Clinically Significant Fungal Pathogens Flashcards

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1
Q

What is a hospital aqcuired infection?

A

A hospital-acquired infection is usually one that first appears three days after a patient is admitted to a hospital or other health care facility.

  • 5-10% of patients admitted to hospitals in the US develop a nosocomial infection.
  • The CDC estimate > two million patients develop hospital-acquired infections yearly causing 99,000 deaths a year
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2
Q

Describe Candida auris- (Japanese fungus)

A
  • First isolated in Japan in 2009
  • It has been isolated from a range of body sites, resulting in invasive infections
  • A more common “cousin” in this family is Candida albicans, which causes the yeast infection thrush.
  • Hospital outbreaks have since been reported in the United States, India, Pakistan, Venezuela, Colombia, Israel, Oman, South Africa and Spain, as well as the UK
  • 66% mortality rate
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3
Q

How do I know if someone has a Candida auris infection?

A
  • Most people who get serious Candida infections are already sick from other medical conditions
  • C. auris is still rare
  • Invasive Candida infection causes fever and chills that don’t improve after antibiotic treatment for a suspected bacterial infection
  • Only a laboratory test can diagnose C. auris infection
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4
Q

Describe drug resistance

A
  • Highly transmissible between patients and from contaminated environments
  • Highlighting the importance of instituting effective infection prevention and control practices.
  • All isolates from the UK demonstrated reduced susceptibility to fluconazole, and variable susceptibility to other antifungals.
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5
Q

C.auris- UK data

A
  • The first UK case emerged in 2013, infection rates have been going up - although it remains rare.
  • End of July 2017- affected more than 200 patients in hospitals in England So far, no UK patient has died from it.
  • Often misidentified
  • Approximately ¼ of reported C. auris detections are clinical infections, including 27 candidaemias.
  • Three large nosocomial intensive care unit outbreaks reported.
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6
Q

C.auris-investigation in clinical laboratories

A

• Indistinguishable from most other Candida species

purple

  • Germ tube test negative budding yeast
  • Some strains can form rudimentary pseudohyphae on cornmeal agar.
  • Growth at 42 - 45⁰C
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7
Q

CHROMagar™ Candida

A

Incubate in aerobic conditions

30-37°C for 48 hours.

Typical Appearance of microrganisms:

Candida albicans → green
Candida tropicalis → metallic blue
Candida krusei / auris→ pink/purple, fuzzy
Other species → white to mauve

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8
Q

Sabouraud Dextrose agar (SDA)

A

30⁰C Atmosphere

Aerobic

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9
Q

Front line tests

A
  • API AUX 20C
  • VITEK-2 YST
  • BD Phoenix
  • MicroScan
  • Misidentifed as a wide range of Candida species and other genera
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10
Q

Confirmation Testing -MALDITOF

A

Any Candida spp isolates associated with:

1) Invasive infections and isolates from superficial sites in patients from high intensity/augmented care settings
2) Transferred from an affected hospital (UK or abroad)

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11
Q

What further work should be undertaken to ensure that they are not C. auris?

A
  • Molecular sequencing of the D1/D2 domain or MALDI-TOF Biotyper analysis with C. auris either already present or added to the database
  • Pure isolates on Sabouraud slopes sent to PHE
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12
Q

Antifungal Susceptibility Testing

A
  • There are no established minimum inhibitory concentration (MIC) breakpoints at present for C. auris.
  • Using breakpoints for other Candida spp, CDC) demonstrated that, of the global outbreaks they investigated, nearly all of 54 isolates were highly resistant to fluconazole.
  • More than half of C. auris isolates were resistant to voriconazole
  • Some isolates have demonstrated elevated MICs to all three major antifungal classes, including azoles, echinocandins, and polyenes.
  • WGS of the organism has found resistant determinants to a variety of antifungal agents.
  • PHE Mycology Reference Laboratory indicates in the UK all isolates are resistant to fluconazole
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13
Q

Decribe treatment

A
  • First-line therapy remains an echinocandin pending specific susceptibility testing which should be undertaken as soon as possible.
  • Evidence that resistance can evolve quite rapidly in this species, ongoing vigilance for evolving resistance is advised in patients who are found to be infected or colonised
  • No evidence to support combination therapy in bloodstream infections with this organism, although if the urinary tract or central nervous system (CNS) is involved dual therapy may be necessary.
  • Currently UK strains remain susceptible to the topical agents nystatin and terbinafine
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14
Q

Describe Colonisation

A

Colonisation tends to persist and is difficult to eradicate making infection prevention and control strategies particularly important:

  1. Strict adherence to central and peripheral catheter care bundles, urinary catheter care bundle and care of the tracheostomy site
  2. Prompt removal of venous cannulas if there is any sign of infection
  3. High standards of aseptic technique when undertaking wound care
  4. Skin decontamination with chlorhexidine washes in critically ill patients.
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15
Q

Suggested screening sites, based on the predilection of Candida spp to colonise the skin and mucosal surfaces i.e. genitourinary tract, gastrointestinal, mouth and respiratory tract, are:

A
  • Groin and axilla
  • Urine
  • Nose and throat
  • Perineal swab
  • Rectal swab or stool sample
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16
Q

Describe Infection control

A
  • Effective handwashing
  • Isolate the patient
  • Waste disposal in clinical waste bins
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17
Q

What is ring worm?

A
  • Ringworm is a common skin disorder otherwise known as “tinea” or “dermatophytosis.”
  • First discovered in 1841 by Hungarian physician David Gruby
  • 1934 Chester Emmons published study of several species of dermatophytes
  • WWII, American servicemen contracted ringworm in the humid Pacific Theater
  • Following which U.S. government launched an intensive study of fungal diseases.
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18
Q

How can you catch ringworm?

A
  • From person to person
  • Touching items which have been in contact with an infected person eg towels, clothes,
  • From animals, such as dogs, cats, guinea pigs and cattle have fungal infections on their skin.
  • Farm animals- Touching a farm gate where infected animals pass through may be enough to infect your skin.
  • From soil- rare
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19
Q

Ring worm presentation: Tinea Capitis

A
  • Scalp ringworm and is the most common ringworm infection in children.
  • Causes the infected area to scale and may involve temporary hair loss.
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20
Q

Ring worm presentation: Tinea Corporis

A
  • Ringworm on the arms and legs.
  • Ring-like patch or plaque with an advancing, elevated, scaling border and a central clearing.
21
Q

Ring worm presentation: Tinea Pedis

A
  • Ringworm on the feet, (Athlete’s Foot)
  • Exposure to moist environments and maceration of the skin.
  • White macerated area
  • Dermatophytes can cause a more dry scaling process.
22
Q

Ring worm presentation: Tinea Cruris

A
  • Ringworm on the groin, otherwise known as Jock Itch.
  • Infects adolescent and young adult men.
  • Contains pustules or vesicles
  • The background rash is red in colour
23
Q

Ring worm presentation: Tinea Unguium

A
  • Ringworm on the fingernails or toenails.
  • Common cause of nail dystrophy
  • May be brought about by tinea pedis, improperly fitting shoes, and diabetes.
24
Q

What are the symptoms of ringworm?

A
  • A rounded, red, inflamed patch of skin.
  • The outer edge is more inflamed and scaly than the paler centre.
  • One patch of infection usually occurs
  • Rash is usually mildly irritating, very itchy and inflamed.
25
Q

What samples are required?

A
  • Microscopic examination of nail or skin scrapings
  • Culture
  • Examination under UV Wood’s light - brilliant green fluorescence if microsporum infection (1); dull green if Trichophyton schoenlenii - favus
26
Q

Woods lamp examination

A
  • Emits ultraviolet (UV) light in the 365 nanometer range
  • The examination is performed in a dark room
  • Wood’s light shines directly on the affected area for a few seconds and looking for any changes in colour or fluorescence.
  • Normal skin does not fluoresce under the light of a Wood’s lamp.
  • If a fungal or bacterial infection or pigment disorder is present, Wood’s lamp examination can strengthen or lessen the suspicion of a particular diagnosis, based on the colour of fluorescence of the affected skin being illuminated.
27
Q

Tests in the laboratory: KOH prep (potassium hydroxide solution)

A

Sample type:

Skin scrapings, hair or nail clippings, tissue, vaginal swab, body fluids, sputum

Description:

The sample is placed on a slide and the chemical solution dissolves non-fungal elements; reveals yeast cells and fungal hyphae (branching filaments) on a microscope slide; examined by a healthcare practitioner or trained laboratorian.

Uses:

Primary screening tool; detects fungi but does not tell what specific fungus is present.

Time for results:

Rapid

28
Q

Tests in the laboratory: Calcofluor white stain

A

Sampple types:

Skin scrapings, hair or nail clippings, vaginal swab, body fluids, sputum

Description:

Stain binds to fungal elements in a sample and fluoresces (glows) under ultraviolet light; allows visualization on microscope slide; more sensitive means of visualizing fungi.

Uses:

Detects fungi but does not tell what specific fungus is present.

Time for results:

Rapid

29
Q

Tests in the laboratory: Fungal culture

A

Sample types:

Skin, nail, hair, body fluids, tissue, vaginal swab, sputum, blood

Description:

A sample is placed on or into nutrient media and incubated to grow any fungi present in sample.

Uses:

Primary tool to diagnose a fungal infection; grows fungi for identification tests and subsequent susceptibility testing.

Weeks

Time for results:

30
Q

What are the targets for antifungal therapy?

A

Cell membrane: Fungi use principally ergosterol instead of cholesterol

DNA synthesis: Some compounds may be selectively activated by fungi, arresting DNA synthesis

Cell wall: Unlike mammalian cells, fungi have a cell wall

31
Q

Treatments for ringworm- antifungal creams/tablets:

Clotrimazole

A

Apply 2-3 times a day for at least four weeks.

32
Q

Treatments for ringworm- antifungal creams/tablets:

Miconazole

A

Apply twice a day and continue for 10 days after the skin is back to normal.

33
Q

Treatments for ringworm- antifungal creams/tablets:

Econazole

A

Apply twice a day until the skin is back to normal

34
Q

Treatments for ringworm- antifungal creams/tablets:

Ketoconazole

A

Apply once or twice a day and continue for a few days after the skin is back to normal.

Cannot be used for children.

35
Q

Treatments for ringworm- antifungal creams/tablets:

Terbinafine

A

Apply once or twice a day for one to two weeks. Cannot be used for children.

Terbinafine, Griseofulvin, or Itraconazole tablets.

36
Q

Describe Aspergillus Fumigatus

A
  • Aspergillus is a group of moulds, of which about 200 species have been identified.
  • 16 species of Aspergillus moulds are known to be dangerous to humans
  • Aspergillus spp. distributed fungal moulds found in soil & other organic matter
  • Human disease is caused by Aspergillus fumigatus or Aspergillus niger
  • Inhalation of the fungal spores
  • Respiratory tract
  • Onychomycosis (fungal nail infection)
  • Otomycosis (fungal infection of the external auditory canal)
  • Implicated in sinus infection
37
Q

Where is Aspergillus found?

A
  • rotting leaves and compost
  • plants, trees and crops
  • air conditioning and heating systems
  • insulation material
  • dust

Develops if you have a pre-existing lung condition, such as asthma or cystic fibrosis, or if you have a weakened immune system.

Most tolerant to temperature and can grow in environments between 20- 55˚c

aspergillosis isn’t contagious, so it can’t be passed from person to person.

38
Q

What are the five main clinical syndromes caused by Aspergillus spp. gaining entry via the respiratory tract?

A
  1. Allergic bronchopulmonary aspergillosis (ABPA)
  2. Severe asthma with fungal sensitisation (SAFS)
  3. Aspergilloma
  4. Invasive aspergillosis
  5. Chronic necrotising pulmonary aspergillosis (CNPA)
39
Q

Describe allergic bronchopulmonary aspergillosis (ABPA)

A

A hypersensitivity reaction to the colonisation of the airways/sinuses/lungs. This predominantly affects patients with asthma, cystic fibrosis (CF) and bronchiectasis.

40
Q

Describe severe asthma with fungal sensitisation (SAFS)

A

Severe asthma (despite standard treatment) with evidence of fungal sensitisation who do not meet the criteria for ABPA.

41
Q

Describe aspergilloma

A

The presence of a mycetoma (fungal ball) of aspergilli in a pre-existing pulmonary cavity (eg, secondary to tuberculosis (TB) or sarcoid)

42
Q

Describe Invasive aspergillosis

A

Disseminated infection affecting the immunocompromised, which often starts in the lungs but may involve other organs and tissues through haematogenous spread

43
Q

Describe chronic necrotising pulmonary aspergillosis (CNPA)

A

Subacute pulmonary infection affecting those with moderate immunosuppression ± pre-existing lung disease, causing a cavitating pulmonary infiltration.

44
Q

Pathophysiology

A
  • Immunocompetent individual, macrophages and neutrophils normally defend against the inhaled fungus.
  • Toxic metabolites attack neutrophils and macrophages
  • Underlying immunosuppression affects neutrophil numbers and function
45
Q

Draw a table of the main approaches to laboratory diagnosis

A
46
Q

Treatment-depends on type: ABPA and SAFS

A

Are usually treated with steroid medication to dampen the reaction of the immune system to the aspergillus particles, and antifungal medication to help kill the mould.

47
Q

Treatment-depends on type: CPA and aspergilloma

A

Can be treated with long-term antifungal medication. In some cases, surgery may be needed to remove an aspergilloma from the lungs, prevent bleeding in the lungs, or remove infected tissue.

48
Q

Treatment-depends on type: IPA

A

Treated in hospital with powerful antifungal medications given by a drip into a vein. Around half of those with the condition die from it.