Loffler Syndrome 

  • Author: Girish D Sharma, MD; Chief Editor: Michael R Bye, MD   more...
 
Updated: Apr 4, 2012
 

Background

Initially described by Löffler in 1932, Löffler syndrome is a transient respiratory illness associated with blood eosinophilia and radiographic shadowing. In 1952, Crofton included Löffler syndrome as one of the 5 categories for conditions that cause pulmonary infiltrates with eosinophilia. The original description of Löffler syndrome listed parasitic infection with Ascaris lumbricoides as its most common cause; however, other parasitic infections and acute hypersensitivity reactions to drugs are included as etiologies for simple pulmonary eosinophilia.

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Pathophysiology

Löffler syndrome has classically been related to the transit of parasitic organisms through the lungs during their life cycle in the human host. After ingestion of Ascaris lumbricoides eggs, larvae hatch in the intestine and penetrate the mesenteric lymphatics and venules to enter the pulmonary circulation. They lodge in the pulmonary capillaries and continue the cycle by migrating through the alveolar walls. Finally, they move up the bronchial tree and are swallowed, returning to the intestine and maturing into adult forms. This process takes approximately 10-16 days after ingestion of the eggs. Other parasites, such as Necator americanus, Ancylostoma duodenale, and Strongyloides stercoralis, have a similar cycle to Ascaris, with passage of larval forms through the alveolar walls. These parasites are not orally ingested but enter the human host through the skin.

A recent review of the parasitic infections of the lung provides an excellent guide for the pulmonary physician.[1]

Researchers initially thought that transit of parasitic forms through the lung was cardinal in the pathogenesis of Löffler syndrome; however, pulmonary eosinophilia has been described in association with parasites whose life cycle does not include passage through the alveoli and also in association with an increasing number of medications. Additionally, eosinophilic pulmonary infiltrates have appeared in mice challenged with a transnasal Ascaris extract. In these situations, accumulation of eosinophils in the lungs is likely secondary to immunologic hyperresponsiveness. The exact immunopathogenic mechanism for this reaction remains unknown.

Animal models demonstrated that development of pulmonary eosinophilia is T cell–dependent because challenged athymic mice do not develop pulmonary eosinophilia. Production of cytokines such as interleukin-5 (IL-5) is necessary for development of pulmonary eosinophilia. Recent data suggest that circulating, but not local, lung IL-5 is critically required for the development of antigen-induced pulmonary eosinophilia.

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Epidemiology

Frequency

United States

Intestinal helminthiases associated with Löffler syndrome, such as ascariasis, have a reported prevalence of 20-67% among children in rural southern communities. No specific statistics have been reported for the occurrence of Löffler syndrome. Because of widespread globalization, immigration, and travel, US physicians may now more commonly encounter imported tropical diseases that may present with Löffler syndrome.

International

Intestinal helminthiases associated with Löffler syndrome are distributed worldwide; however, they are more prevalent in tropical climates, especially in communities with poor sanitary conditions.

Mortality/Morbidity

No deaths due to Löffler syndrome have been reported. Löffler syndrome is considered a benign, self-limiting disease without significant morbidity. Symptoms usually subside within 3-4 weeks or shortly after the offending medication is withdrawn in drug-induced pulmonary eosinophilia.

Age

Because young children are exposed to contaminated soil and exhibit hand-to-mouth behavior more often than adults, they have a higher incidence of intestinal helminthiases and Löffler syndrome.

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Contributor Information and Disclosures
Author

Girish D Sharma, MD  Professor of Pediatrics, Rush Medical College; Senior Attending, Department of Pediatrics, Director, Section of Pediatric Pulmonology and Rush Cystic Fibrosis Center, Rush University Medical Center

Girish D Sharma, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American Thoracic Society, and Royal College of Physicians of Ireland

Disclosure: Nothing to disclose.

Coauthor(s)

Michael J Vinikoor, MD  Fellow in Infectious Diseases, Department of Internal Medicine, University of North Carolina at Chapel Hill School of Medicine

Michael J Vinikoor, MD is a member of the following medical societies: American Academy of Pediatrics

Disclosure: Nothing to disclose.

Specialty Editor Board

Girish D Sharma, MD  Professor of Pediatrics, Rush Medical College; Senior Attending, Department of Pediatrics, Director, Section of Pediatric Pulmonology and Rush Cystic Fibrosis Center, Rush University Medical Center

Girish D Sharma, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American Thoracic Society, and Royal College of Physicians of Ireland

Disclosure: Nothing to disclose.

Mary L Windle, PharmD  Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Charles Callahan, DO  Professor, Deputy Chief of Clinical Services, Walter Reed Army Medical Center

Charles Callahan, DO is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American College of Osteopathic Pediatricians, American Thoracic Society, Association of Military Surgeons of the US, and Christian Medical & Dental Society

Disclosure: Nothing to disclose.

Mary E Cataletto, MD  Director of Children's Sleep Services, Winthrop Sleep Disorders Center; Professor of Clinical Pediatrics, State University of New York at Stony Brook

Mary E Cataletto, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Chest Physicians

Disclosure: Shering Plough Pharmaceuticals Honoraria Consulting

Chief Editor

Michael R Bye, MD  Professor of Clinical Pediatrics, Division of Pulmonary Medicine, Columbia University College of Physicians and Surgeons; Attending Physician, Pediatric Pulmonary Medicine, Morgan Stanley Children's Hospital of New York Presbyterian, Columbia University Medical Center

Michael R Bye, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, and American Thoracic Society

Disclosure: Nothing to disclose.

References

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Initial chest radiograph of a 54-year-old man showing subtle opacity (arrows) in the right middle lung zone.
Follow-up chest radiograph of a 54-year-old man showing migrating opacity in the left lower lobe (arrows) obtained 20 days after the previous image.
High-resolution CT scan (1 mm collimation) obtained in a 54-year-old man showing consolidation with surrounding ground-glass opacity in the left lower lobe. Dilated airways are observed within the lesion. This CT scan was obtained between the first and second images above.
 
 
 
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