Candida albicans is a yeast that can cause infections in humans. It exists in different morphological forms, including yeast, hyphae, and pseudohyphae. Its cell wall contains beta-glucan, chitin, lipids, and mannans. Morphological shifting between forms is associated with invasion of tissues and regulated by environmental conditions and adherence factors. C. albicans binds to epithelial cells using adhesins like Hwp1 and mannoproteins, and secretes proteinases and phospholipases to aid invasion. It evades the immune system using surface receptors that bind complement components and immune regulators. Infections can be diagnosed using KOH preparations of samples and are usually treated with ant

1. Pathogenesis of Candida Albicans
Madiha Siddiqui
M.Phil-1st
Molecular Mechanism of
Pathogenesis

2. General characteristics
• Round yeast cells.
• Belong to ascomycetes
• Produce smooth white colonies.
• Grow on blood or Sabouraud’s agar.
• Identified through:
 Carbohydrate assimilation
 Fermentation
• Distinguishing through the
formation of:
 Hyphae
 Chlamydoconidia
 Germ tubes

3. Candida Albicans
Different Morphological forms:
 Yeast
 Hyphae
 Pseudohyphae
When incubated
at 37°C, C. albicans
rapidly
forms elongated
hyphae called
germ tubes.
On specialized
media,
C. albicans forms
thick walled
chlamydoconidia,
which
differentiate it
from other
Candida
species.
Cell wall includes:
 β-glucan
 Chitin
 Lipid
 Mannan covalently bonded
with protein Cell wall
Structure
observed
through
TEM

4. Pathogenesis
Morphological shifting is
associated with invasion.
Shifting is regulated by:
• Environmental
conditions
• Factors associated with
tissue adherence.
entry

5. Candida binds to the epithelial cells
through the Hwp1 which is
complementary to the amino acid
sequence present in mammalian
keratinocyte transaminases,
Hwp1 forms the cross
links between squamous
epithelial specific
protein
Other mannoproteins that have
similarities to vertebrate integrins such as
glycans, mannoproteins,
phospholipidomannan may also mediate
binding to components of the
extracellular matrix, such as fibronectin,
collagen, and laminin.
A C. albicans strain that produces a
protease is seen producing cavity-like
depressions in the cell
surface.
BINDING

6. Hyphae also secrete proteinases and
phospholipases that are able to digest
epithelial cells and probably facilitate
invasionC. albicans attachment and
invasion
are shown.
Surface glucomannan
receptor(s) on the yeast may
bind to fibronectin covering the
epithelial cell or to elements of
the (ECM)
Invasion is associated with
formation of hyphae and
production of proteinases,
which may digest tissue
elements.
invasion

7. C. albicans has protein surface receptors that bind the
C3 component of complement in a manner similar to
that of the receptors on neutrophils.
At present five candida proteins are identified which bind
human complement- and immune regulators:
 Pra1
 Gpd 2
 Hgt1
 Gpm1
Immune and tissue evasion

8. Gpm1 binds to the complement regulators:
 Factor H
 FHL-1
 Plasminogen.
Gpm1 -bound Factor H and FHL-1 are functionally
active and act as cofactors for degradation of C3b.
Gpm1 binds plasminogen, and plasminogen bound to
Gpm1, and activated plasmin degrades host ECM
proteins and C3b.
Gpm1 catalyzes
glycolysis and
glyconeogenesis.
Thus, Gpm1 bound plasminogen
contributes to immune and tissue
evasion
Receptors bind C3
in an
antiopsonic
manner
Continue…

9. Colonization VS Invasion

10. Antimicrobics and immunosuppression
increase risk local and invasive infection
 Antibacterial therapy
 Leukopenia or corticosteroid therapy
 Acquired immunodeficiency
syndrome
Mechanical disruptions may provide access to
ECM
 Indwelling devices
 Cancer chemotherapy
Vulnerability
Diabetes mellitus also predisposes to C. albicans
infection,
 Greater production of the surface
mannoproteins
in the presence of high glucose

11.  Neutrophils are the primary first-line
defense.
 Candida mannan may downregulate CMI
responses.
 Modulation of tryptophan metabolism
by C. albicans hyphae can down-
modulate TH17-type responses
IMMUNITY

12.  C. albicans produces a white, cheesy plaque that is loosely adherent to
the mucosal surface.
 The lesion is usually painless,
 Oral lesions, called thrush, occur on the tongue, palate, and other
mucosal surfaces as single or multiple, ragged white patches.
 C.albicans skin infection occurs on the moist places.
 Chronic mucocutaneous candidiasis is associated with specific T-cell
cell defects
Clinical manifestation

13. diagnosis
A direct aspirate, biopsy, or bronchoalveolar lavage is often required
to establish the diagnosis.
Exudate or epithelial scrapings examined by potassium hydroxide
(KOH) preparations

14. treatment
C. albicans is usually susceptible to amphotericin B,
nystatin, flucytosine, and the azoles

15. Thank
you