1
Q
Enumerate the tissues dermatophytes are confined to.
A
Hair, skin, nails (keratinized tissues)
2
Q
Identify the type of infection caused by dermatophytes.
A
Superficial or cutaneous infections
3
Q
Identify the disease caused by dermatophytes.
A
Ringworm
(e.g., tinea capitis, tinea pedis)
4
Q
Identify where inflammation is greatest in dermatophyte infections.
A
the advancing edge of the lesion
5
Q
Identify the morphological form of all dermatophytes.
A
Molds
6
Q
Enumerate the three genera of dermatophytes.
A
Epidermophyton, Microsporum, Trichophyton
7
Q
Enumerate the number of species per dermatophyte genus:
A
Epidermophyton – 2 species;
Microsporum – 16 species;
Trichophyton – 24 species
8
Q
Enumerate common indirect transmission routes for dermatophytes.
A
Combs, hats, showers, desquamated skin, and hair
9
Q
Enumerate the diagnostic methods used for dermatophyte detection.
A
Direct examination of scrapings and culture on selective media
10
Q
Identify the type of infection caused by Chromoblastomycosis.
A
Slow, progressive, granulomatous infection
11
Q
Identify the microscopic structure found in the lesions of Chromoblastomycosis.
A
Dark brown sclerotic bodies
12
Q
Describe the appearance of the skin lesions in Chromoblastomycosis.
A
Warty or tumor-like lesions with a cauliflower appearance
13
Q
Enumerate the genera of dematiaceous (black) molds that cause Chromoblastomycosis.
A
Cladosporium and Phialophora
14
Q
Identify the characteristic feature of Mycetoma lesions.
A
Swollen lesions with granules containing organisms draining from sinuses
15
Q
Enumerate the sequence of lesion development in Mycetoma.
A
Nodule formation → collection of pus → formation of draining sinuses
16
Q
Enumerate the causative agents of Mycetoma.
A
Fungi (e.g., Pseudoallescheria) and actinomycetes (prokaryotes)
17
Q
Identify the genus responsible for candidiasis.
A
Candida
18
Q
Identify the general morphology of Candida.
A
Budding yeast, Gram-positive
19
Q
Enumerate the bases for identification of Candida species.
A
Biochemical tests and morphology on corn meal agar
20
Q
Identify the most important pathogenic species of Candida.
A
Candida albicans
21
Q
Enumerate the morphological forms of C. albicans.
A
Budding yeast, pseudohyphae, true hyphae
22
Q
Identify the special structure formed by C. albicans in serum.
A
Germ tubes
23
Q
Identify the usual origin of most Candida infections.
A
Endogenous (from normal flora)
24
Q
Enumerate the normal flora sites where Candida is found.
A
Oral cavity, gastrointestinal tract, vagina
25
Identify the essential pathogenic factor for mucosal infection.
Mucosal adherence
26
Enumerate factors that predispose to symptomatic Candida infection.
Alterations in micro-environment and/or microbial flora
27
Enumerate enzymes that may contribute to local invasion by C. albicans.
Germ tube formation, proteinases, phospholipases
28
Enumerate the common cutaneous infections caused by Candida.
Nails, diaper rash
29
Enumerate the mucosal infections caused by Candida.
Thrush (tongue, oral mucosa), esophagitis, vulvovaginitis
30
Identify the microscopic findings in vulvovaginitis due to Candida.
Discharge containing epithelial cells, pseudohyphae, and hyphae
31
Enumerate predisposing factors for oral thrush.
Inhaled steroids, cancer, HIV infection
32
Identify the infection where Candida is a major cause of nosocomial bloodstream infections.
Candidemia / disseminated candidiasis
33
Enumerate the risk factors for candidemia.
Antibiotics, intravenous catheters
34
Explain briefly the mechanism by which antibiotics increase candidemia risk.
Eliminate normal GI flora, allowing Candida overgrowth and mucosal entry
35
Explain briefly the mechanism by which IV catheters increase risk.
Provide direct skin entry for Candida
36
Enumerate organs commonly involved in disseminated candidiasis.
Kidney, brain, myocardium, eye
37
Identify the characteristic lesion of ocular candidiasis.
White cotton ball-like lesions on the retina (may cause blindness)
38
Identify the patients in whom urinary tract candidiasis is usually seen.
Patients with urinary catheters
39
Identify the organs involved in hepatosplenic candidiasis.
Liver and spleen
40
Identify the patient group prone to hepatosplenic candidiasis.
Severely immunocompromised or neutropenic patients
41
Identify the microscopic feature of hepatosplenic candidiasis.
Multifocal abscesses
42
Enumerate the diagnostic methods for Candida infections.
Direct microscopic examination and culture
43
Identify the key feature needed in direct exam to confirm infection.
Demonstration of tissue invasion (to distinguish from colonization)
44
Identify the type of media Candida grows well on.
Standard media
45
Identify how candidemia is detected.
Commercial blood culture systems
46
Identify the morphology of Cryptococcus neoformans.
Encapsulated yeast
47
Enumerate the laboratory identification features of Cryptococcus.
Presence of capsule,
urease positive,
growth at 37°C,
melanin synthesis, sugar assimilation
48
Enumerate the major virulence factors of Cryptococcus.
Polysaccharide capsule and melanin synthesis
49
Enumerate the functions of the polysaccharide capsule. (CRYPTOCOCCUS NEOFORMANS)
Antiphagocytic and immunosuppressive
50
Identify the etiologic agent of Cryptococcosis.
Cryptococcus neoformans
51
Identify the environmental source of Cryptococcus neoformans.
Pigeon feces
52
Identify the route of acquisition of Cryptococcosis
Inhalation
53
Identify the form of infection that is fatal in Cryptococcosis
Meningitis form
54
Identify the nature of most infections upon acquisition in cryptococcosis
Asymptomatic
55
Identify the possible presentation of localized infection in cryptococcosis
Isolated pulmonary nodule (may resemble carcinoma)
56
Identify the route of dissemination for cryptococcal meningitis.
From lung to CNS
57
Identify the patient group most at risk in Cryptococcal Meningitis
HIV patients with low CD4 counts
58
Identify whether CSF WBC count is elevated in cryptococcal meningitis.
May not be elevated
59
Identify if a non-elevated WBC count in CSF is a good or poor prognostic sign in Cryptococcal Meningitis
Poor prognostic sign
60
Enumerate the diagnostic tests for cryptococcal meningitis.
Direct detection of capsular antigen (CSF latex agglutination or EIA), and culture
61
Identify which test has high sensitivity and specificity in cryptococcocal meningitis
CSF latex agglutination or EIA
62
Identify which older test was displaced for low sensitivity in cryptococcal meningitis
India ink preparation
63
Identify the gold standard for diagnosis.
Culture
64
Enumerate the drugs used in the treatment of cryptococcosis.
Amphotericin B and 5-fluorocytosine
65
Identify whether Cryptococcus can be eradicated in HIV patients.
Cannot be eradicated
66
Identify what kind of therapy is required in HIV patients with Cryptococcus
Suppressive therapy
67
Identify the form of Histoplasma capsulatum in the environment.
Filamentous mold type
68
Enumerate the microscopic features of the mold form of HISTOPLASMA CAPSULATUM
Thin septate hyphae,
microconidia, and
tuberculate macroconidia (8–14 µm)
69
Identify the form of H. capsulatum found in tissues.
Budding yeast (2–4 µm)
70
Identify what type of dimorphism H. capsulatum exhibits.
Thermally dependent and **reversible dimorphism**
71
Enumerate the temperatures at which H. capsulatum transitions between forms.
25°C (mold form) and 37°C (yeast form)
72
Identify where the yeast forms are commonly located in tissue in HISTOPLASMA CAPSULATUM
Within histiocytes (macrophages)
73
Identify the system of the body primarily infected by H. capsulatum.
Reticuloendothelial system (RES)
74
Identify the characteristic pulmonary lesion associated with H. capsulatum infection.
**Patchy bronchopneumonia** containing **yeast-laden phagocytic cells** within **alveolar spaces**
75
Identify the cell type where the yeast cells multiply in H. capsulatum
Giant cells (phagocytic cells)
76
Identify whether dissemination of H. capsulatum can occur.
Yes, yeast can disseminate to other tissues
77
Identify the natural habitat where H. capsulatum can be cultured
Soil in endemic areas
78
Enumerate the materials that promote abundant growth of H. capsulatum in soil.
Bird feces (starling roosts, chicken houses) and bat guano (caves)
79
Identify the **infective forms** of H. capsulatum.
Conidia or hyphal fragments
80
Enumerate the sequence of infection events for H. capsulatum.
Inhalation → ingestion by macrophages → conversion to yeast phase → proliferation in nonimmune macrophages → spread through RES
81
Identify when dissemination occurs and its usual manifestation in H. capsulatum.
Occurs early; usually asymptomatic
82
Identify the host immune response responsible for controlling infection in HISTOPLASMA CAPSULATUM
Cell-mediated immunity (CMI)
83
Enumerate the effects of CMI response In H. Capsulatum
Macrophage activation and increased fungicidal activity
84
Identify whether infection is eradicated after containment in H. Capsulatum
Contained but not necessarily eradicated
85
Identify the most common form of symptomatic histoplasmosis.
Acute pulmonary histoplasmosis
86
Enumerate the symptoms of acute pulmonary histoplasmosis.
Fever, chills, headache, myalgia, anorexia, nonproductive cough, pleuritic chest pain
87
Enumerate additional findings in acute pulmonary histoplasmosis.
Enlarged lymph nodes and patchy infiltrates
88
Identify the usual duration of recovery in acute pulmonary histoplasmosis.
Improvement within several weeks
89
Enumerate the percentage of symptomatic cases that develop inflammatory syndromes.
5–10% of symptomatic cases
90
Enumerate the inflammatory syndromes that may develop in histoplasmosis
Arthritis, erythema nodosum, pericarditis
91
Identify the nature of chronic pulmonary histoplasmosis.
Slowly progressive pulmonary disease
92
Identify the condition commonly associated with chronic pulmonary histoplasmosis.
Preexisting lung disease
93
Enumerate the symptoms of chronic pulmonary histoplasmosis.
Cough, dyspnea, chest pain, fatigue, fever, night sweats, weight loss
94
Identify the outcome if chronic pulmonary histoplasmosis is untreated.
Usually progresses
95
Enumerate the drugs used for treatment and their purpose.
Amphotericin B or itraconazole
(reduce symptoms, improve radiographs, eliminate H. capsulatum from sputum)
96
Enumerate the tissues that may be examined for rapid presumptive diagnosis and Identify the significance of intracellular yeasts on peripheral smear in histoplasmosis
Bone marrow, liver, skin, gastrointestinal mucosa;
Indicates severe disseminated histoplasmosis
97
Identify the growth form of C. immitis in the environment.
(COCCIDIOIDES IMMITIS)
Hyphal form
98
99
Enumerate the microscopic features of the environmental form.
(COCCIDIOIDES IMMITIS)
Thick-walled arthroconidia alternating with thin-walled cells
100
Identify the tissue form of C. immitis
Spherule filled with endospores
101
What fungal species grows as hyphae in the environment and forms thick-walled arthroconidia alternating with thin-walled cells?
Coccidioides immitis
102
What structure is formed in infected tissue by Coccidioides immitis?
Spherule filled with endospores
103
Enumerate the dimorphic forms of Coccidioides immitis.
→
1. Hyphae with arthroconidia in environment
2. Spherule filled with endospores in infected tissue
104
What form of C. immitis is inhaled to initiate infection?
Arthroconidia
105
Into what structure do arthroconidia convert after inhalation?
Spherules
106
What is the size range of spherules formed by C. immitis?
20–150 µm
107
C. immitis spherules are partially resistant to what?
Killing by phagocytic cells
108
Describe the process of spherule development and endospore release in C. immitis.
1. Spherules undergo multiple nuclear divisions
2. Cytoplasm segments to produce hundreds of endospores (2–5 µm)
3. Spherule ruptures
4. Released endospores form new spherules
109
From where can C. immitis be cultured in endemic areas?
Soil
110
What is the expected annual number of C. immitis infections?
100,000 annually
111
What percentage of pulmonary infections caused by C. immitis are symptomatic?
40%
112
List the general symptoms of symptomatic pulmonary infection by C. immitis.
Fatigue, cough, chest pain, fever, dyspnea, myalgia, headache
113
What percentage of C. immitis infections lead to pulmonary nodules?
4%
114
What is the maximum size of solitary pulmonary nodules caused by C. immitis?
≤ 5 cm
115
What complication can pulmonary nodules from C. immitis occasionally form?
Cavities, infrequent rupture into pleural space
116
In approximately what percentage of infections does dissemination occur?
0.5%
117
Name the conditions that increase the risk of disseminated C. immitis infection.
HIV, organ transplants, steroids, Hodgkin’s disease
118
What is the most common site of dissemination? (C. immitis infection.)
Skin
119
List the bones and joints affected in disseminated C. immitis infection.
1. Joints – prominent synovitis and effusion (knee most common)
2. Bones – vertebrae (multiple) > long bones
120
What diagnostic methods are used for C. immitis in bones and joints?
Culture (50%) and histopathology
121
List the key features of meningitis caused by C. immitis.
1. Headache
2. Vomiting
3. Altered mental status
4. ↑ WBC (mononuclear)
5. ↑ Protein
6. ↓ Glucose in CSF
7. Culture usually negative
122
Describe the culture appearance of C. immitis at 25–30°C.
White fluffy mold
123
What structure in culture is suggestive but not diagnostic of C. immitis?
Arthrospores
124
List the histopathologic findings in C. immitis infection.
1. Acute inflammation (PMNs and eosinophils) with active infection and ruptured spherules
2. Granulomas with chronic infection and unruptured spherules
125
Describe the dimorphism of B. dermatitidis. (BLASTOMYCES DERMATITIDIS)
1. Hyphae with microconidia at room temperature
2. Converts to broad-based budding yeast at 37°C
126
List the disease forms caused by B. dermatitidis.
1. Pulmonary infection (asymptomatic or pneumonia)
2. Chronic pulmonary disease (common)
3. Disseminated disease (skin and bones)
127
Describe B. dermatitidis in culture.
1. White → light tan mold at room temperature
2. Not diagnostic
3. Identification based on conversion to yeast at 37°C
128
Enumeration: Describe the histopathologic features of B. dermatitidis.
Thick-walled broad-based budding yeast
Suppurative and/or granulomatous inflammation
129
Describe the dimorphism of P. brasiliensis. (PARACOCCIDIOIDES BRASILIENSIS)
→
1. Hyphae at room temperature
2. Converts to yeast with multiple buds at 37°C
130
What is the probable mode of acquisition for P. brasiliensis?
Inhalation
131
List the possible pulmonary infection forms of P. brasiliensis.
Asymptomatic, acute, or chronic
132
In adults >30 years old, what areas are usually involved in extrapulmonary P. brasiliensis disease?
Oropharyngeal mucosa and regional lymph nodes
133
What is the only dimorphic species in the genus Penicillium?
*Talaromyces marneffei*
134
What is the probable route of infection of T. marneffei?
Inhalation
135
List the general clinical features of T. marneffei infection.
Chronic illness, low-grade fever, weight loss, skin lesions, disseminated infection
136
Describe the microscopic forms of T. marneffei.
1. Intracellular forms resemble *Histoplasma capsulatum*
2. Extracellular forms **exhibit septa** (cells divide by fission, not budding)
137
Describe the culture features of T. marneffei.
→
1. Mold at 25–30°C producing soluble red pigment
2. Converts to yeast phase at 37°C
138
Describe the hyphal characteristics of Aspergillus spp.
Septate hyphae branching at 45° angle
139
List the common pathogenic species of Aspergillus.
A. fumigatus, A. flavus, A. niger
140
Which Aspergillus species is thermotolerant up to 55°C?
A. fumigatus
141
Where is A. fumigatus commonly found in high concentration?
Compost sites
142
What is the mode of spread for Aspergillus infections?
Airborne
143
List the major forms of Aspergillus infections.
1. Allergic bronchopulmonary aspergillosis
2. Aspergilloma (fungus ball)
3. Invasive pulmonary aspergillosis
144
Describe Aspergilloma (fungus ball).
→
Colonization of preexisting lung cavity (e.g., TB, abscess)
145
Describe the key features of invasive pulmonary aspergillosis.
1. Occurs in immunosuppressed and neutropenic patients
2. Vascular invasion, infarction, cavitation
3. Hematogenous dissemination (ocular, cerebral, cutaneous involvement)
146
Why is direct examination of Aspergillus spp. difficult?
Branching septate hyphae resemble other opportunistic fungi (e.g., Pseudallescheria, Fusarium)
147
Describe the culture requirements and identification notes for Aspergillus spp.
1. Grow well on standard media
2. Airborne contaminants common
3. Must observe several colonies from one specimen or same organism in multiple specimens
148
Name the fungi included under Mucoraceae that cause mucormycosis.
Mucor, Rhizopus, Absidia
149
Describe the morphological characteristics of Mucoraceae fungi.
Broad, nonseptate hyphae with sporangia
150
List the natural sources/environments of Mucoraceae.
Decaying vegetables, fruits, soil, old bread, materials containing carbohydrates
151
What is the most common clinical isolate of mucormycosis?
*Rhizopus oryzae*
152
List the three main clinical forms of mucormycosis.
1. Rhinocerebral/craniofacial mucormycosis
2. Pneumonia
3. Cutaneous infection
153
Describe rhinocerebral/craniofacial mucormycosis.
1. Infection of paranasal sinuses
2. Extension from ethmoid into orbit or frontal lobe
3. May involve cavernous sinus thrombosis
4. Prompt diagnosis essential via direct exam of turbinate scrapings and/or sinus aspirate
154
What condition does mucormycotic pneumonia resemble?
Invasive pulmonary aspergillosis
155
Enumeration: Describe the features of cutaneous mucormycosis.
1. Associated with localized trauma
2. Cellulitis with central necrotic area
156
Break
❤️🩹
Microbiology
flashcards
Decks in class (22)
# Cards
-
Module 6106
-
Module 7181
-
Module 8. 1132
-
Module 8.2115
-
Module 8.3283
-
Module 9188
-
9191
-
11.1191
-
11.2170
-
Module 11.2160
-
Module 12 (Slide 1 To 39)94
-
Module 12 (Slide 40 To 65)76
-
Module 12 (66-101)156
-
Module 12 (-110 Last)25
-
LAB EXAM 1 EXERCISES31
-
LAB EXAM 1 PPT CULTURE MEDIA107
-
Module 13 (VIRUSES)64
-
Module Virology Pt.1 (RNA VIRUSES)85
-
Module Virology Part 2 (DNA)57
-
Module VIROLOGY Part 3 (Introduction)98
-
RNA (Picorna-Coronaviridae)83
-
RNA VIRUS (REO - RHABDOVIRIDAE)49
