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Fungi- Cryptococcus and Candida Flashcards

1
Q

What is an opportunistic infection?

A

Infections that develop as a result of damage to the immune system are called opportunistic infections or OIs
These infections take advantage of the opportunity provided by a weakened immune system

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2
Q

When do opportunistic infections appear?

A

Infections tend to appear at predictable stages of immune deterioration

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3
Q

What are the endogenous causes?

A

causes - cancer, leukaemia

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4
Q

What are the exogenous causes?

A

Exogenous causes - immunosuppressive therapy, AIDS.

An important cause of morbidity & mortality in hospitalized patients.

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5
Q

What is the pathogenesis of the fungi that cause opportunistic infections?

A

Produced by relatively non-pathogenic or contaminant fungi in a host whose immunological defence mechanisms are weakened by

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6
Q

What are examples of opportunistic mycoses?

A

Candidiasis

            - Cryptococcosis
            - Aspergillosis		
            - Zygomycosis / Mucormycosis
            - Pneumocystosis
            - Penicilliosis
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7
Q

Candidiasis can take the form of ?

A

superficial, mucocutaneous or systemic disease

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8
Q

What is the habitat for candida?

A

Harmless inhabitants of the skin and mucous membranes of all humans…………………………Found in the gastrointestinal tract, upper respiratory tract, buccal cavity, and vaginal tract.

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9
Q

Most common fungal infection in immunocompromised patients

A

candida

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10
Q

4TH most common cause of nocosomial bs infection

A

candida

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11
Q

candida species implicated in human disease are

A 
C. albicans
C. tropicalis
C. parapsilosis
C. krusei
C. glabrata
C. lusitaniae
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12
Q

Which candida species is resistant to fluconazole?

A

C krusei

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13
Q

C lusitaniae is resistant to

A

amphotericin B

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14
Q

Where is candida found? What suppresses its growth?

A

Found in the gastrointestinal tract, upper respiratory tract, buccal cavity, and vaginal tract.
Growth is normally suppressed by other microorganisms found in these areas.

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15
Q

What leads to candida GI tract infection?

A

Alterations of gastrointestinal flora by broad-spectrum antibiotics or mucosal injury can lead to gastrointestinal tract invasion.

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16
Q

How does it skin invasion? How does it enter the bloodstream?

A

Skin and mucus membranes are normally an effective barrier but damage by the introduction of catheters or intravascular devices can permit Candida to enter the bloodstream

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17
Q

Describe the structures of candida cell wall- reproduction, cells

A
  1. Thick cell wall of mannan and glucan polysaccharides, unicellular, budding (asexual) reproduction
  2. filament formation
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18
Q

What is filament formation?

A

Pseudohyphae (buds stay attached, constricted, chains of elongated blastospores)
Hyphae (buds germinate)

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19
Q

Which candida species is most virulent?

A

C Albicans

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20
Q

What are the virulence factors?

A
  1. Rapid switching of expressed phenotypes
  2. Hyphal formation
  3. Surface hydrophobicity
  4. Surface Virulence molecules
  5. Molecular Mimicry
  6. Lytic enzymes
  7. Growth rate and nutrients
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21
Q

How does candida rapid switching of expressed phenotype lend to the virulence of the species ? Under what circumstances does this occur?

A 
Enhanced ability to reassort and regulate genetic expression by chromosomal rearrangement and recombination
phenotypic - nutrient stress produces different colony forms
virulence factors (including antifungal resistance, e.g. C. lusitaniae vs. amphotericin B)
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22
Q

The hyphal formation is associated with and colonize?

A

The hyphal formation is associated with tissue invasion ( yeast forms associated with epithelial colonization)

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23
Q

What do the hyphae allow?

A

Hyphae adhere more readily to host epithelial surfaces than do yeast cells (50x more adherent

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24
Q

What does experimentation suggest about hyphal formation vs yeast form?

A

Spontaneous C. albicans non-hyphae-forming mutant shows decreased pathogenicity in a rat Candida vaginitis model
Experimental renal infection - yeast and hyphae initiate renal lesions, but hyphae are essential for invasion of the renal pelvis.

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25
Hydrophobic vs hydrophilic , which is more virulent
Hydrophobic C. albicans at 25 C >>virulent than more hydrophilic C. albicans at 37 C
26
Hydrophobic CA shows
) show increased adherence and more rapid hyphal germ tube formation
27
What are the surface virulence molecules?
(receptors, adhesins, pyrogens, and immunomodulators)
28
Candida adheres to
epithelial cells (buccal, cervical, corneal, urinary, gastrointestinal mucosa), vascular endothelial cells, spermatozoa, plastics
29
Candida forms
form ligands to host components - C3d, iC3b, fibrinogen, laminin, fibronectin, fucose receptors, N-acetylglucosamine receptors
30
What is molecular mimicry and how does candida do that?
Surface coat of molecules that mimics host components (decreases recognizability) C. albicans cells in the bloodstream become rapidly coated with host platelets via the fibrinogen-binding ligand.
31
What are lytic enzymes ?
Hydrolases with broad substrate specificities (proteinase, phospholipase(s), lipase(s), acid phosphomonoesterase). Aspartyl proteinase
32
How do the growth rate and undemanding nutrient requirements relate to the virulence of candida?
Virulent strains have shorter doubling times than attenuated strains C. albicans not fastidious, but nutritionally deprived mutants (auxotrophs for adenine, lysine, serine, uracil and heme) show decreased virulence
33
What are the 5 most important risk factors for developing candidiasis?
Neutropenia 2. Diabetes mellitus 3. AIDS 4. Myeloperoxidase defects 5. Broad-spectrum antibiotics
34
Other risk factors
Indwelling catethers 8. Major surgery 9. Organ transplantation 10. Neonates 11. Severity of any illness 12. Intravenous drug addicts
35
What is the epidemiology of candidiasis?
candidiasis is endogenous in most cases, cross infections are described, especially in intensive care unit patients.
36
Examples of mucosal candidiasis
Thrush (oropharyngeal) Esophagitis Vaginitis
37
Examples of cutaneous candidiasis
``` Paronychia (skin around nail bed) Onychomycosis (nails) Diaper rash Balanitis Chronic mucocutaneous candidiasis children with T-cell abnormality ```
38
Invasive candidiasis
(systemic, disseminated, hematogenous) candidiasis
39
Invasive candidiasis begins with
Usually begins with candidemia (but in only about 50% of cases candidemia can be proven) If the phagocytic system is normal, invasive infection stops here If the phagocytic system is compromised, infection spreads to many organs and causes focal infection in these organs
40
Clinical features of candida
fungemia, uti, disseminated(systemic, invasive) infection
41
Invasive infections
kidneys, skin, lungs, eyes, immunocompromised (cancer/chemotherapy, neonatal candidiasis)
42
What is the main defence mechanism?
``` Skin and mucous membranes integrity presence of normal bacterial flora Phagocytosis killing, mostly in polymorphonuclear cells, less in macrophages T-cells (CD4) ```
43
What specimens are taken?
Blood, tissue (biopsy or autopsy), sterile fluid, urine, CSF, skin, respiratory secretions
44
What are the tests carried out?
Microscopy (direct on specimen - except blood and urine) Gram stain, Calcofluor Histopathology (tissues
45
Is C.albicans dimorphic? What occurs at 25 or 37 degrees?
``` C.albicans is not a dimorphic fungus, as both yeast & hyphae are seen in tissue In vitro (25o C): mostly yeast; In vivo (37o C): Yeast, hyphae and pseudohyphae ```
46
Pathology of disseminated candidiasis
yeast-like cells | Esophagus, vascular invasion, blastoconidia and pseudohyphae, PAS
47
What is the media used?
sabouroud’s dextrose blood agar, trypticase soy, and many other media
48
What is the morphology of candida?
Creamy yeast colonies are formed after overnight incubation at a temperature of 21 or 37 ; the optimum growth temperature is around 30
49
What is the shape of the candida colonies?
as round-to-oval yeast cells that are 4-6µm in diameter.
50
When are the hyphae and pseudohyphae?
Psudohyphae and hyphae are also seen; especially at lower incubation temperature (i.e. 22-25) and on nutritionally poor media.
51
What is lab identification?
Unique color on chromagar Chlamydospore production (terminal vesicle) Germ tube production (in horse serum) Carbohydrate assimilation and fermentation (API 20C, Vitek2, RapID and reference) Urea and nitrate Microscopic morphology on Cornmeal Tween 80
52
C glabrata colonies
Light-turquoise colonies (white periphery and turquoise centre), with a flat, shiny, smooth morphotype
53
C krusei
Turquoise-blue colonies, with a characteristically rough morphotype, a dry appearance and an irregular outline
54
C tropicalis
Intense turquoise pigmented colonies, with a mat, uniformly coloured, convex, smooth morphotype
55
C Albicans
pink to purple
56
What is used to identify yeast? At what temp?
Budding of yeast cell. Germ-tube test: Chlamydospore formation when incubated at 22c on cornmeal agar
57
What is the appearance of candida on Sabouraud agar?
Morphology: Creamy white yeast, may be dull, dry irregular and heaped up, glabrous and tough
58
Morphology on chromagar
producing green pigmented colonies on specially designed medium to separate certain yeasts based on color they produce
59
Which candida species are germ +ve?
Germ Tube: Positive Germ tube is a continuous filament germinating from the yeast cell without constriction at the point of attachment. (beginning of true hypha ) e.g. C. albicans, C. dubliniensis
60
Germ tube test
inoculation of yeast in horse serum incubated at 370C for 2 to 3 hours
61
Germ tube negative
Shows constriction at the attachment site | e.g. other Candida species, esp. C. tropicalis
62
Oxgall agar
large round and thick | walled chlamydospores
63
Cornmeal agar
clusters of blastospores along pseudohyphae at regular intervals
64
Is candida antigen, antibody and metabolite detection useful?
NOT useful in routine practice Low sensitivity and specificity Polymerase chain reaction
65
What is the treatment for candida?
remove IV infection and antifungal therapy
66
Antifungal treatment
Amphotericin B IV Azoles (fluconazole, itraconazole, voriconazole, posaconazole) orally, intravenous Flucytosine (only with Ampho B because of resistance) Echinocandins (caspofungin, micafungin)
67
What species show primary resistance?
C. lusitaniae (amphotericin B) C. glabrata (fluconazole) C. krusei (fluconazole)
68
Secondary or acquired resistance is seen with what therapy?
Fluconazole, other azoles Amphotericin B 5-FC
69
Which encapsulated yeast is pathogenic to man?
cryptococcous infections
70
Cryptococcosis infects
occurs in sporadic form and as an opportunistic infection associated with immunosupperession 2nd most common fungal infection after candidiasis in HIV - infected individuals
71
Fungal infections in HIV patients
Most - candida 2nd-cryptococcus
72
Cryptococcus is isolated from
pigeon nests, droppings, old buildings & nitrogenous soil - Creatine favour the growth.
73
Virulence factors of cryptococcus
Capsule – Inhibits phagocytosis. Melanin production by the enzyme phenol oxidase. L- DOPA Melanin Antioxidant - protects the organism from intracellular killing by phagocytes
74
What is the pathogenesis of cryptococcus?
Infection occurs by inhalation, but sometimes through skin or mucosa. Weakening of immune system leads to reactivation & dissemination to CNS and other sites.
75
What is seen in the visceral and cutaneous forms of cryptococcus?
Visceral forms simulate tuberculosis & cancer clinically. | Cutaneous form varies form small ulcers to granulomas.
76
What are the clinical types of cryptococcosis?
Pulmonary(Primary infection) Extrapulmonary – CNS, viscera, bones & skin Cryptococcal meningitis is the most serious type of infection, resembles TB and is often seen in AIDS patients.
77
What are the clinical features of cryptococcosis?
Seen in HIV +ve patients when CD4+ count falls below 200 cells / mm3 Extra pulmonary cryptococcosis is one of the AIDS – defining disease.
78
Primary cryptococcosis can be discovered by
chest x-ray
79
Pulmonary cryptococcosis - who will have asymptomatic carriage
Asymptomatic carriage of Cryptococcus  In addition, patients with chronic lung disease, such as bronchitis and bronchiectasis, may also have asymptomatic colonization. Subclinical cryptococcosis.
80
Chronic pulmonary cryptococcosis increases risk of
also increases the risk of dissemination to the central nervous system.
81
Patients with Invasive pulmonary cryptococcosis may present with
Patients may become pyrexic and have cough, however many pulmonary lesions are often asymptomatic, especially when chronic granulomas are formed.
82
What are the symptoms related to CRYP dissemination to the brain?
Symptoms- headache, drowsiness, dizziness, irritability, confusion, nausea, vomiting, neck stiffness and focal neurological defects, such as ataxia.
83
Dissemination to the brain and meninges cause?
causes meningitis, meningoencephalitis or expanding cryptococcoma.
84
What are the symptoms related to meningoencephalitis?
Symptoms include slow response to treatment and signs of cerebral edema or hydrocephalitis, especially papilledema -- rapid infection leading to com and death
85
What areas are affected in meningoencephalitis?
cerebral cortex, brain stem and cerebellum
86
Cryptococcoma
Characterized by localized, solid, tumor-like masses
87
What specimens are taken?
serum, csf, body fluids
88
What does the gram stain show?
gram +ve budding yeast cells
89
India ink stain
CRYP-Wet mount: India ink - budding yeast cells 5-20, with a distinct halo
90
SDA cryptococcus shows
highly mucoid, cream to buff colored.
91
What is seen of birdseed agar?
Birdseed (Niger seed) agar – selective media | - Brown colored colonies due to melanin production
92
What serology tests are taken?
Crypto LA test –Capsular Ag detection in Serum, CSF & Urine using anticapsular antibodies - Titer > 18 is significant. Antibodies can be detected in the serum of patients.
93
What is the drug of choice for cryptococcosis? Other treatment and prophylaxis?
Antifungals - AMB: Drug of choice - Flucytosine Vaccine - conjugate vaccine developed

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