Loeffler syndrome

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Soroush Seifirad, M.D.[2]

Loeffler syndrome is rare a form of eosinophilic pulmonary disease, which is characterized by mild respiratory symptoms such as dry cough, wheezing, dyspnea, fever, and blood-tinged sputum containing eosinophil-derived Charcot-Leyden crystals, fleeting migratory pulmonary opacities in chest x-ray, and peripheral blood eosinophilia. Parasitic infections, especially Ascaris lumbricoides, may be the cause, but an identifiable etiologic agent is not found in up to one-third of patients. Transpulmonary passage of helminth larvae is the most precise definition of Loeffler syndrome in the literature, nevertheless, there are plenty of controversial definitions under the cluster of eosinophilic pulmonary disorders. The diagnosis of Löffler syndrome is based on characteristic and often transient respiratory symptoms, chest x-ray findings, and peripheral blood eosinophilia. It requires the exclusion of other types of eosinophilic lung disease. such as acute eosinophilic pneumonia which is a distinct entity with acute onset, severe hypoxemia, and a lack of increased blood eosinophils at the onset of disease. Löffler syndrome is a self-limiting condition which is usually resolved within 3-4 weeks.

In 1932, Wilhelm Löffler drew attention to the disease in cases of eosinophilic pneumonia caused by the parasites such as Ascaris lumbricoides, Strongyloides stercoralis and the hookworms, such as Ancylostoma duodenale and Necator americanus. Although Löffler only described eosinophilic pneumonia in the context of infection, many authors give the term “Löffler’s syndrome” to any form of acute onset pulmonary eosinophilia no matter what the underlying cause. If the cause is unknown, it is specified and called “simple pulmonary eosinophilia“.

It is understood that Löffler syndrome is the result of transpulmonary passage of helminth larvae. Helminths, with a pulmonary life cycle are responsible for this syndrome, among them are Ascaris lumbricoides, Ascaris suum, Ancylostoma duodenale, Necator americanus, and Strongyloides stercoralis.

Loeffler syndrome may be caused by Ancylostoma duodenale, Ascaris lumbricoides, Ascaris suum, Necator americanus, Strongyloides stercoralis.

Loeffler syndrome must be differentiated from other diseases that cause pulmonary eosinophilia, such as Churg-Strauss, drug and toxin-induced eosinophilic lung diseases, other helminthic and fungal infection related eosinophilic lung diseases, and nonhelminthic infections such as Coccidioidomycosis, and Mycobacterium tuberculosis.

Löffler syndrome is due to intestinal helminth infections with a pulmonary cycle which is distributed worldwide; nonetheless, parasitic infections such as Ancylostoma duodenale, Ascaris lumbricoides, Ascaris suum, Necator americanus, Strongyloides stercoralis are more prevalent in tropical areas particularly in communities with low socioeconomic status and poor sanitary conditions. In the United States, 20-67% of children in rural southern communities have been reported to suffer from ascariasis; Nevertheless, there are no specific statistics for the occurrence of Löffler syndrome. Globalization increased immigration, and travel warrants alertness of US physicians and the other health care works of developed countries, because an encounter with imported tropical diseases and thus the resulted Löffler syndrome could be more likely nowadays. The case-fatality rate/mortality rate of Löffler syndrome is literally zero. There has been no report of deaths due to Löffler syndrome. Löffler syndrome is a self-limiting, benign condition without significant morbidity. Symptoms usually subside within 3-4 weeks.

There are no established risk factors for Loffler syndrome. Nevertheless, it has been shown that Indians, children, people live in tropical areas are at increased risk for developing the Loeffler syndrome. Common risk factors in the development of helminthic disorders such as ascariasis are often associated with poor sanitary conditions and environmental fecal contamination. Poor socioeconomic conditions, use of human feces as fertilizer, lack of hand washing, eating unwashed fruits and vegetables, environmental contamination with feces are among known conditions which were correlated to ascariasis. Common risk factors in the development of strongyloidiasis include: Occupations that increase contact with contaminated soil such as farming and coal mining, barefoot walking (cultural or low socioeconomic status), Human T-cell lymphotropic virus-1 (HTLV-1) infection, Immunosuppressive therapy with corticosteroids and other medications, Immune reconstitution syndrome, Hematologic malignancies (lymphoma), Tuberculosis, Malnutrition, Diabetes mellitus, chronic obstructive pulmonary disease, (COPD), chronic renal failure, Living in endemic regions, Alcoholics, Travelers, and immigrants.

Löffler syndrome generally presents as a mild syndrome which spontaneously resolves after 2-4 weeks. The symptoms of Löffler syndrome usually develop 10-16 days after ingestion of Ascaris eggs, or N americanus, A duodenale, S stercoralis infection, and start with common symptoms such as fever, malaise, cough, wheezing, and dyspnea. Cough is the most common symptom, which is generally dry and nonproductive but might be productive or even present with small amounts of blood-tinged mucoid sputum. A less common presentation is accompanied by myalgia, anorexia, and urticaria. In order to identify risk factors for exposure to parasites, immigration status, socioeconomic status, hygiene, sanitation, as well as travel history should be carefully elicited. Prognosis is generally excellent, and the 1/5/10-year mortality/survival rate of patients with Loffler syndrome is approximately 100%. The case-fatality rate of Löffler syndrome is literally zero. There has been no report of deaths due to Löffler syndrome. Löffler syndrome is a self-limiting, benign condition without significant morbidity. Symptoms usually subside within 3-4 weeks.

The majority of patients with Löffler syndrome generally presents as a mild syndrome which spontaneously resolves after 2-4 weeks. The symptoms of Löffler syndrome usually develop 10-16 days after ingestion of Ascaris eggs, or N americanus, A duodenale, S stercoralis infection, and start with common symptoms such as fever, malaise, cough, wheezing, and dyspnea. Cough is the most common symptom, which is generally dry and nonproductive but might be productive or even present with small amounts of blood-tinged mucoid sputum. Less common symptoms of Löffler syndrome include myalgia, anorexia, and urticaria. In order to identify risk factors for exposure to parasites, immigration status, socioeconomic status, hygiene, sanitation, as well as travel history should be carefully elicited.

Usually, physical examination reveals no abnormality. Cutaneous features of hypereosinophilic syndrome. Lung auscultation might have crackles on physical examination (common), with or without wheezing. Hence, common physical examination findings of Löffler syndrome include wheezing, rash, and mild fever.

A complete blood count (CBC) with differential may show increased white blood cells, particularly eosinophils. In Loeffler syndrome eosinophilia is generally mild to moderate, usually 5-20%. On the other hand, in certain types of pulmonary eosinophilia, higher percentages are reported. For example, in drug-induced eosinophilia, eosinophils may account for as much as 40% of the WBCs. Generally, the result of stool examination is negative at the time of the Loeffler syndrome presentation. Nevertheless, parasites and ova can be found in the stool 6-12 weeks after the initial parasitic infection. Pulmonary symptoms usually have been resolved when parasitic forms are found in the stool. Immunoglobulin E (IgE) level might be elevated. A bronchoscopy with bronchoalveolar lavage may show increased eosinophilic count. Sputum analysis or gastric lavage may occasionally show larvae of Ascaris or the other parasites with pulmonary cycle.

There are no ECG findings associated with Löffler syndrome.

A chest x-ray may be helpful in the diagnosis of Löffler syndrome. Findings on an x-ray suggestive of Löffler syndrome include migratory densities. Chest x-ray usually shows abnormal shadows that can be unilateral or bilateral. Generally, densities are peripheral and present with both interstitial and alveolar pattern (at the same time), they are a few centimeters in diameter, and are transient, migratory, and disappear completely within 2-4 weeks. Pleural effusions is not common in Loeffler syndrome, but there are reports of pleural effusion in patients with drug-induced pulmonary eosinophilia. (nitrofurantoin, valproic acid)

Chest CT scan may be helpful in the diagnosis of Löffler syndrome. Findings on CT scan suggestive of Löffler syndrome include areas of ground-glass opacity (halo) around consolidation, nodules, and dilated airways within the lesion.

There are no echocardiography/ultrasound findings associated with Löffler syndrome.

There are no other imaging findings associated with Löffler syndrome.

Bronchoscopy and bronchoalveolar lavage may be helpful in the diagnosis of Löffler syndrome. Findings suggestive of Löffler syndrome include increased cell count in bronchoalveolar lavage fluid (BALF), specifically, lymphocytes and eosinophils and neutrophils.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Soroush Seifirad, M.D.[2]

In 1932, Wilhelm Löffler drew attention to the disease in cases of eosinophilic pneumonia caused by the parasites such as Ascaris lumbricoides, Strongyloides stercoralis and the hookworms, such as Ancylostoma duodenale and Necator americanus. Although Löffler only described eosinophilic pneumonia in the context of infection, many authors give the term “Löffler’s syndrome” to any form of acute onset pulmonary eosinophilia no matter what the underlying cause. If the cause is unknown, it is specified and called “simple pulmonary eosinophilia“.

• In 1909, H. French described three categories of eosinophilia in a clinical lecture later published in the Guy’s Hospital Gazett (1909;23:533-537). The three categories he included were:“Guy’s Hospital Gazette – Google Books”.

• Asthma
• Parasitic infections, such as “Anchylostomiasis, Bilharzia huematobia, Trichina spiralis, Hydatid disease; and to less extent with Taenia solium, Taania medio canellata, and Bothriocephalus latus; whilst it does not occur at all with Trichocephalus dispar, Oxyuris vermicularis, or Scabies; and Ascaris lumbricoides.”
• Skin diseases such as bullous dermatoses: “Pemphigus, Erythema bullosiim, Erythema iris, Dermatitis herpetiformis, and Herpes gestationis.”

• In 1922, Koino, a dedicated Japanese clinician scientist studied Ascaris on humans.

• He himself ingested 2000 mature eggs of human Ascaris, which produced symptoms of pneumonia, including fever, dyspnea, productive cough, hemoptysis, and sputum containing larvae. Koino named it ‘Ascaris pneumonia’.
• He also made an experiment on his brother , he fed his younger brother 500 mature Ascaris eggs from the pig, and observed and episode of fever, dyspnea, and productive cough without blood or sputum containing larvae. “CAB Direct”.

• Then in 1932, Wilhelm Löffler drew attention to the disease in cases of eosinophilic pneumonia caused by the parasites such as Ascaris lumbricoides, Strongyloides stercoralis and the hookworms, such as Ancylostoma duodenale and Necator americanus.^[1]

• In his first report, Löffler described four cases of transient (lasting 3-8 days) pulmonary infiltrates on chest X-ray, with very little to no symptoms, and normal white cell counts, except eosinophilia in two of the cases. He discovered these infiltrates while performing mass X-ray surveillance of tuberculosis patients in Zürich at the time.“Zur Differential-Diagnose der Lungeninfiltrierungen | SpringerLink”.
• In 1936 Löffler published 51 additional cases of the syndrome he had observed.^[1]

• In 1940, Freund and Samuelson reported 105 documented cases of Löffler syndrome, which included the 51 cases Löffler described in 1936.“TRANSITORY INFILTRATION OF THE LUNG WITH EOSINOPHILIA: LÖFFLER’S SYNDROME | JAMA Internal Medicine | JAMA Network”.
• In 1942, Vogel and Minning performed human experimentation with Ascaris.“Beiträge zur Klinik der Lungen-Ascariasis und zur Frage der flüchtigen cosinophilen Lungeninfiltrate | SpringerLink”.

• They fed six volunteers with small amount of Ascaris eggs (6 to 45 eggs) which produced significant symptoms in five of the volunteers.
• This demonstrated an allergic element to the Löffler syndrome.

• In 1943, Weingarten published 81 cases from the coastal areas of India with a gradual onset of chronic (lasting up to years) spasmodic bronchitis, leucocytosis, massive blood eosinophilia, and X-ray of lung infiltrates in the acute phase.“TROPICAL EOSINOPHILIA – The Lancet”.

• He named this syndrome ‘tropical eosinophilia’, and directly stated it to be different from the milder symptoms and transient nature of Löffler syndrome.^[2]
• Tropical eosinophilia has occasionally been referred to as Weingarten syndrome and thought to be due to an immune response to microfilariae.
• Nevertheless, plenty of clinician scientists believe that the so-called tropical eosinophilia is a mere modality of Loeffler’s syndrome.^[3]

• In 1943, Maier published 100 cases of the syndrome he observed in Löffler’s clinic. He believed the lung infiltrates to be similar to the temporary infiltrations from eosinophilic pneumonia observed in asthma.
• In 1948, Löffler injected Ascaris into guinea pigs which induced the syndrome in these animals.^[4]
• In 1952, Crofton proposed the term pulmonary eosinophilia to include the range of diseases with pulmonary infiltration and blood eosinophilia.^[5]
• The classification of pulmonary eosinophilia into five groups included:

• Löffler syndrome (transient infiltrations)
• Prolonged pulmonary eosinophilia without asthma
• Prolonged pulmonary eosinophilia with asthma
• Tropical pulmonary eosinophilia usually with asthmatic symptoms
• Polyarteritis nodosa.

• Although Löffler only described eosinophilic pneumonia in the context of infection, many authors give the term “Löffler’s syndrome” to any form of acute onset pulmonary eosinophilia no matter what the underlying cause. If the cause is unknown, it is specified and called “simple pulmonary eosinophilia”.^[6][7][8]
• Cardiac damage caused by the damaging effects of eosinophil granule proteins (ex. major basic protein) is known as Loeffler endocarditis and can be caused by idiopathic eosinophilia or eosinophilia in response to parasitic infection.

• The most well-known case of Löffler’s syndrome was in a young boy from Louisiana. He arrived at the hospital reporting a high fever after three days, as well as having rapid breathing. ”He was hospitalized and treated with supplemental oxygen, intravenous methylprednisolone, and nebulized albuterol.” The boy’s symptoms quickly subsided and upon further investigation, it was discovered that the boy worked caring for pigs. A test was then performed on the pigs’ fecal matter and surrounding soil; it contained the parasite that had caused the boy’s ailment.^[9]
• Another incident again involved a young boy who had suffered from vomiting and a fever for a span of 3 months. When the doctors finally took an echocardiograph of the child they discovered that the “patient’s admission blood count showed leukocytosis with an abnormally elevated level of peripheral eosinophils.” The child was then diagnosed with Löffler’s endocarditis and immediately began immunosuppressive therapy to decline the eosinophilic count.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Soroush Seifirad, M.D.[2]

It is understood that Löffler syndrome is the result of transpulmonary passage of helminth larvae. Helminths, with a pulmonary life cycle are responsible for this syndrome, among them are Ascaris lumbricoides, Ascaris suum, Ancylostoma duodenale, Necator americanus, and Strongyloides stercoralis.

• It is understood that Löffler syndrome is the result of the transpulmonary passage of helminth larvae. Helminths, with a pulmonary life cycle are responsible for this acute hypersensitivity reaction syndrome, among them are Ascaris lumbricoides, Ascaris suum, Ancylostoma duodenale, Necator americanus, and Strongyloides stercoralis.
• Pathogen is usually transmitted via the oral route (Ascaris) or penetrate the skin (Necator) to the human host.^{[1][2][3][4][5]}
• Following transmission/ingestion, infecting larvae reach the lungs via the bloodstream, penetrate into alveoli, mature, and ascend the airways before descending the alimentary tract into the small bowel
• Ascaris is the most common cause of Löffler syndrome worldwide. On the other hand, migrating larvae of hookworms (Ancylostoma duodenale, Necator americanus) and Strongyloides are less likely to elicit symptoms or pulmonary eosinophilia.

• Pulmonary eosinophilia is a different term, with a wider range of infectious and noninfectious pathophysiology.
• Parasites without pulmonary cycle has been linked to pulmonary eosinophilia.
• It is believed that pulmonary eosinophilia is a hypersensitivity reaction due to circulating, but not local inflammatory mediators such as likeinterleukin-5 (IL-5).
• Since challenged athymic mice have not developed pulmonary eosinophilia, it has been suggested that pulmonary eosinophilia is aT cell-dependent phenomenon.

Conditions associated with Loeffler syndrome include subjects infected with:

• Ascaris lumbricoides,
• Ascaris suum, Ancylostoma duodenale,
• Necator americanus,
• Strongyloides stercoralis.

• Loeffler syndrome has its own characteristic imaging findings.
• Biopsy is rarely performed
• Diagnosis is based on clinical findings, radiographic findings, and shreds of evidence of parasite presence in pulmonary secretions.
• Blood-tinged sputum might be presented.

• Eosinophils may be present in sputum
• Eosinophil-derived Charcot-Leyden crystals may be present in blood-tinged sputum
• Stool examinations are generally negative at the time of pulmonary symptoms and thus not useful in the diagnosis of Löffler syndrome.
• Ascaris, Strongyloides, or hookworm larvae might be detected in the respiratory secretions

• Since biopsy is not indicated in patients with the lofeffler syndrome, reported pathological presentations of Loeffler syndrome are based on the autopsy of patients who passed away from another cause while they concomitantly had simple pulmonary eosinophilia.
• It has been shown that eosinophilic infiltration occurs in the bronchi and bronchioles and in the alveolar and interstitial spaces.
• Usually no parasitic form has been found in the lungs.^[6][7]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Soroush Seifirad, M.D.[2]

Loeffler syndrome may be caused by Ancylostoma duodenale, Ascaris lumbricoides, Ascaris suum, Necator americanus, Strongyloides stercoralis.

• There are no life-threatening causes of Loeffler syndrome.
• It is a self-limiting condition which generally resolves by itself in 3-4 weeks.
• Nevertheless, there are rare life-threatening conditions related to the helminths responsible for Loeffler syndrome, although Loeffler syndrome itself has never killed a patient.

Common causes of Loffler syndrome may include:^[1]

• • Ascaris lumbricoides,^[2][1][3]

• • Ascaris suum,^[4]

Less common causes of [disease name] include:

• Ancylostoma duodenale,^[5][6]
• Necator americanus,^[5][6]
• Strongyloides stercoralis.^[7][8]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Soroush Seifirad, M.D.[2]

Loeffler syndrome must be differentiated from other diseases that cause pulmonary eosinophilia, such as Churg-Strauss, drug and toxin-induced eosinophilic lung diseases, other helminthic and fungal infection related eosinophilic lung diseases, and nonhelminthic infections such as Coccidioidomycosis, and Mycobacterium tuberculosis.

Template:WH Template:WS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Soroush Seifirad, M.D.[2]

Löffler syndrome is due to intestinal helminth infections with a pulmonary cycle which is distributed worldwide; nonetheless, parasitic infections such as Ancylostoma duodenale, Ascaris lumbricoides, Ascaris suum, Necator americanus, Strongyloides stercoralis are more prevalent in tropical areas particularly in communities with low socioeconomic status and poor sanitary conditions. In the United States, 20-67% of children in rural southern communities have been reported to suffer from ascariasis; Nevertheless, there are no specific statistics for the occurrence of Löffler syndrome. Globalization increased immigration, and travel warrants alertness of US physicians and the other health care works of developed countries, because an encounter with imported tropical diseases and thus the resulted Löffler syndrome could be more likely nowadays. The case-fatality rate/mortality rate of Löffler syndrome is literally zero. There has been no report of deaths due to Löffler syndrome. Löffler syndrome is a self-limiting, benign condition without significant morbidity. Symptoms usually subside within 3-4 weeks.

The epidemiological aspect of Löffler’s syndrome isn’t well known since there have been minimal statistics reported on the topic.^[1][2][3]

• The incidence of Löffler syndrome is not well studied, neither worldwide nor in the US.

• The prevalence of Löffler syndrome is not well studied, neither worldwide nor in the US.
• In the United States, 20-67% of children in rural southern communities have been reported to suffer from ascariasis; Nevertheless, there are no specific statistics for the occurrence of Löffler syndrome.

• The case-fatality rate/mortality rate of Löffler syndrome is literally zero.
• There has been no report of deaths due to Löffler syndrome.
• Löffler syndrome is a self-limiting, benign condition without significant morbidity.
• Symptoms usually subside within 3-4 weeks.^[4]

• Patients of all age groups may develop Löffler syndrome.
• Nevertheless, Löffler syndrome more commonly affects young children.
• A higher incidence of intestinal helminthiases and hence, Löffler syndrome has been reported in young children because they are more exposed to contaminated soil and because young children exhibit hand-to-mouth behavior more often than adults

• Löffler syndrome usually affects Indians, nevertheless, it has not been well studied whether it is because of the tropical climate, poor sanitary condition or there is a genetic tendency which is very unlikely.^[5]

• Löffler syndrome affects men and women equally.

• The majority of Löffler syndrome cases are reported in tropical areas with poor sanitation. Particularly India.^[6]

• In the United States, 20-67% of children in rural southern communities have been reported to suffer from ascariasis;^[7][8]
• Nevertheless, there are no specific statistics for the occurrence of Löffler syndrome.
• Globalization increased immigration, and travel warrants alertness of US physicians and the other health care works of developed countries, because an encounter with imported tropical diseases and thus the resulted Löffler syndrome could be more likely nowadays.

• Löffler syndrome is due to intestinal helminth infections with a pulmonary cycle which is distributed worldwide;^{[9][10][11][12]}
• Nonetheless, parasitic infections such as Ancylostoma duodenale, Ascaris lumbricoides, Ascaris suum, Necator americanus, Strongyloides stercoralis are more prevalent in tropical areas particularly in communities with low socioeconomic status and poor sanitary conditions.

Template:WH Template:WS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Soroush Seifirad, M.D.[2]

There are no established risk factors for Loffler syndrome. Nevertheless, it has been shown that Indians, children, people live in tropical areas are at increased risk for developing the loffler syndrome. Common risk factors in the development of helminthic disorders such as ascariasis are often associated with poor sanitary conditions and environmental fecal contamination. Poor socioeconomic conditions, use of human feces as fertilizer, lack of hand washing, eating unwashed fruits and vegetables, environmental contamination with feces are among known conditions which were correlated to ascariasis. Common risk factors in the development of strongyloidiasis include: Occupations that increase contact with contaminated soil such as farming and coal mining, barefoot walking (cultural or low socioeconomic status), Human T-cell lymphotropic virus-1 (HTLV-1) infection, Immunosuppressive therapy with corticosteroids and other medications, Immune reconstitution syndrome, Hematologic malignancies (lymphoma), Tuberculosis, Malnutrition, Diabetes mellitus, chronic obstructive pulmonary disease, (COPD), chronic renal failure, Living in endemic regions, Alcoholics, Travelers, and immigrants.

There are no established risk factors for Loffler syndrome itself. Nevertheless, it has been shown that Indians, children, people live in tropical areas are at increased risk for developing loffler syndrome.Common risk factors in the development of helminthic disorders such as ascariasis are often associated with poor sanitary conditions and environmental fecal contamination.

The risk factors for ascariasis are often associated with poor sanitary conditions and environmental fecal contamination. Risk factors for ascariasis include:^[1][2][3]

• Poor socioeconomic conditions
• Use of human feces as fertilizer
• Lack of hand washing
• Eating unwashed fruits and vegetables
• Environmental contamination with feces

Common risk factors in the development of strongyloidiasis include:^[4][5]

• Occupations that increase contact with contaminated soil such as farming and coal mining
• Human T-cell lymphotropic virus-1 (HTLV-1) infection
• Immunosuppressive therapy with corticosteroids and other medications,
• Immune reconstitution syndrome
• Hematologic malignancies (lymphoma)
• Tuberculosis
• Malnutrition
• Diabetes mellitus, chronic obstructive pulmonary disease (COPD), chronic renal failure.
• Living in endemic regions.
• Alcoholics
• Travelers, immigrants

Template:WH Template:WS

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Soroush Seifirad, M.D.[2]

Löffler syndrome generally presents as a mild syndrome which spontaneously resolves after 2-4 weeks. The symptoms of Löffler syndrome usually develop 10-16 days after ingestion of Ascaris eggs, or N americanus, A duodenale, S stercoralis infection, and start with common symptoms such as fever, malaise, cough, wheezing, and dyspnea. Cough is the most common symptom, which is generally dry and nonproductive but might be productive or even present with small amounts of blood-tinged mucoid sputum. A less common presentation is accompanied by myalgia, anorexia, and urticaria. In order to identify risk factors for exposure to parasites, immigration status, socioeconomic status, hygiene, sanitation, as well as travel history should be carefully elicited. Prognosis is generally excellent, and the 1/5/10-year mortality/survival rate of patients with Loffler syndrome is approximately 100%. The case-fatality rate of Löffler syndrome is literally zero. There has been no report of deaths due to Löffler syndrome. Löffler syndrome is a self-limiting, benign condition without significant morbidity. Symptoms usually subside within 3-4 weeks.

• Löffler syndrome generally presents as a mild syndrome which spontaneously resolves after 2-4 weeks.^[1]
• The symptoms of Löffler syndrome usually develop 10-16 days after ingestion of Ascaris eggs, or N americanus, A duodenale, S stercoralis infection, and start with common symptoms such as fever, malaise, cough, wheezing, and dyspnea.
• Cough is the most common symptom, which is generally dry and nonproductive but might be productive or even present with small amounts of blood-tinged mucoid sputum.^[2]
• Less common presentation is accompanied by myalgia, anorexia, and urticaria.^[3]
• In order to identify risk factors for exposure to parasites, immigration status, socioeconomic status, hygiene, sanitation, as well as travel history should be carefully elicited.

• Löffler syndrome is a self-limiting, benign condition without significant morbidity.

• Prognosis is generally excellent, and the 1/5/10-year mortality/survival rate of patients with Loffler syndrome is approximately 100%. ^[4]
• The case-fatality rate of Löffler syndrome is literally zero.
• There has been no report of deaths due to Löffler syndrome.
• Löffler syndrome is a self-limiting, benign condition without significant morbidity.^[5]
• Symptoms usually subside within 3-4 weeks.

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