Mycoses

Mycoses

5 groups of mycoses are there according to the type of infected tissue in the host:-

1. Superficial mycoses
2. Cutaneous mycoses
3. Subcutaneous mycoses
4. Systemic mycoses
5. Opportunistic mycoses

Superficial Mycoses

 Fungal infection is limited to outer surface of hair and skin.
 Fungi live exclusively on dead layers of the skin and its appendages.
 They have no contact with living tissue and hence don’t induce inflammatory response.

Infection of hair shaft is called as Piedras.

1. Black Piedra – Piedraia hortae
2. White Piedra – Trichosporon beigelii
• Tineas – Superficial infection involving outer layers of skin

a. Tinea versicolor – is a chronic mild superficial infection of stratum corneum
caused by Malassezia globosa, M. restricta, and other members of the M. furfur
complex.

b. Tinea nigra - is a superficial chronic and asymptomatic infection of the stratum
corneum caused by the dematiaceous fungus Hortaea (Exophiala) werneckii.

 More prevalent in warm coastal regions and among young women
 Lesions appear as dark (brown to black) discoloration mostly on the palm

Cutaneous Mycoses

• Cutaneous mycoses are caused by fungi that infect only the superficial keratinized
tissue (skin, hair, and nails).

• Most important of these are the dermatophytes, a group of 40 related fungi that
belong to 3 genera:

1. Microsporum
2. Trichophyton

3. Epidermophyton

Properties of Dermatophytes:-

1. Restricted to non-viable skin ∵ mostly they are unable to grow at 37 °C or in the
presence of serum

2. Most prevalent infections (Dermatophytoses) in world. These infection can be
persistent but they are not life-threatening

3. Dermatophytes are classified as geophilic, zoophilic, or anthropophilic depending on
whether their habitat is soil, animals, or humans.

4. source of infection is soil or an infected animal in the case of geophilic and zoophilic
dermatophytes

5. Anthropophilic species is transmitted by direct contact or through fomites eg
contaminated towel

6. Dermatophytes are acquired by contact with contaminated soil or with infected
animals or humans. Dermatophyte infections begin in the skin after trauma and
contact.

7. Anthropophilic species causes greatest number of human infections and cause mild
and chronic infections in humans, produce few conidia in culture, and may be
difficult to eradicate.

8. Geophilic and zoophilic dermatophytes are less adapted to human hosts produce
acute inflammatory infections that tend to resolve quickly.

9. Host susceptibility is enhanced by moisture, warmth, specific skin chemistry,
composition of sebum and perspiration, youth, heavy exposure, and genetic
predisposition.

10.Higher Incidence in hot, humid climates and under crowded living conditions.

11.Wearing shoes provides warmth and moisture, a setting for infections of the feet.

12.Conidia can remain viable for long periods.

13.Trichophytin is a crude Ag preparation that can be used to detect immediate- or
delayed-type hypersensitivity to dermatophytic Ags.

14.Patients who develop chronic, non-inflammatory dermatophyte infections have poor
cell-mediated immune responses to dermatophyte antigen.

15.These patients are atopic (genetic tendency to develop allergies) and have
immediate-type hypersensitivity and elevated IgE concentrations.

16.In normal host, immunity to dermatophytosis varies in duration and degree
depending on host, the site, and the species of fungus causing the infection.

Tinea pedis (Athlete’s Foot)

1. Chronic infection of toe webs

2. There is itching b/w toes and development of small vesicles that rupture and
discharge a thin fluid.

3. Skin of toe webs becomes smooth and peels, where upon cracks appear that are prone
to develop secondary bacterial infection.

T rubrum, T mentagrophytes, E floccosum

Treatment

1. Effective drugs are itraconazole and terbinafine

2. Numbers of topical preparations (which are applied in/on to particular part of the
body) may be used eg miconazole nitrate, tolnaftate, and clotrimazole.

3. If applied for at least 2–4 weeks, the cure rates are 70–100%. Treatment should be
continued for 1–2 weeks after clearing of the lesions.

4. For troublesome cases, a short course of oral griseofulvin can be administered.

Tinea corporis

1. Dermatophytosis of the glabrous skin (smooth and devoid of hair) gives rise to the
annular lesions of ringworm, with a clearing; scaly center surrounded by a red
advancing border that may be dry or vesicular.

2. Dermatophyte grows only within dead, keratinized tissue, but fungal metabolites,
enzymes, and antigens diffuse through the viable layers of the epidermis to cause
erythema, vesicle formation, and pruritus.

3. Lesions expand centrifugally and active hyphal growth is at the periphery.

Eg T rubrum, E floccosum

Tinea cruris (Jock Itch)

1. Groin area (Area of hip b/w stomach and thigh)

2. Dry, itchy lesions that start on the scrotum and spread to the groin.

T rubrum, T mentagrophytes, E floccosum

Tinea manus

1. Hands or fingers

2. Dry scaly lesions may involve one or both hands, single fingers, or two or more fingers.

T rubrum, T mentagrophytes, E floccosum

Tinea capitis

1. Scalp and hair

2. Infection begins with hyphal invasion of the skin of the scalp, with subsequent spread
down the keratinized wall of the hair follicle.

3. Infection of the hair takes place just above the hair root.

4. Hyphae grow downward on the non-living portion of the hair and at the same rate as
the hair grows upward.

5. The infection produces dull gray, circular patches of alopecia, scaling, and itching.

6. As the hair grows out of the follicle, the hyphae of Microsporum species produce a
chain of spores that form a sheath around the hair shaft (ectothrix).

7. These spores impart a greenish to silvery fluorescence when the hairs are examined
under Wood’s light (365 nm).

8. T tonsurans, the chief cause of “black dot” tinea capitis, produces spores within the hair
shaft (endothrix).

9. These hairs do not fluoresce; they are weakened and typically break easily at the
follicular opening.

10.Manifestation of tinea capitis is favus, an acute inflammatory infection of the hair
follicle caused by T schoenleinii, which leads to the formation of scutula (crusts)
around the follicle.

11.In favic hairs, the hyphae don’t form spores but can be found within the hair shaft.

Tinea barbae

 Bearded region
 Especially when a zoophilic dermatophyte is involved, a highly inflammatory reaction

that closely resembles pyogenic infection.
 T mentagrophytes

Trichophytid Reaction

 In the course of dermatophytosis, the individual may become hypersensitive to
constituents or products of the fungus and may develop allergic manifestations— called
dermatophytids (vesicles)—elsewhere on the body, most often on the hands.

Tinea unguium (Onychomycosis)

 Nail infection may follow prolonged tinea pedis.
 With hyphal invasion, the nails become yellow, brittle, thickened, and crumbly.
 One or more nails of the feet or hands may be involved.

T rubrum, T mentagrophytes, E floccosum

Subcutaneous Mycoses

• Fungi that cause subcutaneous mycoses normally reside in soil or on vegetation.
• They enter the skin or subcutaneous tissue by traumatic inoculation with contaminated

material.
• Lesions become granulomatous and expand slowly from the area of implantation.
• Extension via lymphatics draining the lesion is slow except in sporotrichosis.
• Mycoses are confined to subcutaneous tissues, but in rare cases they become systemic

and produce life-threatening disease.

Systemic Mycoses
 Blastomycosis

 Coccidioidomycosis
 Cryptococcosis

 Histoplasmosis

Histoplasmosis

• Histoplasma capsulatum

• dimorphic soil saprophyte

Antigen

• Histoplasmin is a crude mycelial broth culture filtrate antigen. After initial infection,
which is asymptomatic in over 95% of individuals, a positive delayed type skin test to
histoplasmin is acquired. Antibodies to both yeast and mycelial antigens can be
measured serologically.

Pathogenesis

• After inhalation, conidia develop into yeast cells and are engulfed by alveolar
macrophages, where they are able to replicate.

• Within macrophages, the yeasts may disseminate to reticuloendothelial tissues such as
liver, spleen, bone marrow, and lymph nodes. The initial inflammatory reaction
becomes granulomatous.

• In over 95% of cases, the resulting cell-mediated immune response leads to the
secretion of cytokines that activate macrophages to inhibit the intracellular growth of
the yeasts.

• Some individuals, such as immunocompetent persons who inhale a heavy inoculum,
develop acute pulmonary histoplasmosis, which is a self-limited flu-like syndrome with
fever, chills, myalgias, headaches, and nonproductive cough.

• On radiographic examination, most patients will have hilar lymphadenopathy and
pulmonary infiltrates or nodules.

• These symptoms resolve spontaneously without therapy, and the granulomatous
nodules in the lungs or other sites heal with calcification.

• Chronic pulmonary histoplasmosis occurs most often in men and is usually a
reactivation process, the breaking down of a dormant lesion that may have been
acquired years before.

• This reactivation is usually precipitated by pulmonary damage such as emphysema.

• Severe disseminated histoplasmosis develops in a small minority of infected individuals
particularly infants, the elderly, and the immunosuppressed, including AIDS patients.

• The reticuloendothelial system is involved, with lymphadenopathy, enlarged spleen
and liver, high fever, anemia, and a high mortality rate without antifungal therapy.

• Mucocutaneous ulcers of the nose, mouth, tongue, and intestine can occur. In such
individuals, histologic study reveals focal areas of necrosis within granulomas in many
organs.

• The yeasts may be present in macrophages in the blood, liver, spleen, and bone
marrow.

Treatment
• Acute pulmonary histoplasmosis is managed with supportive therapy and rest.
• Itraconazole is the treatment for mild to moderate infection.
• In disseminated disease, systemic treatment with amphotericin B is curative, though

patients may need prolonged treatment and monitoring for relapses.
• Patients with AIDS typically relapse despite therapy that would be curative in other

patients. Therefore, AIDS patients require maintenance therapy with itraconazole.
Opportunistic Mycoses
• Patients with compromised host defenses are susceptible to ubiquitous fungi to which

healthy people are exposed but usually resistant.

• In patients with AIDS, the susceptibility and incidence of opportunistic mycoses are
inversely correlated with the CD4 lymphocyte count.

Candida

C albicans, C tropicalis, C parapsilosis, C glabrata, C guilliermondii, C dubliniensis, C krusei
and C lusitaniae

• Superficial (cutaneous or mucosal) candidiasis is established by an increase in the local
census of Candida and damage to the skin or epithelium that permits local invasion by
the yeasts and pseudohyphae.

• The local histology of cutaneous or mucocutaneous lesions is characterized by
inflammatory reactions varying from pyogenic abscesses to chronic granulomas. The
lesions contain abundant budding yeast cells and pseudohyphae.

Thrush

• Thrush can occur on tongue, lips, gums, or palate.

• It is patchy to confluent, whitish pseudomembranous lesion composed of epithelial cells,
yeasts, and pseudohyphae.

• Thrush develops in most patients with AIDS. Other risk factors include treatment with
corticosteroids or antibiotics, high levels of glucose, and cellular immunodeficiency.

Vulvovaginitis

• invasion of the vaginal mucosa

• Characterized by irritation, pruritus, and vaginal discharge.

• This condition is often preceded by factors such as diabetes, pregnancy, or antibacterial
drugs that alter the microbial flora, local acidity, or secretions.

Cutaneous candidiasis

• Invasion of skin

• This occurs when skin is weakened by trauma, burns, or maceration.

• Intertriginous infection occurs in moist, warm parts of the body such as the axillae,
groin, and intergluteal or inframammary folds

• It is most common in obese and diabetic individuals.

• Infected areas become red and moist and may develop vesicles. Interdigital
involvement between the fingers follows repeated prolonged immersion in water.

• Systemic candidiasis occurs when Candida enters the bloodstream and the phagocytic
host defenses are inadequate to contain the growth and dissemination of the yeasts.

• From the circulation, Candida can infect the kidneys, attach to prosthetic heart valves, or
produce candidal infections almost anywhere (eg, arthritis, meningitis,
endophthalmitis).

• Systemic candidiasis is mostly associated with chronic administration of corticosteroids
or other immunosuppressive agents; with hematologic diseases like leukemia,
lymphoma, and aplastic anemia; or with chronic granulomatous disease.

• Candidal endocarditis is associated with deposition and growth of yeasts and
pseudohyphae on prosthetic heart valves.

• Kidney infections are systemic manifestation, whereas urinary tract infections are
associated with Foley catheters, diabetes, pregnancy, and antibacterial antibiotics.

Onychomycosis

• Candidal invasion of the nails and around the nail plate

• Erythematous swelling of the nail fold resembling a pyogenic paronychia, which may
eventually destroy the nail

Aspergillosis

Aspergillosis is caused by a number of Aspergillus species

Allergic Asthma

In some atopic individuals, development of IgE antibodies to the surface antigens of
aspergillus conidia elicits an immediate asthmatic reaction upon subsequent exposure.

Allergic bronchopulmonary aspergillosis

 In some individuals, the conidia germinate and hyphae colonize the bronchial tree
without invading the lung parenchyma.

 Clinically defined as asthma, recurrent chest infiltrates,
 Eosinophilia, and both type I (immediate) and type III (Arthus) skin test hypersensitivity

to Aspergillus antigen.
 Many patients produce sputum with Aspergillus and serum precipitins. They have

difficulty breathing and may develop permanent lung scarring.

Aspergilloma and Extrapulmonary Colonization

 Aspergilloma occurs when inhaled conidia enter an existing cavity, germinate, and
produce abundant hyphae in the abnormal pulmonary space.

 Patients with previous cavitary disease (eg, tuberculosis, sarcoidosis, emphysema) are at
risk.

 Some patients are asymptomatic; others develop cough, dyspnea, weight loss, fatigue,
and hemoptysis.

 Cases of aspergilloma rarely become invasive.
 Localized, non-invasive infections (colonization) by Aspergillus species may involve the

nasal sinuses, the ear canal, the cornea, or the nails.

Invasive Aspergillosis

 Following inhalation and germination of the conidia, invasive disease develops as an
acute pneumonic process with or without dissemination.

 Hyphae invade the lumens and walls of blood vessels, causing thrombosis, infarction,
and necrosis.

 From the lungs, the disease may spread to the gastrointestinal tract, kidney, liver, brain,
or other organs, producing abscesses and necrotic lesions.

 Symptoms include fever, cough, dyspnea, and hemoptysis.