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Prevention and Treatment

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  stop exposure / acute disease usually self-limiting
  
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  dust control / protective masks / cleaning of wet ventilation systems
  
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  steroids may help in severe acute/subacute cases but have not been shown to alter eventual outcome in chronic disease / prednisone 60 mg/d for 1-2 wk then tapered over the next 2 wks to 20 mg/d, followed by weekly decrements of 2.5 mg until off / antibiotics only if superimposed infection
  
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  bronchodilators and antihistamines not shown to help
  

repeated inhalation of dusts from hay containing thermophilic actinomycetes / worse in rainy season / delayed type hypersensitivity

fever, chills, cough occurring within hours of massive exposure to moldy silage (e.g., when uncapping a silo) / (+) pulmonary infiltrates

Note: different from silo filler’s disease (toxic oxides of nitrogen given off by fresh silage)
Organic dust toxic syndrome (e.g., grain fever)

transient fever, muscle aches +/- respiratory symptoms / no sensitization after exposure / ?endotoxin

contaminated heating, cooling, and humidifying / ?endotoxin

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  eosinophilic pneumonias associated with bronchial asthma (more common)
  

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  extrinsic bronchial asthma with the PIE syndrome, often is allergic bronchopulmonary aspergillosis
  
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  intrinsic bronchial asthma with the PIE syndrome (chronic eosinophilic pneumonia), characteristic peripheral infiltrates on CXR
  
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  allergic granulomatosis (Churg-Strauss syndrome) or simple eosinophilic pneumonia (Löffler’s syndrome)
  

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  eosinophilic pneumonias NOT associated with asthma
  

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  Acute eosinophilic pneumonia, a distinct entity of unknown cause, results in acute fever, severe hypoxemia, diffuse pulmonary infiltrates, and > 25% eosinophils in bronchoalveolar lavage fluid; it resolves promptly and completely with corticosteroid therapy
  
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  eosinophilia-myalgia syndrome is associated with ingestion of large doses of contaminated L-tryptophan used as a dietary supplement. Pulmonary infiltrates occasionally occur along with the expected features of myalgia, muscle weakness, skin rash, and soft tissue induration resembling scleroderma
  
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  hypereosinophilic syndrome are persistent eosinophilia > 1500 eosinophils/mm³ for more than 6 mo, lack of evidence for other known causes of eosinophilia, and systemic involvement of the heart, liver, spleen, CNS, or lungs. The heart is commonly affected. Fever, weight loss, and anemia are common. Thromboembolic disease, arterial more commonly than venous, occurs often.
  

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  Löffler’s syndrome may include low-grade fever, minimal (if any) respiratory symptoms, and prompt recovery
  
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  other forms of the PIE syndrome may produce fever and symptoms of bronchial asthma, including cough, wheezing, and dyspnea at rest
  
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  chronic eosinophilic pneumonia is often progressive and life threatening (if not treated
  

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  Labs: marked blood eosinophilia (between 20-40% and higher) is usually striking
  
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  CXR: rapidly developing and disappearing infiltrates in various lobes (migratory infiltrates) / chronic EP described as “photographic negative” of pulmonary edema.
  

Note: hypersensitivity pneumonitis and Wegener’s are not commonly associated with eosinophilia

allergic reaction / not same as invasive aspergillosis (see below)

Causes: rarer organisms, such as Penicillium, Candida, Curvularia, or Helminthosporium sp, may cause identical syndromes more accurately termed allergic bronchopulmonary mycoses.

Mechanism: types I, III (and possibly type IV) hypersensitivity reactions

Pathology: alveoli full of eosinophils / granulomatous interstitial pneumonitis / proximal bronchiectasis develops in advanced cases / fibrosis can lead to severe, irreversible airway obstruction

Presentation: exacerbation of bronchial asthma, intermittent low-grade fever and systemic symptoms.

Radiology

CXR (serial) show migratory opacities/shadows and/or atelectasis

Chest CT may show bronchiectasis in proximal airways

Sputum same as typical asthma with Curschmann’s spirals (mucoid casts), Charcot-Leyden crystals (eosinophilic debris), mucus, and eosinophils but may also have A. fumigatus mycelia; sputum culture may or may not be positive

Labs: peripheral eosinophil count usually > 1000/µL and IgE and IgE to A. fumigatus may be very high

Diagnosis: extrinsic (atopic, allergic) asthma (usually long-standing), pulmonary infiltrates, sputum and blood eosinophilia, and hypersensitivity to Aspergillus or another relevant fungus as shown by a wheal and flare skin test, precipitating antibodies in the serum, and high levels of total and specific IgE. The presence of these features makes the diagnosis very likely / unlike hypersensitivity pneumonitis wherein PFT’s show restrictive rather than obstructive pattern and eosinophilia is rare
Bronchocentric granulomatis

Usually targets small airways sparing adjacent pulmonary vasculature; may result in association with allergic aspergillosis or other infections such as Tb, histoplasmosis, blastomycosis, mucormycosis

usually occurs as a serious opportunistic pneumonia in immunosuppressed patients / in old cavitary disease (e.g., TB) or, rarely, in rheumatoid spondylitis due to colonization within cystic airspaces of the upper lobes

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  antiasthmatic drugs (theophylline, sympathomimetics) usually successful in allowing expectoration of the mucus plugs and the Aspergillus with them
  
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  prednisone as for hypersensitivity pneumonitis (may require long-term treatment, to prevent progressive, irreversible disease / success for maintenance therapy with inhaled corticosteroids is not established
  
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  immunotherapy and fungicidal or fungistatic drugs are not recommended
  

population at highest risk for pneumonia

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  early (first 2 weeks): GNR (Enterobacteriaceae), pseudomonas, S. aureus, aspergillus, candida
  
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  middle (1 to 6 months): primary or reactivation of CMV (hard to distinguish from acute rejection; CMV may be cause of rejection and BOOP) / RSV causes post-transplant pneumonitis
  
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  late (> 6 months): Pneumocystis, nocardia, listeria, other fungi, intracellular pathogens / any transplant patient at risk for EBV-associated lymphomas
  

Neurology