Fungal Infections Flashcards
Aspergillosis basic aetiology
Caused by Aspergillus Fumigatus
- not part of normal human flora
- Opportunistic fungal infection, spores released from farm animals, birds, soil and water.
Practically inhaled by humans and pathogenic species replicate at body temperature
it infects immunocompromised patients
what are the sub types of Aspergillosis ?
Aspergillosis is divided into 3 sub types
- Non-invasive infection ( immunocompetent )
- Invasive infection ( immunosuppressed )
- Disseminated ( severely immunosuppressed )
Describe the possible manifestations of non-invasive infection of aspergillosis
Aspergilloma - The fungi colonise paranasal sinuses - causes low-grade infection, form mass of fungal hyphae. it may calcify to form a anthrolith
Dystrophic calcification -> Anthrolith
Allergic Disease - Allergic fungal sinusitis
bronchopulmonary tract asthma
Superficial disease - Infection after tooth extraction ( port of entry ), through external ear canal
this leads to painful gingival ulcerations, can lead to extensive necrosis if left untreated
Invasive forms of aspergillosis present as…?
Generally the invasive of damaged tissue of immunocompetent host ( leukemia , pts on high doses of steroids )
Oral lesions
- enters through marginal gingiva and gingival sulcus
- Painful gingival ulcerations
- Ulcer edge - soft tissue swelling with grey hue —> progress to extensive necrosis with facial swelling
The oral ulcerations generally start on the gingival margin and spread to adjacent mucos with a dark purple to black colour.
The dark discolouration is due to the pathogenesis of this lesion where hyphae invade the blood vessels in the area and then proliferate to the point of occlusion, this cuts of blood supply to the area leading to necrosis.
Difference between non-invasive and invasive forms of Aspergillosis with regard to sinus involvement
Non-invasive - Fungae colonize the paranasal sinuses and causes low grade infection - and forms a mass of fungal hyphae
Invasive form invades the mucosa of the paranasal sinuses and causes tissue destruction
The clinical features of the disseminated form of Aspergillosis
Initial symptoms = Chest pain, fever and cough
Very poor prognosis
spreads via blood vessels and can affect multiple systemic organs
may disseminate to - CNS, eye, skin, liver, GIT, bone, thyroid
Diagnosis of Aspergillosis
Clinical
radiographic
Histological features
culture - PCR is faster
The invasive disease requires an incisional biopsy
Biopsys submitted in formalin to histopathology lab for quick ID or fresh to the microbiology lab for MC and S which may take longer but aids in the selection of the correct hyphae.
Treatment of aspergillosis
Localized Disease
Aspergilloma - Surgical debridement
Allergic Disease - Debridement and corticosteroids
Superficial Disease - Debridement, removal of sequestrated bone and antifungals ( voriconazole )
Invasive disease
Aggressive debridement of necrotic tissue
IV anti-fungals for extended period
Monitor renal function
Address underlying immune suppression
Management of Aspergillosis
Diagnosis will depend on clinical form
Appropriate referrals - Aspergilloma and allergic form to ENT
Disseminated form to GP
Treatment — >
Investigate and address underlying immunosuppression
Follow-up to evaluate healing, reconstructive surgery — after healing is completed
follow up after reconstructive surgery
Path of Mucormycosis
Opportunistic infection
Caused by mucormycotina
from soil and decaying organic materials
we are constantly expose but only those who have underlying predisposing factors acquire the disease
Inhalation of spores
entry through damaged skin/mucosa
- Vascular invasion
- Thrombosis
- Tissue Infarction
- Necrotising inflammation
REFERRAL NB - dude to systemic spread of hyphae
Predisposing factors Mucormycosis
Immunocompromised
- Bone marrow transplant recipients
- AIDs
- Systemic corticosteroid therapy
Uncontrolled Diabetes
- ketoacidosis
Patients taking deferoxamine
how can uncontrolled diabetes result in increased fungal growth?
Due to ketoacidosis ( too little insulin, shift in metabolic cycle to use fat-ketones as by product- which inhibt iron binding )
Inhibits iron binding to transferrin
Rise in serum iron levels
Enhances growth of fungus
why do patients taking deferoxamine have an increased risk of acquire mucormycosis?
Iron-chelating agent
It transports iron from blood across fungal wall whihc promotes fungal growth.
Clinical features of mucormycosis
The rhinocerebral form is the most common, intracranial extension is also seen.
large areas of necrosis
fever
cellulitis
it is associated with patients who have uncontrolled diabetes
Orbital involvement leads to conjunctival edam and erythema with loss of muscular function.
Brain abscess and cavernous sinus thrombosis may also occur, often then giving bilateral cranial nerve signs
Radiographic diagnosis of mucorycosis
Opacification of sinuses
Patchy effacement of sinus walls
MRI - to check extent of infection
