3.1 Introduction To Fungi and Mycoses

Introduction to
Fungi & Mycoses
Dr Gina Mulundu
UNZA SOM
Key Concepts
• Mycology - the study of fungi (molds, yeasts, and mushrooms).
• All fungi are Eukaryotic
– true nucleus,
– 80S ribosomes,
as are humans
– Mitochondria
• The have complex CHO CW s, chitin, glucan, &mannan.
• Ergosterol is their major membrane sterol
• Imidazole used to inhibit synthesis of ergosterol.
• Polyene bind more tightly to ergosterol than cholesterol.
• They are heterotrophic (require organic carbon)
• They’r also Saprophytic or saprobic (live on dead organic material)
• Some are Parasitic (live on other living organisms)
Key Concepts….
They constitute a separate kingdom – FUNGI
Able to be multicellular and comprise:
Filamentous strucs  moulds
Unicellular forms  yeasts
Some are dimorphic – exist in either form depending
on environ condtns (almost always as yeast in infection)
Cause superficial, Cutan, subcut, & systemic infections
Are typically free living, acquired from environ
sources & others are part of norm flora
Cause disease by inflamm resp, direct invasion or
tissue destruction
Introduction
Fungal infections or MYCOSES, usually classified by

body area affected & type of infection induced
1. Endemic mycoses ↘ from geog restricted true pathogens
2. Opportunistic mycoses ↘ from non-true pathogens but cause

severe diseases in immune compro patients
3. Subcutaneous mycoses ↘ diseases involve the skin, subcut tissue

& lymphatics
4. Superficial & cutaneous mycoses ↘ common, limited to skin &

skin structures
Types of Pathogenic Fungi
Fungi belong to a discrete kingdom- the FUNGI/

EUMYCOTA, and are classified on the basis :-
Mode of sexual & asexual reproduction
Morphology
Life cycle
Physiology (to some extent)

Comprises at least 100 thou spp found world wide
Most are ubiquitous in nature & > 1% cause disease in man
They play a crucial role in biodegradation of waste material
They are also economically destructive, causing widespread

damage to food and fabrics
Fungi are used commercially in industrial processes such as

fermentation and in the production of important metabolites
such as antibiotics and steroid hormone derivatives
Are eukaryotes, defined nucleus, CM with lipids,
glycoproteins, sterols, mitocond, GA, Robos bound to ER,
Cytoskel, microtub, microfilaments
 Have CW of chitin, mannan, glucans
 In nature they derive nutrients from decaying matter
 They lack chlorophyll and do not do photosynthesis
 They are almost all strict aerobes and favour 35 -37◦C temps
Fungi that cause disease exists in:
filamentous (moulds) - multicellular
2 forms
unicellular (yeasts)
• Moulds branch in threadlike filaments
→ hyphae, collectively called mycelium
• Hyphae maybe septate (partitioned) or coenocytic (multinucleate
with no cross walls)
• Yeasts are single cells, ovoid or spherical, with a rigid cell wall
• Yeasts divide by budding or binary fission (asexual)
• Some produce polysaccharide capsule

YEAST
• Multiple solitary small rounded

forms, actively dividing, growing,
and metabolising form of the
fungus.
• Reproduction occurs via

budding (or fission) and the
colonies are typically moist
and mucoid
2. Yeast cells are medium size with thick walls.
walls
Saprobic Phase BUDDING YEAST

CELLS
3. Yeast cells often show multiple buds
Saprobic Phase Yeast cells with buds

4. Yeast capsule is extremely large.
Yeast showing large capsule

On agar, yeast
forms moist
colonies that
appear to, but are
larger than
bacteria
FUNGI
Grow as microscopic branching
threadlike filaments
Filaments are called hyphae
Hyphae are collectively called
mycelium
The hyphae grow by elongation at
their tips
At the ends of hyphae are rounded
forms that could be confused with
yeast, called conidia or spores.
• Hyphae are either septate or
coenocytic
Mould growth on Agar

Fungal Dimorphism
Many display both forms and able to exist as moulds

or yeasts
This is known as Dimorphism, and occurs when

fungi infect living host
The Yeast is the parasitic form in most cases
Occasionally this rule maybe reversed

Fungal Dimorphism
1. when infecting susceptible species fungi can change
from mould to yeast transition
Mould
Yeast
Human Mycotic Encounter
Humans encounter pathogenic fungi via one of 2

ways:
freely in nature/environment
a. By entry into their geographic confines
b. Natural encounter with immunocompromised
individuals
Normal Human Fungal Flora

– Has ability to cause severe infection in
immunocompromised individuals
Diagrammatic representation of the saprophytic and
invasive tissue forms of pathogenic fungi.
fungi
Entry Into Host
Innate immunity protects from fungal inversion –
skin & mucosal surface, hence most are mild & self
limiting
Desiccation, Epeth cell t/over, fatty acids, low pH, bacterial
flora + mucous membranes
alterations in normal flora (via Abios) or nutritional

changes allow fungi (C albicans) to proliferate and may
allow entry and even infection
violation of natural barriers – trauma/foreign bodies

allow entry of fungi into sterile areas of the body
Spread & Multiplication
• Tissue reaction to fungal presence varies with:
– Spp; site affected; duration of infection
• Some mycoses are typical of causing low-grade inflamm response

that fails to clear the fungi leaving a low virulent infection
• Gen nonspecific inflammatory reactions are very critical in
eliminating fungi
• Neutrophils phagocytosis & killing are of primary importance and
is most effective
• Phagocytosis may fail with some fungi part. those surrounded by
thick viscous capsule
Fungal cells are highly antigenic and evoke both
cellular and humoral responses
Antibodies and complement play a role in

extracellular killing of some fungi → by secreting lethal
lysosomal enzymes
Resistance to fungal infections is due to cellular or

T-lymphocyte-mediated immunity
Damage From Mycoses
outcome of infection is determined by:
Virulence of infecting organism
Size of inoculum
Adequacy of host defense
Tissue damage varies with each spp and organ involved

but typically is due to direct invasion of organism + assoc
displacement or destruction of vital structures & toxic
effects of inflamm response
Fungi that cause invasive disease are not known to secrete

toxins harmful to host
Diagnosis
Lab via:
direct microscopy(some large enough for direct exam)
histopath,
culture,
serology, and
antigen detection
Morphological characteristics can be distinctive enough

in some to aid identification
This is useful in some serious systemic infn to provide

immediate diagnosis
Gen cultural growth of fungi fro sterile areas implies
infection
Culture must guard vs contamination
Serum antibody detection is useful in diagnosis of endemic

infections but rarely in opportunistic infections
Direct detection of fungal antigens proving more useful
PCR continues to prove useful and holds great potential

Mycotic Treatment
Not all mycoses require treatment
for those that require antifungal agents, toxicity is a

prob due to struc & pathway similarity in fungi &
mammalian cells
Thus very few antifungal agents available

Conclusions
Fungi comprise a separate kingdom with 100s of 000s of
spp
They are eukaryotic
Many encounters with fungi do not produce disease
However large infection doses and immunocomp is
enough to produce disease serious/life threatening disease.
a variety of diagnostic tests are now available to
determine presence of fungal infection

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Introduction to

Fungi & Mycoses

Fungal infections or MYCOSES, usually classified by

2. Opportunistic mycoses ↘ from non-true pathogens but cause

3. Subcutaneous mycoses ↘ diseases involve the skin, subcut tissue

4. Superficial & cutaneous mycoses ↘ common, limited to skin &

Fungi belong to a discrete kingdom- the FUNGI/

Physiology (to some extent)

Most are ubiquitous in nature & > 1% cause disease in man

They play a crucial role in biodegradation of waste material

They are also economically destructive, causing widespread

Fungi are used commercially in industrial processes such as

 In nature they derive nutrients from decaying matter

 They lack chlorophyll and do not do photosynthesis

• Yeasts divide by budding or binary fission (asexual)

• Some produce polysaccharide capsule

• Multiple solitary small rounded

• Reproduction occurs via

Saprobic Phase BUDDING YEAST

Saprobic Phase Yeast cells with buds

Yeast showing large capsule

Mould growth on Agar

Many display both forms and able to exist as moulds

This is known as Dimorphism, and occurs when

The Yeast is the parasitic form in most cases

Occasionally this rule maybe reversed

Humans encounter pathogenic fungi via one of 2

Normal Human Fungal Flora

alterations in normal flora (via Abios) or nutritional

violation of natural barriers – trauma/foreign bodies

– Spp; site affected; duration of infection

• Some mycoses are typical of causing low-grade inflamm response

Antibodies and complement play a role in

Resistance to fungal infections is due to cellular or

Tissue damage varies with each spp and organ involved

Fungi that cause invasive disease are not known to secrete

Morphological characteristics can be distinctive enough

This is useful in some serious systemic infn to provide

Culture must guard vs contamination

Serum antibody detection is useful in diagnosis of endemic

Direct detection of fungal antigens proving more useful

PCR continues to prove useful and holds great potential

Not all mycoses require treatment

for those that require antifungal agents, toxicity is a

Thus very few antifungal agents available

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