Internal Medicine_Infectious Diseases_16 Flashcards

Fungal infections

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1
Q

What is Sporothrix schenckii and what disease does it cause?

A

Sporothrix schenckii is a dimorphic fungus that causes sporotrichosis, also known as rose gardener’s disease.

Mold in the cold (25 - 30 C)
Yeast in the heat (35 - 37 C)

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2
Q

Where is Sporothrix schenckii commonly found?

A

Found in soil, plant debris, tree bark, and bushes.
Associated with rose thorns and other contaminated plant materials.

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3
Q

How does Sporothrix schenckii enter the body?

A

Through physical trauma, such as a puncture wound from a thorn or contaminated material. Infection often occurs after handling plants contaminated with Sporothrix schenckii, such as being pricked by rose thorns.

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4
Q

What are the characteristic microscopic features of Sporothrix schenckii in its yeast form?

A

Cigar-shaped cells are seen microscopically in its yeast form.

Can be visualized with methanemine silver.

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5
Q

What is the pattern of lesion spread in lymphocutaneous sporotrichosis?

A

Lesions spread in an ascending pattern along the lymphatic channels.
Start as local pustules or ulcers, progressing to subcutaneous nodules.

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6
Q

What is the gold standard for diagnosing sporotrichosis?

A

Culture of the organism.

Biopsy showing granulomas with histiocytes, multinucleated giant cells, and yeast cells is also diagnostic.

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7
Q

What is the preferred treatment for sporotrichosis?

A

Itraconazole is the first-line treatment for cutaneous and lymphocutaneous sporotrichosis.

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8
Q

What historical treatment is sometimes used for sporotrichosis?

A

Saturated solution of potassium iodide (SSKI), though modern antifungal medications are preferred.

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9
Q

Where is Histoplasma capsulatum geographically endemic?

A

The Midwestern and Central United States, particularly along the Mississippi and Ohio River Valleys.

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10
Q

How is Histoplasma capsulatum transmitted?

A

Inhalation of airborne fungal spores from soil or mold.
Often associated with bird droppings and bat guano.

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11
Q

What type of individuals are at increased risk of histoplasmosis?

A

Most are asymptomatic.

Immunocompromised patients, such as those with HIV/AIDS or undergoing chemotherapy, are the people most at risk, as are individuals exposed to bird or bat droppings.

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12
Q

What are the key clinical features of histoplasmosis?

A

Constitutional symptoms:
Fever, Fatigue, Malaise, weight loss

Pulmonary symptoms:
Cough, lung cavitations (resembles tuberculosis), patchy/nodular infiltrates, Hilar lymphadenopathy.

Disseminated disease:
Arthalgias, Hepatosplenomegaly, skin nodules, ulcers and other skin manifestations like erythema nodosum.

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13
Q

What dermatologic finding is associated with histoplasmosis?

A

Erythema nodosum, characterized by painful red nodules on the shins.

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14
Q

What is the role of lung calcifications in histoplasmosis?

A

Chronic histoplasmosis can lead to calcified mediastinal and hilar lymph nodes, as part of the healing process.

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15
Q

What would pertinent lab findings show in a patient with histoplasmosis?

A

Pancytopenia

Elevated AST/ALT

Elevated LDH

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16
Q

What is the histological hallmark of Histoplasma capsulatum on microscopy?

A

Small intracellular oval yeast bodies within macrophages.
These yeast cells are smaller than red blood cells.

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17
Q

What diagnostic tests are available for histoplasmosis?

A

Antigen testing of serum or urine (SAg, UAg).

Tissue biopsy or respiratory specimen staining.

Culture is the gold standard.

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18
Q

What is the treatment for mild histoplasmosis?

A

Itraconazole (an azole antifungal).

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19
Q

What is the treatment for severe or disseminated histoplasmosis?

A

Amphotericin B is the drug of choice for severe cases, followed by itraconazole as step-down therapy.

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20
Q

Where is Blastomyces dermatitidis geographically endemic?

A

Eastern and Central United States
Near the Ohio and Mississippi River Valleys
The Great Lakes region

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21
Q

What is Blastomyces dermatitidis and what disease does it cause?

A

Blastomyces dermatitidis is a dimorphic fungus that causes blastomycosis, a systemic fungal infection.

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22
Q

Which populations are at higher risk for disseminated blastomycosis?

A

Immunocompromised individuals, such as those with HIV/AIDS or undergoing chemotherapy.

Can disseminate even if immunocompetent.

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23
Q

How is Blastomyces dermatitidis transmitted?

A

Through inhalation of mold spores.
The spores convert to yeast form upon entering the lungs.

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24
Q

What are the common pulmonary manifestations of blastomycosis?

A

Known to cause acute and chronic pneumonia

Patchy alveolar infiltrates or “haziness” on chest X-rays (CXR).
May include mass-like lesions or cavitations.
Granulomatous infection, with the lungs being the most commonly affected organ.

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25
Q

What systemic organs are affected in disseminated blastomycosis?

A

Lungs (most common), skin, and bones.
Skin lesions: Papules, pustules, ulcers, or verrucous growths.
Bone involvement: Painful lytic lesions, osteomyelitis.

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26
Q

What is the characteristic morphology of Blastomyces dermatitidis in its yeast form?

A

Yeast form exhibits broad-based budding with a double refractile cell wall.
Similar in size to a red blood cell (RBC).

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27
Q

What diagnostic methods are used for blastomycosis?

A

Urine antigen test.

Microscopy, culture, or histopathology (gold standard).

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28
Q

What is the treatment for mild to moderate blastomycosis?

A

Itraconazole or fluconazole.

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29
Q

What is the treatment for severe or disseminated blastomycosis?

A

Amphotericin B is the drug of choice.

Followed by Itraconazole.

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30
Q

What is Coccidioides immitis, and what disease does it cause?

A

Coccidioides immitis is a dimorphic fungus that causes coccidioidomycosis, also known as San Joaquin Valley fever.

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31
Q

Where is Coccidioides immitis geographically endemic?

A

Southwestern United States (e.g., California, Arizona)
Northern Mexico
Found in desert soils.

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32
Q

How is Coccidioides immitis transmitted?

A

Through inhalation of airborne arthroconidia (mold spores).

Spores become airborne when soil is disturbed (e.g., farming, construction, earthquakes, or dust storms).

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33
Q

What is the characteristic morphology of Coccidioides immitis in tissue samples?

A

Appears as large yeast-like spherules containing endospores.
These spherules are larger than red blood cells (RBCs).

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34
Q

Which patients are at risk for disseminated coccidioidomycosis?

A

Immunocompromised patients, such as those with HIV/AIDS or undergoing immunosuppressive therapy.

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35
Q

What are the common clinical features of coccidioidomycosis?

A

Acute pneumonia: Cough, fever, chest pain, and arthralgia.

Erythema nodosum: Painful red nodules on the lower extremities.

In some cases, hilar lymphadenopathy and lung nodules or cavities.

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36
Q

What are the manifestations of disseminated coccidioidomycosis?

A

Systemic symptoms: fever, night sweats, weight loss.

Skin lesions: Papules, pustules, ulcers, verrucous growths.

Osteolytic bone lesions.

CNS involvement, such as meningitis.

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37
Q

What imaging findings are associated with primary coccidioidomycosis?

A

Unilateral infiltrates.
Hilar lymphadenopathy.
Nodules or cavities (though imaging may be normal in some cases).

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38
Q

How does Coccidioides immitis exhibit dimorphism?

A

Grows as mold in cooler environments (25–30°C).
Converts to yeast at human body temperature (35–37°C).

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39
Q

How is coccidioidomycosis diagnosed?

A

Serology using IgM

Cultures

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40
Q

What are the treatments for coccidioidomycosis?

A

Mild to moderate disease: Itraconazole or fluconazole.

Severe or disseminated disease: Amphotericin B, followed by Itraconazole.

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41
Q

What is Paracoccidioides brasiliensis, and what disease does it cause?

A

Paracoccidioides brasiliensis is a dimorphic fungus that causes paracoccidioidomycosis, a systemic fungal infection.

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42
Q

Where is Paracoccidioides brasiliensis geographically endemic?

A

Central and South America, particularly in Brazil.

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43
Q

What is the characteristic morphology of Paracoccidioides brasiliensis in its yeast form?

A

Multipolar budding radiating from a central cell, resembling a captain’s wheel.

The yeast is larger than red blood cells (RBCs).

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44
Q

How is Paracoccidioides brasiliensis transmitted?

A

Through inhalation of mold spores.

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45
Q

What are the common clinical features of paracoccidioidomycosis?

A

Coughing and lymphadenopathy affecting cervical, axillary, and inguinal lymph nodes.

Granulomas in the lungs.

Mucosal ulcers in the upper respiratory tract.

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46
Q

Which organs are commonly affected in disseminated paracoccidioidomycosis?

A

Lungs, oral mucosa, and lymph nodes.

In severe cases, other organs may also be involved.

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47
Q

What are the treatments for paracoccidioidomycosis?

A

Mild to moderate disease: Azoles (e.g., itraconazole).

Severe disease: Amphotericin B.

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48
Q

What is Malassezia furfur, and what conditions does it cause?

A

Malassezia furfur is a fungus that is part of the normal skin flora.

Thrives in hot and humid conditions.

It causes pityriasis versicolor and seborrheic dermatitis.

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49
Q

How does Paracoccidioides brasiliensis exhibit dimorphism?

A

Grows as mold in cooler environments (25–30°C).

Converts to yeast at human body temperature (35–37°C).

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50
Q

How does Malassezia furfur appear on a KOH prep?

A

It has a characteristic “spaghetti and meatballs” appearance due to its yeast and hyphae forms.

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51
Q

What are the typical clinical features of pityriasis versicolor?

A

Hypopigmented or hyperpigmented macules or patches, often with fine scaling.

Commonly affects the back and chest.

Patches can merge into larger areas.

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52
Q

What environmental conditions favor the pathogenic form of Malassezia furfur?

A

Hot and humid conditions.

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53
Q

What layer of the skin does Malassezia furfur primarily infect?

A

The stratum corneum, the most superficial layer of the epidermis.

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54
Q

What systemic complication is associated with Malassezia furfur in neonates?

A

Malassezia fungemia, particularly in neonates receiving total parenteral nutrition (TPN) through central venous catheters.

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55
Q

What is the pathogenesis of the skin lesions in pityriasis versicolor?

A

Lipid degradation by the fungus produces acid, which damages melanocytes, leading to pigmentation changes (inhibiting tyrosinase).

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56
Q

How is pityriasis versicolor treated?

A

Topical selenium sulfide (e.g., Selsun Blue).
Promotes the shedding of the stratum corneum where the fungus resides.

Oral ketoconazole.

Terbinafine.

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57
Q

What are the three genera of dermatophytes responsible for tinea infections?

A

Trichophyton

Epidermophyton

Microsporum

58
Q

Seborrheic dermatitis is caused by over secretion of the sebaceous glands due to a hypersensitivity reaction to _____________ .

A

Seborrheic dermatitis is caused by over secretion of the sebaceous glands due to a hypersensitivity reaction to Malassezia spp.

59
Q

What can be used to determine the extent of the disease caused by Malassezia spp.?

A

Use of a Woods Lamp.

60
Q

What are the common species categories of dermatophytes based on their habitat preference?

A

Anthropophilic (human-loving)

Zoophilic (animal-loving)

Geophilic (soil-loving)

61
Q

Tinea capitis is and infection of the … ?

A

Scalp

62
Q

Tinea corporis is and infection of the … ?

A

Body

63
Q

Tinea cruris is and infection of the … ?

A

Groin (jock itch)

64
Q

Tinea pedis is and infection of the … ?

A

Feet (athlete’s foot)

65
Q

Tinea unguium is and infection of the … ?

A

Nails (onychomycosis)

66
Q

What are the diagnostic tools for dermatophyte infections?

A

Usually clinically diagnosed

Recommended for support of diagnosis:
KOH prep to visualize hyphae.
Wood’s lamp for fluorescenceof Microsporum, Trichophyton, or Epidermophyton.

67
Q

What are the common risk factors for tinea corporis (ringworm)?

A

Skin-to-skin contact
Contact with infected animals
Humid environments

68
Q

What is the appearance of tinea infections on the skin?

A

Red, scaly, and annular (ring-like) plaques with central clearing and pruritus.

69
Q

how is tinea corporis (ringworm) treated?

A

Topical azoles

oral terbinafine

70
Q

What are common clinical features of tinea capitis?

A

Scaly patches with alopecia (hair loss).

Often fluoresces under Wood’s lamp in cases caused by Microsporum.

Black dots with hair shaft.

71
Q

How does tinea capitis spread?

A

Combs, pillows, hats.

Prevent by not sharing these items with others.

72
Q

What are the treatments for tinea capitis infections?

A

oral terbinafine or griseofulvin.

73
Q

What is onychomycosis, and how is it treated?

A

A fungal infection of the nails causing thickened, discolored nails.

Subungual debris can lead to the separation of nail plate from bed.

Treated with oral terbinafine, griseofulvin, or azoles.

74
Q

What are the risk factors for tinea unguium (onychomycosis)?

A

Nail trauma
Prolonged exposure to moisture (e.g., wet environments)
Diabetes or peripheral vascular disease
Poor nail hygiene

75
Q

What are the risk factors for tinea pedis (athlete’s foot)?

A

Wearing tight, non-breathable shoes
Walking barefoot in communal showers or locker rooms
Excessive sweating

76
Q

What are the subtypes of tinea pedis (athlete’s foot)?

A

Interdigital

Moccasin

Vesiculobullous

All can cause redness and scaling between toes and on the foot.

77
Q

How is tinea pedis (athlete’s foot) treated?

A

topical azoles or oral terbinafine.

78
Q

What are the risk factors for tinea cruris (jock itch)?

A

Obesity
Wearing tight or wet clothing
Excessive sweating, especially in hot climates
Shared gym equipment

79
Q

How is tinea cruris treated?

A

topical azoles or oral terbinafine.

80
Q

Which dermatophyte infection commonly affects wrestlers?

A

Tinea corporis (ringworm).

81
Q

What are the risk factors for tinea capitis (scalp infection)?

A

Sharing combs or hats
Contact with infected individuals or animals
Poor scalp hygiene

82
Q

Are dermatophytes part of the normal skin flora?

A

No

83
Q

What microorganism is most commonly involved in the pathogenesis of tinea capitis?

A

Trichophyton tonsurans

84
Q

Which subtype of tinea pedis (athlete’s foot) is most common?

A

Interdigital

85
Q

What type of fungus is Candida albicans?

A

Candida albicans is a catalase-positive, urease-positive, dimorphic fungus that exhibits pseudohyphae and budding yeast.

86
Q

How is Candida albicans tested in a laboratory?

A

Candida albicans can produce germ tubes when incubated in serum at 37°C.

87
Q

What populations are particularly vulnerable to Candida infections?

A

Neutropenic individuals
Diabetics
People with HIV/AIDS
Intravenous drug users

88
Q

What are the common clinical manifestations of Candida infections?

A

Oral candidiasis (thrush)
Candidal esophagitis (AIDS-defining illness, often with CD4 <200)
Candidal vulvovaginitis
Diaper rash
Candidal endocarditis

89
Q

What condition is associated with candidal esophagitis?

A

Candidal esophagitis is an AIDS-defining illness, often observed when CD4 counts drop below 200.

90
Q

Which populations are at risk for candidal endocarditis?

A

Intravenous drug users are at higher risk for candidal endocarditis, which can affect the heart valves.

Candida endocarditis predominantly affects the tricuspid valve in IV drug users and individuals with prosthetic heart valves and indwelling
catheters.

91
Q

What condition is associated with obese patients or those with diabetes and candidal infection?

A

Candidal intertrigo

Burning red plaques in the skin folds with surrounding satellite macules.

Affects the gluteal creases, inframammary folds, inguinal creases, and abdominal pannus.

Diagnosed clinically but supported with KOH prep or fungal culture
Treated with topical azoles or nystatin.

92
Q

What makes Candida albicans dimorphic?

A

Candida albicans is a dimorphic fungus, but differs from other dimorphic fungi in that it exists in its yeast-form at 23-25 °C and a multicellular hyphal form at 37°C.

93
Q

Vulvovaginal candidiasis often presents with

A

Burning, irritation, pruritus and a thick white vaginal discharge.

Usually odorless.

94
Q

what is the underlying cause of Vulvovaginal candidiasis?

A

Overgrowth of normal vaginal flora.

Other species possible like glabrata.

95
Q

what increases the risk of Vulvovaginal candidiasis?

A

Diabetes, antibiotics, IUDs, hormonal pills, or immunosuppression.

96
Q

In vulvovaginal candidiasis, the vaginal pH typically remains within the normal range of

A

3.8 - 4.5

97
Q

What is the treatment for Vulvovaginal candidiasis?

A

Topical azoles (clotrimazole, miconazole), or nystatin

then

PO Fluconazole

Amphotericin B can be used in cases of severe or fluconazole-resistant
Candida infections

98
Q

Vulvovaginal candidiasis caused by glabrata is treated with … ?

A

intravaginal boric acid.

99
Q

What is characteristic of oral thrush?

A

Candida albicans causes oral thrush, which is characterized by white, scrapable lesions in the mouth; oral thrush is frequently seen in individuals using inhaled steroids and in immunocompromised patients

100
Q

What is used for disseminated candidiasis?

A

Echinocandins, such as caspofungin and micafungin, are options for treating severe or refractory cases of candidiasis, including esophageal and systemic infections.

101
Q

A 10-year-old boy is brought to the clinic by his parents due to a long history of recurrent oral thrush, nail infections, and persistent skin rashes. On examination, there are white plaques on the tongue and buccal mucosa that scrape off easily, erythematous skin lesions, and thickened, discolored fingernails. Laboratory workup reveals normal neutrophil count, normal immunoglobulin levels, but low T-cell-mediated responses on in vitro stimulation tests. Genetic testing confirms a mutation in the autoimmune regulator (AIRE) gene.

Which of the following is the most likely underlying mechanism of this patient’s condition?

A. Impaired B-cell development
B. Neutrophil dysfunction
C. Defective T-cell immunity
D. Complement deficiency
E. Increased pro-inflammatory cytokine production

A

C. Defective T-cell immunity

Explanation:

The patient presents with chronic mucocutaneous candidiasis (CMC), characterized by recurrent Candida infections involving the skin, nails, and mucosal surfaces. CMC is most commonly associated with T-cell dysfunction, specifically an impaired Th17 response, which is crucial for defense against fungal infections.

The mutation in the AIRE gene points to an association with autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED) syndrome, a rare autosomal recessive condition that includes endocrine abnormalities and chronic Candida infections. In this case, defective T-cell-mediated immunity allows Candida overgrowth despite normal neutrophil and antibody responses. The other associated issues may be type 1 diabetes or thyroiditis.

102
Q

A 45-year-old male with a history of acute myeloid leukemia undergoing chemotherapy presents with fever, pleuritic chest pain, and hemoptysis. His absolute neutrophil count is 100/μL. Chest CT reveals a nodular infiltrate with surrounding ground-glass opacity (halo sign).

What is the most likely diagnosis, and what is the first-line antifungal treatment?
A. Candidiasis; Amphotericin B
B. Mucormycosis; Posaconazole
C. Invasive Aspergillosis; Voriconazole
D. Cryptococcosis; Fluconazole
E. Histoplasmosis; Itraconazole

A

C. Invasive Aspergillosis; Voriconazole

Explanation: Immunocompromised state and imaging findings are classic for invasive aspergillosis. Voriconazole is the treatment of choice for this condition.

103
Q

What are the characteristics of Aspergillus spp.?

A

Catalase-positive fungi. Catalase allows them to neutralize reactive oxygen species, enhancing survival.

Aspergillus spp. is considered to be opportunistic.

Aspergillus spp. exhibit characteristic septate hyphae with acute branching angles, often around 45 degrees.

104
Q

How is Aspergillus transmitted?

A

Aspergillus spores are inhaled, often from fruiting bodies in decaying organic matter.

105
Q

Which Aspergillus species produces aflatoxins, and what condition does it cause?

A

Aspergillus flavus produces aflatoxins, which are linked to hepatocellular carcinoma.

106
Q

What is ABPA, and who is at risk?

A

Allergic Bronchopulmonary Aspergillosis (ABPA)

Hypersensitivity reaction to Aspergillus spp., is characterized by migratory pulmonary infiltrates, fever, wheezing, and elevated serum IgE levels, and it most commonly affects individuals with cystic fibrosis or asthma.

107
Q

Bronchiectasis is associated with ________, which is a hypersensitivity reaction to Aspergillus

A

Allergic bronchopulmonary aspergillosis (ABPA)

Note: Bronchiectasis is the permanent dilation of airways.

108
Q

Key Features of Allergic Bronchopulmonary Aspergillosis (ABPA) include …

A

Fever
Migratory pulmonary infiltrates
Recurring episodes or exacerbations
Wheezing
Elevated IgE
Coughing up brown mucous plugs

109
Q

Lung cavities secondary to Aspergillus from conditions like tuberculosis, leading to symptoms such as cough and hemoptysis is likely a(n) …. ?

A

Aspergilloma (Fungus Ball)

110
Q

Where do aspergillomas typically form?

A

In pre-existing lung cavities caused by conditions like TB, sarcoidosis, or emphysema.

111
Q

Symptoms of aspergillomas include … ?

A

Cough
Hemoptysis
Visible as gravity-dependent mass on imaging (shifting with positional changes).

112
Q

In the context of Aspergillus, what does a previous TB infection predispose a patient to and how does this present?

A

History of lung disease or TB infection (cavitation) can lead to Chronic pulmonary aspergillosis which presents as an illness with a subacute onset. Symptoms include weight loss, productive cough, hemoptysis, dyspnea, fever and night sweats.

113
Q

Management of Allergic Bronchopulmonary Aspergillosis (ABPA) includes …

A

Serological testing of Aspergillus IgE or skin testing

Acute flares treated with corticosteroids to reduce inflammation and voriconazole or itraconazole to decrease fungal load.

114
Q

Aspergillus accounts for ____ % of fungal infective endocarditis

A

30

115
Q

What is the management of Chronic pulmonary aspergillosis?

A

Imaging of the upper lobes for a possible fungus ball

Serology for IgG

Treatment is surgical resection and Voriconazole.

116
Q

Who is at risk for invasive aspergillosis, and what are the clinical features?

A

Seen in immunocompromised patients (e.g., neutropenia, organ transplant).

117
Q

Symptoms of invasive aspergillosis include .. ?

A

Fever
Chest pain
Hemoptysis
Dissemination to CNS, kidneys, sinuses, and heart.

118
Q

What are the hallmark radiological features of invasive aspergillosis?

A

Nodular infiltrates with halo sign (ground-glass opacity)
Air crescent sign in later stages.

Gravity-dependent lesion that moves with changes in position.

119
Q

How is Invasive Aspergillus infection diagnosed?

A

Sputum stain or culture

Biomarkers (beta-D-glucan or galactomannan)

Tissue biopsy if uncertain

120
Q

How is Invasive Aspergillus infection treated?

A

Voriconazole (with caspofungin if severe)

Amphotericin B is used for severe or refractory infections.

121
Q

What is Cryptococcus neoformans?

A

An opportunistic fungus that is urease-positive and heavily encapsulated.

122
Q

What is the role of the polysaccharide capsule in Cryptococcus neoformans?

A

It inhibits phagocytosis and is a diagnostic feature of the fungus.

123
Q

What environmental exposure is commonly associated with Cryptococcus neoformans?

A

Pigeon droppings.

124
Q

Which population is most at risk for Cryptococcus neoformans infections?

A

Immunocompromised individuals, particularly those with HIV/AIDS.

125
Q

What are common pulmonary symptoms of Cryptococcus infections?

A

Cough, chest pain, or asymptomatic presentation.

Commonly causes pneumonia in the HIV patient population.

126
Q

What clinical manifestation is most commonly associated with Cryptococcus?

A

Meningoencephalitis

Characterized by fever, N/V, headache, neck stiffness, and sensitivity to light.

127
Q

What staining technique is used to visualize Cryptococcus neoformans?

A

India ink stain, revealing encapsulated cells with clear halos against a dark background.

This is largely replaced by the latex agglutination test or ELISA with CSF

128
Q

What is the latex agglutination test used for in Cryptococcus infections?

A

Detecting the polysaccharide capsule antigen in serum and CSF.

129
Q

What imaging finding is associated with Cryptococcal meningitis?

A

“Soap bubble” lesions in the brain’s gray matter on MRI.

130
Q

What is the initial treatment for Cryptococcal meningitis?

A

A combination of amphotericin B and flucytosine for 2 weeks.

Followed by maintenance therapy with fluconazole for 1 year.

131
Q

What is used to diagnose pneumonia secondary to Cryptococcus?

A

Bronchoalveolar lavage samples can be prepared with mucicarmine (red) or methenamine (silver) stain for diagnosis of pulmonary
cryptococcosis.

132
Q

Opportunistic fungi causing mucormycosis

A

Mucor and Rhizopus spp. are opportunistic fungi that primarily affect immunocompromised individuals (steroid users), including those with leukemia, neutropenia, and diabetes.

133
Q

Primary risk factor for mucormycosis

A

Diabetic ketoacidosis (DKA) is strongly associated with mucormycosis due to elevated glucose and ketone levels that create an ideal environment for fungal growth.

134
Q

Primary mode of entry for Mucor and Rhizopus spp.

A

Entry typically occurs via spore inhalation, with the fungi colonizing blood vessel walls.

135
Q

Histologic appearance of Mucor and Rhizopus

A

Non-septate hyphae with wide-angle (90°) branching, often seen in tissue samples.

136
Q

Common sites of mucormycosis invasion

A

The fungi can invade the cribriform plate to access the brain, leading to rhinocerebral mucormycosis and tissue necrosis.

137
Q

Clinical hallmark of rhinocerebral mucormycosis

A

Black eschar visible in the nasal cavity or on the palate/turbinates, indicative of necrosis.

138
Q

Imaging finding in rhinocerebral mucormycosis

A

Tissue necrosis and invasion of adjacent structures, often seen in advanced cases. Proliferation within blood vessel walls leads to thrombosis, ischemia, and tissue necrosis.

139
Q

How is mucormycosis diagnosed?

A

tissue biopsy

140
Q

Common environmental source of Rhizopus species

A

Rhizopus spp. are commonly known as bread molds and are found in decaying organic material.

141
Q

Primary treatment for mucormycosis

A

Combination of amphotericin B (antifungal therapy) and surgical debridement to remove necrotic tissues.