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A YOUNG WOMAN WITH RESPIRATORY FAILURE AFTER A VISIT TO COMPOST STATION

Case Editor - Judd Flesch

Reviewed By Clinical Problems Assembly

Submitted by

Eugene Shostak, MD

Department of General Internal Medicine

Lahey Clinic Medical Center

Burlington, MA

Timothy Liesching, MD

Assistant Professor of Medicine, Tufts University School of Medicine

Department of Pulmonary and Critical Care Medicine

Lahey Clinic Medical Center

Burlington, MA

Kenneth Wener, MD

Assistant Professor of Medicine, Tufts University School of Medicine

Department of Infectious Diseases

Lahey Clinic Medical Center

Burlington, MA

Submit your comments to the author(s).

History

A 32 year-old woman with a medical history notable only for mild intermittent asthma presented to her primary care physician's office with a seven day history of fevers and dyspnea one week after heavy gardening and working in at local compost station. She complained of nocturnal sweats and non productive cough but denied wheezing and hemoptysis. The patient had already completed a 5 day course of azithromycin without improvement in symptoms. Prior to her acute illness she had been in good health. She was an avid marathon runner and exercised regularly. She resided in New England and worked as a district attorney. The patient denied any recent travels or any HIV or tuberculosis risk factors. She was a lifetime nonsmoker with no history of drug or alcohol abuse. She owned a pet dog for many years. Her parents and her 5 adult siblings were all healthy.

Physical Exam

The patient's vital signs were notable for oxygen saturation of 85% on room air, which increased to 93% with 2 liters of oxygen. Her temperature was 102.5ºF and respiratory rate was 24/minute. The patient appeared mildly short of breath but spoke in full sentences. Her oropharynx was clear and nasal passages were patent. There was no palpable lymphadenopathy. Auscultation of the lungs revealed diffuse bilateral crackles with no wheezing. Cardiac exam revealed a regular rhythm without murmurs. Abdomen was soft and non-tender with no organomegaly. There was no clubbing or edema of the extremities.

Lab

Laboratory data revealed white blood cell count of 6000/µL with 13% peripheral eosinophilia. Arterial blood gas was notable for partial pressure of oxygen of 70mm Hg on 3 liters of oxygen. Kidney and liver metabolic screening was unremarkable. Chest radiograph (Figure 1) showed diffuse bilateral reticular nodules. The finding was confirmed by a computed tomography of the thorax (Figure 2) which further characterized the bilateral reticular nodular densities as coexisting with a degree of groundglass opacification throughout all lobes but with a slight upper lobe predominance. There were also small bilateral pleural effusions.

 Figure 1

Figure 1: Chest radiograph demonstrating diffuse bilateral reticulonodular infiltrates.

Figure 2

Figure 2: Computed tomography demonstrating diffuse reticular-nodular densities and bilateral groundglass opacities.

Question 1

Which of the following is the most likely diagnosis in this patient?

References

  1. Hayakawa H, Sato A, Toyoshima M et al. A clinical study of idiopathic eosinophilic pneumonia. Chest 1994;105:1462.
  2. Badesch DB, King TE Jr, Schwarz MI. Acute eosinophilic pneumonia: a hypersensitivity phenomenon? Am Rev Respir Dis 1989;139:249.
  3. Khuroo MS. Ascariasis. Gastroenterol Clin North Am 1996;25:553.
  4. Wilson ME, Weller PF. Eosinophilia. In: Tropical Infectious Diseases: Principles, Pathogens and Practice. 2nd ed. Guerrant RL, Walker DH, Weller PF eds. Elsevier, Philadelphia, 2006. p. 1478.
  5. Guidelines for the clinical evaluation of hypersensitivity pneumonitis. Report of the Subcommittee on Hypersensitivity Pneumonitis. J Allergy Clin Immunol 1989;84:839.
  6. Richerson HB, Bernstein IL, Fink JN. Guidelines for the clinical evaluation of hypersensitivity pneumonitis. Report of the Subcommittee on Hypersensitivity Pneumonitis. J Allergy Clin Immunol 1989;84:839.
  7. Fenoglio CM, Reboux G, Sudre B. Diagnostic value of serum precipitins to mould antigens in active hypersensitivity pneumonitis. Eur Respir J 2007;29:706.
  8. Lalancette M, Carrier G, Laviolette M. Farmer's lung: Longterm outcome and lack of predictive value of bronchoalveolar lavage fibrosing factors. Am Rev Respir Dis 1993;148:216.
  9. Klech HH, Pohl WW. Use of bronchoalveolar lavage in interstitial lung disease. In: Pulmonary and Critical Care Medicine, Bone, RC, (Ed), Mosby, St. Louis, part M, chapter 2, 1997, p. 1.
  10. Gibson PG. Allergic bronchopulmonary aspergillosis. Semin Respir Crit Care Med. 2006;27:185.
  11. Azar AE, Ballas ZK. Evaluation of the adult with suspected immunodeficiency. Am J Med 2007;120:764.
  12. Denning DW, Lee JY, Hostetler JS, Pappas P, Kauffman CA, Dewsnup DH, Galgiani JN, Graybill JR, Sugar AM, Catanzaro A. NIAID Mycoses Study Group Multicenter Trial of Oral Itraconazole Therapy for Invasive Aspergillosis. Am J Med 1994;97:135.
  13. Bodey GP. 1992. Azole antifungal agents. Clin. Infect. Dis. 14(Suppl 1):S161.
  14. Denning DW, Hanson LH, Perlman AM, Stevens DA. In vitro susceptibility and synergy studies of Aspergillus species to conventional and new agents. Diagn. Microbiol. Infect. Dis 1992;15:21.
  15. St-Germain G, Dion C, Espinel-Ingroff A, Ratelle J, de Repentigny L. Ketoconazole and itraconazole susceptibility of Candida albicans isolates from patients infected with HIV. J. Antimicrob. Chemother. 1995;36:109.
  16. Como JA, Dismukes WE. Oral azole drugs as systemic antifungal therapy. N. Engl. J. Med. 1994;330:263.
  17. Winkelstein JA, Marino MC, Johnston RB Jr. Chronic granulomatous disease. Report on a national registry of 368 patients. Medicine (Baltimore) 2000;79:155.
  18. Jones LB, McGrogan P, Flood TJ, Gennery AR, Morton L, Thrasher A, Goldblatt D, Parker L, Cant AJ. Special article: chronic granulomatous disease in the United Kingdom and Ireland: a comprehensive national patient-based registry. Clin Exp Immunol 2008;152:211.
  19. Martire B, Rondelli R, Soresina A. Clinical features, long-term follow-up and outcome of a large cohort of patients with Chronic Granulomatous Disease: an Italian multicenter study. Clin Immunol 2008;126:155.
  20. Segal BH, Leto TL, Gallin JI. Genetic, biochemical, and clinical features of chronic granulomatous disease. Medicine (Baltimore) 2000; 79:170.
  21. Nauseef WM. Assembly of the phagocyte NADPH oxidase. Histochem Cell Biol. 2004;122:277.
  22. Roos D. X-CGDbase: a database of X-CGD-causing mutations. Immunol Today 1996;17:517.
  23. Cross A, Curnutte J, Heyworth P. Hematologically Important Mutations: The Autosomal Recessive Forms of Chronic Granulomatous Disease. Blood Cells, Molecules, and Diseases 1996;22:268.
  24. Repine JE, Clawson CC, White JG, Holmes B. Spectrum of function of neutrophils from carriers of sex-linked chronic granulomatous disease. J Pediatr 1975;87:901.
  25. Schoenborn JR, Wilson CB. Regulation of interferon-gamma during innate and adaptive immune responses. Adv. Immunol 2007;96: 41.
  26. A controlled trial of interferon gamma to prevent infection in chronic granulomatous disease. The International Chronic Granulomatous Disease Cooperative Study Group. N Engl J Med 1991;324:509.
  27. Martire B, Rondelli R, Soresina A. Clinical features, long-term follow-up and outcome of a large cohort of patients with Chronic Granulomatous Disease: an Italian multicenter study. Clin Immunol 2008;126:155.
  28. Martire B, Rondelli R, Soresina A. Clinical features, long-term follow-up and outcome of a large cohort of patients with Chronic Granulomatous Disease: an Italian multicenter study. Clin Immunol 2008;126:155.