Understanding Fungal Skin Infections and Ringworm: Causes, Symptoms, and Treatment Options.pdf

NOOR-UL-AIN MEHMOOD
25
2nd PROFF / PHARM-D
MICROBIOLOGY
SUBMITTED TO: MA’AM HINA TARIQ
Friday, September 29,
2023
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2023
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I. Fungi
II. Fungal skin infections / Mycoses
a. Epidimology
b. Classification of Mycoses
1. Cutaneous Mycoses
a. Types of Cutaneous mycoses
2. Sub-cutaneous Mycoses
a.Types of Sub-cutaneous Mycoses
3. Systemic Mycoses
a.Types of Systemic Mycoses
4. Opportunistic Mycoses
a.Types of Opportunistic Mycoses
LIST OF CONTENTS

I. FUNGI :
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 Fungi (singular: fungus) are a kingdom of usually multicellular
eukaryotic organisms that are heterotrophs (cannot make their
own food).
 includes microorganisms such as yeasts and molds, as well as
the more familiar mushrooms.
 classified as a kingdom, fungi, which is separate from the
other eukaryotic life kingdoms of plants and animals.
 Mycology is the branch of biology concerned with the
systematic study of fungi, including their genetic and
biochemical properties, their taxonomy, and their use to humans
as a source of medicine.
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II. FUNGAL SKIN INFECTIONS
o MYCOSIS:
(PLURAL: MYCOSES)
 Mycosis is a fungal infection
of animals, including humans.
 mycosis often start on the
skin or in lungs.
Micrograph showing a
mycosis (aspergillosis). The
Aspergillum (which is
spaghetti-like) is seen in the
center and surrounded by
inflammatory cells.
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a. EPIDIMOLOGY:
Fungal infections of the
skin were the 4th most
common skin disease in
2010 affecting 984 million
people. 6%
11%
21%
62%
percentages
opputunistic cutaneous
subcutaneous systemic
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b. CLASSIFICATION OF MYCOSIS:
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mycosis
subcutaneous
mycoses
Cutaneous
mycoses
Systemic
mycoses
Opportunistic
mycoses

1. CUTANEOUS MYCOSIS:
 INTRODUCTION:
 Also called dermatophytoses
 these common diseases are caused by a group of related
fungi, the dermatophytes (RING WORM)
 Dermatophytes fall into three genera, each with many
species:
Trichophyton (skin, hair and nails), Epidermophyton
(skin and hair) and Microsporum (skin and nails)
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EPIDIMOLOGY:
32%
7%
1%
7%
53%
percentages
T.pedis
T.corporis
T,capitis
T.cruris
T.unguium
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ETIOLOGY:
 The causative organisms of the dermatophytoses are
often distinguished according to their natural habitats:
anthropophilic (residing on human skin), zoophilic
(residing on the skin of domestic and farm animals), or
geophilic (residing in the soil).
 Most human infections are by anthropophilic and
zoophilic organisms.
 Transmission from human to human or animal to human
is by infected skin scales.
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CLINICAL MANIFESTATIONS:
 DURATION:
months to years or life time
 SYMPTOMS:
• Usually asymptomatic
• Pruritus
• Pain with bacterial super infection
 RISK FACTORS:
• late childhood or young adult life, commonly 20-25 years
• Males > females
• Predisposing factors: hot and humid weather, occlusive
footwear, excessive sweating.
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PATHOPHYSIOLOGY:
 dermatophytes have the ability to use keratin as a
source of nutrition
 This ability allows them to infect keratinized tissues and
structures, such as skin, hair, and nails
 all three genera attack the skin, Microsporum does
not infect nails and Epidermophyton does not infect
hair.
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CLINICAL SIGNIFICANCE:
 Dermatophytoses are characterized by itching, scaling
skin patches that can become inflamed and weeping
 Specific diseases are usually identified according to
affected tissue (for example, scalp, pubic area, or feet),
but a given disease can be caused by any one of several
organisms, and some organisms can cause more than
one dis-ease depending, for example, on the site of
infection or condition of the skin.
 The following are the most commonly encountered
dermatophytoses.
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Tinea
pedis
Tinea
unguium
Tinea
cruris
Tinea
capitis
Tinea
corporis
TYPES OF CUTANEOUS MYCOSIS:

 TINEA PEDIS:
Also known as “Athlete’s foot”
Causative agents:
Trichophyton rubrum, Trichophyton
mentagrophytes, and Epidermophyton
floccosum
 Site of Attack:
initially between the toes, but can
spread to the nails, which become yellow
and brittle. Skin fissures can lead to
secondary bacterial infections, with
consequent lymph node inflammation
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 TINEA CORPORIS:
 Also known as “Ringworm”
 Causative Agent:
E.floccosum and several species of
Trichophyton and Microsporum
 Site of Attack:
Although any site on the body can
be affected, lesions most often occur on
non-hairy areas of the trunk.
Lesions appear as advancing annular
rings with scaly centers. The
periphery of the ring, which is the
site of active fungal growth, is usually
inflamed and vesiculated.
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 TINEA CAPITIS
Also known as “Scalp Ringworm”
Causative Agent:
Several species of Trichophytonand
Microsporumhave been isolated from scalp
ringwormlesions, the predominant infecting
species depending on the geo-graphic
location of the patient. In the United
States, for example,the predominant
infecting species is Trichophyton
tonsurans.Disease manifestations range
from small, scaling patches,
toinvolvement of the entire scalp with
extensive hair loss (Figure20.5C). The
hair shafts can become invaded by
Microsporumhyphae, as manifested by
their green fluorescence in long-
waveultraviolet light (Wood lamp
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 TINEA CRURIS:
 Also known as “jock itch”.
 Causative agents:
Causative organisms are E. floccosum and
T. rubrum.
 Disease Manifestations:
Disease manifestations are similar to
ringworm,except that lesions occur in the
moist groin area, where they canspread from
the upper thighs to the genitals.
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 TINEA UNGUIUM:
Also known as “onychomycosis”
Causuative Agent:
The causative organism is most
often T. Rubrum
 The nails are thickened,
discolored, andbrittle. Treatment
must be continued for three to four
months untilall infected portions
of the nail grow out and are
trimmed off
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LABORATORY DIAGNOSIS
 Skin scales should be examined microscopically in a KOH
preparation for the presence of hyphae.
 The organism is identified by the apperance of its
mycelium and it’s asexual spores on Sabouraud’s
Dextrose Agar.
 Serologic tests are not useful.
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TREATMENT:
● PHARMACOLOGICAL:
 Removal of infected skin, followed by topical application of
antifungal antibiotics such as miconazole or clotrimazole
(applied to effective area for 2-4 weeks), is the first course of
treatment.
 Refactory infections such as tinea unguium and tinea capitis
usually respond well to oral griseofulvin (500 mg/OD or 250
mg/BD)
 Infections of the hair and nails usually require systemic
(oral) therapy which includes:
Topical anti-fungal treatment 2x/week; (selenium
sulphide shampoo or terbinafine cream
 Terbinafine (250 mg/OD) is the drug of choice for
onychomycosis.
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TREATMENT
•NON-
PHARMACOLOGICAL:
Avoid sharing of towels or
clothing.
Keep the affected area cool
and dry.
Frequent washing of
clothes.
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COMPLICATIONS
 If not treated in time, cutaneous mycoses leads to;
 Cellulitis
 Alopecia
 Autoeczematization
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2. SUBCUTANEOUS MYSOSES:
 These are caused by fungi that grow in soil and on
vegetation and are introduced into dermis, subcutaneous
tissues and bone.
 EPIDIMOLOGY:
 The high prevalence of subcutaneous mycotic infections
shows that 20-25% of the world's population has skin
mycoses, making these one of the most frequent forms
of infection.
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a. TYPES OF SUBCUTANEOUS MYCOSES
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SPOROTRICHOSIS
 CASUATIVE AGENT:
Sporothrix schenckii
 CHARACTERISTICS:
• Also known as “Gardener’s
Rose Disease.”
• Thermally dimorphic.
• Habitat is soil or vegetation.
 TRANSMISSION:
• Mold spores enter skin in
puncture wounds caused by rose
thorns and other sharp objects in
garden.
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PATHOPHYSIOLOGY:
When introduced into the skin,
typically by a thorn, it causes a
local pustule or ulcer with nodules
along the draining lymphatics.
• There is a little systemic illness.
• Lesions may be chronic.
 RISK FACTORS:
• It occurs most often in
gardeners, especially those
who prone roses, because
they may be struck by a rose
thorn.
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 LABORATORY DIAGNOSIS:
• Cigar-shaped budding yeasts
visible in pus or tissue specimens.
• Culture on Sabouraud’s agar
shows typical morphology of
hyphae bearing oval conidia in
clusters at the tip of slender
conidiophores (resembling a
daisy).
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TREATMENT:
Oral Itraconazole is the
choice of drug for skin lesions,
prescribed as;
 200 mg, BD × 1 wk.
Mycological cure rate is 63%.
PREVENTION:
It can be prevented by
protecting skin by touching
Plants
Moss
Wood
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 CASUATIVE AGENTS:
Soil fungi such as Fonsecaea,
Phialophora, Cladosporium etc.
• Slowly progressive
granulomatous infection.
 TRANSMISSION:
• The fungi is introduced into skin
through trauma. These fungi
are collectively called as
“dematiaceous fungi”.
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• They are named so because their
conidia or hyphae are dark-
coloured, either gray or black.
• Wart-like lesions with crusting
abcesses extend along the
lymphatics.
 DISEASE OCCURANCE:
• This disease occurs mainly in
Tropics and is found on bare feet
and legs.
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• In the clinical laboratory, dark
brown, round fungal cells are seen
in leukocytes of giant cells.
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 TREATMENT:
 This disease is treated with;
 Oral Flucytosine + local
surgeory:
 Dosage Forms & Strengths;
o Capsule:
 250mg
 500mg
‡ Adults, 50-150 mg/kg/d div
q6hr PO
‡ Child, same as adult dosing; 50-
150 mg/kg/d div q6hr PO
‡ Neonates (<28 days old), 80-
160 mg/kg/d div q6hr PO
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 CAUSATIVE AGENTS:
Soil organisms like Petriellidium
& Madurella.
 TRANSMISSION:
• These organisms enter through
wounds on the feet, hands or
back and cause abcessions with
pus discharge through sinuses.
The pus contains compact
coloured granules.
• Actinomycetes such as
Nocardia can cause similar
lesions known as
“Actinomycotic mycetoma.”
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 TREATMENT:
• There is no effective drug
against the fungal form;
surgical excision is
recommended.
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3. SYSTEMIC MYCOSIS
 These infections results from inhalation of the spores of dimorphic
fungi that have their mold forms in soil.
 Within the lungs, the spores differentiate into yeasts or other
specialized forms. Most lung infections are asymptomatic and
self-limited.
 However, in some patients, disseminated disease develops in which
the organisms grow in other organs, cause destructive lesions and
may result in death.
 Infected persons do not communicate these diseases to
others.
 EPIDIMOLOGY:
• Systemic mycoses showed a very low prevalence of eight per
100,000 persons and three per 1 million persons.
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TYPES OF SYSTEMIC MYCOSIS
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HISTOPLASMOSIS
CAUSATIVE AGENT:
• Histoplasma capsulatum
CHARACTERISTICS:
• Thermally dimorphic i.e. a yeast
at body temperature and a mold
in the soil at ambient
temperature.
• The mold grows prefrentially in
soil enriched with bird droppings.
• Mostly endemic in central &
eastern United States, especially
in Ohio and Mississipi River
Valleys.
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 TRANSMISSION:
• Inhalation of airborne asexual
spores (microconidia)
 PATHOPHYSIOLOGY:
• Spores enter the lungs and
diffrentiate into yeast cells.
• The yeast cells are ingested by
alveolar macrophages and
multiply within them.
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• An immune
response is
mounted and
granulomas forms.
• Most infections are
contained at this
level but
suppression of
cell-mediated
immunity can lead
to disseminated
disease.
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 RISK FACTORS:
 The risk factors include
• AIDS
• Primary immunodeficiencies
• Drug-induced immunosuppressive states
• The extremes of age.
 SKIN TESTS:
• Histoplasmin, a mycelial extract, is the antigen. Useful for
epidemiologic purposes to determine the incidence of infection.
• A positive result indicates only that infection has occured; it can
not be used to diagnose active disease. Because skin testing can
induce anti-bodies, serologic tests must be done first.
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• Sputum or tissue can be examined microscopically and cultured on
SDA.
• Yeasts are visible in macrophages.
• The presence of tuberculate chlamydospores in culture at 25°C
is diagnostic.
• A rise in anti-body titer is useful for diagnosis, but cross-section
with other fungi (e.g. Coccidioides) occurs.
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 TREATMENT:
• Amphotericin-B
 Dosage Forms & Strengths;
 powder for injection
• 50mg/vial
 ADULTS:
 Test dose: 1 mg IV x1 infused over 20-30 min
 Load: 0.25-0.5 mg/kg IV infused over 2-6 hr
 Maintenance: 0.25-1 mg/kg IV qDay OR up to 1.5 mg/kg IV
qOD (may increase gradually by 0.25 mg-increments/day)
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PEDIATRIC:
Test dose: 0.1 mg/kg IV, not to
exceed 1 mg; administer over 20-60
min
Initial dose: 0.25 mg/kg/dose IV
qDay/qOD
Maintenance: Increase by 0.25
mg/day increments as tolerated to
1-1.5 mg/kg/day
PREVENTION:
•No vaccine is available.
•Itraconazole can be used for
chronic suppresion in AIDS patients.
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COCCIDIOIDOMYCOSIS
• Coccidioides immitis
• Thermally dimorphic. At 37°C in
the body, it forms spherules
containing endospores. At
25°C, either in soil or on agar
in the laboratory, it grows as a
mold.
• The cells at the tip of hyphae
grows into asexual spores
(arthrospores).
• Natural habitat is soil.
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 TRANSMISSION:
• Inhalation of airborne arthrospores.
• In the bronchioles, the arthroconidia enlarge to form spherules,
which are round double-walled structures measuring
approximately 20-100 μm in diameter.
• The spherules undergo internal division within 48-72 hours and
become filled with hundreds to thousands of offspring (ie,
endospores).
• Rupture of the spherules leads to the release of endospores,
which mature to form more spherules, thereby disseminating
the infection within the body.
• A cell-mediated response containes the infection in some
people , but those who are immunocompromised are at high
risk.
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 RISK FACTORS:
 This risk persists when analyses are controlled for;
o Age
o Sex
o additional demographic features
o concurrent medical problems
o duration of exposure
o occupation
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• Sputum or tissue can be
examined microscopically for
spherules and cultured on
SDA.
• A rise in IgM (using precipitin
test) anti-bodies indicate
recent infection.
• An increase in IgG anti-bodies
(using complement-fixation
test) indicates dissemination.
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 SKIN TEST:
• Either Coccidiodin, a mycelial extract, or Spherulin, an
extract of spherules, is an antigen.
• Useful in determining whether the patient has been
infected.
• A positive test indicates prior infection but not
necessarily active disease.
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 TREATMENT:
 Amphotericin-B for disseminated disease;
 Dosage Forms & Strengths:
 powder for injection; 50mg/vial
 Test dose: 1 mg IV x1 infused over 20-30 min
 Load: 0.25-0.5 mg/kg IV infused over 2-6 hr
 Maintenance: 0.25-1 mg/kg IV qDay OR up to 1.5 mg/kg IV qOD
(may increase gradually by 0.25 mg-increments/day)
 PREVENTION:
• No prophylactic drug is available.
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BLASTOMYCOSIS
 CAUSATIVE AGENT:
Blastomyces dermatitidis
• thermally dimorphic. Mold in
soil and yeast in the body at
37°C.
• The yeast form has a single,
broad-based bud and a thick,
refractive wall.
• Natural habitat is rich soil (e.g.
near beaver dams), especially in
the upper midwestern region of
United States.
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mold
yeast

TRANSMISSION:
•Inhalation of air borne
spores (conidia).
PATHOGENESIS:
• Inhaled conidia
differentiate into yeasts,
which initially causes
abscesses followed by
formation of
granulomas.
• Dissemination is rare,
but when it occurs,
bones and skin are most
commonly involved.
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 RISK FACTORS:
 The mean age at diagnosis is approximately 45 years, with
most patients aged 30-69 years. However, persons of any
age can acquire the disease, including infants and very
elderly persons.
 The disease is rare in children and adolescents.
• Sputum or skin lessions are examined microscopically for
yeasts with a broad-based bud culture on SDA. Serological
tests are not useful.
 SKIN TEST:
• The skin test lacks specificity and has little value.
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 PREVENTION:
• No vaccine or prophylactic drug is available.
 TREATMENT:
• Itraconazole is the drug of choice given as;
 Dosage Forms & Strengths;
 capsule
65mg (Tolsura)
100mg (Sporanox, generic)
 oral solution
10mg/mL (Sporanox, generic)
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• Sporanox
200 mg PO qDay
If no improvement, or evidence of
progressive fungal disease, increase
dose in 100-mg increments to a
maximum of 400 mg/day
Divide doses >200 mg/day into 2
doses
• Tolsura
130 mg PO qDay
If no improvement, or evidence of
progressive fungal disease, increase
dose in 65 mg increments to a
maximum of 260 mg/day (130 mg
BID)
Divide doses >130 mg/day into 2
doses
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PARACOCCIDIOIDOMYCOSIS
 CAUSATIVE AGENT:
• Paracoccidioides
brasiliensis
• Thermally dimorphic. Mold in
soil, yeast in body at 37°C.
• The yeast form has multiple
buds (resembles the steering
wheel of a ship).
 TRANSMISSION:
• Inhalation of airborne conidia
(spores).
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• After inhalation of the conidia, the
fungus transforms into yeast cells
within the alveolar macrophages.
• This transformation induces a
nonspecific inflammatory response,
which generally limits the disease at
this point. Therefore, in most patients
who are immunocompetent, the
infection is asymptomatic and resolves
without medical intervention.
• Less commonly, after an incubation
period of weeks to decades, the
fungus can disseminate through the
venous and lymphatic systems,
causing granulomatous disease in
multiple tissues.
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 SIGNS AND SYMPTOMS:
 rimary lung infection - Cough (productive or nonproductive),
dyspnea, malaise, fever, and weight loss are common symptoms
 Chronic pulmonary sequelae - Develop in one third of patients; can
include pulmonary fibrosis, bullae, and emphysematous changes that
can contribute to pulmonary hypertension and cor pulmonale in 5%
of cases.
 Mucous membrane involvement - Occurs in 50% of patients with
acute pulmonary infection; includes laryngeal and pharyngeal lesions
 Oral lesions - May be associated with nasal and pharyngeal ulcers
(Aguiar-Pupo stomatitis) and with mandibular or cervical lymph node
enlargement
 Cutaneous lesions - Caused by hematologic dissemination from the
lungs; occur in 25% of patients; crusted papules, ulcers, nodules,
plaques, and verrucous lesions are typical
 Lymphadenopathy - Most common in the cervical region
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 The diagnosis of paracoccidioidomycosis is most commonly
made by visualization of the yeast cells in tissue, wet
preparations (eg, sputum), or superficial scrapings (eg, skin
lesions).
 Serological tests are available in areas of highest endemicity.
In patients with active paracoccidioidomycosis, chest
radiography reveals interstitial infiltrates (in 64% of cases) or
mixed lesions with linear and nodular infiltrates.
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 TREATMENT:
 Itraconazole is considered the drug of choice for
paracoccidioidomycosis, with a reported effectiveness of 95%.
The course of therapy is typically 200 mg/day for 6 months.
itraconazole is considered superior to ketoconazole because of
shorter treatment course, lower toxicity profile, and lower
relapse rate (3-5%)
 Ketoconazole is also an effective agent for
paracoccidioidomycosis, with a cure rate of 85-90% and an
associated relapse rate of less than 10%. A dose of 200-400
mg/day in adults or 5 mg/kg/day in children for 6-18
months is required.
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4. OPPORTUNISTIC MYCOSES
 Opportunistic mycoses occurs in immunocompromised
individuals but rare in healthy persons.
 The organisms involved are cosmopolitan fungi which
have a very low inherent virulence. The increased
incidence of these infections and the diversity of fungi
causing them, has parallelled the emergence of AIDS,
more aggressive cancer and post-transplantation
chemotherapy and the use of antibiotics, cytotoxins,
immunosuppressives, corticosteroids and other macro
disruptive procedures that result in lowered resistance of
the host.
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EPIDYMOLOGY
 The epidemiologic features, including incidence, of some
of these mycoses are markedly different in Latin
America than they are in other parts of the world. The
most consistent epidemiologic data are available for
candidemia, with a large prospective study in Brazil
reporting an incidence that is 3- to 15-fold higher than
that reported in studies from North America and
Europe. Species distribution also differs: in Latin
America, the most common Candida species (other
than Candida albicans) causing bloodstream infections
are Candida parapsilosis or Candida tropicalis,
rather than Candida glabrata.
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TYPES
OPPORTUNISTIC
candidiasis
cryptococco-
sis
aspergillosis
Mucormyco-
sis
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CANDIDIASIS:
Candida albicans
• It is a yeast when part of
normal flora of mucous
membranes but forms
pseudohyphae and hyphea
when invades tissue.
• Not thermally dimorphic.
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 TRANSMISSION:
• Part of normal flora of mucous membranes, skin and GI tract.
• No person-to-person transmission.
• Opportunistic pathogen.
• When local or systemic host defenses are impaired, disease may
result.
• C.albicans causes;
 Thrush (white patches) in mouth.
 Vulvovaginitis with itching.
 Skin invasion occurs in warm, moist areas which become red and
weeping.
 Fingers and nails are involved when repeatedly immersed in
water.
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SIGNS AND SYMPTOMS:
• Sore and painful mouth
• Dysphagia
• Thick, whitish patches on the
oral mucosa
• Retrosternal pain
• Epigastric pain
• Nausea and vomiting
• Abdominal pain
• Fever and chills
• Erythematous vagina and
labia; a thick, curdlike
discharge
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 LABORATORY DIAGNOSIS
• Microscopic examination of tissue reveals yeasts and
pseudohyphae.
• If only yeasts are found, colonization is suggested.
• The yeast is gram positive and forms colonies on SDA.
• Serologic tests are not useful.
 TREATMENT:
• Skin and mucous membrane disease can be treated with any
oral or topical anti-fungal agents such as;
 Miconazole (50mg); Apply buccal tab to gum region qDay for 14
consecutive days.
• Disseminated disease requires;
 Amphotericin-B (50mg/vial); 0.25-0.5 mg/kg IV infused over 2-
6 hr
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 RISK FACTORS:
 Granulocytopenia
 Bone marrow transplantation
 Solid organ transplantation (liver, kidney)
 Recent chemotherapy or radiation therapy
 Corticosteroids
 Broad-spectrum antibiotics
 Burns
 Prolonged hospitalization
 Acute and chronic renal failure
 Mechanical ventilation for longer than 3 days
 PREVENTION:
• Predisposing factors should be reduced or eliminated.
• There is no vaccine.
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ASPERGILLOSIS
Aspergillus fumigatus
• Mold with septate hyphae that
branch at a V-shaped angle .
• Not dimorphic.
• Habitat is soil.
 TRANSMISSION:
• Inhalation of airborne spores.
• Aspergillus primarily affects the
lungs.
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• Aspergillus causes a spectrum of disease, from colonization to
hypersensitivity reactions to chronic necrotizing infections to
rapidly progressive angioinvasion, often resulting in death.
• Rarely found in individuals who are immunocompetent, invasive
Aspergillus infection almost always occurs in patients who are
immunosuppressed by virtue of underlying lung disease,
immunosuppressive drug therapy, or immunodeficiency.
• Human host defense against the inhaled spores begins with the
mucous layer and the ciliary action in the respiratory tract.
Macrophages and neutrophils encompass, engulf, and eradicate
the fungus. However, many species of Aspergillus produce
toxic metabolites that inhibit macrophage and neutrophil
phagocytosis. Corticosteroids also impair macrophage and
neutrophil function.
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SIGNS AND SYMPTOMS:
•Fever
•Cough
•Night sweats
•Weight loss
•Leukemia
•Lymphoma
•Cough with mucous plugs
•Subacute pneumonia
•Pleuritic chest pain
DIAGNOSIS:
• Chest radiographs show a
mass in a preexisting cavity,
usually in an upper lobe,
manifested by a crescent of air
partially outlining a solid mass.
76

• Definitive diagnosis of invasive aspergillosis or CNPA
depends on the demonstration of the organism in tissue, as
follows:
• Visualization of the characteristic fungi using Gomori
methenamine silver stain or Calcofluor
• Positive culture result from sputum, needle biopsy, or
bronchoalveolar lavage (BAL) fluid (however, a negative
result does not exclude pulmonary aspergillosis)
 SKIN TEST:
• Not available.
77

 TREATMENT:
 Amphotericin-B (50mg/vial); 0.25-0.5 mg/kg IV infused over 2-6
hr
 Some lesions (e.g. fungal balls) can be surgically removed.
 Steroid therapy is recommended for allergic brochopulmonary
aspergillous.
 RISK FACTORS:
• Occurs in persons with asthma and those with cystic fibrosis (CF)
• Occurs in patients with underlying disease (eg, steroid-dependent
chronic obstructive pulmonary disease [COPD], alcoholism)
• Occurs in patients with prolonged neutropenia or immunosuppression
• Organ transplantation, especially bone marrow but also lung, heart,
and other solid organ transplants
78

80
 ALL CONTENT:
i. Warren Levinson (ninth edition);Review of Medical Microbiology
and Immunology.
ii. https://archive.org/details/Lippincotts_Illustrated_Reviews_Microbi
ology_3rd_Edition_by_Richard_A._Harvey Cy
iii. https://emedicine.medscape.com/article/296052
iv. https://www.dermnetnz.org/topics/skin-manifestations-of-
systemic-mycoses
v. https://en.wikipedia.org/wiki/Mycosis#Epidemiology
 ALL PICTURES:
i. https://www.google.com

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