Fungal lung diseases Occupational lung diseases Edit Csada, MD 19.11.2014.

Fungal lung diseasesOccupational lung diseases

Edit Csada, MD

19.11.2014.

PATHOGEN FUNGIFacultative pathogens

 Saprophyte Aspergillus fumigatus

Aspergillus flavus

Cryptococcus neoformans

Mucoraceae

Parasite Candida albicans

Candida tropicalis

Obligate pathogens Histoplasma capsulatum

Coccidioides immitis

Blastomyces dermatitidis

Sporothrix shenckii

RISK FACTORS

Immuncompromised state, treatment

Cytostatic treatment

Antibiotic and steroid treatment

Leukemy

Neutropenic patients

Malignancies

Diabetes mellitus

AIDS

After intensive therapy

After transplantation

PATHOLOGICAL FINDINGS

Epitheloid hyperplasia

Histocyte granulomas

Thrombotic arteriitis

Caseation granuloma

Fibrosis

Calcification

DIAGNOSTIC METHODSMicroscopic examination

native smeardifferent stainings

CultureSpecial culture media

Histology+ culture

Skin testSerology

Differential diagnosistumortuberculosischr pneumonia

THERAPYMedical treatment

Polyens Amphotericin B (Fungisone)

Nystatin

Pimafucin

5 fluorocytosin Ancotil

Azoles Ketoconazole (Nizoral)

Clotrimazole (Canesten)

Caspofungin (cancidas)

Fluconazole (Diflucan)

Itraconazole (Orungal)

Voriconazole (Vfend) (2. gen.)

Surgery

CLINICAL MANIFESTATION OF ASPERGILLOSIS

Allergic aspergillosisExtrinsic allergic alveolitis

hypersensitivity pneumonitisAllergic bronchopulmonary aspergillosis

AspergillomasInvasive aspergillosisRare manifestations

Aspergillus endocarditisAspergillus pneumoniaEndophthalmitis

ALLERGIC BRONCHOPULMONARY ASPERGILLOSIS

Type I immediate hypersensitivity reactionType III antigen, antibody, immune komplex reactionDiagnosis

Bronchial obstructionFeverEosinophyliaSkin testIgG se precipitating antibody Total, specific IgE

X-ray Small, fleeting inflitratesHilar, paratracheal adenopathy

Chronic consolidationAlveolitis – fibrosisBronchiectasis

TherapyChromoglycateCorticosteroid

ASPERGILLOMA

Saprophytic colonisation of fungi in pulmonary cavities

Manifestation No symptoms Haemoptysis Fever Cachexia

Chraracteristic x-ray picture!Therapy: surgery

INVASIVE ASPERGILLOSIS

Immuncompromised host!Necrotising pneumoniaEmpyemaPulm., extrapulm. Dissemination

Symptoms: fever, pleural pain, haemotysisTherapy: Amphotericin B

or voriconazole

itraconazole, caspofungin

CANDIDIASISNormal inhabitants of mucocutaneous body surfaces.

80% of all systemic fungal infection

Manifestation

Disease of skin and mucosa

Gynecological disease

Oesophagitis

In the lung: Bronchitis

Pneumonia

Pleurisy

Therapy: Amphotericin B, caspofungin, fluconazole, itraconazole, voriconazole

CRYPTOCOCCOSISIt is the 4. Most common cause of opportunistic infections in AIDS patients in the US.

Manifestations:

asymptomatic colonisation

ext. All. Alveolitis

primary complex

toruloma

Diagnosis: Masson-Fontana staining

Complication: meningoencephalitis

Therapy: spontaneous healing, amphotericin B, fluconazole, flucytosine

HISTOPLASMOSISIt is the most common systemic mycosis in the USA.

Manifestation

Subclinical

Acute form: Influenzalike disease

X-ray: small scattered, patchy infiltrates

calcification

Progressive, disseminated form

Rare (AIDS)

Chr. pulmonary form

(COPD)

Segmental, interstitial pneumonitis

Chr cavitary disease

Diagnosis: Wright’s or Giemsa staining

Prognosis: good

Therapy: itraconazole, amphotericin B

COCCIDIOIDOMYCOSISAcute, benign disease

Primary infection: infuenzalike symptoms

Radiological findings:

Segmental pneumonia

Minimal infiltrates

Adenopathy, pleural effusion

Nodular lesions, cavities

Prognosis is good without any therapy.

Diagnosis: eosinophilia, IgGProgressive, extrapum. manifestation

COCCIDIOIDOMYCOSIS• Risk factors for dissemination of Coccidioides Immitis infection

• Older age• Males• Non-caucasians, Filipinos• Immunsuppression• Gravidity

• Therapy• Azoles• Fluconazole > Itraconazole• Ketoconazole: less effective

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Occupational lung diseases

Pneumoconiosis

Hypersensitivity pneumonitis

Obstructive airway diseases

Toxic damages

Malignant lung diseases

Pleural diseases

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Common causes of occupational asthmaAgents

Isocyanates

Flour

Epoxy resins

Animals (rats, mice)

Wood dusts

Azodicarbonamide

Persulphate salts

Latex

Drugs

Grain dust

Occupational exposure

Spray paints, varnishes,adhesives, polyurethanefoam manufacture

Bakers

Hardening agents,adhesives

Laboratory workers

Sawmill workers, joiners

Polyvinyl plasticsmanufacture

Hairdressers

Healthcare workers

Pharmaceutical industry

Farmers, millers, bakers

Occupational asthma• Diagnosis:

– Asthma diagnosis– Causative connection between asthma and working place

• Clinical manifestations– Immediate asthmatic response– Delayed asthmatic response– Combined response

• Therapy:– Avoidance of exposition– Protective devices– Asthma treatment

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PNEUMOCONIOSIS

Etiologic agents: inhalation of inorganic dusts

metal dusts

free silica

coal dusts

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SILICOSIS

The base of disease is the progressive concentric fibrosis with hyalinisation in the centre.

Free silica: mining

stone cutting

road and building construction

blasting

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DETERMINING FACTORS IN DEVELOPMENT OF SILICOSIS

Silicic acid content

Content of dusts in the place of work

(200 000/m3)

Size of dust (<2 micron)

Time of exposure

Individual inclination (smoking)

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SILICOSISSymptoms: no symptoms

dyspnoehypoxaemia, hypercapnia=>ventilatory failure=>cor pulmonale

X-ray: nodular disseminationsilicomas (=>emphysematic bullae)hilar adenopathycalcification, egg shell pattern

Complications: chr. bronchitisemphysemaptx

Tb is more frequentCaplan’s syndromaTherapy: symptomaticProphylaxis!

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Silicosis

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ASBESTOSIS

• Hydrosilicate – fibre, thread

• Pulmonal clearence depends on the ratio of length and diameter of fibers

• 50-100 asbest particula/cm3 → mesothelioma

• Basal and subpleural fibrosis

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HYPERSENSITIVE PNEUMONITIS(Extrinic allergic alveolitis)It is an immunologically induced inflammation of lung

parenchyma involving alveolar walls and terminal airways secondary to repeated inhalation of a variety of organic dusts and other agents by susceptible host.

Manifestations:Farmer’s lung (1932) – thermophylic actinomycetesBird fancier’s breeder’s or handler’s lung

Miller’s lungBagassosisByssinosis

Air conditioner’s lungCoffee worker’s lung

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HYPERSENSITIVE PNEUMONITIS

Clinical forms:

Acute: (type III. reaction) cough, fever, chills, malaise, dyspnoe may occur 6-8 hours after exposure and usually clear within few days

Subacute: (type IV reaction) symptoms appear over a period of week( cough, dyspnoe, cyanosis). Symptoms disappear within weeks, or months, if causative agent is no longer inhaled.

Chronic: (type IV reaction) gradually progressive intersistial disease associated with cough, exertional dyspnoe without a prior history of acute or subacute disease.

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HYPERSENSITIVE PNEUMONITISDiagnosis:

anamnesisx-ray: normal

poorly defined patchy or diffuse infiltrates reticulonodular lesions

lung function tests:impaired diffusing capacity, decreased comliance exercise induced hypoxaemia

Se precipitins against suspected antigensBAL: acute : neutrophyls, monocytes(5%)

chr: lymphocytes(60-70%)Lung biopsy: intersitial alveolar infiltrates

bronchiolitisTherapy:

avoidance of antigenscorticosteroids

40Thank you for your attention!