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Fungal infections Flashcards

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1
Q

what does dimorphic mean?

A

Has active and passive form

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2
Q

What is the active form of candida?

A

Hyphal form which is the infective form

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3
Q

what 3 factors determine whether clinical evidence of candida infection exists?

A
  1. Immune status of host
  2. oral environment (like wearing a denture)
  3. stain of C.albicans
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4
Q

Name immunocompromising infections

A

Diabetes, alcoholism, bone marrow pathology, chemotherapy, malnutrition, HIV infection

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5
Q

Give the pathogenesis of candida albicans

A

C.albicans is commensal in the oral cavity. Local or systemic factors predispose to the fungus becoming pathogenic (hyphal form present) and locally invasive. Dissemination occurs in severe immunocomp patients. NB host defence is CD4 T-lymphocyte which gives immunity.

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6
Q

Give the clinical variants of candida albicans under Acute and Chronic infections

A

Acute: 1. pseudomembranous

  1. erythematous (atrophic) candida
    chronic:
  2. chronic pseudomembranous (HIV) candida
  3. chronic atrophic (erythematous)- denture stomatitis, angular chellitis and median rhomboid glossitis
  4. hyperplastic
  5. mucocutaneous
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7
Q

pseudomembraneous candida explain the clinical picture

A

creamy white, removable plaques. Also get a burning sensation in the mouth. Foul taste present. Should not bleed after removal but erythematous candida area under sometimes. IF it bleeds when removing then there is another process such as lichen planus present.

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8
Q

Why does antibiotics cause candida?

A

The elimination of competing bacteria allows candida to grow in the mouth or even impairment of the immune system occurs with corticosteroids.

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9
Q

Give the clinical picture of erythematous candida

A

Usually if immunocompromised or broad spectrum antibiotics are used. Erythema of oral mucosa and a burning sensation is felt. Patients complain as if the mouth has been burnt almost. On the tongue the burning sensation is accompanied by loss of filiform papillae on dorsum of tongue. Therefore the tongue looks red and bald.

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10
Q

Denture stomatitis. Give the clinical picture

A

Red, asymptomatic palatal denture bearing mucosa. Asymptomatic and painless. Due to less saliva flow. Persistant infection causes papillary hyperplasia in palatal vault. Denture shows colonization by hyphae. Candida bound to the acrylic due to acrylic having porocity. Therefore hyphae seen on the denture and not keratinized mucosa.

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11
Q

Give the clinical picture of angular chelitis

A

Erythema, erosion and crusting at skin folds at commisures of the lips. Due to loss of vertical dimention of the dentures. This causes saliva to accumulate in skin folds and secondary infection by C.albicans to occur. 60% of the cases are due to combined C.albicans and S.aureus. 20% S.aureus alone and other 20% candida alone.

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12
Q

What treatment would you give for a patient with Angular chelitis?

A
  1. Check the vertical dimention and fix dentures (in test go more into what you’d do with dentures)
  2. Give clotrimazole as it is antibacterial and antifungal.
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13
Q

Cheilocandidiasis. GIve the clinical picture

A

Candida infection involving the perioral skin, usually due to actions of keeping the skin moist like licking lips, putting petroleum based salves on (vaseline) and thumb sucking. Creates a red area around the lips.

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14
Q

median rhomboid glossitis/central papillary glossitis. Give the clinical picture

A

red, atrophic area, asymptomatic.
Midline of posterior dorsum tongue.
occurs because congenital lack of langerhans cells in the posterior of tongue. Erythema is due to loss of papillae (filiform) in the area.
Lesion is symmetrical and surface range from smooth to lobulated.
Resolves with antifungals

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15
Q

Give the clinical picture of chronic multifocal candidasis

A

Addition to dorsal of the tongue there are other sites like the soft and hard palate and angles of the mouth affected.
Palatal lesion appears erythematous area, when”tongue is at rest and touching the palate it results in a “kissing lesion” because of intimate proximity of involved areas.
Also asymptomatic.

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16
Q

Chronic hyperplastic candiasis give the clinical picture.

A

Rough, non-removable white plaques on dorsum of dorsum tongue or buccal mucosa.
Mid aged men who smoke. Rough white plaques.
Cannot remove by scraping it.
Will dissapear with antifungals.
If it persists then likely leukoplakia with secondary candida infection. Wait 2 weeks then recall patient to see if the lesion is gone.

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17
Q

Give the clinical picture of mucocutaneous candida

A

Its a heterogenous group of syndromes.
Recurrent infections by candida in skin and nails.
NOT A SPECIFIC DISEASE
Oral lesions are thick, white plaques that dont rub off.
Patient must be checked for endocrine abnormalities and iron deficiency anaemia.
Endocrine abnormalities include hypothroidism, hypoparathyroidism, hypoadrenocorticism, diabetes mellitis. Often give patients systemic antifungals and disease dissapears.

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18
Q

Pseudomembranous candida:

  1. give the appearance of symptoms
  2. common sites
  3. associated factors
A
  1. Creamy white plaques which are removable, burning sensation and foul taste.
  2. buccal mucosa, tongue, palate
  3. antibiotic therapy and immunosupressed.
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19
Q

Erythematous candida:

  1. give the appearance of symptoms
  2. common sites
  3. associated factors
A
  1. Red macules and burning sensation
  2. posterior hard palate, buccal mucosa, dorsal tongue.
  3. Antibioitics, xerostomia, immune supression, idiopathic
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20
Q

median rhomboid glossitis:

  1. give the appearance of symptoms
  2. common sites
  3. associated factors
Study These Flashcards
A
  1. red, atrophic mucosal areas, asymptomatic.
  2. midline posterior dorsal of tongue
  3. Idiopathic and immunosupression.
21
Q

chronic multifocal candida:

  1. give the appearance of symptoms
  2. common sites
  3. associated factors
Study These Flashcards
A
  1. red areas, removable white plaques, burning sensation, asymptomatic
  2. post palate, posterior dorsal tongue, angles mouth.
  3. immunesupressed and idiopathic
22
Q

Angular chelitis:

  1. give the appearance of symptoms
  2. common sites
  3. associated factors
Study These Flashcards
A
  1. red, fissured lesions, irritated, raw feeling
  2. angles of mouth
  3. idiopathic, immunosupression, loss vertical dimention
23
Q

denture stomatitis:

  1. give the appearance of symptoms
  2. common sites
  3. associated factors
Study These Flashcards
A
  1. red and asymptomatic
  2. denture bearing areas
  3. not true infection, denture is positive on culture but the mucosa is not. Hyphae in the denture.
24
Q

Hyperplastic candida:

  1. give the appearance of symptoms
  2. common sites
  3. associated factors
Study These Flashcards
A
  1. White plaques not removable. asymptomatic
  2. anterior buccal mucosa most of time
  3. idiopathic, immunosupression
25
Mucocutaneous candida: 1. give the appearance of symptoms 2. common sites 3. associated factors
1. white plaques, some removable, red areas 2. tongue, buccal mucosa and palate. 3. Rare, inherited, sporadic idiopathic immune dysfunction.
26
endocrine-candida syndromes: 1. give the appearance of symptoms 2. common sites 3. associated factors
1. white plaques most which aren't removable. 2. tongue, buccal mucosa, palate 3. Rare, endocrine disorder develops after candida
27
How would you diagnose candida?
Smear biopsy (fungal elements are identified by histochemical stains) such as periodic acid schiff (PAS)= PURPLE and the grocott gomori methenamine silver stain (GMS)= black green colour Culture= sabourauds agar Incisional biopsy in chronic hyperplastic candida.
28
Aspergillosis how is it seen under histology?
Septate and branch at acute angles (think A- acute angles and aspergillosis)
29
Aetiology of aspergillus species?
A.fumigatus (90%) and A.flavis (10%)
30
pathogenesis of aspergillosis?
- Not part of normal human flora but can get easy from environment - infection can stay as localised sinus infection or invade the immunocompromised. Non-invasive: aspergilloma: fungi colonises paranasal sinuses causes low grade infection. The fungus sends out mass of fungal hyphae. Allergic disease: frequent IgG and IgE allergic reactions account for nr of sinus pathologies such as aspergilloma. Superficial disease: infection after tooth extraction or ERCt in mx especially post segment. Tissue damage predisposes the sinus to infection. then symptoms localise pain and tenderness and get nasal discharge. Can be seen external ear, skin and nails. Aspergilloma mass can undergo dystrophic calcification and form a antrolith. Invasive: Primarily in the immuocompressed. Its painful ulceration, diffuse grey swelling if not treated then vascular invasion occurs, then necrotising inflammation, infarction of tissues, enters sinuses, lungs, mastoids. Disseminated disease: occurs in VERY immunocomp pt. Primary site is the lungs (chest pain, cough, fever), possible spread to CNS, eyes, skin, bone.
31
Give the clinical features of aspergillosis:
- Fungi colonise the paranasal sinus called aspergilloma - This mass undergoes dystrophic calcification then forms an antrolith. - Invasive infections (immunocomp): oral lesions enter the marginal gingiva and sulcus causing painful uclers. If not treated then necrosis occurs seen as yellow/black ulcer. -ulcers common on soft palate, tongue, pharynx
32
How do you diagnose aspergillosis?
- Clinical and radiological. - histology uses PAS/GMS - Do a culture but need to give treatment immediately.
33
Give the treatment of localised Aspergillosis:
- aspergilloma: surgically debride - allergic disease: debridement and corticosteroids. - superficial disease: debride, remove sequestrated bone and give antifungals (vorconazole) NB important.
34
Give the treatment of invasive disease of aspergillosis:
- Agressive debridement of necrotic tissue - IV antifungals (amphoteracin B) for extended time - Monitor renal fx - address underlying immune supression.
35
Mucormycosis is also known as?
Zygomycosis or phycomycosis
36
How does mucormycosis present under histology?
Non septae branch at right angles
37
Give the aetiology of mucormycosis:
Fungal opportunistic infection with phylum zygomycota.
38
Give the pathogenesis of mucomycosis.
Opportunistic fungal infection which is uncommon. Found in soil and decaying organic material. Inhalation of spores or entry through damaged skin or mucosa. Mainly immunocomp pts. Infection is characterised by vascular invasion, necrotising inflammation, and infarction of tissue. Also often seen in insul-dependent diabetics who have uncontrolled diabetes and ketoacidosis which inhibits binding of iron to transferin. (therefore iron levels high in the blood). Patient who also take deferoxamine (iron chelating agent used to treat diseases such as thalassemia) also at risk of forming mucormycosis!
39
Give the clinical features of mucomycosis
Rhinocerebral form is most common, affects the nose, maxilary sinus and the mid face. Patients feel as if they have a nasal constriction, bloody nasal discharge, facial pain, headaches, face swelling, sometimes cellulitis, visual disturbances can also occur. Can even get cranial nerve involvement! Presents as facial paralysis. Also present with fever, orbital cellutitis after the blood vessels are invaded, thrombosis occurs, blockages, necrosis and large tissue defects. Orbital involvement leads to conjunctional oedema and erythema: loss of muscle function of eye then occurs which leads to proptosis. Intraoral: black necrotic areas common on palate. Extraoral: skin involved gives black necrotic skin due to vessel invasion and thrombosis. Eventually into cranial vault invasion occurs: blindness, lethargy, seizures and death. Main thing to know is that it spreads throughout the face and occludes blood vessels causes areas to necrose.
40
How do we diagnose mucomycosis?
Radiological: opacification of the sinuses. Patchy sinus wall also present. Difficult to distinguish from a malignancy. Usually do MRI. Diagnosis also based on histology so do a biopsy of it if you can.
41
Give the treatment of mucomycosis:
Need to diagnose fast and do surgical debridement of infected, necrotic tissue and give systemic antifungals (such as amphoteracin B) but amphoteracin B can cause renal failure so monitor this patient renally! Prognosis is still poor even if treatment is given. 40-50% of patients die. ALSO REMEMBER ALWAYS CORRECT UNDERLYING PROBLEM OF IMMUNITY OR GET NO MARKS.
42
Histoplasmosis aetiology?
Histoplasma capsulatum. Humid areas. Bird and bat excrement in soil great place for growth. In natural environment its a mould. At body temp its a yeast which is dimorphic. Spores inhaled and germinate in lungs.
43
Can histoplasmosis be deadly?
Yes, it disseminates in the immunocompromised! Person gets a fever, weight loss, splenomegaly, pulponary infiltrates. Oral lesions can occur caused from spread from lungs
44
Give the clinical presentation of histoplasmosis:
Acute pulmonary infection, chronic pulm infection, disseminated miltary disease. Most people have mild symptoms or none. Mild symptoms: flulike (fever), splenomegaly, Acute histoplasmosis: fever,headache, myaligia, non productive cough, calcification of lymph nodes similar to TB Chronic histoplasmosis: Affects lungs, immunocomp pts, similar to TB= weightloss fever, chest pain. Disseminated histoplasmosis: immunocomp pts, affects spleen, adrenal glands, liver, GIT, oral mucosa (can produce addisons diease)
45
Explain how the oral lesions of histoplasmosis look and occur
Occur with disseminated form of disease (so pt immuno comp). Common sites are tongue, palate, buccal mucosa. Some lesions appear erythematous or white with irregular surface. Chonric ulcers: solitary, painful, firm rolled margins NB look like malignancy but malignancy isn't usually painful!
46
How do we diagnose histoplasmosis?
Histopathological identification of orgasnism or culture.
47
Treatment of histoplasmosis?
Acute histoplasmosis: no specific treatment other than analgesics and anti-pyretics. Chronic: Needs treatment. Itraconazole for 3 months. Severe cases use IV ampohteracin B. Disseminated: Death in most patients if untreated. Ampohteracin B. Also treat the underlying immunosupression.
48
Give the principles of management for fungal diseases in general
1. Remove fungal component 2. Give antifungals 3. Address predisposing factors 4. prevent recurrences

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