Hypersensitivity Pneumonitis Om P Sharma
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Hypersensitivity Pneumonitis: A Historical PerspectiveChapter 1

Om P Sharma
 
In 1555, Olaus Magnus in Sweden cautioned us, “When sifting the chaff from the whole wheat one must carefully consider the time when a suitable wind is available that sweeps away the harmful dust. The fine grained material readily makes its way into the mouth, congests the throat and threatens the organs of the threshing men”.1 This most likely was the first description of hypersensitivity pneumonitis (HP) or extrinsic allergic alveolitis. Even Hippocrates had instructed that one should always take in to account the patient's environmental history.2
In the latter half of the eighteenth century, De Morbis Artificum Diatriba, one of the most influential documents of occupational medicine appeared in Modena, Italy. The treatise was by Bernardino (Bernardini) Ramazzini da Capri (1633–1714) (Figure 1-1), who studied medicine at University of Parma. He became professor of the Theory of Medicine at the University of Modena. After 20 years in Modena, he moved to Padua in 1670 to accept the University's first chair of medicine oriented to epidemiologic problems. His book was reprinted in Padua in 1713. In the chapter, Sifters and Measurers of Grain, the author wrote, “…the men who sift and measure are so plagued by this kind of dust that when the work is finished they heap a thousand curses on their calling. The throat, lungs, and eyes are keenly aware of serious damage; the throat is choked and dried up with dust, the pulmonary passages become coated with crust formed by dust, and results in a dry and obstinate cough; the eyes are much inflamed and watery; and almost all who make a living by sifting or measuring grain are short of breath and cachectic and rarely reach old age; in fact, they are very liable to lapse in orthopnea and finally dropsy. Moreover, the dust is so irritating that it excites intense itching over the whole body, of the sort that is sometimes observed in nettle rash. I have often wondered how so noxious a dust can come from grain as wholesome as wheat, and I began to suspect that in that dust there lurk minute worms imperceptible to our senses and they are set in motion by the sifting and measuring of the grain and broadcast by the air; then they readily adhere to the skin and excite that great heat and itching all over the body; thus connecting the observation of Leeuwenhoek in 1695 of the presence of ‘little worms’ (little wolves) in the corn dust”.3,4
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Figure 1-1: De Morbis Artificum Diatriba, a treatise by Bernardino Ramazzini (1633–1714) (Courtesy of University of Padual Italy).
2Authonie van Leeuwenhoek (Figure 1-2) was born in Delft on October 24, 1632. He came from a family of tradesmen, received no higher education, had no fortune, and knew no languages other than his native language, Dutch. Yet, he made some of the most important discoveries in the history of biology. He discovered bacteria, free living and parasitic microscopic protists, sperm cells, blood cells, microscopic nematodes and rotifers, and much more. His observations opened up an entire world of microscopic life to scientific awareness. Ramazzini was the first to give the clinical description and etiology of HP related to biological microparticles (extrinsic allergic alveolitis, farmer's lung). Ramazzini also made a similar observation about bakers and millers, “In the first place, then, those who separate flour from the bran with sieves or shake and turn over sacks; however, they may protect their faces, cannot help taking in the floating particles of flour with the air they breathe…”3
Jean Francois Millet painted many great rural scenes immortalizing the elegant motions of the sowers, threshers, and the gleaners of hay (Figure 1-3). In one of his paintings, the thick white smoke from the winnowing basket portends danger to the thresher. Theophile Gautier (1811–1872), a poet, dramatist, and literary critic, looked at these scenes and observed, “To look at this picture can make one sneeze”.5 Despite these observations, the syndrome of HP was forgotten for more than 200 years. In 1932, Campbell gave a classic description of farmer's lung disease in a report describing the occurrence of a peculiar pneumonia-like illness seen in Westmorland, England.6 Later, accounts of farmer's lung (haysott or hay sickness) appeared in Icelandic literature. Bjornsson reported that his grandfather, an Icelandic farmer born in 1855, also suffered from the disease. An English physician, Fawcitt discussed seven new cases of farmer's lung in 1936 and called the disease a mycosis caused by Aspergillus, Penicillium, and Mucor species.7 In 1946, Tornell of Sweden, coined the term 3‘thresher's lung’ for a pneumonia-like illness occurring in individuals exposed to moldy grain during the threshing process.8 He concluded that the disease was due to Monilia (Candida) infection. His fellow countryman, Zettergren, laid strong support to this hypothesis and distinguished the illness from Besnier-Boek-Schaumann disease (sarcoidosis) and miliary tuberculosis.9 Thresher's lung has almost disappeared since the threshing is done in open air and by machines.10
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Figure 1-2: Anthonie van Leeuwenhoek (1632–1723), a painting by Jan Verkolje (Courtesy of University of California, Museum of Paleontology).
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Figure 1-3: Rural scenes painted by Jean Francois Millet. A, The haystacks (Courtesy of Metropolitan Museum of Art, New York, NY, USA). B, the gleaners (Courtesy of Museed' Orsay, Paris, France).
The term farmer's lung is attributed to Pickles, but it was Fuller who gave us the first clinical review of the topic.11,12 He divided the illness into three different phases: acute (phase 1), subacute (phase 2), and chronic (phase 3).
Jack (Jacob) Pepys, a British immunologist (Figure 1-4) was the first to provide the serologic link between moldy hay and HP. Pepys was Professor of Clinical Immunology at the Brompton Hospital, London from 1967 to 1979. He founded and was the first editor of the journal Clinical Allergy (now Clinical and Experimental Immunology), which was to become one of the most popular journals in the field. He showed that the chief culprit in moldy hay was a thermophilic actinomycete, Thermopolyspora polyspora that caused the illness.13 He developed a blood test for farmer's lung which has remained routine in clinical practice ever since. Soon after, it became a common practice to advise farmers with farmer's lung disease to quit farming. Further studies, however, showed that most farmers could continue farming, if they could avoid inhaling the organic particles. Unfortunately, some farmers who stayed away from the dust but stayed on the farm developed progressive disease and some progressed to respiratory failure. It is well known that multiple or even a single episode of farmer's lung inflammation can lead to irreversible lung damage in the form of interstitial fibrosis.
Molina has drawn attention of French practitioners to the frequency of the disease in the agricultural areas in the center of France and has contributed 4to a number of reports both on the clinical and etiological aspects and on the immunological and mycological features. The disease is found to a certain extent throughout the world but particularly in the cold and humid regions of Wales, Auvergne, Switzerland, Alps, and Pyrenees. On the other hand, it is rare in sunny dry parts of Africa and Mediterranean regions. It has been a subject of a considerable number of reports from Europe.14
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Figure 1-4: Professor Jack Pepys, FRCP (1914–1996).
In 1954, the first report of HP in the USA was presented by Soucheray.15 In 1958, Frank reviewed the literature and outlined the clinical course of 127 patients.16 The first lung biopsy description of granulomatous pneumonitis was made by Dickie and Rankin.17 Totten et al.18 recognized foreign body particles in many of the granulomas. Cooper19 first reported the use of corticosteroids in treating farmer's lung disease.
Over the last five decades, different forms of hypersensitivity pneumonitides have been described.20
In the USA, in the early 1930s, Towey et al.21 described the maple-bark lung. Maple trees are used for the construction of railway sleepers and manufacturing paper. Corticosterona corticale, a mold, germinates and houses between the wood and the bark. Inhalations of the spores result in what is popularly known as maple bark stripper's lung characterized by granulomatous alveolitis.
In 1965 Reed, Sosman, and Barbee described in pigeon fanciers a lung disease they considered to be a hypersensitive reaction to the inhalation of protein antigens contained in pigeon excreta.22 Of all the types of hypersensitivity pneumonitides, chronic pigeon breeder's disease is now the most common interstitial lung disease in many parts of the world and is the most extensively studied. Here, the interstitial alveolitis is acquired by the inhalation of protein material derived from excreta, feather-particles, and saliva of certain birds. Many birds, including pigeons, 5ducks, canaries, pheasants, and geese can induce bird fancier's disease. Parakeets give rise to a severe form of the disease and progressive dyspnea. Unlike farmer's lung, there seem to be no geographical factors that influence the prevalence of bird fancier's lung as domestic pets, such as canaries, pigeons, and parakeets are kept within the home. Seasonal factors are less significant. Cases are reported from Belgium, England, France, the USA, Mexico, as well as other countries with smaller numbers of bird fanciers and breeders. The disease can be caused by exposure to just one bird or many birds. Many reports have described individuals with HP who had owned one or two pet birds. This is particularly common to pigeon fanciers. Pigeons and other birds excrete nitrogenous wastes, the form of uric acid. Because very little water is needed in the release of excreta, the droppings dry up quickly and form miniature dust storms when cages are cleaned, shaken, or disturbed in any manner. Bird fancier's lung predominantly affects women, aged 20-65. This is because on most breeding farms and even in domestic situations, women are more often responsible for the care of birds. In Mexico, the disease is produced by low-grade domestic exposure to pigeon proteins, mainly in women who develop an insidious clinical illness punctuated by acute episodes.23
Poultry workers, who clean, sort, and process duck and goose feathers, may develop fatigue, general malaise, nausea, headache, cough, and dyspnea. The symptoms usually subside after 3–4 days because a certain tolerance develops. The type, extent, and histology of the pulmonary malady, called feather picker's disease, are incompletely understood.24
Bagassosis, described by Jamison et al.,25 is acquired by inhaling bagasse-particles, the residual product of the extraction of sugar juice from sugar cane. Bagasse is also used in the manufacture of insulation panels, paper, and some explosives. Almost always, the bagasse is allowed to sit in the humid and hot weather. During this period, the once fibrous bagasse becomes powdery and moldy. The moldy bagasse may contain over 240 million spores per gram and numerous other organisms. The workers, commonly men between 18 and 50 years of age, who handle the bagasse dust often suffer from this type of HP. The disease has been reported from all parts of Europe, Cuba, India, Puerto Rico, South America, Madagascar, Hawaii, and other sugar cane growing areas of the world. Modern studies have clarified the nature, immunopathogenesis, course, treatment, and prognosis of HP.2630
Sisal fibers, used in manufacturing threads, bags, and welcome mats, are derived from the leaves of an agave from Mexico. Serum precipitins against sisal antigen are present and helpful in establishing diagnosis in individuals with a positive occupational history.31 New Guinea lung was reported first by Blackburn and Green from the population of Papua in New Guinea. It is thought to be caused by inhalation of fungal and vegetable matter used in constructing thatched huts. The thatches are made of grasses and dried roots. During the rainy season, the thatches 6become damp and moldy. The patients have precipitin antibodies against the organic matter.32
There are many of the other hypersensitivity pneumonitides, which are less frequent or have completely disappeared and been pushed to the shelves of medical history. Humidifier lung results from inhalation of thermophilic actinomycetes that grow in humidifier vents, air conditioners, heating system, and saunas. Although mainly restricted to a specific occupation, it can occur in rural and urban life. An office worker, a sauna-bather, and even a driver of a car with a contaminated air conditioner can be at risk.3336
Fuel chip-induced HP is caused by fuel chips made of wood and peat. An alternative to electrical heating, fuel chips are used in only a few countries. The microorganism most likely to cause the disease is Penicillium sp., the most abundant of the molds that grow in fuel chips.37
Mushroom worker's lung, a little known HP is caused by the thermophilic actinomycete found in mushroom compost and Actinobifida dichotomica, a microorganism present in mushrooms themselves.38 Alex Sakula discovered precipitin antibodies against M. faeni and T. vulgaris in these patients.39
Spaetlese lung, a rare disease, is caused by inhalation of gray and moldy substance that covers the surface of grapes used to make wine. Chemical analysis shows the thrush to consist largely of Botrytis cenerea and small amounts of Alternaria tenuis and Arthrobotrys superba.40 The workers having to harvest and prepare the grapes for fermentation are exposed to dust formed by the thrush.
Cheese worker's disease is caused by the organism Penicillium roqueforti, a distinctive ingredient of blue cheese.41 This unusual disease should not be confused with cheese washer's disease, which is caused by the inhalation of Penicillium casei, the mold, which develops on the surface of cheese aged in damp cellars.42
Suberosis or cork worker's lung disease is caused by inhalation of dust formed in the production of bottle corks, disks, and insulation sheets. The particles of cork are small enough to enter the airways and continue to interstitial and alveolar-capillary junction.5,43
Vineyard sprayer's lung disease is caused not by the inhalation of organic particles but by inorganic copper sulfate. Copper sulfate solution is sprayed on grapevines by vineyard workers in order to eliminate the growth of mildew. The specific solution, known as Bordeaux mixture, is utilized predominantly in Italy and France.44
Coffee worker's lung disease, reported by van Toorn in 1970, occurred in a man who had worked in a coffee roasting factory for 20 years. His serum had antibodies against coffee bean dust.45
Paprika splitter's lung occurred in paprika splitters, mainly in women, who cut open the fruit in order to strip out a series of thin pale ribs, which were discarded because of their high content of capsaicin. The Turkish invaders to Eastern Europe 7introduced paprika in the 16th century. The plant became popular for its medicinal value and pepper became an important source of revenue. The mold, Mucor stolonifer, infests the paprika and is inhaled during the splitting process. Now red pepper is obtained by grinding paprika and the disease no longer occurs because paprika is no longer subjected to splitting.46
Smallpox handler's lung is now only of historical interest because pox no longer remains a scourge of the human race. The doctors, nurses, paramedical staff, and respiratory therapists, who looked after the patients suffering from smallpox, were in danger of developing clinical syndrome, characterized by fever, cough, headache, tightness of the chest, and dyspnea. Fine, diffuse, and nodular infiltrates are present on chest X-ray films. The pneumonitis, most likely, was caused by inhalation of clouds of smallpox scabs released during bed-making, combing, or drying the patient.47,48
Grain weevil disease, potato-riddler's lung, and saxophone player's lung have disappeared, as a result of awareness and the proper use of mask and extractor fans.4952
HP, like other granulomatous lung diseases, can also affect animals. In England, Jenkins and Pepys made extensive studies of fog fever, an HP, affecting cows.13 Cattle in the Toulouse region of France are known to suffer from a similar illness.5 Fog fever in cattle and broken wind in horses produce shortness of breath. Horses can also develop sarcoidosis.53
HP, in man or in beast, is an immunological reaction to inhaled organic antigens. Similar illness has also occurred in patients exposed to low molecular weight chemicals. The diagnosis is secured by the combination of clinical features, radiographic abnormalities, lung function abnormalities, immunological changes, and bronchoalveolar findings.5356 The important diagnostic test, however, is a complete occupational history. Always ask the question, first recommended by Hippocrates: What is your occupation? The treatment is then mostly avoidance of the offending agent.57
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