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Dentistry Year 2 - Pathology > Fungal Infections > Flashcards

Fungal Infections Flashcards

1
Q

What are fungi?

A

They are eukaryotic (making it hard to differentiate between between human and fungal cells) and obtain nutrients from environment .

They are occur worldwide and may be environmental, commensal or pathogenic.

They can be divided into yeasts and moulds.

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2
Q

What are the characteristics of yeasts and moulds?

A

Yeasts:

  • unicellular
  • reproduce by budding
  • some may produce hyphae and pseudohyphae

Moulds:

  • multicellular
  • reproduce using specialised spore structures
  • produce hyphae
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3
Q

What are structures produced by yeasts?

A
  • yeasts reproduce via budding by making copies
  • pseudohyphae produced by bud elongation , can resemble a string of sausages
  • true hyphae produced by apical extension, have even and parallel sides
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4
Q

What do moulds produce/

A

True hyphae.
Mould forms a colony on solid media that is round, sub-surface growth occurs and special spore structures may be on the surface.

Moulds are multicellular so have filaments all over. Can see these coming through the agar.

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5
Q

Are any fungi commensals to humans?

A

Yeasts are but moulds are not.

Yeast examples are candida albicans in GI tract, other candida species in GI tract and malassezia in skin.

Too many candida species can lead to infection.

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6
Q

What are factors can can increase risk of candidiasis?

A

Age - very young = no immune system, older = declined immune system

Endocrine disorders - diabetes changing the body biochemistry

Defects in cell mediated immunity - no way to defend against fungal infection

Cancer - treatments take away the cell mediated immunity

Drug addiction - specifically to heroin use, candida was being injected with it

Drug therapy - antibiotics due to bacterial flora dying and allowing yeast flora to thrive, corticosteroids (e.g. inhalers) take away local immunity

Surgery - abdominal surgery, can get a leakage of the bacteria from the gut and can leak around the body

Intravenous catheters- candida can colonise a catheters and cause an infection through this.

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7
Q

What is candidiasis?

A

Candida species are commensal to GI tract, most infections arise from endogenous flora.
Commenest fungi found = candida albicans, C.glabrate, C.tropicalis, C. parapsolosis and C.krusei.

Occasionally the endogenous sources is implicated e.g. hospital outbreaks and the commnest cause of these is C.albicnas.

Latest nosocomial problem is candida auris. this colonises readily. persists in environment and is highly resistant to antifungals.

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8
Q

What can candidiasis cause in mouth?

A

Detachable plaques, AIDS present, angular chelitis.

Extra - can cause skin and nail infections. Linked to frequency of moisture in skin.
Obesity is a risk factor as more skin rolls can cause it.

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9
Q

Where is candidiasis likely to form in children?

A

During nappy rash.
Satellite lesions form.
Due to the presence of moisture in nappy.

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10
Q

What is chronic mucocutaneous candidiasis?

A

Presents in childhood or infancy.
Recurrent oral, skin and nail infection.
Skin lesions can form on face and scalp.
Linked to immunological deficiencies.

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11
Q

What is systemic candidiasis? Details

A

Predisposing factors include: age, antibiotic treatment, abdominal surgery, immune suppression, catheterisation, prolonged hospitilsation.

Affects blood, lungs, skin.

Endogenous source - results from predisposing factors

Exogenous source - outbreaks can occur in wards with severely debilitated hosts

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12
Q

What species of candida is most likely to cause infection?

A

Candida albicans

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13
Q

How can infection be detected in fungi?

A

Use a stain to pick up chitin in fungal cell walls.
Grow it to identify species.

If budding can be seen, its a candida infection.

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14
Q

List the 7 ways that candida albicans can cause infection?

A
  1. Ability to adapt to changes in environment e.g. pH, sites including mouth, GI, skin.
  2. Ability to adhere to different surfaces - have surface molecules that bind to fibrinogen, fibronectin, epithelial cells.
  3. Production of destructive enzymes - proteinase, phospholipase, extracellular matrix proteins
  4. Changes in cellular morphology e.g. yeast, hyphae, pseduohyphae
  5. Production of biofilms e.g. offers protection from environment, phagocytosis and antifungals.
  6. Evasion of host defence mechanisms e.g. block oxygen radical production and degradation of PMN, kill monocytes, may stimulate cytokine release, may activate complement caspase
  7. Toxin production
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15
Q

Explain the yeast called Crytococcosis

A
  • Chronic, subacute to acute pulmonary infection from inhalation of cryptococcus yeasts
  • On dissemination the yeast shows a predilection for the CNS and cryptococcal meningitis occurs
  • Systemic spread may result in skin lesions and infection of bone and internal organs
  • Worldwide yeast associated with bird droppings
  • Risk factors are aids and hiv
  • Crytococcus gattii and related species can also infection of mostly immune competents host. This species is associated with trees and soil
  • Virulence factors is capsule for protection and prevents phagocytosis
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16
Q

Mould infections:

Give 3 examples

A

No commensal mould in human body. Infections always exogenously.

  1. Dermatophytes (common, superficial, sources include human, animal and soil, healthy host)
  2. Aspergillosis (uncommon, systemic, environmental, immune compomsied host or predisposing factors underlie disease)
  3. Mucormycosis (rare, environmental, subcutaneous, systemic, route of entry determines disease type)
17
Q

What factors predispose to mould infections?

A
  • History of trauma to site of infection
  • Host immune status (can determine the extent of disease, duration, outcome)
  • Underlying disease (may influence susceptibility to certain types of infection)
  • Exposure to a source
  • Portal of entry
18
Q

Give details on a dematophyte mould infection

A
  • Dermatophytes are a family of fungi that use keratin as a substrate
  • Species can infect skin, nail, hair
  • Infections result from contact with a source
  • Affect healthy and immune compromise people
  • Commonest cause of human mould infection
  • Commonest cause of skin and nail infection
  • Species are linked to primary hosts - human, animals or soil

Risk factors:

  • Age (most infections before puberty, uncommon in adults)
  • Contact with infection (relevant history of exposure such as human, animal, soil)
  • Minor trauma to inoculate (scratching, hair dressing, barbers, sharing hates/towels)
  • Affects healthy hosts (not more common in immune compromised hosts, but infections may be more florid)
19
Q

What are the pathogenicity mechanisms for tinea capitis (dermatophyte scalp infection)?

A
  1. Adherence: adhesins, enzymes, fibrillar projections on fungal cell surface
  2. Invasion: phospholipase, subtilisins, mellatoproteinases. Complex process regulated by protein content and pH
  3. Utilise ketain - cornified layers of skin are rich in disulphide bridges. Dermatophytes reduce this bind and then cleave the protein.
  4. Manipulation of the immune response - cell wall suppress lymphoproliferative activity
  5. Adaptation on host - passed between humans causes a less reactive response
20
Q

Give details on the fungi we use for aspergillosis

Give info on the common species

A

Causes systemic disease following inhalation of spores. Type of disease is determined by host status. Commonest causes: Aspergillus fumigatus, A. flavus, A. nidulans, A. niger, A.terreus. All are referred to as species complex as each comprises closely related organisms that are only distinguished genetically.

 Allergic aspergillosis - temporary presence of aspergillus in respiratory tract, healthy host. Agricultural link, or exposure to large nos. spores
 Aspergilloma - colonisation of pre-existing cavities, fungal ball in lung, predisposing factors for lung cavitation but may otherwise be healthy
 Invasive aspergillosis - pulmonary focus, dissemination possible, immune compromised host
 Systemic aspergillosis - lungs, brain, other organs, immune compromised host

The primary infection is due to skin damage, secondary infection is due to disseminated disease.
Risk factors = trauma, immune compromised host.

21
Q

Give some details on Mucormycosis (a mould)

A

 Disease depends on host status, predisposing factors (eg medical history), and the portal of entry
 Rare
 Usually acute and rapidly progressing as Mucoraceous moulds are angioinvasive and infection progresses via blood vessels
 Rhinocerebral - inhalation, uncontrolled diabetes mellitus
 Pulmonary & disseminated - inhalation, immune compromised host
 Gastrointestinal – ingestion of contaminated food linked with malnutrition, dissemination of lung infection in immune compromised host
 Wounds and burns - traumatic inoculation, can be a healthy host

22
Q

Summarise host factors predisposing to infection

A

 Risk factors for candidiasis include: age, pregnancy, occlusion, antibiotic therapy, endocrine disorders, immune defects, immune suppression, Fe or Zn deficiency, catheterisation, abdominal surgery
 Infections of skin, nails, mucous membranes, and systemic infections occur according to underlying risk factors
 The host immune status is important for systemic manifestations of fungal infections, eg. aspergillosis
 Opportunity for infection - exposure and trauma are frequently required for mould infections

23
Q

Summarise fungal pathogenicity factors

A
  • Adherence to tissue
  • Ability to invade tissue - protease production, other enzymes, changes in morphology
  • Ability to spread in tissue - budding yeasts, hyphal production
  • Ability to form biofilms – on implants, catheters, in cavities which prevent phagocytosis and penetration of drugs
  • Ability to evade or modify the immune response - capsule production, cell wall constituents
  • Ability to disperse to other hosts – spores in the environment, infected tissue, contact

Dentistry Year 2 - Pathology (25 decks)

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