Mycologists estimate that there are 100,000 species of fungi in
nature. These fungi inhabit different niches, a number of them
are symbiotic and may live in commensalism, mutualism or
parasitism with other organisms. However, only some of the
fungal species are pathogenic to man, a fact that has led to
several studies providing a better understanding of the
relationshipamong parasite, host and virulence factors 14,93.
The symbiotic-parasitic relationship produces an infectious
process leading to lesions of the host tissues and establishment of
disease due to a direct imbalance in parasite-host interaction. The
host provides conditions for growth that usually differ markedly
from the ecological niche that the fungus normally inhabits. In
order to survive inthis new environment, potential pathogens
must withstand high temperatures, hormonal influences and
attacks by phagocytes cells of the immune system 93 (Figure 1).
Fig. 1 - Factors that affect the transition from the saprophytic to parasite
form in host-fungus relationship.
This process of adaptation to a more resistant form to the new
microenvironment frequently results in aggression tohost tissues.
Some fungi, such as dimorphic fungi, have a greater ability to
grow in adverse conditions provided by the host, and to produce
disease. This process called pathogenicity is considered to be the
result of direct interaction between the pathogen and host.
Several fungal factors may help in this relationship and are
frequently studied being known as virulence factors 14,38.
For anorganism to cause disease it must (1) enter the host, (2)
multiply in host tissues, (3) resist or not stimulate host defense
mechanisms, and (4) damage the host. The success of all these
processes will depend on which virulence factor the fungus
Some virulence factors are of obvious importance. For example,
the ability of a fungus to grow at 37ºC is a virulence factor for
invasivefungi, representing the transition to a parastic form
essential for the pathogenicity of dimorphic fungi 38. It is worth
pointing out that not all fungal products may be considered as
virulence factors. An example is the production of chitinase and
ß-glucanase by spherules of Coccidioides immitis during the
transition from the mycelial to parasitic form. Chitinase and ßglucanase can only beconsidered as virulence factors if a
probable interaction of the above-mentioned proteins with the
host is suggested 38.
The ability to survive and replicate at 37°C seems to be a
common property of pathogenic fungi. This phenomenon, known
as thermotolerance, is observed in Cryptococcus
neoformans, Histoplasma capsulatum andSporothrix schenckii 56,
. Most isolates of C.neoformans var. gattii that do not grow
efficiently at 37oC are not able to produce fatal infection in mice,
whereas isolates of var. neoformans germinate and grow at 37°C
producing lethal infection93. Low-virulence strains of H.
capsulatum require more time for mycelium-to-yeast-phase
transition at 37ºC, whereas the more virulent strains are capable
of withstanding drastic temperaturechanges and of transforming
more quickly 72. Isolates of S. schenckii from systemic lesions can
grow at 35ºC and at 37ºC, but isolates from fixed cutaneous
lesions can only grow at 35ºC 56. It is believed that even small
differences in temperature tolerance can influence the pathogenic
potential of a microorganism as well as the form of disease
presented by the host 93.
Resistance totemperature changes is also related to the
synthesis of heat-shock proteins 48. Production of these proteins
seems to play an important role not only in thermo-adaptation,
but also in the mycelium-to-yeast-phase transition in dimorphic
fungi 36. The temperature change from 25ºC to 37ºC induces a
significant synthesis of the heat-shock proteins in Trypanosoma
cruzi and Leishmania major 112....