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MDSC 3312 MB > Fungi- Cryptococcus and Candida > Flashcards

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
Q

Hydrophobic vs hydrophilic , which is more virulent

A

Hydrophobic C. albicans at 25 C&raquo_space;virulent than more hydrophilic C. albicans at 37 C

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26
Q

Hydrophobic CA shows

A

) show increased adherence and more rapid hyphal germ tube formation

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27
Q

What are the surface virulence molecules?

A

(receptors, adhesins, pyrogens, and immunomodulators)

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28
Q

Candida adheres to

A

epithelial cells (buccal, cervical, corneal, urinary, gastrointestinal mucosa), vascular endothelial cells, spermatozoa, plastics

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29
Q

Candida forms

A

form ligands to host components - C3d, iC3b, fibrinogen, laminin, fibronectin, fucose receptors, N-acetylglucosamine receptors

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30
Q

What is molecular mimicry and how does candida do that?

A

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.

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31
Q

What are lytic enzymes ?

A

Hydrolases with broad substrate specificities (proteinase, phospholipase(s), lipase(s), acid phosphomonoesterase).
Aspartyl proteinase

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32
Q

How do the growth rate and undemanding nutrient requirements relate to the virulence of candida?

A

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

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33
Q

What are the 5 most important risk factors for developing candidiasis?

A

Neutropenia

  1. Diabetes mellitus
  2. AIDS
  3. Myeloperoxidase defects
  4. Broad-spectrum antibiotics
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34
Q

Other risk factors

A

Indwelling catethers

  1. Major surgery
  2. Organ transplantation
  3. Neonates
  4. Severity of any illness
  5. Intravenous drug addicts
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35
Q

What is the epidemiology of candidiasis?

A

candidiasis is endogenous in most cases, cross infections are described, especially in intensive care unit patients.

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36
Q

Examples of mucosal candidiasis

A

Thrush (oropharyngeal)
Esophagitis
Vaginitis

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37
Q

Examples of cutaneous candidiasis

A 
Paronychia (skin around nail bed)
Onychomycosis (nails)
Diaper rash
Balanitis
Chronic mucocutaneous candidiasis
children with T-cell abnormality
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38
Q

Invasive candidiasis

A

(systemic, disseminated, hematogenous) candidiasis

39
Q

Invasive candidiasis begins with

A

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
Q

Clinical features of candida

A

fungemia, uti, disseminated(systemic, invasive) infection

41
Q

Invasive infections

A

kidneys, skin, lungs, eyes, immunocompromised (cancer/chemotherapy, neonatal candidiasis)

42
Q

What is the main defence mechanism?

A 
Skin and mucous membranes integrity presence of normal bacterial flora 
Phagocytosis killing, 
mostly in polymorphonuclear cells, 
less in macrophages
T-cells (CD4)
43
Q

What specimens are taken?

A

Blood, tissue (biopsy or autopsy), sterile fluid, urine, CSF, skin, respiratory secretions

44
Q

What are the tests carried out?

A

Microscopy (direct on specimen - except blood and urine)
Gram stain, Calcofluor
Histopathology (tissues

45
Q

Is C.albicans dimorphic? What occurs at 25 or 37 degrees?

A 
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
Q

Pathology of disseminated candidiasis

A

yeast-like cells

Esophagus, vascular invasion, blastoconidia and pseudohyphae, PAS

47
Q

What is the media used?

A

sabouroud’s dextrose blood agar, trypticase soy, and many other media

48
Q

What is the morphology of candida?

A

Creamy yeast colonies are formed after overnight incubation at a temperature of 21 or 37 ; the optimum growth temperature is around 30

49
Q

What is the shape of the candida colonies?

A

as round-to-oval yeast cells that are 4-6µm in diameter.

50
Q

When are the hyphae and pseudohyphae?

A

Psudohyphae and hyphae are also seen; especially at lower incubation temperature (i.e. 22-25) and on nutritionally poor media.

51
Q

What is lab identification?

A

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
Q

C glabrata colonies

A

Light-turquoise colonies (white periphery and turquoise centre), with a flat, shiny, smooth morphotype

53
Q

C krusei

A

Turquoise-blue colonies, with a characteristically rough morphotype, a dry appearance and an irregular outline

54
Q

C tropicalis

A

Intense turquoise pigmented colonies, with a mat, uniformly coloured, convex, smooth morphotype

55
Q

C Albicans

A

pink to purple

56
Q

What is used to identify yeast? At what temp?

A

Budding of yeast cell.
Germ-tube test:
Chlamydospore formation when incubated at 22c
on cornmeal agar

57
Q

What is the appearance of candida on Sabouraud agar?

A

Morphology: Creamy white yeast,
may be dull, dry irregular and
heaped up, glabrous and tough

58
Q

Morphology on chromagar

A

producing green pigmented colonies
on specially designed medium to
separate certain yeasts based on
color they produce

59
Q

Which candida species are germ +ve?

A

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
Q

Germ tube test

A

inoculation of yeast in horse serum incubated at 370C for 2 to 3 hours

61
Q

Germ tube negative

A

Shows constriction at the attachment site

e.g. other Candida species, esp. C. tropicalis

62
Q

Oxgall agar

A

large round and thick

walled chlamydospores

63
Q

Cornmeal agar

A

clusters of
blastospores along
pseudohyphae at regular
intervals

64
Q

Is candida antigen, antibody and metabolite detection useful?

A

NOT useful in routine practice
Low sensitivity and specificity
Polymerase chain reaction

65
Q

What is the treatment for candida?

A

remove IV infection and antifungal therapy

66
Q

Antifungal treatment

A

Amphotericin B IV
Azoles (fluconazole, itraconazole, voriconazole, posaconazole) orally, intravenous
Flucytosine (only with Ampho B because of resistance)
Echinocandins (caspofungin, micafungin)

67
Q

What species show primary resistance?

A

C. lusitaniae (amphotericin B)
C. glabrata (fluconazole)
C. krusei (fluconazole)

68
Q

Secondary or acquired resistance is seen with what therapy?

A

Fluconazole, other azoles
Amphotericin B
5-FC

69
Q

Which encapsulated yeast is pathogenic to man?

A

cryptococcous infections

70
Q

Cryptococcosis infects

A

occurs in sporadic form and as an opportunistic infection associated with immunosupperession
2nd most common fungal infection after candidiasis in HIV - infected individuals

71
Q

Fungal infections in HIV patients

A

Most - candida 2nd-cryptococcus

72
Q

Cryptococcus is isolated from

A

pigeon nests, droppings, old buildings & nitrogenous soil - Creatine favour the growth.

73
Q

Virulence factors of cryptococcus

A

Capsule – Inhibits phagocytosis.
Melanin production by the enzyme phenol oxidase.
L- DOPA Melanin

Antioxidant - protects the organism from  intracellular killing by phagocytes
74
Q

What is the pathogenesis of cryptococcus?

A

Infection occurs by inhalation, but sometimes through skin or mucosa.
Weakening of immune system leads to reactivation & dissemination to CNS and other sites.

75
Q

What is seen in the visceral and cutaneous forms of cryptococcus?

A

Visceral forms simulate tuberculosis & cancer clinically.

Cutaneous form varies form small ulcers to granulomas.

76
Q

What are the clinical types of cryptococcosis?

A

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
Q

What are the clinical features of cryptococcosis?

A

Seen in HIV +ve patients when CD4+ count falls below 200 cells / mm3
Extra pulmonary cryptococcosis is one of the AIDS – defining disease.

78
Q

Primary cryptococcosis can be discovered by

A

chest x-ray

79
Q

Pulmonary cryptococcosis - who will have asymptomatic carriage

A

Asymptomatic carriage ofCryptococcus

In addition, patients with chronic lung disease, such as bronchitis and bronchiectasis, may also have asymptomatic colonization.

Subclinical cryptococcosis.

80
Q

Chronic pulmonary cryptococcosis increases risk of

A

also increases the risk of dissemination to the central nervous system.

81
Q

Patients with Invasive pulmonary cryptococcosis may present with

A

Patients may become pyrexic and have cough, however many pulmonary lesions are often asymptomatic, especially when chronic granulomas are formed.

82
Q

What are the symptoms related to CRYP dissemination to the brain?

A

Symptoms- headache, drowsiness, dizziness, irritability, confusion, nausea, vomiting, neck stiffness and focal neurological defects, such as ataxia.

83
Q

Dissemination to the brain and meninges cause?

A

causes meningitis, meningoencephalitis or expanding cryptococcoma.

84
Q

What are the symptoms related to meningoencephalitis?

A

Symptoms include slow response to treatment and signs of cerebral edema or hydrocephalitis, especially papilledema – rapid infection leading to com and death

85
Q

What areas are affected in meningoencephalitis?

A

cerebral cortex, brain stem and cerebellum

86
Q

Cryptococcoma

A

Characterized by localized, solid, tumor-like masses

87
Q

What specimens are taken?

A

serum, csf, body fluids

88
Q

What does the gram stain show?

A

gram +ve budding yeast cells

89
Q

India ink stain

A

CRYP-Wet mount: India ink - budding yeast cells 5-20, with a distinct halo

90
Q

SDA cryptococcus shows

A

highly mucoid, cream to buff colored.

91
Q

What is seen of birdseed agar?

A

Birdseed (Niger seed) agar – selective media

- Brown colored colonies due to melanin production

92
Q

What serology tests are taken?

A

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
Q

What is the drug of choice for cryptococcosis? Other treatment and prophylaxis?

A

Antifungals - AMB: Drug of choice
- Flucytosine

Vaccine - conjugate vaccine developed

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