Pulmonary Eosinophilia Clinical Presentation
- Author: Jussi J Saukkonen, MD; Chief Editor: Zab Mosenifar, MD, FACP, FCCP more...
Methodical history taking, to exclude infections, foods, medications, or other precipitants, is important before labeling a pulmonary eosinophilic syndrome as intrinsic or idiopathic. The duration of symptoms and the presence of concomitant medical illnesses, such as collagen vascular disease, may be relevant.
- Query patients about the usage of all medications, including dietary supplements, and illicit drugs.
- Loeffler syndrome is precipitated by food, medications, or infections. It is self-limited (usually < 1 mo duration). Symptoms are mild, and the syndrome is characterized by blood eosinophilia and fleeting pulmonary infiltrates, with or without dyspnea.
- AEP: An acute onset of rapidly progressing dyspnea, often accompanied by abdominal complaints and myalgias, usually occurs within 1 week of presentation. Commonly, recent antecedent outdoor activity with considerable dust exposure has occurred. Marked acute hypoxemia, often progressing to respiratory distress, is typical. AEP is distinguished from CEP by its rapid progression, the presence of fever and severe hypoxemia, and no associated history of hypersensitivity to drugs.
- Obtaining a careful travel history is important for assessing the risk of fungal or parasitic infection. Travel to or from areas endemic for parasites (eg, Asia, Africa, Latin America, South America, southeast region of the United States) is of particular relevance to parasitic infection. Parasitic infections tend to cause fever, weight loss, fatigue, dyspnea, dry cough, wheezing, chest discomfort, and, occasionally, hemoptysis. Relevant historical elements for parasitic infections are provided below.
- Strongyloidiasis: Patients may report skin contact with sand or soil, abdominal pain or distension, and/or diarrhea, with or without immunocompromise. Marked wheezing and/or respiratory distress may occur.
- Ascariasis: Mild pulmonary symptoms are accompanied by pruritic dermatitis.
- Schistosomiasis: Patients may report contact with contaminated water and the presence of skin lesions. Symptoms of early infection are mild, but the manifestations of chronic infection include chronic dyspnea. Other symptoms are bladder and gastrointestinal dysfunction, cirrhosis, and, commonly, pulmonary hypertension.
- Clonorchis sinensis infection: Patients may relate a history of ingestion of inadequately cooked or pickled fish, abdominal pain, nausea, vomiting, and/or diarrhea.
- Paragonimiasis: Ingestion of inadequately cooked or pickled crustaceans, abdominal pain, nausea, vomiting, diarrhea, testicular pain, and/or CNS manifestations are reported findings. Patients may develop significant hemoptysis or extensive infiltration.
- Toxocariasis: Findings include skin or oral contact with soil contaminated by canine feces, contact with puppies, and/or seizures. This condition can lead to significant wheezing and, occasionally, respiratory distress. Patients with toxocariasis may also be asymptomatic.
- Fungal infections associated with pulmonary infiltrates and eosinophilia include Aspergillus infections, Coccidioides immitis infections, and other less common infections.
- Aspergillus infections: Although Aspergillus species are ubiquitous, ask about contact with soil or contaminated water sources.
- ABPA: Although technically not an infection because it is the host response to colonization by Aspergillus that is etiologic, it is considered here. Wheezing may be severe, and patients eventually develop prominent central bronchiectasis. The mildest form of ABPA is serologically positive (ABPA-S), the moderate form has central bronchiectasis (ABPA-CB), and the severe form includes both central bronchiectasis and other radiologic features (ABPA-CB-ORF). Early treatment has been suggested to prevent progression to more severe parenchymal disease.
- C immitis infection: Inquire about recent travel to the southwestern United States.
- The clinical course of coccidioidomycosis is highly variable, with more than 60% of patients being asymptomatic, while most of the remainder have mild symptoms.
- For intrinsic syndromes, seek the historical elements described below.
- CEP: Gradual onset of cough, fever, dyspnea, constitutional symptoms, and weight loss occurs. Wheezing, night sweats, chest pain, and, occasionally, hemoptysis may be reported. Respiratory failure is occasionally reported. Half the patients with CEP have a history of asthma.
- IHES: Patients may complain of constitutional symptoms, dyspnea, cough, wheezing or angioedema (occasionally), and symptoms related to multiple affected organs, particularly those in the cardiovascular, gastrointestinal, and musculoskeletal systems. Symptoms related to arterial and venous thromboembolic disease may be present (eg, pulmonary emboli, vascular insufficiency, cerebrovascular accident).
- CSS: Patients often have antecedent rhinitis, sinusitis, and nasal polyps, followed by the development of asthma symptoms. Symptoms related to vasculitis occur years later and include mononeuritis multiplex, abdominal pain, gastrointestinal bleeding, symptoms of heart failure, arthralgias, myalgias, urticaria, purpura, and nodular skin lesions.
- EG: Approximately one fourth of patients are asymptomatic. Most have a cough, dyspnea, fever, and chest discomfort. Wheezing may be reported. Patients may develop symptoms related to the pneumothorax, bony lesions, and diabetes insipidus. Cigarette smoking is nearly universal in these patients and is considered etiologic. The course of EG is highly variable. Patients at age extremes, those with multiorgan or skin involvement, and those with pneumothoraces tend to have a poor prognosis.
A complete physical examination of these patients is necessary. For this heterogeneous group of diseases, clues to establishing a diagnosis are found in virtually every portion of the examination.
- Skin examination
- A pruritic rash, which may be raised or serpiginous, is often seen.
- Medication-related syndromes may result in skin manifestations.
- Parasitic infection, commonly with Strongyloides, Ascaris, Toxocara, Ancylostoma, Necator, and Trichinella species, may cause skin symptoms.
- Disseminated coccidioidomycosis is related to patients' skin symptoms.
- A rash associated with IHES may be due to skin infiltration by eosinophils. Splinter hemorrhages and evidence of vascular occlusion may be seen.
- Head, eyes, ears, nose, and throat examination
- Evidence of rhinitis/sinusitis may be observed in persons with CSS and CEP.
- Vascular occlusion may be observed during the eye examinations of patients with IHES.
- Proptosis may be seen in patients with CSS.
- Chest examination
- All the syndromes discussed can cause rales and wheezing.
- Physical signs of cardiac decompensation (eg, valvular insufficiency, S3, rales, jugular venous distension [JVD], peripheral edema) may be present in patients with IHES and CSS.
- Patients with chronic schistosomiasis may present with signs of pulmonary hypertension (eg, loud P2, JVD, peripheral edema, right-sided S3).
- Abdominal examination
- Patients with chronic schistosomiasis may present with signs of cirrhosis (eg, distended abdomen, shifting dullness, peripheral edema, telangiectasias, icterus).
- Nonspecific abdominal tenderness is common in patients with parasitic diseases and intrinsic diseases.
- Neurologic examination
- Neuropathy may be observed in patients with IHES and CSS.
- Evidence of CNS deficits due to cerebrovascular accident may be observed in patients with IHES.
See the list below:
- Extrinsic syndromes and the eosinophilic immune response can be triggered by inhaled or ingested substances, including medications, drugs (eg, cocaine), food (eg, contaminated cooking oil), dietary supplements (eg, L-tryptophan), and infections (eg, parasites, fungi, mycobacteria).
- Medications that have been implicated include the following:
- Antibiotics (among the most common offending agents)
- Nonsteroidal anti-inflammatory drugs (among the most common offending agents)
- Leukotriene inhibitors
- Parasitic infections due to nematodes, filariae, and helminths may cause pulmonary infiltrates and eosinophilia. Such infections include strongyloidiasis, ascariasis, paragonimiasis, schistosomiasis, dirofilariasis, ancylostomiasis, trichomoniasis, clonorchiasis, and visceral larva migrans.
- Fungal processes, such as ABPA and coccidioidomycosis, may also cause pulmonary eosinophilia. Bronchocentric granulomatosis is most commonly related to Aspergillus infection.
- Other infections may include tuberculosis and Pneumocystis carinii pneumonia.
- Medications that have been implicated include the following:
- Intrinsic syndromes (ie, CEP, IHES, CSS, EG) are idiopathic.
- Asthma can cause pulmonary eosinophilia.
- Occasionally, eosinophilia and pulmonary infiltrates have been associated with AIDS, bronchiolitis obliterans organizing pneumonia (BOOP), hypersensitivity pneumonitis, idiopathic pulmonary fibrosis, sarcoidosis, Hodgkin disease, rheumatoid lung disease, and other collagen vascular diseases.
Sharma P, Sharma A, Vishwakarma AL, Agnihotri PK, Sharma S, Srivastava M. Host lung immunity is severely compromised during tropical pulmonary eosinophilia: role of lung eosinophils and macrophages. J Leukoc Biol. 2015 Oct 21. [Medline].
Bafadhel M, Saha S, Siva R, et al. Sputum IL-5 concentration is associated with a sputum eosinophilia and attenuated by corticosteroid therapy in COPD. Respiration. 2009. 78(3):256-62. [Medline]. [Full Text].
Gonlugur U, Gonlugur TE. Eosinophilic bronchitis without asthma. Int Arch Allergy Immunol. 2008. 147(1):1-5. [Medline].
Kawabata Y, Takemura T, Hebisawa A, et al. Eosinophilia in bronchoalveolar lavage fluid and architectural destruction are features of desquamative interstitial pneumonia. Histopathology. 2008 Jan. 52(2):194-202. [Medline].
Lee JH, Park HK, Heo J, et al. Drug Rash with Eosinophilia and Systemic Symptoms (DRESS) syndrome induced by celecoxib and anti-tuberculosis drugs. J Korean Med Sci. 2008 Jun. 23(3):521-5. [Medline]. [Full Text].
Vijayan VK. Tropical pulmonary eosinophilia: pathogenesis, diagnosis and management. Curr Opin Pulm Med. 2007 Sep. 13(5):428-33. [Medline].
Swartz J, Stoller JK. Acute eosinophilic pneumonia complicating Coccidioides immitis pneumonia: a case report and literature review. Respiration. 2009. 77(1):102-6. [Medline].
Uchiyama H, Suda T, Nakamura Y, et al. Alterations in smoking habits are associated with acute eosinophilic pneumonia. Chest. 2008 May. 133(5):1174-80. [Medline].
Yoshimi M, Nannya Y, Watanabe T, et al. Acute eosinophilic pneumonia is a non-infectious lung complication after allogeneic hematopoietic stem cell transplantation. Int J Hematol. 2009 Mar. 89(2):244-8. [Medline].
Cottin V, Frognier R, Monnot H, Levy A, DeVuyst P, Cordier JF. Chronic eosinophilic pneumonia after radiation therapy for breast cancer. Eur Respir J. 2004 Jan. 23(1):9-13. [Medline].
Hartl D, Latzin P, Zissel G, Krane M, Krauss-Etschmann S, Griese M. Chemokines indicate allergic bronchopulmonary aspergillosis in patients with cystic fibrosis. Am J Respir Crit Care Med. 2006 Jun 15. 173(12):1370-6. [Medline].
Saito H, Tsurikisawa N, Tsuburai T, Akiyama K. Involvement of regulatory T cells in the pathogenesis of Churg-Strauss syndrome. Int Arch Allergy Immunol. 2008. 146 Suppl 1:73-6. [Medline].
Wechsler ME, Wong DA, Miller MK, Lawrence-Miyasaki L. Churg-strauss syndrome in patients treated with omalizumab. Chest. 2009 Aug. 136(2):507-18. [Medline].
Kumar R. Mild, moderate, and severe forms of allergic bronchopulmonary aspergillosis: a clinical and serologic evaluation. Chest. 2003 Sep. 124(3):890-2. [Medline].
Kaliterna DM, Perkovic D, Radic M. Churg-Strauss syndrome associated with montelukast therapy. J Asthma. 2009 Aug. 46(6):604-5. [Medline].
de Gorgolas M, Casado V, Renedo G, Alen JF, Fernandez Guerrero ML. Nodular lung schistosomiais lesions after chemotherapy for dysgerminoma. Am J Trop Med Hyg. 2009 Sep. 81(3):424-7. [Medline].
Velthove KJ, Bracke M, Souverein PC, et al. Identification of exacerbations in obstructive lung disease through biomarkers. Biomarkers. 2009 Sep 7. [Medline].
Hillas G, Loukides S, Kostikas K, Bakakos P. Biomarkers Obtained by Non-Invasive Methods in Patients with COPD: Where do we Stand, what do we Expect?. Curr Med Chem. 2009. 16(22):2824-38. [Medline].
Agarwal R, Gupta D, Aggarwal AN, Saxena AK, Chakrabarti A, Jindal SK. Clinical significance of hyperattenuating mucoid impaction in allergic bronchopulmonary aspergillosis: an analysis of 155 patients. Chest. 2007 Oct. 132(4):1183-90. [Medline].
Chung SY, Lee JH, Kim TH, et al. F-18 FDG PET scan findings in patients with Loeffler's syndrome. Clin Nucl Med. 2009 Sep. 34(9):570-5. [Medline].
Chu E, Whitlock WL, Dietrich RA. Pulmonary hyperinfection syndrome with Strongyloides stercoralis. Chest. 1990 Jun. 97(6):1475-7. [Medline].
Tsurikisawa N, Taniguchi M, Saito H, et al. Treatment of Churg-Strauss syndrome with high-dose intravenous immunoglobulin. Ann Allergy Asthma Immunol. 2004 Jan. 92(1):80-7. [Medline].
Hellmich B, Gross WL. Recent progress in the pharmacotherapy of Churg-Strauss syndrome. Expert Opin Pharmacother. 2004 Jan. 5(1):25-35. [Medline].
[Guideline] Dicpinigaitis PV. Chronic cough due to asthma: ACCP evidence-based clinical practice guidelines. Chest. 2006 Jan. 129(1 Suppl):75S-79S. [Medline].
[Guideline] Tarlo SM. Cough: occupational and environmental considerations: ACCP evidence-based clinical practice guidelines. Chest. 2006 Jan. 129(1 Suppl):186S-196S. [Medline].
Wark P. Pathogenesis of allergic bronchopulmonary aspergillosis and an evidence-based review of azoles in treatment. Respir Med. 2004 Oct. 98(10):915-23. [Medline].
Allen JN, Davis WB. Eosinophilic lung diseases. Am J Respir Crit Care Med. 1994 Nov. 150(5 Pt 1):1423-38. [Medline].
Allen JN, Pacht ER, Gadek JE, Davis WB. Acute eosinophilic pneumonia as a reversible cause of noninfectious respiratory failure. N Engl J Med. 1989 Aug 31. 321(9):569-74. [Medline].
Barrett-Connor E. Parasitic pulmonary disease. Am Rev Respir Dis. 1982 Sep. 126(3):558-63. [Medline].
Cordier JF. Eosinophilic pneumonias. Schwarz MI, King TE, eds. Interstitial Lung Disease. Hamilton, Ontario: BC Decker; 1998. 559-95.
Davis WB, Fells GA, Sun XH, Gadek JE, Venet A, Crystal RG. Eosinophil-mediated injury to lung parenchymal cells and interstitial matrix. A possible role for eosinophils in chronic inflammatory disorders of the lower respiratory tract. J Clin Invest. 1984 Jul. 74(1):269-78. [Medline]. [Full Text].
Fauci AS, Harley JB, Roberts WC, Ferrans VJ, Gralnick HR, Bjornson BH. NIH conference. The idiopathic hypereosinophilic syndrome. Clinical, pathophysiologic, and therapeutic considerations. Ann Intern Med. 1982 Jul. 97(1):78-92. [Medline].
Jederlinic PJ, Sicilian L, Gaensler EA. Chronic eosinophilic pneumonia. A report of 19 cases and a review of the literature. Medicine (Baltimore). 1988 May. 67(3):154-62. [Medline].
Lanham JG, Elkon KB, Pusey CD, Hughes GR. Systemic vasculitis with asthma and eosinophilia: a clinical approach to the Churg-Strauss syndrome. Medicine (Baltimore). 1984 Mar. 63(2):65-81. [Medline].
Naughton M, Fahy J, FitzGerald MX. Chronic eosinophilic pneumonia. A long-term follow-up of 12 patients. Chest. 1993 Jan. 103(1):162-5. [Medline].
Ottesen EA, Nutman TB. Tropical pulmonary eosinophilia. Annu Rev Med. 1992. 43:417-24. [Medline].
Peros-Golubicic T, Smojver-Jezek S. Hypereosinophilic syndrome: diagnosis and treatment. Curr Opin Pulm Med. 2007 Sep. 13(5):422-7. [Medline].
Pinkston P, Vijayan VK, Nutman TB, et al. Acute tropical pulmonary eosinophilia. Characterization of the lower respiratory tract inflammation and its response to therapy. J Clin Invest. 1987 Jul. 80(1):216-25. [Medline]. [Full Text].
Powers MA, Askin FB, Cresson DH. Pulmonary eosinophilic granuloma. 25-year follow-up. Am Rev Respir Dis. 1984 Mar. 129(3):503-7. [Medline].
Slavin RG, Hutcheson PS, Chauhan B, Bellone CJ. An overview of allergic bronchopulmonary aspergillosis with some new insights. Allergy Asthma Proc. 2004 Nov-Dec. 25(6):395-9. [Medline].
Sterk PJ, Hiemstra PS. Eosinophil progenitors in sputum: throwing out the baby with the bath water?. Am J Respir Crit Care Med. 2004 Mar 1. 169(5):549-50. [Medline].
Tillie-Leblond I, Tonnel AB. Allergic bronchopulmonary aspergillosis. Allergy. 2005 Aug. 60(8):1004-13. [Medline].
Wardlaw A, Geddes DM. Allergic bronchopulmonary aspergillosis: a review. J R Soc Med. 1992 Dec. 85(12):747-51. [Medline].
Weller PF. The immunobiology of eosinophils. N Engl J Med. 1991 Apr 18. 324(16):1110-8. [Medline].
Woolnough K, Wardlaw AJ. Eosinophilia in Pulmonary Disorders. Immunol Allergy Clin North Am. 2015 Aug. 35 (3):477-92. [Medline].