At the World Budgerigar Convention held in 1975 in Harrogate, Yorkshire, the question of respiratory disorders, from which many bird fanciers suffer, was raised. Several cases of such disorders were cited. This article, attempts to transcribe a subject of considerable technical difficulty into an easily understandable form. In doing so, the author realises that this entails some sacrifice of scientific exactitude.
A chance conversation led to a contact with a member of a research group at the Institute of Diseases of the Chest, Brompton Hospital, London, where studies of bird fancier's lung disease have been in progress for some years. We are indebted to this Specialist (Dr. Joan L. Longbottom), firstly, for loaning to us a number of publications concerning research work carried out in this field at the Institute and abroad and, for sending us her constructive comments and those of a Consultant Chest Physician on the first draft of this paper.
Respiratory Disorders In Bird Fanciers
The respiratory disorders we shall deal with belong to a growing group of disorders which appear to be the result of a specially high sensitivity (or "hypersensitivity") to inhaled organic dusts. Such a hypersensitivity is called an "allergy".
When something, such as a germ, comes into contact with an individual, the human body produces "antibodies" which help to fight the intruder so as to resist infection, and give immunity against a similar intruder, even if such immunity is, in some cases, only relatively short-lived. The foreign body is called an "antigen", that is to say, it triggers the generation of antibodies. There are some antigens, such as grass pollens, feathers, household dust, animal hairs, insect bites and items of food (for example, shellfish, strawberries and chocolate) which do not produce any reactions in most people. However, in the case of about 10 per cent of the whole population of the United Kingdom, there is a hypersensitivity to one or more antigens, resulting in reactions like hay fever, breathlessness, asthma, headaches, skin irritations and spasms in the digestive tract. The antigens which have been mentioned - and these are but a few of the many hundreds now known - are called "allergic antigens" or "allergens".
In bird fanciers, two types of respiratory disorders can occur, both of which result from antibody effects in allergic individuals. The type of disorder depends on the allergen, on the individual, and on the circumstances of exposure in some persons, asthma occurs though this, if due solely to exposure to birds is, we are informed, probably quite rare. In most cases, where a bird fancier has asthma, this is due to the individual being hypersensitive to other allergens. The other type of disorder in bird fanciers if "bird fancier's lung disease".
We have already referred to the reaction of the human body to germs, and it is common knowledge that, in some cases, respiratory disease is caused by the inhalation of microbial antigens. However, we shall see that, in the case of the two respiratory disorders in bird fanciers, the offending agents which are inhaled are present in the blood serum, droppings, feathers, skin and contents of eggs of the birds.
We propose now to go into this subject in more detail. Firstly, an attempt will be made to provide as simplified a picture as possible of the structure, functions and defences of the respiratory system. Secondly, we will summarise the findings of some of the research publications already referred to.
The Respiratory Tract
1. Structure
One might look upon the middle and lower sections of the respiratory tract as being like a tree upside down. The air which is breathed in through the upper section - nose or mouth - passes into the trachea or windpipe, which is in the equivalent of the tree trunk. The air then passes to each being via the left and right branch, which are the main branches of the tree. The air passages continue to divide into smaller and smaller branches, ending in minute air sacs called "alveoli". The walls of these sacs contain a network of fine capillaries and it is in this area that the interchange of oxygen from the lungs and carbon dioxide from the blood takes place. Any inflammation or blockage of these capillaries affects breathing.
The respiratory tract, like many other organs of the body, is lined with a soft "mucous membrane". The outer layer of this membrane contains cells which secrete a substance which combines with body water to form mucous. The lower layer contains muscle fibres which, under certain circumstances, contract and thus reduce the respiratory volume of the lungs and cause breathlessness..
In parts of the respiratory tract, the mucous membrane is covered with a large number of microscopic hair-like projections called "cilia". These are in constant motion and serve to "sweep" the mucous back up the respiratory tract until it reaches a point where it is either swallowed or expectorated.
2. Deposition Model
As might be expected, dust particles greater than a certain size and density fall to the ground, because the gravitational force is greater than the force of intake of air into the nose or mouth. Of those particles which can be inhaled, some are exhaled again. The retained portion is dependent on the size and density of the inhaled particles. The largest of the particles are deposited in the nose and pharynx; the smaller the particles that are inhaled, the further they will penetrate into the respiratory tract. The smallest of all reach as far as the alveoli.
3, Clearance Model
The process and rate of clearance of dust particles from the respiratory tract depend on the degree of solubilities, of the particles and on the site of their deposition. One clearance path is by direct uptake into the systemic blood. Another clearance path is by mucous transport by ciliary action back up the tract.
Composition Of Blood
Blood consists of red and white cells, blood platelets and watery plasma (serum). Since the research studies on bird fancier's lung disease have paid particular attention to the effects of allergic reactions on two of the five types of white cells, our comments will be confined to the white cells. The normal number of such cells per millilitre of blood is around 7,000, the two most abundant of the five types are neutrophils (about 60 per cent) and lymphocytes (about 30 per cent). The former have an important role in inflammation and the lymphocytes are believed to participate in the early phases of the formation of antibodies. The three smaller components of white cells are (a) eosinophils which become abnormally abundant in allergic reactions, (b) basophils which re thought to play a significant part in some of the phenomena of hypersensitivity, and (c) monocytes which take part in inflammatory reactions.
Research Studies
In this section, we shall use the phrase "bird owners" rather than "budgerigar breeders". One reason is that the first symptoms of lung disease resulting from contact with birds and their habitat occurred in pigeon fanciers. Another reason is that, in the case of owners of budgerigars, nearly all of the patients referred for investigation at the Brompton Hospital have not been breeders. We have also been informed that, in a recent survey carried out by a research team at the Churchill Hospital and Radcliife Infirmary, Oxford, of the 117 budgerigar owners attending four outpatient clinics, none was a budgerigar breeder but people with the birds, as pets, in their homes, where often such birds are allowed to fly round the room. These persons are thus subjected to a continuous, "low-level" exposure to the offending agents, resulting in a more insidious form of lung disease than is the case with breeders who, although exposed to more birds, spend much less time with them in the aviaries.
The first report we have seen regarding pigeon fanciers was of a study begun in 1959 in U.S.A. The general symptoms observed were high temperature (103 degrees F and 104 degrees F), malaise, coughs and breathlessness, which occurred some 4 to 8 hours after exposure to the pigeons and their habitat. Furthermore, in the case of the first 3 patients examined, there had been weight losses of 10 to 25 lb over a period of a few months.
Blood tests showed high levels of white cells (as high as 23,000 per ml of blood in one case). There was also a high, but transient, level of eosinophils in one man.
Each patient was subjected to an inhalation test with an aerosol extract of pigeon droppings to see whether this would provoke a reaction. In the main, the responses were the same as those experienced by the patients after exposure to their pigeons or after cleaning the pigeon lofts. Thus there was something in the droppings which was the allergen.
In one kind of allergic mechanism, when a clear solution containing an antigen is mixed with a clear solution containing the related antibody, there is a reaction between the two and a finely divided powder, or precipitate, is formed. The precipitating antibody is called a "precipitin". hence one method of testing whether a person is hypersensitive to a particular antigen is to take a sample of that person's blood, extract the serum and mix it with a clear solution of the antigen. If the antibody is present in the person's blood serum, a precipitate will be formed.
Such a test was carried out on the 3 patients referred to. Blood serum from each was mixed with extracts of pigeon droppings and also of pigeon feathers. All three samples of blood serum showed high concentrations of precipitins. Subsequently, the researchers found antigens in the blood serum and egg white of pigeons and they tracked down the offending agents which were producing the allergy in their patients to certain proteins (globulins) present in the pigeon blood serum, droppings, feathers and eggs. (The probable antibody which produces the precipitate is now believed to be "immunoglobulin G", or Ig G).
When the research team carried out similar tests on the blood serum from 30 normal persons, not exposed to pigeons, no precipitins were found. Tests were then conducted on 43 members of a pigeon-flying club. In 7 of these, some precipitins were found but the amounts present were very low and none of these persons had any symptoms when handling the birds.
Up to 1971, publications reporting studies on bird owner's lung disease were, with one exception, confined to pigeon owners. The exception was a publication in 1966 by a team at the Institute of Diseases of the Chest, Brompton Hospital. They examined 12 patients, 7 being pigeon owners and 5 budgerigar owners. All had high precipitins in their blood sera against antigens from their birds. The general symptoms were fever, cough, breathlessness (asthma in the case of one budgerigar owner) and loss of weight. The lung capacities were lower than normal, being less than 80 per cent in 6 of the 12 cases.
Provocative inhalation tests were carried out on 10 of the patients but not on the remaining 2 cases, because they already had severe respiratory disability. The most consistent reaction observed was a high rise of temperature a few hours after inhalation, the temperature falling to normal at 24 hours. (This is a common observation reported in other publications.) When the temperature was highest, there was a high white-cell level which returned to normal after some 24 to 48 hours. There was also a raised eosinophil count.
In 1971, the Institute reported on tests on 118 budgerigar owners. Of these, 43 showed no respiratory disease and when their blood sera were tested for reactions to budgerigar blood serum, no precipitins were found. Of those with respiratory troubles, 42 had diseases not connected with budgerigars. Of the remaining 23, 19 had budgerigar owner's lung disease (nearly all resulting from the keeping of pet birds), and 14 had asthma (which, mentioned earlier, is considered to be rare if the asthma is due solely to exposure to budgerigars; hence the asthma was probably due to other causes.
In those few individuals in whom exposure to budgerigars produces asthma, a different mechanism from that leading to lung disease is operative. When budgerigar allergen which causes asthma enters the respiratory tract for the first time, the antibodies produced (now said to be "immunoglobulin E" or Ig E) attach themselves to cells known as "mast cells". A second exposure and subsequent exposure of these mast cells to the same allergen results in the cells breaking up, with the production of "histamine". This causes the muscular contractions referred to in an earlier section resulting in impaired respiratory function. To overcome these contractions and restore the respiratory performance, treatment consists in the administration of antihistamine drugs. There are many drugs in this category but, since a preparation which may relieve symptoms in one person may prove ineffective and even harmful in another, self-medication should never be attempted. One's doctor should be consulted.
In the most recent publication we have seen (8th July, 1978), 4 out of 117 current budgerigar owners were found to have "budgerigar fancier's lung", none, it appears, being budgerigar breeders. It is stated that in the early stages of the disease, the characteristic physical signs, chest radiographic appearances and disturbances of pulmonary function, many be unimpressive. It is claimed that provocation inhalation tests rather than precipitin tests are the most reliable method of confirming or excluding the disease.
To sum up, one concludes from the research studies that certain proteins (globulins) present in the blood serum, droppings, feathers and eggs of birds, are the cause of asthma (which is rare in the case of exposure to budgerigars) and of bird owners' lung disease, which is called "allergic alveolitis", meaning inflammation of the alveoli in the lungs as a result of an individuals allergic reaction to the birds and their habitat. The problem one is faced with is what measures can be taken by those who, whether obviously allergic or not, wish to minimise the risks and effects.
Protective Measures And Treatment
The first line of action which can be taken in the case of, say, an allergy to a particular food, is to avoid that food in future. This cannot be followed in the case of hay fever, because of the presence of pollens in the atmosphere, even in that of major towns and cities.
When my Son, G.S. Binks, was a youngster, he had an asthmatic attack following inhalation of pollens in a hay field. Tests which were carried out indicated hypersensitivity to grass pollens, feathers, dogs and horses. Desensitization was carried out which, though not wholly effective, reduced the severity of future attacks of hay fever and appeared to eliminate asthmatic attacks.
We understand that desensitization for asthma due to exposure to birds is not recommended, since it may induce antibodies of the type that produce bird owner's lung disease.
The question is what should a budgerigar fancier do? Clearly when the lung disease is severe or tending towards severity, there is no alternative but to avoid all future contact with the birds since the disease is said to be irreversible. We understand that a few have had to adopt this step, which must cause considerable regret at having to give up one's hobby.
To return to the case of G.S. Binks, since he had been desensitized against dust and feathers, the family saw no reason for not allowing him to pursue his hobby as a budgerigar breeder. However, some years later, he suffered repeated throat infections, necessitating long periods of recovery. He rejected any suggestions from his doctor that the aviary was the source of infection, since he was afraid to give up his hobby. Later on, microscopic examination of the aviary dust revealed that this contained not only feather fibre but also dried droppings from the birds. He then used a mask which covered the mouth and nose, yet permitted easy breathing. The throat and chest infections ceased. It is realised that masks may not be sufficient but they should reduce the intake of aviary dust. Doubtless, many of those who have aviaries spray the floor with fine water spray before sweeping it. It seems worthwhile to spray the trays similarly before cleaning off the droppings.
Another measure which might be adopted is to wear special clothing, say, overalls which are used only in the aviary and kept in a separate locker, preferably outside the aviary.
We are advised that the best procedure for any "sufferers" would be to have confirmation as to whether any asthma or other respiratory disorder is related to the birds. They should, therefore, consult their doctors who could refer them to a local Chest Clinic for fuller examination by a Chest Consultant, most of whom are now fully aware of the existence of "Bird Fancier's Lung".
"© The content of The Best of Budgerigar World Volume 1 is copyrighted and may not be used for any purpose without prior permission. However, Internet links are most welcome".