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Infection > Fungal infections > Flashcards

Fungal infections Flashcards

1
Q

Please explain the grand mycological challenge:

A
  • 1.5 billion fungal infections of humans
  •  > 3 million life threatening infections /year  Mortality rates typically > 50%
  •  >400,000 cases of blindness per year
  •  Allergens and asthma (>20 million)
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2
Q

What are the three main fungal pathogens?

A
  • Aspergillus species 
    • Aspergillus fumigatus
  •  Candida species
    •  Candida albicans
  •  Cryptococcus species
    •  Cryptococcus neoformans
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3
Q

Which patients are suspectible to fungal infection and why?

A

They are opportunistic in nature.

  • Affecting patients with an impaired immune system 
    • Patients with primary immunodeficiencies
    •  Patients with HIV/AIDS
    •  Patients with malignancies (neutropenia) & transplants
    •  Premature neonates (immature immune system)
  •  Affecting patients with chronic lung diseases (pulmonary
  • aspergillosis and other moulds) 
    • Asthma
    •  Cystic Fibrosis
    •  Chronic obstructive lung disorders
  •  Affecting patients in ICU settings
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4
Q

Who is susceptibile for mucocutaneous candidiasis?

A
  • Antibiotic use
  •  Moist areas
  •  Inhalation steroids
  •  Neonates < 3 months
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5
Q

What are the presenting symptoms of mucocutaneous candidiasis?

A
  • Neutropenia
  • Low CD4+ T-cells
  • impaired IL-17 immunity
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6
Q

What are notable features of candidiasis?

A
  • Gut commensal
  • Infections mostly endogenous of origin
  •  4th most common bloodstream
  • infection (BSI) in adults: 30/100.000 admissions
  •  Premature neonates (< 1000 g):
  • 150/100.000 admissions
  •  Clinical presentation as bacterial BSI
  •  Mortality up to 40%
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7
Q

How do we diagnose invasive candidiasis?

A
  • Blood culture or culture from normally sterile site
  •  β-d-glucan high NPV and performs very well to exclude invasive candidiasis
  •  Recent developments in PCR assays very promising
  •  In infants and children performance lower due to sampling issues
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8
Q

How is aspergillus transmissioned?

A
  • sporulation
  • hydrophobic conidia
  • diameter 2-3 μm
  • airborne / inhalation
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9
Q

What is invasive pulmonary aspergillosis?

A

Asperigillus infection of the ciliated cells of the lungs.

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10
Q

What are the classifications of aspergillus infection?

A
  • Acute invasive pulmonary aspergillosis
    • Neutropenic patients (incidence 1-10%)
    • Post transplants: stem cell > solid organ (incidence up to 8%)
    • Patients with defects in phagocytes
  • Chronic pulmonary aspergillosis (> 3 months)
    • • Patients with underlying chronic lung conditions
  • Allergic aspergillosis
    • Allergic bronchopulmonary aspergillosis in CF and asthma (incidence 10-15%)
    • Asthma or CF with fungal sensitisation (incidence 5-15%)
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11
Q

Notable features and SSx of Acute Invasive Pulmonary Aspergillosis:

A
  • Rapid and extensive hyphal growth
  • Thrombosis and hemorrhage
  • Angio-invasive and dissemination
  • Absent or non-specific clinical signs and symptoms
  • Persistent febrile neutropenia despite broad-spectrum antibiotics
  • Mortality rates around 50% (but depending on immune recovery)
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12
Q

Notable features/SSx of (sub) Acute Invasive Pulmonary Aspergillosis:

A

non-neutropenic host (graft-versus-host disease, neutrophil disorders)

  • Non-angioinvasive
  •  Limited fungal growth
  •  Pyogranulomatous infiltrates
  •  Tissue necrosis
  •  Excessive inflammation
  •  Non-specific clinical signs and symptoms  Mild to moderate systemic illness
  •  Mortality 20-50%
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13
Q

How can invasive aspergillosis present as primary immunodefiency?

A

Congenital neutropenia Chronic granulomatous disease

 Phagocytic disorder
Hyper IgE syndrome (Job’s syndrome)

 Phagocytic disorder and impaired IL-17 pathway CARD-9 deficiency

 Innate immune pathways, killing defect

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14
Q

Notable features/SSx for chronic pulmonary aspergillosis?

A

asthma, cystic fibrosis, chronic obstructive lung disorders

  • Pulmonary exacerbations (not responding to antibiotics)
  •  Lung function decline
  •  Increased respiratory symptoms as cough,
  • decreased exercise tolerance and dyspnea
  •  Positive sputum cultures for Aspergillus
    •  50% of CF patients are infected
  •  High morbidity but causative mortality rates less
  • clear
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15
Q

What is Allergic Bronchopulmonary Aspergillosis?

A

Immunological responses to a variety of A. fumigatus antigens in the CF-host (10-15%) that result in:

  • Acute/subacute deterioration of lung function and respiratory symptoms
  •  New abnormalities chest imaging
  •  Elevated immunoglobulin E (IgE) level
  •  Increased Aspergillus specific IgE or positive skin-test
  •  Positive Aspergillus specific IgG
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16
Q

What is pulmonary aspergilloma?

A

A fungal mass that usually grows in lung cavities

  • Tuberculosis
    •  In 22% if residual cavities
  •  Sarcoidosis
  •  Bronchiectasis
  •  Bronchial cysts and bullae  After pulmonary infections
17
Q

How do we diagnose pulmonary aspergillosis in non-neutropenic patients?

A
  • Cultures of sputum and/or bronchoalveolar lavage, and/or biopsy
  • Aspergillus specific IgG and IgE in chronic and allergic pulmonary aspergillosis
18
Q

How do we diagnose pulmonary aspergillosis in neutropenic patients?

A
  • High resolution CT-chest
    •  ‘halo-sign’ and ‘air-crescent sign’
  • Molecular markers in blood: galactomannan and PCR-Aspergillus (high NPV and are suited for screening purposes)
  • BAL and biopsies if clinical condition allows
19
Q

How is cryptococcus transmitted?

A
  • Transmission by inhalation: can be found on the bark of a variety of trees, bird faeces and organic matter
20
Q

How can cryptoccus present?

A

Pulmonary infection from asymptomatic to pneumonia

21
Q

What is the brain risk from cryptoccocal infection?

A
  • Dissemination to brain: meningoencephalitis in HIV/AIDS patients (CD4 < 100 cells/ul)
22
Q

How does cryptococcus clinically present?

A
  • headache, confusion, altered behaviour, visual disturbances, coma (due to raised intracranial pressure in 60-80%)
23
Q

How do we diagnose cyptococcal disease?

A
  • Cerebrospinal fluid: Indian Ink preparation (80% sensitivity), culture, high protein and low glucose, Cryptococcus antigen (lateral flow assay)
  •  Blood: culture, Cryptococcus antigen
24
Q

What are the outcomes for cryptococcal meningitis?

A
  • Africa: 3-month mortality 70%
  •  US: 3-months mortality 25%
  •  Factors associated with mortality:
    •  Delay in presentation and diagnosis
    •  Lack of access to antifungals
    •  Inadequate induction therapy
    •  Delays in starting antiretroviral therapy  Immune reconstitution syndrome
25
Q

How do Amphotericin B formulations (iv) work?

A

• Acting on ergosterol > lysis

26
Q

How do azoles work?

A

inhibit ergosterol synthesis

27
Q

How do echinocandins function?

A

Inhibiting glucan synthesis

28
Q

How does flucytosine work?

A

Inhibiting fungal DNA synthesis

29
Q

Which is the broadest antifungal?

A
30
Q

What are the drugs of choice for invasive candidiasis?

A

Echinocandins and fluconazole

31
Q

What are the drugs of choice for (acute) invasive aspergillosis ?

A

Voriconazole and Isavuconazole

32
Q

What are the drugs of choice for antifungal prophylaxis?

A

Itraconazole and Posaconazole

33
Q

What are the drugs for maintenance for cryptococcal meningitis?

A

AmB + flucytosine followed by fluconazole

Infection (12 decks)

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