ASPERGILLOSIS.pptx

ASPERGILLOSIS -DR NITIN WADHWANI

1. ASPERGILLOSIS BY-DR NITIN WADHWANI

2. ASPERGILLUS INFECTION INTRODUCTION: Aspergillus infections of the lung are caused by Aspergillus fumigatus which are ubiquitous fungi found throughout nature. Results in disease in susceptible hosts when inhaled. The pathogenesis of Aspergillus infection varies with quality and virulence of the inhaled organism and the status of the host defence mechanisms. Characterised by spectrum of pathology related to an immune response of individual to the organism.

3. ETIOLOGY:

4. IMMUNE SYSTEM MILD IMMUNOCOMPROMISED HYPERSENSITIVITY NORMAL SEVERELY IMMUNOCOMPROMISED ABPA MYCETOMA SEMIINVASIVE /CHRONIC NECROTIZING ASPERGILLOSIS INVASIVE PULMONARY ASPERGILLOSIS

5. MYCETOMA: Is non invasive colonization of preexisting cavity in immunologically normal pt with cavitatory disease Mycetoma is a ball of coalscent mycelial hhyphae that typically colonize pre- existing cavity. Clinical features : Cough and expectoration Hemoptysis -frequently seen in almost ½ of cases Bleeding is usually due to friction between fungal ball and hypervascular wall which releases endotoxins from fungus and causes type-3 reaction in cavity wall.

6. LOCATION : UPPER LOBES SUPERIOR SEGMENT OF LOWER LOBE

7. TB SARCOIDOSIS BRONCHIECTASIS LUNG ABSCESS NF-1 EMPHYSEMATOUS BULLA PREDISPOSED PT:

8. XRAY CT SCAN Round to oval mass of soft tissue density lying within preexisting cavity. Taken in supine and prone position Air crescent sign Mass within the cavity Decubitus xray – to demonstrate mobility of fungal ball Air crescent sign Thickening of cavity wall –s/o signs of early aspergillus infection Mobile intracavitatory mass is characteristic of aspergilloma. Irregular air spaces within Fungal strands bridging the fungus ball &cavity wall maybe seen. IMAGING FINDINGS:

9. D/D of fungal ball and air crescent sign : Infection Cavitating neoplasm Trauma Hydatid cyst Tuberculoma Bacterial lung abscess Bronchial adenoma Cystic hamartoma Pulmonary hematoma

10. Allergic aspergillosis is a result of hypersensitivity reaction that produce ABPA or less commonly extrinsic allergic pneumonitis or Loeffler syndrome. It is airway disease. Only seen in patients with asthma and cystic fibrosis. There is airway colonization -> complex hypersensitivity reaction (1 > III). ALLERGIC BRONCHOPULMONARY ASPERGILLOSIS: C/F: Cough Wheezing a/s allergic symptoms

11. Eosinophil derived inflammation (fleeting infiltration). Plugging of bronchial wall with mucus plugs (contain septate hyphae) Th2 mediated inflammation (IL-5, 4,13) of bronchial wall cough with sputum (hyphae) Longterm - Irreversible dilatation Bronchiectasis. Pathogenesis :

12. Bronchiectasis – more in upper lobe , central, proximal airways and is B/L Mucus plugging with hyphae can also lead to atelectatsis . Adherence of conidia to respiratory epithelial cells cellular dysfunction Initially cilial disruption The fungal colony grows,hyphae are produced invade between & through epithelialcells Leading to substantial tissue disruption Pathogenesis :

13. ABPA: CHRONIC ABPA: ACUTE ABPA: TYPE I REACTION :IMMEDIATE IgE MEDIATED TYPE III REACTION:DELAYED IMMUNE COMPLEX IgA MEDIATED

14. Pathology Allergic bronchopulmonary aspergillosis is the result of hypersensitivity towards  Aspergillus   spp ( esp   fumigatus ) . It grows within the lumen of the bronchi, without invasion .   The hypersensitivity initially causes bronchospasm and bronchial wall edema, which is IgE -mediated. Ultimately, there is bronchial wall damage with loss of muscle and bronchial wall cartilage resulting in  bronchiectasis  (typically  central bronchiectasis )  7 . Both types I and III  allergic reactions  have been implicated  4 .

15. XRAY CT SCAN Non segmental consolidation in upper lobe Bronchiectasis Lobar collapse Mucoid impaction Branching thick tubular opacity bronchial wall thickening: common Pul cavitation cavitation: 10% Hyperinflated lung fields Gloved finger sign Central bronchiectasis ACUTE ABPA :

16. Gloved finger sign :

17. CHRONIC ABPA : IMAGING FEATURES: Bronchiectasis : Bronchial wall thickening Tramline shawdows Ring formation Fibrosis: linear fibrotic band , can also cause traction bronchiectasis Loss of volume in upper lobe

18. A clinical staging system has been developed   : stage I : acute stage II : remission stage III : recurrent exacerbation stage IV : steroid-dependent asthma stage V : pulmonary fibrosis Major and minor criteria have also been established . major criteria clinical asthma  (approximately 90% of patient may have asthma ) radiographic features pulmonary opacities (transient or chronic) central  bronchiectasis immune system blood eosinophilia immediate skin reactivity to  Aspergillus  antigen (elevated IgG and/or IgE against  A. fumigatus ) increased serum IgE (>1000 IU/ml) minor criteria fungal elements in sputum expectoration of brown plugs/flecks delayed skin reactivity to fungal antigens

19. This form typically occurs in patients with a depressed immune system, but not as profoundly immunocompromised as bone marrow patients who more frequently develop  angioinvasive aspergillosis . Patients are typically middle-aged. Risk factors, therefore, include  1-3 : corticosteroids - most common systemic immunodepressant   3 diabetes mellitus alcoholism chronic liver disease malnutrition SEMI-INVASIVE(CHRONIC NECROTIZING ASPERGILLOSIS)

20. IMAGING FEATURES : AREA OF CONSOLIDATION IN UPPER LOBE PROGRESSES TO THICK WALLED CAVITY ADJACENT PLEURAL THICKENING .

21. CONFINED TO IMMUNOCOMPROMISED HOST. INVASIVE PULMONARY ASPERGILLOSIS: IMAGING FEATURES: MULTIPLE/ SINGLE ILLDEFINED OPACITIES DIFFUSE B/L CONSOLIDATION LARGE WEDGE SHAPED PLEURAL BASED LESION CAVITATION OF NODULE AIR CRESCENT SIGN

22. IMAGING FEATURES: CT SCAN: 1-3 CM NODULES SEGMENTAL CONSOLIDATION CT HALO SIGN : ggo around the nodules