infections such as the central nervous system
or the necrotic tissue with poor blood supply;
(vi) reduced blood concentration of the
antifungal agent due to drug interaction,
especially during voriconazole therapy;
(vii) suboptimal duration of the antifungal
therapy; and (viii) the underlying disease as the
main barometer of clinical success and failure
in antifungal therapy.
Like bacteria, fungi also produce a biofilm
in vitro. It is well known that the biofilm is an
important obstruction in antibacterial therapy.
In fungal infections similar studies have been
conducted. Enhanced extracellular matrix
especially beta glucan synthesis during biofilm
growth has been shown to prevent penetration
of antifungal agents such as azole and
polyene29. It is believed that the echinocandins
and lipid formulations of amphotericin B can
penetrate biofilm better than amphotericin
B deoxycholate and azoles19. The clinical trials
also indicate the importance of the biofilm.
Numerous clinical trials on candidemia have
demonstrated that the treatment failure and
mortality are high in patients who are on
catheters for long periods
Conclusion
With increase in the incidence and spectrum of
invasive fungal infections, antifungal drug
resistance has become an important
consideration in the management of patients.
Though unlike bacteria, the level of resistance
to antifungal agents is relatively low due to the
possible absence of drug-resistant plasmid or
transposons in fungi, the recently conducted
experiment of horizontal gene transfer in
pathogenic Fusarium species shows that there
is no scope of complacency. The emergence
of intrinsically resistant fungal species as a
human pathogen is compounding the
challenge of planning treatment strategies.
Beyond these confounding factors, the
conditions leading to clinical resistance should
be kept in mind while managing invasive
fungal infections in immunocompromised
patients.
Acknowledgement
The author acknowledges the help of
M. Manpreet Dhaliwal for organizing the
references.