This presentation provides an overview of fungal infections, including their cell structure, epidemiology, pathogenesis, diagnosis, and treatment. It discusses several common fungal infections in depth. Major topics covered include superficial and subcutaneous fungal infections caused by dermatophytes, dimorphic fungi that cause endemic mycoses, opportunistic fungi that can cause disease in immunocompromised hosts, and miscellaneous opportunistic fungi. Treatment involves antifungal drugs like amphotericin B and azoles. Prevention focuses on reducing exposure to fungal spores through masks, clothing, and hygiene practices.

1. A PRESENTATION
ON FUNGAL
INFECTIONS

2. FUNGAL INFECTIONS
• THE INFECTIONS CAUSED
BY FUNGI ARE KNOWN AS
FUNGAL INFECTIONS/
MYCOSIS.
• Once exotic and rare
• Now increasingly common
• Fungi are not “virulent"
But they are good at
taking advantage
"Opportunistic”

3. FUNGI CELL STRUCTURE:
• Yeasts (unicellular, budding)
• Molds (mycelial, spores)
• Dimorphs (both)
3

5. Epidemiology of the Mycoses
• Most fungal pathogens do not require a host to
complete their life cycles and infections are not
communicable.
• Dermatophytes and Candida sp naturally inhabit
human body and are transmissible.
• True fungal pathogens are distributed in a
predictable geographical pattern - climate, soil.
• Dermaphytoses most prevalent
• Cases go undiagnosed or misdiagnosed.
• Systemic, subcutaneous, cutaneous or superficial
infections
5

6. Pathogenesis of the Fungi
• Portal of entry
– primary mycoses – respiratory portal; inhaled spores
– subcutaneous - inoculated skin; trauma
– cutaneous and superficial – contamination of skin
surface
• Virulence factors – thermal dimorphism, toxin production,
capsules and adhesion factors, hydrolytic enzymes,
inflammatory stimulants
• Antifungal defenses are the integrity of the barriers and
respiratory cilia.
• Most important defenses are cell-mediated immunity,
phagocytosis, and inflammation.
• Long-term immunity can only develop for some. 6

7. Diagnosis of Mycotic Infections
• Diagnosis and identification require
microscopic examination of stained
specimens, culturing in selective and enriched
media and specific biochemical and
serological tests.
7

8. 8

9. Control of Mycotic Infections
• Immunization is not usually effective.
• Control involves intravenous amphotericin B,
flucytosine, azoles and nystatin.
• In some cases surgical removal of damaged tissues.
• Prevention is limited to masks and protective clothing
to reduce contact with spores.
• Few communicable infections (ringworm) requires
isolation and separate washing of clothes.
• Towels and clothes must not be shared.
9

10. Overview of fungal infections
• Superficial (skin or mucosa)
• Subcutaneous (hypodermal layers)
• Systemic:
– “True pathogens” – infect healthy hosts, although
disease worsens with immunocompromised
– “Opportunists” – disease almost exclusively in
immunocompromised

12. 12

13. 1. SYSTEMIC FUNGAL
INFECTIONS:
THE “TRUE PATHOGENS”
Histoplasmosis, Coccidioidomycosis,
Paracoccidioidomycosis and Blastomycosis
• Dimorphic
• Respiratory acquisition
• Restricted geographic distribution
• Infect normal hosts
• Disease reminiscent of TB

14. HISTOPLASMOSIS: OHIO VALLEY FEVER
• Organism: Histoplasma
capsulatum
– Dimorphic soil organism
• Habitat: soils with high N content
• Ohio-Mississippi valley; Puerto Rico,
Central and S. America
• Guano(droppings) of bats, birds, poultry
(chicken coops and caves)
• Pathogenesis: inhalation of spores
Pathophysiology:
• Spores transform to yeast in lung, elicit
cellular immunity as per TB
– Hematogenous dissemination
– skin test reactivity (histoplamin)
Clinical Features: mimics
TB
• May disseminate early
(infancy, immunodef.)
• May cause acute
nodular/cavitary lung
disease
• May reactivate years
later

15. 15

16. 16

17. 17

18. COCCIDIOIDOMYCOSIS: VALLEY FEVER
• Organism: Coccoides immitis
– Dimorphic soil organism with
spherules and endospores in host
• Habitat:
– Southwest US, Mexico, Central and
South America
• Pathogenesis: inhalation of spores
Pathophysiology:
• Spores transform to spherules in
lung, elicit cellular immunity as per
TB
• Hematogenous dissemination
• Skin test reactivity (coccoidin)
Clinical Features:
Acute self-limited flu-
like seroconversion
(Valley fever)
Dissemination (pregnancy,
dark skin, immuno-
compromised)
Treatment:
• Amphotericin B

19. BLASTOMYCOSIS
• Organism: Blastomyces
dermatitidis
– Dimorphic soil organism
• Habitat: humid woodlands
– MidAtlantic countryside
– Beaver dams, peanut farms
– Organic debris
• Pathogenesis: inhalation of spores
Pathophysiology:
• Spores transform into yeast in
lung, disseminate.
• No good antigen test to describe
exposed population
Clinical:
• Acute or chronic
lung disease
(nodular/cavitary)
• Disseminated
disease
– skin
– bone
– urinary tract

20. 20

22. PARACOCCIDIOIDOMYCOSIS
• Paracoccidioides brasiliensis
• Distributed in Central and South America
• Lung infection occurs through inhalation or
inoculation of spores.
• Systemic disease is not common.
• Ketoconazole, amphotericin B, sulfa drugs
22

23. 2.PATHOGENS WITH
INTERMEDIATE VIRULENCE
I. SUBCUTANEOUS FUNGAL
INFECTIONS
• Lymphocutaneous sporotrichosis
• Chromoblastomycosis
• Mycetoma
Pathogenesis: Introduced through skin, grow in
subcutaneous tissues, spread via lymphatics. May
reach distant organs especially bone, joints in path.
Most common in nonindustrialized world (“Madura
foot”)

24. SPOROTRICHOSIS (ROSE-GARDENER’S
DISEASE)
• Organism: Sporothrix schenkii
– Dimorphic soil organism, Worldwide distribution
Pathogenesis: Splinters or thorns inoculate organism into
subcutaneous tissues & forms nodules, then Yeast travels
along lymph nodes. Elicit mixed pyogenic/ granulomatous
reaction
Clinical Features:
• Gardners and sports person
• Ulcerating nodules along hard cord
• Bone and joint destruction
• Occasional dissemination
• Infects appendages and lungs.

25. CHROMOBLASTOMYCOSIS
• A progressive subcutaneous mycosis
characterized by highly visible verrucous
lesions
• Etiologic agents are soil saprobes with dark-
pigmented mycelia and spores
• Fonsecaea pedrosoi, Phialophora verrucosa,
Cladosporium carrionii
• Produce very large, thick, yeastlike bodies,
sclerotic cells
25

26. MYCETOMA
• When soil microbes are accidentally
implanted into the skin
• Progressive, tumor like disease of the hand
or foot (madura foot) due to chronic fungal
infection; may lead to loss of body part
• Caused by Pseudallescheria or Madurella
26

27. II. CUTANEOUS MYCOSES
• Infections strictly confined to keratinized
epidermis (skin, hair, nails) are called
dermatophytoses- ringworm and tinea
• 39 species in the genera Trichophyton,
Microsporum, Epidermophyton
• Closely related and morphologically similar
• Causative agent of ring worm varies case to
case
27

28. 28

29. RINGWORM
• Also known as
dermatophytosis
• Natural reservoirs-
humans, animals, and
soil
• Infection facilitated by
moist, chafed skin
• Long infection period
followed by localized
inflammation and
allergic reactions to
fungal proteins 29

30. • Ringworm of scalp (tinea capitis) affects scalp and
hair-bearing regions of head; hair may be lost.
• Ringworm of beard (tinea barbae) affects the chin
and beard of adult males; contracted mainly from
animals.
• Ringworm of body (tinea corporis) occurs as
inflamed, red ring lesions anywhere on smooth
skin.
• Ringworm of groin (tinea cruris) “jock itch” affects
groin and scrotal regions.

31. • Ringworm of foot and hand
(tinea pedis and tinea manuum)
is spread by exposure to public
surfaces; occurs between digits
and on soles also known as
atheletes foot.
• Ringworm of nails (tinea
unguium) is a persistent
colonization of the nails of the
hands and feet that distorts the
nail bed.
• Treatment of dermatophytes
includes topical antifungal agents
– tolnaftate, miconazole applied
for several weeks.
• Lamisil or griseofulvin 1-2 years
31

32. III. SUPERFICIAL MYCOSES
• Tinea versicolor – caused by Malassezia furfur;
elicits mild, chronic scaling, mottling of skin;
also implicated in folliculitis, psoriasis, and
seborrheic dermatitis
• White piedra – caused by Trichosporon
beigelii; whitish or colored masses develop on
scalp, pubic, or axillary hair
• Black piedra – caused by Piedraia hortae; dark-
brown to black gritty nodules, mainly on scalp
hairs
32

33. SYSTEMIC FUNGAL INFECTIONS:
THE “OPPORTUNISTS”
True pathogens Opportunists
geographic restriction Omnipresent
Dimorphic Yeasts or molds
Infection by inhalation Various routes
Pyogenic (pus)/granulomatous host
response
Host response varies
Similar to TB Widely variable
Infection = immunity No lasting immunity

34. 34

35. CRYPTOCOCCOSIS
• Organism: Cryptococcus neoformans
– yeast with thick polysaccharide
capsule
• Habitat:
– Bioterrorism of a sort, worldwide
• Pathogenesis: inhalation of yeast
Pathophysiology:
• transient colonization
OR
• acute/chronic lung disease
OR
• CNS invasion
Clinical features:
Meningoencephalitis
• acute or chronic
• fever, headache, stiff neck,
loss of vision
• complicated by
hydrocephalus
• cryptococcal antigen for
diagnosis

38. CANDIDIASIS
• Organism: Candida
albicans et al
• Habitat: normal
human flora
• Pathogenesis:
– colonized areas:
overgrowth
– noncolonized areas:
invasion

39. Candidiasis
Pathogenesis:
• Breach in
• Skin or mucosal integrity
• Normal bacteriologic flora
• Neutrophil function or CMI
Diagnosis:
• Gram stain may help
• Infection and colonization may
be difficult to distinguish
Treatment:
• Remove the breach in defenses,
if possible
Types of Candidiasis:
• Cutaneous candidiasis
• Oral candidiasis(oral thrush)
• Vaginal candidiasis(vaginal
thrush)
Clinical settings:
• Moisture, antibiotics,
pregnancy
• HIV infection
• Intravenous catheters
• Chemotherapy or marrow
ablation

42. ASPERGILLOSIS
• Organism: Aspergillus fumigatus and
others
– Mold without a yeast phase
• Habitat:
– everywhere, worldwide
• Pathogenesis:
– Inhalation of spores
Pathophysiology:
Spores in lung may
• elicit allergy
• grow in preexisting cavity
• invade vasculature, disseminate
(neutrophils key)
Clinical Features:
• Allergic broncho-
pulmonary
aspergillosis
• Aspergilloma
• Invasive, with
pneumonia,
other end-organ
disease
• TREATMENT:
Amphotericin B
and nystatin

43. 43
PNEUMOCYSTIS PNEUMONIA
• Pneumocystis (carinii) jiroveci
• A small, unicellular fungus that causes
pneumonia (PCP), the most prominent
opportunistic infection in AIDS patients
• This pneumonia forms secretions in the
lungs that block breathing and can be
rapidly fatal if not controlled with
medication.
• Pentamidine and cotrimoxazole

44. MUCORMYCOSIS
• Organism: species of Mucorales,
genera Rhizopus and Mucor
– Mold without a yeast phase
• Habitat:
– Everywhere, worldwide
• Pathogenesis:
– Inhalation of spores
Pathophysiology:
• Alveolar MPH/PML clear organisms
BUT Acid, Sugar, Neutrophil
dysfunction may enable relentless
growth.
Clinical Features:
The most acute and
fulminant fungal infection
known
Pneumonia progressing to
infarction
Sinusitis progressing to
brain abscess

45. ZYGOMYCOSIS
• Zygomycota are extremely abundant saprobic fungi
found in soil, water, organic debris, and food.
• Genera most often involved are Rhizopus, Absidia,
and Mucor.
• Usually harmless air contaminants invade the
membranes of the nose, eyes, heart, and brain of
people with diabetes and malnutrition, with severe
consequences.
45

46. 46
MISCELLANEOUS OPPORTUNISTS
• Any fungus can be implicated in infections
when immune defenses are severely
compromised.
• Geotrichum candidum – geotrichosis; mold
found in soil, dairy products; primarily
involved in secondary lung infections
• Fusarium species – soil; occasionally infects
eyes, toenails, burned skin

47. REFERENCES
• 1. PHARMACOTHERAPY HANDBOOK, NINTH
EDITION, McGraw Hill Education, Pg No.:347-
360
• 2. TEXTBOOK OF MICROBIOLOGY, SIXTH
EDITION, McGraw Hill Education.