Given the severe morbidity and mortality from Fusarium infections, it is important to understand the sources of these organisms and determine the extent to which fusaria may be transmitted in the hospital. One such study by Anaissie in 2001 implicated hospital water systems (drains, faucet aerators, shower heads) as potential reservoirs for Fusarium, and suggested that these fungi can be transmitted through the water system due to their persistence in plumbing systems
. In the United States, Short et al. recently confirmed these findings by performing an extensive MLST study of fusaria recovered from plumbing drains in the United States
. They found that the 6 most common sequence types in drains (FSSC 1-a, 1-b, 2-d, 2-k, FOSC 33 and Fusarium dimerum) were also the six most commonly associated with human infection. Our study bolsters the findings of Short et al. with regard to common Fusarium STs isolated from water-related sources, since we also found that FOSC 33 was the most common ST isolated in drains, faucets, and tiles of showers and sinks in the hospital. Unlike Short et al., we found FSSC 1-a and FSSC 1-b to be more commonly found in these sources, as opposed to FSSC 2-d. Our study differs in two ways, however, since environmental sampling was conducted in Brazil, and only exterior plumbing surfaces were sampled.
Several studies have shown that MLST of three loci (EF-1α, rRNA and RPB2) have the highest discriminatory power in delineating FSSC using comparative sequence analyses
[7, 15, 16]. We used this three-locus method and found that subtypes of most BTMU inpatient clinical isolates belonged to FSSC species 2 (69%, 38/55), and were primarily 2-d (recovered from 36% of patients) and 2-f (recovered from 18% of patients). In contrast, FSSC isolates comprised 36% of the environmental samples and were shown to be predominantly species type 1-a (18%) and 1-b (13%), while only four environmental samples were FSSC 2. The remaining environmental samples were predominantly FOSC from swabs and water (50% of environmental samples) and FIESC from air (79% of air samples). We did not find any FIESC clinical isolates, although we did find two FOSC clinical cases. Our data suggest that most of the clinical cases of fusariosis in this immunosuppressed population could not be traced to a specific water-related environmental source in the hospital ward. However, because we found a small number of species type-level matches between clinical and environmental isolates, we believe that in this institution, environmental water-related sources and even air must be considered as possible reservoirs for patient infection.
In this study, we were unable to find any temporal association between BMTU patient fusarial infections and contaminated water-related sources in the BMTU environment. We explored the epidemiology of community acquisition by studying a population of dermatology outpatients diagnosed with skin or nail fusariosis who were seen at the hospital during the same period. The spectrum of Fusarium STs recovered from these patients largely mirrored those recovered from BMTU inpatients (Figure
1). A study by Raad et al. used RAPD subtyping to demonstrate that Fusarium DNA collected from 10 infected patients did not match DNA from 15 environmental isolates collected from shower head water, sink water, and drains in their institution
. Our study was far more extensive and yielded similar results.
Both Anassie and Short
[13, 14] have implicated water systems as reservoirs of fusariosis, but in our study we found only FSSC 1 to be common in both hematology patients and the environment. It is possible that Fusarium patient subtypes could have been missed in the hospital environment because of limitations in the environmental investigation. Environmental sampling was sporadic and was limited in scope, so potential sources of contamination may have been missed. Few samples were collected from air in the BMTU, and surfaces of other fomites in the patient rooms were not sampled; rather focus was placed on the patient bathrooms, pursuing the hypothesis that water-related sources were Fusarium reservoirs. Additionally, the methods used for environmental sample collection may not have been optimal for Fusarium recovery.
The diversity of Fusarium STs among dermatology patients with superficial infections was greater than that of BMTU patients, and the distribution of STs was highly similar between these patient populations. We found that a single species, FSSC 2-d, predominated in both inpatient hematology and outpatient dermatology samples. Certainly, our combined patient data suggest that FSSC species remain a cause of superficial colonization, and under appropriate circumstances of immunosuppression, could cause disease in an IHC patient population. The increase in fusariosis in this and other hospitals (personal communication, Marcio Nucci) suggests that there may be a significant increase in circulating Fusarium conidia in this geographical region. Our findings raise important questions for future research, including a search for the environmental reservoirs of Fusarium spp., an explanation for this surge of environmental Fusarium, and the potential implications of these findings in infection control measures.