Diagnosis

Diagnosing fusariosis involves a combination of clinical assessment and laboratory

investigations:

1. Clinical Examination:
o Detailed history and physical examination to identify characteristic signs and
symptoms.
o Assessment of risk factors, including immunosuppression, recent trauma, and
exposure to contaminated environments.

2. Microbiological Tests:
o Direct Microscopy: Examination of clinical specimens (e.g., skin scrapings,
corneal scrapings, tissue biopsies) using stains such as potassium hydroxide
(KOH) or calcofluor white to visualize fungal elements.
o Culture: Isolation of Fusarium species on Sabouraud dextrose agar or other
mycological media. Cultures typically show rapid growth and characteristic
hyphal structures.
o Histopathology: Tissue biopsies stained with periodic acid-Schiff (PAS) or
Gomori methenamine silver (GMS) stains to demonstrate fungal hyphae within
tissues.

3. Molecular Methods:
o Polymerase Chain Reaction (PCR): Rapid and specific identification of
Fusarium species through amplification of fungal DNA.
o Sequencing: Genetic sequencing of fungal isolates to confirm species
identification and assess antifungal resistance patterns.

Treatment

The treatment of fusariosis is challenging due to the intrinsic resistance of many Fusarium
species to common antifungal agents. Management strategies include:
 1. Antifungal Therapy:
o Voriconazole: Often considered the first-line treatment due to its broad-spectrum
activity and good tissue penetration.
o Amphotericin B: Used for severe infections, particularly in disseminated disease.
However, its use is limited by significant nephrotoxicity and infusion-related
reactions.
o Posaconazole and Isavuconazole: Alternative agents for refractory cases or
when voriconazole is not tolerated. These drugs have a broad spectrum of activity
against Fusarium species.

2. Surgical Debridement:
o Necessary for removing necrotic tissue and reducing fungal load in localized
infections, such as cutaneous lesions or keratitis.
o May involve procedures such as excision of infected skin, nail removal, or corneal
debridement.

3. Supportive Care:
o Management of underlying conditions that predispose to infection, such as
neutropenia or immunosuppression.
o Supportive measures to maintain hemodynamic stability and organ function in
severe cases of disseminated fusariosis.

4. Adjunctive Therapies:
o Use of granulocyte colony-stimulating factor (G-CSF) or granulocyte-
macrophage colony-stimulating factor (GM-CSF) to boost neutrophil counts in
patients with neutropenia.
o Hyperbaric oxygen therapy has been explored as an adjunctive treatment in some
cases, although evidence for its efficacy is limited.

Epidemiology

Fusariosis is more prevalent in tropical and subtropical regions where the fungi thrive. It is an
important health concern in Africa, particularly among immunocompromised individuals, such
as those with HIV/AIDS, cancer patients undergoing chemotherapy, and organ transplant
recipients.

Prevention and Control

Preventive measures include:

 Good Hygiene Practices: Proper wound care and hand hygiene to prevent skin
infections.
 Protective Measures: For high-risk individuals, such as using protective gloves in
agricultural settings.
 Prophylactic Antifungals: In immunocompromised patients to prevent systemic
infections.
 Public Health Education: Raising awareness about fusariosis and its risk factors.

Conclusion

Fusariosis is a significant fungal infection with varied clinical presentations, primarily affecting
immunocompromised individuals. Effective management requires a combination of prompt
diagnosis, appropriate antifungal therapy, and preventive measures to reduce the risk of
infection. Understanding the pathogenesis, clinical manifestations, and treatment options is
crucial for healthcare providers in managing this challenging infection.

In-depth explanation of Fusariosis with Relevant References

Introduction

Fusariosis is a fungal infection caused by species of the genus Fusarium. These fungi are widely
distributed in soil and plants and can cause a range of infections in humans, particularly in
immunocompromised individuals. The clinical manifestations of fusariosis vary from superficial
skin infections to severe, disseminated disease.

Epidemiology
Diagnosis

1. Clinical Examination

 Symptoms vary depending on the site of infection. Skin lesions may appear as painful,
erythematous nodules that can ulcerate. Keratitis presents with eye pain, redness, and
visual impairment.

2. Laboratory Tests

 Microscopy and Culture: Direct microscopy of clinical specimens (skin scrapings,

corneal scrapings, tissue biopsies) can reveal fungal elements. Cultures on Sabouraud
dextrose agar help identify Fusarium species.
 Histopathology: Tissue biopsies stained with periodic acid-Schiff (PAS) or Gomori
methenamine silver (GMS) stains can show characteristic hyphae.
 Molecular Methods: PCR and DNA sequencing can provide rapid and specific
identification of Fusarium species.

Treatment

1. Antifungal Therapy

 Treatment of fusariosis is challenging due to the intrinsic resistance of Fusarium species

to many antifungal agents. The choice of antifungal depends on the severity and site of
infection.
 Voriconazole: Often the drug of choice for invasive fusariosis.
 Amphotericin B: Used for severe infections, though it has significant toxicity.
 Posaconazole and Isavuconazole: Alternative options for refractory cases or when other
antifungals are not tolerated.

2. Surgical Intervention

 Surgical debridement of infected tissue may be necessary, especially in cases of localized

cutaneous infection or keratitis.
 3. Supportive Care

 Immunocompromised patients may require supportive care, including hematopoietic

growth factors to address neutropenia and broad-spectrum antibiotics to manage
secondary bacterial infections.

Prevention and Control

1. Public Health Measures

 Awareness and Education: Educating healthcare workers and the public about fusariosis
and its risk factors is crucial.
 Hygiene Practices: Promoting proper wound care, hand hygiene, and contact lens care
can reduce the risk of infection.

2. Protective Measures for High-Risk Groups

 Prophylactic Antifungals: In high-risk patients, prophylactic antifungal treatments may

help prevent infection.
 Environmental Controls: Reducing exposure to contaminated soil and plant material for
immunocompromised individuals can help prevent infections.

3. Strengthening Healthcare Infrastructure

 Diagnostic Capabilities: Enhancing laboratory facilities and training healthcare

personnel can improve early detection and management of fusariosis.
 Access to Treatment: Ensuring the availability of effective antifungal medications is
essential for controlling the disease.

Conclusion

Fusariosis is a significant fungal infection with varied clinical presentations, primarily affecting
immunocompromised individuals. Understanding its pathogenesis, epidemiology, and treatment
options is crucial for effective management. Recent studies, such as those examining the
population structure of Fusarium species, provide valuable insights into the disease's dynamics
in Africa. Ongoing research and public health initiatives are essential to mitigate the impact of
fusariosis and improve patient outcomes.

The genus Fusarium is a common soil saprophyte and an important plant pathogen. The
organism causes a broad spectrum of human disease, including mycotoxicosis and infections
which can be locally invasive or disseminated.
Microbiology
Fusarium spp. are agents of hyalohyphomycosis along with other fungi such
as Penicillium spp., Scedosporium spp., Acremonium spp., Paecilomyces spp., Aspergillus spp.,
Scopulariopsis spp. and others [1]. ‘Hyalohyphomycosis’ is a term that describes fungal
infections caused by moulds whose basic tissue form is like hyaline, light-colored, hyphal
elements that are branched or unbranched, occasionally toruloid, and without pigment in their
wall [2].
Fusarium spp. grow rapidly on many media (without cycloheximide which is inhibitory). On
potato dextrose agar, Fusarium spp. produce white, lavender, pink, salmon, or grey colonies
(which readily change colour) with velvety to cottony surfaces [3].
Microscopically, the hyphae of Fusarium in tissue resemble those of Aspergillus spp.; the
filaments are hyaline, septate and 3–8 μm in diameter. They typically branch at acute or right
angles. The production of both fusoid macroconidia (hyaline, multicellular, banana-like clusters
with foot cells at the base of the macroconidium) and microconidia (hyaline, unicellular, ovoid to
cylindrical in slimy head or chains) are characteristic of the genus Fusarium. If microconidia are
present, the shape, number of cells (usually one to three), and mode of cell formation (chains or
false heads) are important in identification. Chlamydospores are sometimes present and appear
singly, in clumps or in chains, and their walls may be rough or smooth [3].
Fusarium can be distinguished from Acremonium by its curved, multicellular macroconidia,
while Cylindrocarpon is distinguished from Fusarium by its straight to curved macroconidia that
lack foot cells [3]. The identification of Fusarium spp. may be difficult and is well described by
Nelson et al.[4].
Fusarium spp. possess several virulence factors including the production of tricothecene and
other mycotoxins. These mycotoxins can suppress humoral and cellular immunity, and cause
tissue breakdown. Fusarium spp. also have the ability to adhere to prosthetic material (contact
lenses, catheters), and to produce proteases and collagenases [4].
Epidemiology
Fusarium spp. are widely distributed in soil, plants and air. They are common in tropical and
temperate regions but are also found in desert, alpine and arctic areas [4]. In a survey of airborne
fungi conducted in the USA, Fusarium spp. were more commonly recovered from air samples
than were Aspergillus spp. [5]. Fusarium spp. colonised 17% of throat specimens of 27
nonhospitalised healthy adults [6]. These organisms can also colonise the conjunctival sac,
especially in diseased eyes [7]. Wind and rain effectively Fusarium disperse [8].
Fusarium spp. are the most common cause of fungal keratitis world-wide. In a series of 391
incidences of infectious keratitis in Thailand, 34 (12%) were fungal and Fusarium was the most
common fungus recovered [9]. Another series of 1352 fungal keratitis cases in India confirmed
this finding (37%).
In severely immunocompromised patients, this fungus can cause disseminated disease and has
recently emerged as the second most common pathogenic mould (after Aspergillus) in high-risk
patients with haematological cancer, and in recipients of solid organ [10] and allogeneic bone
marrow or stem cell transplants [11, 12, 13]. In the latter patient population, the distribution of
fusariosis is bimodal, with peaks observed before and several weeks after engraftment. At one
US institution, the incidence of fusarial infection was 1.2% among 750 allogeneic and 0.2%
among 1537 autologous marrow transplant recipients during a 10-year period [11]. A review of
fusarial infections in patients with acute leukaemia in Italy showed an incidence of 0.06%[14].
While the incidence in Europe has remained stable over the past 20 years, it has significantly
increased at one US institution from 0.5 to 3.8 cases per year from 1975 to 1995 [11]. In this
institution, the hospital water system was found to be a reservoir for Fusarium spp. [15]. In
another US institution, 31 cases of invasive fusariosis were documented among 5589 stem cell
transplant recipients (0.55%) during a 14-year period, with an increase in the number of these
patients during the late 1990s [13].
Risk Factors
Tissue breakdown from direct trauma or the presence of a foreign body in a colonised patient are
the usual risk factors for infections in nonimmunosuppressed patients. These infections are
mainly localised and include keratitis after trauma or among contact lens wearers [16],
onychomycosis among individuals who walk barefooted and, rarely, peritonitis in patients
undergoing continuous ambulatory peritoneal dialysis, cellulitis after injury [17] and others.
Disseminated fusariosis among previously healthy individuals can develop in the setting of a
severe burn injury [18, 19].
Risk factors for disseminated fusariosis include severe immunosuppression (mainly patients with
haematological malignancies) in addition to colonisation and tissue damage. More specifically,
neutropenia, lymphopenia, graft-versus-host disease, corticosteroid therapy or any other
immunosuppressive treatment, are considered risk factors for disseminated fusariosis
[11, 20, 21, 22]. In a recent review of invasive fungal infections among stem cell transplant
recipients, multiple myeloma, and receipt of a graft from an HLA-mismatched or unrelated
donor were significantly associated with Fusarium infections [13].
Clinical manifestations
Infections by Fusarium spp. can be divided into foreign-body associated, single organ invasion
and disseminated fusariosis [4]. Mycotoxicosis caused by Fusarium spp. will not be included in
this review.
Single organ invasion

Keratitis

Fusarium spp. are a frequent cause of corneal damage in developing countries in the tropics [23],
and are the most frequent cause of fungal keratitis in the USA [24]. The main predisposing factor
is ocular trauma due to the implantation of vegetable or soil matter [16, 25, 26]. An additional
risk factor for Fusarium keratitis is the presence of a pathological corneal condition and
concomitant therapy with topical steroids and antibacterial antibiotics. Topical natamycin is the
treatment of choice because of its excellent antifusarial activity, corneal penetration and safety
profile, but amphotericin B ointment can also be used [27, 28]. Chlorhexidine may have potential
as an inexpensive topical agent for fungal keratitis and warrants further assessment as a first-line
treatment in conditions where microbiological facilities and a range of antifungal agents may not
be available [29]. Systemic antifungal treatment may be useful in severe mycotic keratitis and
surgery may be required in refractory infections or when serious complications are likely to
occur.
Endophthalmitis

Fusarial endophthalmitis can develop between 2 and 22 weeks after the onset of fusarial keratitis
or following surgical and nonsurgical trauma [37].

Onychomycosis

Fusarium spp. may invade the great toenails after soil contamination, especially in individuals
who walk in open sandals or barefooted. The most common clinical presentations include
proximal subungual onychomycosis with or without paronychia, and white superficial
onychomycosis [38, 39]. Distal subungual onychomycosis can also occur following trauma or a
dermatophyte infection [40]. Fusarium spp. were reported to be the causative agent of 9–44% of
the nail invasions caused by nondermatophytic moulds [38, 41, 42, 43]. A combined strategy of
systemic itraconazole, systemic terbinafine, topical terbinafine after nail plate avulsion, and
ciclopirox nail lacquer was able to cure only 40% of 26 patients with Fusarium onychomycosis
[38]. Aspergillus onychomycosis, on the other hand, responded very well to this therapy.
Although onychomycosis as a result of Fusarium spp. infection usually behaves as a localised
infection in immune competent individuals, it could also represent the portal of entry for
disseminated disease in immunocompromised patients [4, 44, 45].

Cutaneous infections

In immune competent individuals, localised cutaneous infections may develop in the setting of
initial colonisation and the presence of excessive moisture or trauma (including burn). Skin
lesions may vary including granulomas, ulcers, nodules, mycetomas, necrosis, panniculitis and
intertrigo [4, 46]. As reported in a recent review of cutaneous infections by Fusarium spp. [45],
in patients presenting with localised cutaneous infections, immunocompetent patients (10 of 13)
had more frequently a history of skin breakdown than those who were immunocompromised (11
of 20). While cutaneous infections in the former population were characterised by localised
involvement, slow progression and good response to therapy, those in the latter population who
presented as rapidly progressive usually disseminated lesions with poor response to antifungal
agents. The cutaneous infections secondary to disseminated disease will be described later.
Foreign-body associated fusariosis

Keratitis in contact lens wearers

Fusarium spp. can also contaminate the contact lens paraphernalia or the lens itself, especially
after improper care. In windy conditions, Fusarium spp. can also contaminate the lens during
use. This fungus can penetrate the matrix of the soft contact lens with increasing microbial
growth in lenses with high water content [30]. Fusarium keratitis can also develop among users
of daily disposable soft contact lenses [31]. Treatment often requires removal of the lens and
topical treatment with natamycin but may require surgery in refractory patients
[31, 32, 33, 34, 35, 36].

Peritonitis following continuous ambulatory peritoneal dialysis

The clinical presentation is usually insidious, with fever, abdominal pain and decreasing drainage
from the peritoneal catheter. Fungi can either plug or invade the catheter. Treatment often
requires catheter removal and systemic antifungal therapy [47, 48, 49, 50, 51, 52, 53, 54, 55].

Catheter-associated fungemia

Fusarium spp. can rarely plug and invade the wall of a central venous catheter and lead to
fungemia [56, 57, 58]. Treatment includes catheter removal and systemic antifungal therapy.
Other single organ infections
Less frequently, Fusarium spp. can also cause osteomyelitis, arthritis, otitis, sinusitis and brain
abscess. Fusarium was the cause of 1% of 83 cases of mycotic otitis of the external ear in Gabon,
Central Africa [59]. F. solani was found in, and was able to germinate in, the middle ear of
agricultural workers [60]. Four of five cases of Fusarium osteomyelitis were reported in healthy
individuals following surgery or trauma [61, 62, 63, 64]. Successful outcome resulted from a
combination of surgical and medical treatment. Bone involvement by Fusarium spp. may also
occur in the setting of disseminated disease [65]. Fusarium septic arthritis has been reported in
two patients after trauma, responded to surgery and amphotericin B [66, 67]. Sinusitis in a
diabetic cancer patient [68] and an isolated brain abscess in a patient with chronic infectious
mononucleosis syndrome [69] have also been reported.
Disseminated disease

Clinical presentation

Disseminated infections occur most commonly in patients with haematological malignancies and
occasionally in patients with extensive burns [11]. The Fusarium spp. most frequently implicated
as human pathogens include F. solani, F. oxysporum, F. moniliforme and less commonly, F.
anthophilum, F. chlamydosporum, F. dimerum, F. equiseti, F. lichenicola, F. napiforme, F.
proliferatum, F. semitecum and F. verticilloides (the less common species listed in alphabetical
order) [11, 12, 70, 71, 72, 73]. Disseminated infection usually presents as persistent fever
refractory to antibacterial and antifungal agents. Other presenting features include sinusitis
and/or rhinocerebral infection, cellulitis at the site of skin breakdown, endophthalmitis, painful
skin lesions, pneumonia, myositis and infections of the central nervous system [11, 21]. Almost
any organ can be involved but the most frequently affected is the skin (70–90%), followed by
lungs and sinuses (70–80%) [11]. Three types of cutaneous lesions can be observed: multiple, at
times painful, subcutaneous nodules and ecthyma-like lesions, and less commonly, bullae or
target lesions consisting of the ecthyma-like lesions surrounded by a thin rim of erythema [ 45].
Some of these lesions represent an evolution of the same lesions observed at different ages.
Extensive cellulitis of the face or the extremities, with or without fascitis, has also been
described [74]. Pleuritic chest pain, fever, cough and haemoptysis occur in patients with
pulmonary involvement and are indistinguishable from pulmonary aspergillosis. Indeed, the
clinical features of patients with disseminated fusarial infection are similar in many respects to
those with disseminated aspergillosis [11]. Unlike aspergillosis, however, infection
with Fusarium spp. is associated with a high incidence of skin and subcutaneous lesions and with
positive blood cultures [11, 21, 45, 75, 76, 77].
Among patients undergoing solid organ transplantation, fusarial infections tend to be more
localised, occur later after transplantation and have a better outcome than among patients with
haematological cancer or recipients of bone marrow transplantation [10].
In a recent review of cutaneous fusariosis in 259 patients including 232 who were
immunocompromised, a higher rate of skin lesions was present among neutropenic (78%) than
non-neutropenic patients (45%) and those with disseminated skin lesions were more likely to
have fusarial fungemia [45]. Skin lesions involved practically any skin site, with predominance
on the extremities, and took different forms as described above. The lesions evolved rapidly,
usually over a few days (range 1–5 days) and lesions at different stages of evolution were
described in many patients (usually a combination of papules, nodules and necrotic lesions),
sometimes along with myalgias (suggesting muscle involvement). The skin was the primary site
of infection leading to disseminated fusariosis in 16 patients (mainly at sites of onychomycosis
and less frequently at sites of trauma or insect bite). The pattern of skin lesions did not appear to
be associated with any particular species of Fusarium.

Diagnosis

In patients with severe immunosuppression, a high index of suspicion for disseminated fusariosis
should be raised when mould fungemia is reported, or when preceding or concomitant toe or
finger cellulitis, or cutaneous or subcutaneous lesions are present [72, 78].
Skin is a very important source for diagnosis. In one report, skin lesions were the single source
of diagnosis of fusarial infection in 55% of patients. In most cases, skin lesions preceded
fungemia by a median of 5 days (range 1–10 days), but they also developed after the diagnosis of
fungemia (up to 13 days later) [45]. Histopathological examination of skin lesions showed
hyaline acute-branching septate hyphae invading the skin and extending into the blood vessels,
with thrombosis and necrosis in those patients with metastatic lesions [45].
In contrast to disseminated aspergillosis, disseminated fusariosis can be diagnosed by blood
cultures in 40% of patients [11, 72]. The rate of positive blood cultures increases to 60% in the
presence of disseminated skin lesions, while fungemia is extremely rare in patients with localised
skin infections [45].
As with aspergillosis, the radiological findings of pulmonary fusarial infection range from
nonspecific infiltrates (most commonly) to nodular and/or cavitary lesions, depending on the
timing of the study.

The definitive diagnosis of fusariosis requires the isolation of Fusarium spp. from clinical
specimens (blood, skin, sinuses, lungs, other). Culture identification is important because of the
histopathological similarities between Fusarium and other members of the
hyalohyphophomycosis family and the different susceptibilities of these pathogens to antifungal
agents. Like Aspergillus spp., Fusarium spp. invade blood vessels causing thrombosis and tissue
infarction and appear in tissues as acute branching septate hyphae [4, 11]. Tissue diagnosis of
fusariosis can be made by immunohistological staining, using polyclonal fluorescent antibody
reagents that distinguish Aspergillus spp. from Fusarium spp. [79]. In-situ hybridisation may
also help to distinguish Fusarium spp. from Aspergillus and Pseudoallescheria in tissue sections
with a 100% positive predictive value [80].

Treatment

Prompt therapy of localised disease is critical to prevent progression to disseminated infection

and includes surgical debridement, and probably systemic antifungal chemotherapy [11, 76, 81].
The optimal treatment for disseminated fusariosis remains unclear. Voriconazole, itraconazole
and the polyenes (amphotericin B and its lipid formulations) [82, 83, 84, 85, 86, 87] have been
associated with some success. In the USA, voriconazole is the only agent with an indication for
treating refractory fusariosis.
Fusarium spp. are some of the most drug-resistant fungi. Data on their in-vitro susceptibility to
various antifungal agents indicate low susceptibility to 5-flucytosine, fluconazole and
amphotericin B [88, 89, 90] and variable susceptibility to itraconazole, voriconazole and
posaconazole [89, 91, 92, 93, 94, 95, 96, 97, 98, 99]. F. solani seems to be somewhat more
susceptible to amphotericin B but less susceptible to voriconazole than F. oxysporum[100].
The echinocandins caspofungin [101], anidulafungin, and micafungin [102, 103] have no in-vitro
activity against Fusarium spp.
In severely neutropenic patients, treatment with granulocyte or granulocyte–macrophage colony-
stimulating factors (G- or GM-CSF) and CSF-stimulated white blood cell transfusions may also
be considered [11, 104, 105, 106]. Recently, a combined approach of liposomal amphotericin B,
voriconazole, surgery and granulocyte transfusions was associated with a successful outcome in
a child with severe aplastic anaemia and disseminated infection by F. oxysporum[106].
Debridement or resection of all infected tissues (sinuses, ocular tissues, soft tissue, bone, other)
is recommend but frequently impossible because of severe thrombocytopenia. Catheter removal
may be of benefit if the catheter is the source of the fusariosis.

Outcome
Disseminated fusariosis is a life-threatening disease whose outcome is very much influenced by
the host immune status. Overall mortality of fusarial infections in immunocompromised patients
ranges from 50% to 80%[11, 45, 72, 107]. In a retrospective study that included 84 patients with
fusariosis, factors associated with poor survival by multivariate analysis included persistent
neutropenia and therapy with corticosteroids. The actuarial survival of patients with both
persistent neutropenia and corticosteroid therapy was 0%, compared to 67% who had neither of
these two factors present, 30% for those on corticosteroids (but with adequate neutrophil counts),
and 4% for those whose only negative prognostic factor was persistent neutropenia [108].
These data are in agreement with other reports that describe very high mortality in persistently
neutropenic patients [11, 45, 72, 107].
Disseminated skin lesions may be a marker of poor outcome in non-neutropenic patients. In a
retrospective study of 259 patients with fusariosis [45], a higher mortality was observed among
patients with skin lesions (70% vs. 56%), particularly among those who had an adequate
neutrophil count throughout the course of their illness. In this group of patients, the mortality rate
for patients with metastatic skin lesions was 67% vs. 21% for those with localised lesions. The
mortality among neutropenic patients was high regardless of whether the lesions were localised
or metastatic (64% vs. 77%), respectively.

Prevention

Because of the high morbidity and mortality of disseminated fusariosis, every effort should be
made to prevent these infections, and to enhance the patient's immune status, perhaps by tapering
or discontinuing immunosuppressive agents or shortening the duration of neutropenia. We also
recommend that patients likely to receive severely immunosuppressive therapy undergo a
thorough skin evaluation prior to commencing immunosuppression, to identify areas of tissue
breakdown and evaluate these lesions with culture and biopsy and antifungal treatment
if Fusarium spp. are identified. In addition, severely immunocompromised patients with skin or
other exposed tissue breakdown should avoid exposure to environmental sources
of Fusarium spp. such as tap water. Indeed, we have shown that hospital water may be
contaminated with Fusarium spp. and can lead to aerosolisation (especially after showering) and
to patient exposure and disease [109]. Avoiding exposure to tap water can be accomplished by
the use of sterile sponge baths instead of showering (to minimise aerosolisation), and by drinking
sterile water only during periods of severe immunosuppression. Cleaning water-related
environmental surfaces (bathroom floors) results in a significant decrease in the airborne
concentration of pathogenic moulds in the bathrooms of a bone marrow transplant unit [110].
Thus, adequate cleaning of the bathroom is recommended prior to showering (for those patients
who insist on showering during the period of major immunosuppression).
Because of the risk of relapse in immunosuppressed patients with prior fusarial infections [111],
secondary prophylaxis should be considered. The agent of choice would be the one associated
with clinical response during the initial infection. Consideration should also be given to using
prophylactic G-CSF or GM-CSF-stimulated granulocyte transfusions following initiation of
severely myelosuppressive chemotherapy.