The temperature difference between the soil and warm-blooded animals is significant in light of the
serious penalties incurred on enzyme function as the temperature increases. Those fungi that cause
infections of the skin (dermatophytes) are restricted to temperatures cooler than 37°C, and may illustrate
the problems of adapting to wider temperatures. For those fungi that do tolerate body temperatures, the
shift in temperature is used as a signal for gene expression (a feature observed in pathogenic bacteria).
The ability of certain fungi to use specialised structures to penetrate the host tissues is widespread
amongst plant pathogens and also occurs in human fungal pathogens. The ability to switch between
hyphal and yeast forms (dimorphism) is commonly observed when infecting animal hosts in the course
of an infection. Candida develop hyphae (pseudohyphae) when invading human tissue. In contrast to
bacterial pathogens, the use of capsules as virulence factors is almost unknown in fungal pathogens with
the exception of Cryptococcus neoformans.
The heterotrophic nature of fungal nutrition means that they secrete numerous degradative enzymes in
large quantities, many of which may attack host tissues. Consequently, it is difficult to assess
experimentally the contribution of individual enzymes as the other enzymes may compensate for any
loss. Furthermore, the property is characteristic of most fungi, yet very few are pathogenic to humans.
Fungal pathogens that persist in human hosts do so by various mechanisms:
1 . infection of immuno-privileged sites (skin, central nervous system),
2 . fungal spores are relatively resistant to phagocytosis compared with hyphae,
3 . release of immunomodulatory substances or molecular mimics.
This chapter has outlined four fungal infections to illustrate the variety in conditions that underlie these
events. They highlight the need to consider both the state of the host and the fungus in conjunction;
viewing either in isolation is insufficient. With fungal infections of humans that are accidental to the
normal lifecycle of the organism, the virulence factors are unlikely to be specific to that organism but
instead common to most fungi. The reason disease has developed is because of an accidental encounter.
Accidental human mycoses have little opportunity for transmission to new hosts in sharp contrast to
well-adapted pathogens, the dermatophytes and Candida albicans. Studies on the pathogenesis of fungi
have lagged behind those of bacteria and viruses, although the rising incidence of mycoses will stimulate
much needed funds for new studies. However, the methodology will be more complicated than with bacteria as genetic complexities of most fungi will complicate the ‘virulence gene’ deletion studies.

As saprophytes, fungi are mostly accidental pathogens of humans. Primary fungal
pathogens (certain dimorphic fungi and the dermatophytes) are able to infect humans
without recognisable predisposing factors in the host. Primary pathogens cause systemic or
superficial (skin) infections. The dimorphic fungi responsible for systemic infections are
acquired via inhalation of spores and are able to replicate in the niche (human tissue). The
superficial dermatophyte infections are restricted to keratinised tissues. Secondary fungal
pathogens replicate in humans only through predisposing factors such as
immunosuppression or traumatic implantation of the organisms into the tissues but, as a
consequence, are more likely to cause systemic disease. The virulence factors recognised
include dimorphism, thermal tolerance and immunomodulatory abilities, but increasing
numbers of immunosuppressed hosts through medical improvements or disease such as
AIDS means that fungal infections are increasing in number. This increase indicates the
importance of host condition in the balance between fungal and human factors in whether
infections are established.
Cutler, J.E. (1991) Putative virulence factors of Candida albicans. Annu. Rev. Microbiol.45, 187–218.
Denning, D.W. (1991) Epidemiology and pathogenesis of systemic fungal infections in the
immunocompromised host. J. Antimicrob. Chemother.28, Suppl. B, 1–16.
Fridkin, S.K. and Jarvis, W.R. (1996) Epidemiology of nosocomial fungal infections. Clin.
Microbiol. Rev.9, 499–511.
Hogan, L.H., Klein, B.S. and Levitz, S.M. (1996) Virulence factors of medically important fungi.
Clin. Microbiol. Rev.9, 469–88.
Kobayashi, G.S. and Medoff, G. (1998) Introduction to the fungi and mycoses, in Schlaecter, M.,
Engelberg, N.C., Eisenstein, B.I. and Medoff, G. (eds) Mechanisms of Microbial Disease, 3rd
edition, Lippincott, Williams & Wilkins, Baltimore, USA.
Richardson, M.D. (1992) Fungal infections, in McGee, J.O.D., Isaacson, P.G. and Wright, N.A. (eds)
Oxford Textbook of Pathology, Oxford University Press, Oxford, UK.
Weitzman, I. and Summerbell, R.C. (1995) The dermatophytes. Clin. Microbiol. Rev.8, 240–59.

Cited By Kamal Singh Khadka
Msc Microbiology, TU.
Assistant Professor In PU, PBPC, PNC, LA, NA.
Pokhara, Nepal.
SOME SUGGESTED REFERENCES: › MicrobiologyBytes Video Library › NCBI › Literature › PubMed Central (PMC


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