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Infection > Fungal Infections > Flashcards

Fungal Infections Flashcards

1
Q

What are the 3 main fungal species?

A

Aspergillus species Candida species Cryptococcus species

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2
Q

Fungal pathogens are _______ in nature.

A

Opportunistic

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3
Q

Give examples of patients who may be more affected by fungal infections

A

Those with impaired immune systems (AIDS, primary immunodeficiencies, malignancies, transplants, premature neonates)

Those with chronic lung dx (CF, asthma, chronic obstructive lung disorders)

Those in ICU

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4
Q

What is candida a type of?

A

Yeast

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5
Q

What is the most common cause of fungal infections worldwide?

A

Candida

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6
Q

What is candidiasis?

A

Candida infection (due to any type of candida)

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7
Q

What is the most common cause of candidiasis?

A

Candida albicans

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8
Q

Most candida are harmless - when do they pose a threat to someone’s health?

A

When mucosal barriers are disrupted/immune system is impaired they can invade and cause disease

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9
Q

What are the risk factors for mucocutaneous candidiasis?

A

Post-antibiotic use

Moist areas

Inhalational steroids (oral thrush)

Neonates (<3m)

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10
Q

Why are neonates more prone to candiasis?

A

As they have an immature immune system

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11
Q

Why are you more prone to candidiasis after a course of antibiotics?

A

Antibiotics lead to imbalance in local flora which allows candida to thrive

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12
Q

Mucocutaneous candidiasis is the presenting symptom of primary immunodeficiency disorders characterised by what things?

A

Neutropenia

Low CD4 T-cells

Impaired IL17 immunity

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13
Q

What is IL-17?

A

Pro-inflammatory cytokine produced by T-helper 17 cells

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14
Q

True or false:

Candida is a respiratory commensal

A

FALSE - it is a gut commensal

Found in low numbers on skin, GI, GU tracts, mouth

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15
Q

What is the most common pathogenesis of invasive candidiasis?

A

Local mucocutaneous infection –> breach of skin/mucosal barrier or translocation (e.g. IV catheterisation) –> direct invasion into bloodstream (candidaemia) –> spread to visceral tissues –> disseminated organ infection

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16
Q

What is the mortality of invasive candidiasis?

A

Up to 40%

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17
Q

What is the clinical presentation of invasive candidiasis?

A

Classical presentation as bacterial bloodstream infection (may vary from fever –> sepsis)

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18
Q

What are the risk factors for invasive candidiasis?

A
  • Broad spectrum antibiotics
  • IV catheters
  • TPN
  • Abdominal surgery
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19
Q

How do you diagnose invasive candidiasis?

A

Blood culture/culture from normally sterile site

?Developments in PCR

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20
Q

Lack of ____________ is a good negative predictor to exclude invasive candidiasis.

A

Beta-d-glucan (naturally occuring polysaccharide in the cell wall of fungi)

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21
Q

How do you treat invasive candidiasis?

A

Enchocandins or fluconazole

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22
Q

Aspergillus is a type of _______.

A

Mould

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23
Q

Aspergillus spores are _______ but do not usually cause infection in patients who are ___________.

A

Ubiquitous

Immunocompetent

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24
Q

Describe the process of sporulation in A. fumigatus

A

A. fumigatus produces a small, hydrophobic conidia (asexual, non-motile fungal spore) which are easily dispersed in air currents

25
Q

How are aspergillus spores spread?

A

Through inhalation of airborne spores

26
Q

What is the most common aspergillus species to cause disease in the immunodeficient?

A

Aspergillus fumigatus

27
Q

Describe the pathogenesis of invasive pulmonary aspergillosis

A

Sporulation of a microbe –> conidia inhaled into alveola –> conidial germination (grows into mould) in absence of pulmonary defences

28
Q

What occurs in those with invasive pulmonary aspergillosus due to corticosteroid induced immunodeficiency?

A

Polymorphonuclear neutrophils are recruited and tissue is damaged

29
Q

What occurs in those with invasive pulmonary aspergillosus due to neutropenia?

A

Excessive hyphal growth and dissemination

30
Q

Describe what hyphi of aspergillus look like

A

Long, branching form of aspergillus

31
Q

What are the three classifications of pulmonary aspergillus disease?

A

Acute invasive pulmonary aspergillosis

Chronic pulmonary aspergillosis (>3m, tends to be those with chronic lung disease)

Allergic aspergillosis (e.g. in those with CF, asthma)

32
Q

What are the clinical consequences of acute invasive pulmonary aspergillosis in the neutropenic host?

A
  • Thrombosis and haemorrhage
  • Angio-invasive and dissemination
    *
33
Q

What are the clues in someone’s presentation that may indicate an acute invasive pulmonary aspergillosis?

A

Persistent febrile neutropenia despite broad-spectrum antibiotics

Absent/non-specific clinical signs and symptoms

34
Q

How do you treat acute invasive aspergillosis?

A

Voriconazole or isavuconazole

35
Q

What is the presentation of sub-acute invasive pulmonary aspergillosis?

A
  • Non-angioinvasive
  • Limited fungal growth
  • Polygranulomatous infiltrates
  • Tissue necrosis
  • Excessive inflammation
36
Q

What primary immunodeficiencies may present as invasive aspergillosis?

A

Congenital neutropenia

Chronic granulomatous disease

Hyper IgE syndrome

CARD-9 deficiency

In these groups, the presentation is often outside the lungs, e.g. bone, spine, brain

37
Q

When should you be suspicious of chronic pulmonary aspergillosis?

A

Pulmonary exacerbations not responding to antibiotics with lung function decline & increased respiratory symptoms

Positive sputum cultures for aspergillus

38
Q

What is allergic bronchopulmonary aspergillosis?

A

Immunological response to A. fumigatus antigens in the CF host resulting in acute/subacute deterioriation of lung function & respiratory symptoms, new abnormalities in chest imaging, elevated IgE levels (incl. IgE specific for aspergillus/+ve skin prick test), positive IgG for aspergillus

39
Q

How do you 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

40
Q

How do you diagnose pulmonary aspergillosis in neutropenic patients?

A

High resolution chest CT (halo sign/air crescent sign)

Molecular markers in blood - galactomannan and PCR-aspergillosis

Bronchoalveolar lavage and biopsies if patient well enough

41
Q

What is glactomannan?

A

Component of cell wall of aspergillus (released during its growth)

42
Q

What is bronchoalveolar lavage?

A

When a bronchoscope is put through the nose/mouth into the lungs and fluid is squirted into a small part of the lung and re-collected for examination

43
Q

What are cryoptococci types of?

A

Yeast

44
Q

Which of the cyrptococci is the main pathogen?

A

Cyrptococcus neoforms

45
Q

Extrapulmonary cryptococcal infection is what kind of disease?

A

AIDS defining illness

46
Q

How is cryptococcus transmitted and where can it be found?

A

Inhalation

Found on trees, bird faeces, organic matter

47
Q

What is the clinical presentation of cryptococcosis?

A

Pulmonary infection, varies from asymptomatic to pneumonia

Dissemination to bring (meningoencephalitis in those with HIV/AIDS)

Clinical presentation: headache, confusion, altered behaviour, visual disturbances, coma

48
Q

At what CD4 count do most cases of cryptococcal meningitis occur in those with HIV?

A

<100

49
Q

How do you diagnose cryptococcal disease?

A

CSF - india ink preparation or culture (high protein, low glucose, cryptococcus antigen)

Blood - culture, cryptococcal antigen

50
Q

What factors are associated with higher mortality in those with cryptococcal meningitis?

A
  • Delay in presentation and diagnosis
  • Lack of access to antifungals
  • Inadequate induction therapy
  • Delays in starting anti-retroviral therapy
  • Immune reconstitution syndrome
51
Q

How do you treat cryptococcal meningitis?

A

AmB + Flucytosine

Followed by fluconazole maintenance

52
Q

How does amphotericin B work?

A

Acts on ergosterol to cause lysis

Ergosterol is a component of the fungi cell membrane

53
Q

Which anti-fungal has the broadest anti-fungal activity?

A

Amphotericin B

54
Q

How do azoles work?

A

Inhibit ergosterol synthesis

55
Q

How do echocandins work?

A

Inhibit glucan synthesis

These can be used for invasive candidiasis

56
Q

How does flucytosine work?

A

Inhibits fungal DNA synthesis

57
Q

What are risk factors for invasive asperigllosis?

A

HIV

Leukaemia

Following broad spectrum antibiotics

58
Q
A

Infection (22 decks)

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