rate to a lipid formulation of amphotericin B appeared superior to that of deoxycholate amphotericin B (46% vs. 32%, respectively), but the difference was not statistically significant (p=0.36) (46). In a retrospective study, amphotericin B lipid complex was given to 28 patients with fusariosis, 8 as first line, and 20 as second line therapy (8 intolerant of and 12 refractory to prior antifungal therapy) (48). At a median daily dose of 4.5 mg/kg (total cumulative dose 5 g), the response rate (cure or improvement) in 26 evaluable patients was 46%. The median duration of treatment was 20 days. However, these numbers should not be taken as a guide, since the duration of treatment should be decided on an individual basis, depending on the clinical is response to treatment.  Voriconazole has been successfully given as primary therapy in some cases of fusariosis in doses of 6 mg/kg q12 h in the first day and then 4 mg/kg q12h thereafter (9,13,17,25,28,62), and may be an alternative for lipid amphotericin B.

Special Infections

Keratitis is usually treated with topical antifungal agents, and natamycin is the drug of choice (16). Localized skin lesions in immunocompromised patients deserve special attention. Since the skin may be the source for disseminated and frequently life-threatening fusarial infections, local debridement should be performed and topical antifungal agents (natamycin, amphotericin B) should be used, prior to commencing immunosuppressive therapies.

Alternative Therapy 

An alternative to a lipid formulation of amphotericin B is voriconazole. In a retrospective study, voriconazole was given to 11 patients with fusariosis, all intolerant of or refractory to primary therapy (49). The dose of voriconazole was 6 mg/kg q12h IV for the first 24 hours, followed by b.i.d.). The response rate (complete + partial response) was 45%, with an actuarial survival at 90 days of 71%. Another option is posaconazole. Twenty-one patients (17 refractory to primary therapy) with proven or probable fusariosis were analyzed (53). All but one patient were initially treated with a lipid-based formulation of amphotericin B. The dose of posaconazole was 800 mg PO in 2 or 4 divided doses. The overall success rate (complete + partial response) was 48%.

Combination Therapy 

Data on combination therapy for fusariosis is limited to a few case reports: caspofungin plus amphotericin B (41), amphotericin B plus voriconazole (1829), amphotericin B and terbinafine (56), and voriconazole plus terbinafine (35). Given the scarcity of data and the potential publication bias, no solid recommendations can be provided.

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In addition to antifungal treatment, the optimal management of patients with fusariosis includes surgical debulking of infected tissues (40) and removal of venous catheters in patients with confirmed catheter-related fusariosis (61). The role of granulocyte or granulocyte-macrophage colony-stimulating factors (G- or GM-CSF) and of G-CSF-stimulated granulocyte transfusions in the adjuvant treatment of fusariosis is not established. However, given the poor prognosis of fusariosis, especially in persistently neutropenic patients, these treatment modalities are frequently used. In support there are isolated case reports of the successful treatment of invasive fusariosis with a combination of medical treatment and some of these measures (55).


Treatment should be monitored taking into account the clinical and laboratory manifestations of infection. Criteria for response in invasive fusariosis include disappearance of fever and clinical symptoms attributed to the infection, and resolution of fungemia and radiologic abnormalities. In patients with fusarial sinusitis, nasal endoscopy should be repeated in order to ascertain that no new necrotic lesions developed. The interpretation of radiologic images may be problematic, since residual (not necessarily active) lesions in the lungs and sinuses may remain. A careful analysis comparing images before and after treatment may be of help. In addition, imaging methods that detect inflammation may be used, such as positron emission tomography (PET) or Indium-labeled white blood cells scintigraphy.

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No vaccines are available for fusariosis.



Because of the poor prognosis associated with fusariosis, and the limited susceptibility of Fusarium spp. to antifungal agents, prevention of infection remains the cornerstone of management. Decreasing immunosuppression should be attempted in patients with prior history of Fusarium infection and can be achieved by a reduction in or discontinuation of immunosuppressive agents, shortening the duration of neutropenia (selection of non-myeloablative as opposed to myeloablative preparative regimens for allogeneic HSCT and use of G-CSF or G-CSF and dexamethasone-elicited white blood cell transfusions) (1532).

Since skin may be the source for disseminated and frequently life-threatening fusarial infections, we recommend that patients likely to undergo severely immunosuppressive therapy undergo a thorough skin evaluation prior to commencing immunosuppression (Table 2). All areas of tissue breakdown should be identified and suspicious skin lesions cultured and biopsied. Local debridment should be performed and topical antifungal agents (Natamycin, amphotericin B) considered if Fusarium spp. are identified (45).

Antifungal Agent Prophylaxis

There are no recommendations for antifungal prophylaxis against Fusarium species either as primary prophylaxis or as secondary prophylaxis (patients with prior fusariosis who will be exposed to periods of prolonged neutropenia or will undergo an allogeneic HSCT). However, the use of an antifungal agent should be considered for secondary prophylaxis, and the choice should be based on the Fusarium species causing infection and/or the results of in vitro susceptibility testing if available.

Infection Control

Since the airways are the principal portal of entry for Fusarium species, the placement of patients at high risk (prolonged and profound neutropenia and allogeneic HSCT recipients) in rooms with HEPA filter and positive pressure may decrease the risk of nosocomial acquisition of fusariosis. In addition, since the water may be a source ofFusarium species in the hospital, every effort should be made to prevent patient exposure (e.g., by avoiding contact with reservoirs of Fusarium spp., such as tap water (6)), and/or cleaning showers prior to use by high-risk patients during periods at risk (7).

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Table 1. Clinical spectrum of fusariosis in immunocompetent and immunocompromised patients









  Skin infection (wounds, burns)






  Septic arthritis

  Septic thrombophlebitis


   Bloodstream (fungemia)


Invasive infection 




   Bloodstream (fungemia)

   Disseminated (may affect any organ, including brain, sinuses, lungs, gastrointestinal tract, kidney, liver, spleen, lymph nodes and skin)


Table 2. Preventive Measures for Fusariosis

a) Educate patients about the need to avoid activities associated with an increased risk of skin breakdown (e.g. clipping nails during periods

    of immunosuppression), and exposure of wounds to contaminated tap water

b) Preventive measures before immunosuppression:

-         Perform debridement of infected wounds and apply topical antifungal agents (terbinafine, natamycin, other) if culture yields Fusarium spp.

c) Preventive measures in patients with prior history of fusariosis:

-         Consider giving less immunosuppressive therapies (e.g. imatinib mesylate instead of bone marrow transplantation to patients with chronic myeloid leukemia, thalidomide or PS-341 instead of aggressive chemotherapy or bone marrow transplantation to patients with multiple myeloma)

-         Search for residual foci of fusariosis with image methods (computerized scan, magnetic resonance imaging, positron emission tomography) and surgically remove these lesions

-         Consider giving G-CSF plus dexamethasone-elicited white blood cell transfusions throughout the period of neutropenia

-         Consider secondary antifungal prophylaxis

What's New

Schaudin C, Stoodley P, Kainovic' A, O'Keeffe T, Costerton B, Robinson D, Baum M, Ehrlich G, Webster P.  Bacterial Biofilms, Other Structures Seen as Mainstream Concepts.  Microbe 2007;2:231-237.



Clinical Manifestations

Laboratory Diagnosis