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Complications
Abnormal beak conformations including beak overgrowth can lead to difficulty eating, resulting in malnutrition or starvation

Care is needed to avoid over-cutting as this will cause bleeding. This can be stopped using a silver nitrate pencil - but often the bird rubs it and bleeding starts again. For this reason beak trimming is best performed by a veterinarian.

Moving the bird into a larger cage may help increase exercise and so increase natural wear of the beak. Contrary to popular belief cuttle bone and mineral blocks are not thought to help with beak growth.

The underlying cause (eg mites) should be treated appropriately. See cnemidocoptes pilae.

Long term problems
Neglected cases may die from starvation and general debilitation.

In 1988-9 it was decided to find out exactly what the causes of death of exhibition budgerigars are. All the birds that died in the large studs of 3 fanciers in the year were post-mortemed. While in some ways 2 of the studs were not typical, at least two of the findings were of general interest. First in all three studs the average age of death was around 2 years whereas the average age of death of pet birds submitted for post-mortem examination is just over 6 years.

Why should this be so? It seemed possible that exhibition birds were either more stressed with showing and breeding than pets or that in breeding for exhibition features, stress susceptibility had been bred into the birds. Microscopical examination of the adrenals, the stress glands, did show marked differences between the pet and exhibition bird but that raised the question as to which was normal, or if either of them were.

After a year's work dealing with Australian bureaucracy and getting a file 2½ thick of forms and correspondence, I eventually managed to get adrenal glands from some wild budgies and it was a surprise at first to find that they were similar to those of the exhibition birds. Should this really have been a surprise? In retrospect I think not; life expectation in the wild is probably less than 1 year and the birds are probably stressed due to predators, and possible competition, in years when numbers are high, for food and nest holes. The second thing to come out of this cause-of-death survey was the importance of quarantine for new birds arriving at a stud. In two of the three studs there were serious disease outbreaks following the introduction of new birds which were mixed immediately with the others in the flight. New birds should be quarantined well away from the resident birds for at least three weeks. During this time disease may develop, the birds can be tested to see if they are carrying disease or they can be given preventative treatment.

In 1990-1 it was decided that we would investigate the condition of clagged vents in which large amounts of droppings accumulate around the vent and eventually block it and the bird then dies of an accumulation of waste products in the body. Unfortunately on this occasion the fancy let the research project down and the number of samples provided meant that only provisional results could be obtained.

While several causes of the condition were found it was predominantly due either to kidney disease or to malfunctioning of the lower part of the bowel. As yet nothing can be done for the former, which frequently rights itself if the vent is kept clear of obstructions. In some circumstances the latter is treatable.

After this success with a disease at the top end of the digestive system (vomiting budgies), in 1986-7 attention was turned to the other end to look at why some birds developed diarrhoea. In some ways this was a less successful investigation, in as much as it did not come up with as neat an answer as the first two. Over 20 different causes of diarrhoea were discovered but none was much more common than the others. Some of the causes were within the digestive system itself; some outside it; some of the conditions were treatable and others were not.

One of the commoner causes of the disease was loss of the bacteria which should be present in the intestine. At the end of the work, all we could do was suggest to the fancy that in cases of diarrhoea if simple remedies such as cold tea do not work and the problem persists, laboratory investigation of both the bird and samples of droppings is essential to find the cause. In many cases antibiotics are not the answer to the problem. If they are used, and in cases where the gut flora has been lost, probiotics have a very useful role to play in restoring the germs which should be present.

DISEASES TRANSMITTED TO EGGS

Early embryonic death, blood-ring, dead-in-shell.., these terms frustrate and confound aviculturists, novice and professional alike. The reasons that embryos die are many, and diagnosing the specific cause of death can prove elusive in some cases. The serious aviculturist, whether a hobbyist or one who makes her living from bird breeding, should work with an experienced avian veterinarian who can help with all facets of aviculture. Every egg that dies prior to hatching should be examined by an avian veterinarian who can perform an egg necropsy and any other tests to determine the cause of death.

Often, histopathology (microscopic examination of tissues) will prove diagnostic, if the embryo has recently died. Bacterial and fungal cultures, stains of egg membranes, viral isolation and DNA PCR probes for specific organisms may also help in diagnosing the cause of death. There are many infectious organisms that can be transferred from the hen to the egg that may cause the egg to die. In some cases, the infectious organism may infect the egg, yet the embryo may continue developing, and may even hatch, carrying the organism at hatch time. If an organism is passed from an infected hen directly into an egg, and then into the developing embryo, this is called vertical transmission. The term vertical transmission also describes the transmission of an infectious agent from a parent to an egg during fertilization, during egg development in the oviduct of the hen, or immediately after oviposition. Once the egg is laid, some infectious organisms can pass through the eggshell upon contact with contaminated feces, urates or bedding. This is also considered vertical transmission if infection occurs immediately after laying. Some organisms are transmitted from the ovary to the egg, and this is called transovarian transmission. Infectious organisms harbored in the oviduct can also be passed into the egg prior to the shell being formed. Some organisms infect eggs if contents from the cloaca contaminate the surface of the egg, and then penetrate the egg. The other method of transmitting infectious organisms is by horizontal transmission. Horizontal transmission can occur by preening, inhalation, copulation, insect or animal bites, ingestion, contact with contaminated equipment or fighting. It seems obvious that prior to the egg membranes and shell being applied to it, the egg would be susceptible to infection by numerous infectious organisms. Even though the eggshell appears solid, it contains microscopic pores that can allow liquids and small organisms into the egg. The pores allow the transfer of gasses, as well.

Bacterial Diseases
Chlamydia psittaci is a primitive bacteria that can be vertically transmitted from an infected hen through the egg to the embryo. Depending on the pathogenicity of the strain and the number of organisms that are passed into the egg, the embryo may die during incubation, or it may actually hatch as a baby bird with chlamydiosis. It should be noted that transovarian transmission of chlamydiosis has not yet been confirmed by researchers, so it may be that the eggs are contaminated with the organism by some other vertical method. One avicultural client of mine with over 100 pairs of large psittacines was having a problem with a pair of blue-and-gold macaws. They pulled all of the pair's eggs for artificial incubation. Several eggs in the incubator died about halfway through incubation. During the egg necropsies, I tested for chlamydiosis by sending in a swab for DNA PCR testing. I also tested the adult breeder pair for Chlamydia, using the University of Georgia tests, which included DNA PCR testing of the blood and DNA PCR testing of a choanal and cloacal swab. A latex agglutination titer, was run through the University of Miami as well. The eggs were positive for Chlamydia, as were the parent birds. I recommended that the breeders remove from the incubator those eggs from the blue & golds, and isolate them in a small incubator. There were five remaining eggs that were in the early stages of incubation. To increase hatchability of the potentially infected eggs, we began a course of egg injections, using injectable doxycycline, which is an excellent drug for chlamydiosis. The eggs, much to our surprise, continued to develop, and all five actually hatched on schedule. As soon as the eggs hatched, I instructed the owners to begin medicating the hatchlings with oral doxycycline, which would be continued for 45 days total. Because all baby birds receiving antibiotic therapy should also be prescribed antifungal medication to prevent infection with Candida sp., we also started the babies on a combination of oral nystatin suspension and fluconizole.

The babies were also prescribed avian lactobacillus and acidophilus to give them some normal, good bacterial flora. The five baby blue & gold’s all developed normally and weaned on schedule. Subsequent testing showed that these babies showed no signs of chlamydiosis. It should be noted that testing is not always 100 percent accurate, and although treatment is often curative, some birds may never completely clear the organism from their system, resulting in asymptomatic carriers. However, these macaws have thrived and all have remained healthy. Bacteria of the genus Salmonella can also cause embryos to die in the shell, or, if the egg is contaminated by a very small number of bacteria, Salmonella can cause weak-hatch babies that may die shortly after breaking out of the egg. The bacteria may cause yolk material to coagulate in the egg, dead embryos may show hemorrhagic streaks on the liver, and the spleen and kidneys may be congested.

Pinpoint areas of the liver may be necrotic. Inflammation of the pericardium may also be seen. Salmonella are motile bacteria that can penetrate the eggshell and are transmitted vertically. Culture of the infected embryo will prove diagnostic. Some Staphylococcus bacteria can kill embryos. The avian embryo can be resistant to some strains of staphylococci, but can be highly susceptible to other strains. Infected wounds on parent birds can infect eggs, as can staph infections found on the hands of aviculturists, if the egg comes in contact with lesions. Artificial incubators will grow staph readily, and it can spread horizontally in this manner. An embryo can die within 48 hours of exposure to some strains of staph, especially Staph, Aureus. The older the embryo is at the time of the first exposure to staph, the less chance of embryonic mortality. Hemorrhages may be found on various internal organs. A laying hen can develop an ovary infected with Staph, Faecalis, which can contaminate the forming egg. Contaminated eggs will have up to 50 percent mortality. Culturing the egg is important for diagnosis. E. coil is a common bacteria normally found in the gastrointestinal (Gl) tract of mammals, and some birds as well.

It can enter the egg from an infected reproductive tract of a hen. E. coil can also penetrate the eggshell if the egg is contaminated with fecal material. E. coli commonly produces yolk sac infection, causing the yolk sac contents to appear a watery yellow-green or yellow-brown. Dirty nests and cages serve as sources of egg contamination. The use of water bottles may reduce the amount of E. coil that builds up in the Gl tract of birds. In my experience, aviaries that use a watering system, as opposed to water bowls, have fewer problems with subclinical bacterial infections in their breeder birds and their off-spring, Many embryos infected with E. coil die late in incubation or shortly after hatching. If an E. coil infection is acquired during incubation, the hatchling may develop an umbilical and yolk sac infection (omphalitis) and may have poor weight gain. Cracked eggs are more easily infected and may serve as a source of infection for other eggs in the incubator. Cracked eggs should be repaired as soon as the damage is discovered, or they should be discarded.

Mycoplasma
Mycoplamatales are one order of microscopic organisms that replicate by binary fission. They have no cell wall, but have a three-layer membrane. They are more primitive than bacteria, and must live and grow inside the host. They live only for a short time. Although we have much to learn about mycoplasmas, they can be involved in problems with Cockatiel conjunctivitis and respiratory infections, as well as respiratory/eye problems in other species of pet and breeder birds. The organism is spread by the respiratory excretions and by the gonads of both sexes, and infection in the air sacs may lead to contact transmission of the ovary and developing follicle. Transovarian transmission can occur. Mycoplasma can spread to the egg from an infected oviduct or from the semen of infected male birds. It is possible to treat eggs infected with Mycoplasma infections. Tylosin is injected into the air cell at the start of incubation. A combination of lincomycin and spectinomycin is also effective for egg injection. Dipping the eggs in antibiotic solutions reduces the incidence of disease; however, I personally, have never used this method. A third treatment that has been useful in breaking the transmission cycle of Mycoplasma gallisepicum and M. synoviae involves elevating the temperature in a forced-air incubator to 46 degrees Celsius for 12 to 14 hours before incubating the eggs normally. This technique inactivates the Mycoplasma organisms, but it will reduce the hatchability by 8 to 12 percent.

Viral Diseases
Several important viral diseases are vertically transmitted in birds. Psittacine beak and feather disease (PBFD) has been demonstrated to be vertically transmitted, since the virus is found in the blood of infected birds. It has been shown that artificially incubated baby birds from PBFD-infected hens will consistently develop PBFD. So, attempting to control PBFD by pulling eggs for artificial incubation is futile. Avian paramyxovirus 1 (Newcastle's Disease or PMV 1) is one of a group of nine distinct serovars (with several more yet to be characterized) of the virus that is dangerous to birds. Although paramyxovirus is theoretically vertically transmissible, this mode of transmission is considered unlikely because infected hens will generally stop laying eggs when they are viremic. Eggs contaminated by virus-laden feces immediately after laying can contaminate an incubator, and serve as a source of virus for recently hatched neonates. Herpesviruses, most of which are quite species-specific, include Pacheco's disease virus, Amazon tracheitis virus, respiratory disease in Neophema sp. and Psittacula sp., wart-like or flat plaque-like lesions on the skin of psittacine birds, budgerigar herpesvirus, pigeon herpesvirus (infectious to budgies and cockatiels), falcon herpesvirus (infectious to budgies and Amazon parrots), and Marek's disease (suggestive lesions in budgies). It has been theorized that some hens latently infected with Pacheco's disease can pass the virus (and antibodies to the virus) to their eggs. The resulting neonates would be latently infected carriers that might not develop detectable levels of antibodies. Herpesvirus of European budgerigars causes feather abnormalities (referred to as "feather dusters") and is thought to be egg transmitted. It has been demonstrated in dead-in-shell embryos and is considered a major cause of early embryonic death in affected flocks, resulting in decreased egg hatchability. Proventricular Dilatation Disease (PDD) is an enigmatic disease that is being diagnosed with increased frequency. Although we have much to learn about this disease, my personal experience indicates that PDD may be vertically transmitted. I am working with an aviary that has a pair of severe macaws whose eggs were taken for artificial incubation because the parents often damaged the eggs after they were laid.

The eggs were placed in a new incubator, and the babies were the only ones in the nursery during hand-feeding. The owner had problems with the babies from day one, as the crops were slow to empty, and they did not gain weight properly. The babies had to be given antibiotics, anti-fungals and motility enhancers (cisapride) to get them to digest their food at all. One baby died at six weeks of age, and histopathology showed all the classic PDD lesions. The second baby died shortly after weaning, and, once again, histopath confirmed PDD. Histopathological examination of tissues from a dead bird (especially the proventriculus, ventriculus, crop, small intestines, and brain) is the only way to confirm PDD in a dead bird as, grossly, many diseases can look like PDD. Dr. Branson Ritchie at the University of Georgia is currently developing PDD tests, and when they are available, we hope to test the parent birds of these two babies. At this time, barium radiographs may render a presumptive diagnosis, and the biopsy of areas of the gastrointestinal tract may prove diagnostic if positive. Once the new testing becomes available, it will be easier to screen for this terrible disease. Some adenoviruses, REO viruses and reticuloendotheliosis viruses can be vertically transmitted. Influenza A may be vertically transmitted, as well.

Parasites
Oddly enough, some parasites have been documented to occur within eggs. Adult ascarids (roundworms) have been found within eggs. These worms get into the egg by moving from the cloaca up into the oviduct, where the eggshell is then formed around the aberrant parasite. The fluke, Prosthogonimus ovatus can be found in the oviduct of Galliformes and Anseriformes, and may also be trapped within an egg, but the flukes are more likely to result in abnormal eggshell formation.

Conclusions
As our knowledge of avian medicine and theriogenology grows, we may discover other organisms that can be vertically transmitted. With the information that is available today, it may be possible to save some eggs that have acquired an infectious agent. Egg injections are routinely performed in my practice, and this has greatly increased the hatchability of infected eggs. By testing for infectious organisms, it is possible to cull eggs, as in the case of PBFD persistently infected birds, or treat the parents, as in the case of many bacterial or chlamydial infections. The result is healthier baby birds.

Margaret A. Wissman, DVM, Dip., ABVP-Avian Practise Dr. Wissman and her husband, Bill Parsons, own and operate Icarus Mobile Veterinary Service and Small World Zoological Gardens in the Tampa, Florida, area.
Dr. Wissman is a frequent author and lecturer.

As long as people breed Budgerigars, French Moult has been the subject of many publications and discussions. One of the first important publications about this feather disease, was presented in Diseases of Budgerigars published in august 1951, Wisconsin USA. At that time French Moult was believed to be caused by faulty diet, overbreeding, and other factors and even a hereditary form was presumed. The term "French Moult" was coined in Europe in the last century where the disease was very prevalent in the 1870's. It had, however been known before that time. The disease has been called French Moult because budgerigars which were shipped all over Europe from the large breeding establishments in southern France, either had the disease in its obvious form or carried it in its hidden form. These birds when bred, would frequently produce a certain percentage of youngsters suffering from French Moult. Two manifestations of F.M. were reported then. The severest form is when young budgerigars in the nest never grow normal feathers. They have been called runners, creepers, crawlers, or bullets. The second, milder form of F.M. includes birds which may eventually grow a normal coat of feathers and become good flyers.

As early as 1888 Dr. Karl Russ made a summary of statements by breeders on the subject of F.M. as they had appeared in early bird journals. Dr. Russ, who was familiar with microscopic work, did not ascribe the cause of F.M. to feather parasites, but to faulty feeding, overbreeding, and breeding in rooms which are too warm. But the most comprehensive study on F.M. has been done in 1932 by Dr. Hans Steiner from the University of Zurich in Switzerland. By continuously inbreeding victims of F.M. he was able to establish a strain in which this disease was carried on in the "hereditary" form from generation to generation according to the Mendelian Law. Dr. Steiner concluded from his experiments that F.M. is the result of degeneration. The view that mites may cause F.M. has been mentioned many times during the last 50 years or more, but has been abandoned each time.

In 1950 scientific work on young Budgerigars suffering from F.M. was done by the Armed Forces Institute of Pathology, Registry of Vetrinary Pathology, Washington, D.C. The report published in All-Pets Magazine in May 1950, was very clear. F.M. is not caused by parasites (including mites) nor by any other "bugs". To find an answer to the question what really causes this unpredictable disease, more scientific work was necessary. However, it was not until 1969 that T.G.Taylor published some experimental investigations on F.M. in Diseases of Cage and Aviary Birds. He came up with a definition and a describtion of the symptoms and stated that the latter vary considerably and depend a great deal on the severety of the attack. He also stated that these variable symptoms have led some people to suggest that F.M. is not a single disease but that it includes several distinct, though related, feather diseases. One of the most interesting findings during these investigations was that a striking difference was found between bone marrow smears obtained from healthy birds and birds suffering from F.M. Red blood cells of diseased birds were abnormally fragile and the life span of the erythrocytes (white blood cells) is unusually short. Taylor concluded, after testing most theories, that the possibility that F.M. may be due to a virus or a virus-like agent, should be taken seriously. However, it was not before 1981 the first serious case report was published in Avian Diseases by Davis and coworkers [5]. They reported high rates of mortality amongst fledgeling budgerigars from aviaries in Georgia and Texas. Affected birds died acutely and exhibited abdomal distention and reddening of the skin. Post mortem they found enlarged heart and liver with areas of necrosis, and swollen, congested kidneys. They examined a variety of tissues and found cells with enlarged nuclei containing inclusions. Electron micrographs revealed the presence of viral particles in the nuclei in the kidneys, feather follicles, liver, heart, bone marrow, spleen and brain. Later on in a separate publication also in Avian Diseases (1981), Bozeman and coworkers isolated a virus that belongs to the Papovaviridae family [4]. They found characteristics that suggest the virus belongs to this family, e.g. the presence of DNA, the side of viral replication appearing to be in the nucleus, and the size of the virus particles ranging from 42 to 49 nm in diameter. (The name Papovavirus was chosen to denote papilloma (PA), polyoma (PO) and vacuolating (VA) viruses). However, they referred to the condition of affected birds as budgerigar fledgling disease (BFD) and characterized a virus (BFDV) isolated from diseased birds.

Again in 1981 another research note was published in Avian Diseases by Bernier, Morin and Marsolais from Canada [2]. They also reported high mortality rates in Budgerigars between one and 15 days of age in 19 aviaries in the Province of Quebec. Signs in adult birds were similar to those described as French Moult. They considered F.M. to be a milder form of the infection described. Surviving birds exhibited a retarded growth of flight and tail feathers. Results of their investigations suggest that this disease of budgerigars is caused by a papova-like agent that can replicate in many tissues of the body, causing widespread lesions responsible for the high mortality rate in very young birds.

In 1982 Dykstra and Bozeman published the results of a light and electron microscopic examination of a "newly" described avian virus in Budgerigars [8]. They found that the virus particles are of the same size and symmetry as members of the polyoma subgroup of the Papovaviridae. The means of transmission of the virus within an aviary population is less clear, though their studies have implicated several possible routes. Adults may pass the virus by feeding their young by regurgitation. Air currents circulating inside affected aviaries may also be responsible for transmission. They also suggest a possible respiratory route of transmission since virions within cells of lung tissue were found.

In 1984 Prof.Dr.Kaleta from Germany and coworkers, published some results obtained by their investigations on young budgerigars showing signs of F.M. [13]. The birds were purchased from five different sources. Infected cells were isolated and examined electronmicroscopically. During this investigation intranuclear virus particles were found with a diameter of 35-45nm.

In the American Journal of Veterinary Research Dykstra and coworkers published a report to characterize a virus linked to Budgerigar Fledgling Disease (BFD) which previously had been identified as a papovavirus [9]. The purpose of this investigation was to prepare further genetic investigations to develop a possible vaccine as has been done for e.g. foot-and-mouth disease of cattle. Their results showed little similarity to simian virus 40 (SV40) or polyomavirus DNA. During the same year Bernier, Morin and Marsolais published an article in The Canadian Veterinary Journal involving clinical and pathological findings in budgerigars suffering from a papovavirus infection [3]. They described one to 15 day old birds displaying a lack of nestling down feathers and filoplumes on the head and neck. Microscopic lesions in the feather follicles of the affected birds less than 15 days of age, were characterized by focal, multifocal or diffuse ballooning degeneration in the plate cells of the barb ridges. Again microscopic examination of these cells showed virus particles similar to those already described by earlier investigators. Results of this investigation suggested that a papovavirus can cause temporary absence, retarded growth and the incomplete development of feathers in young budgerigars. The infection was also suspected to be egg transmitted. The fact that eggs from pairs producing affected young will also give diseased birds when fostered by pairs whose own youngsters are normal, supports the hypothesis of egg-transmission. It was suggested that F.M. is a nonfatal form of the papovavirus infections described in budgerigars.

Lynch and coworkers from the Veterinary Laboratory Services Branch, Ontario, Canada, also published their results in Avian Diseases (1984)[18]. They examined birds from three unrelated outbreaks of disease occurring in Ontario in 1981,1983, and 1984. Egg-inoculation experiments suggested that the disease may be egg-transmitted and that significant virus replication must occur before the budgerigar's immune system matures sufficiently to mount a response.

In the year 1984 many research was carried out on this unpredictable disease. Jacobson and coworkers reported 45 fledling psittacine birds being raised in an avian nursery of which 14 died over a 6-week period [12]. Birds died acutely with full crops, abdominal distention, and hemorrhagic skin. Feather abnormalities were seen in birds older than 15 days. In this report, a die-off of fledgling conures and macaws was described. Electron microscopy demonstrated a virus similar in size and conformation to BFDV (Budgerigar Fledgling Disease Virus). They concluded that the psittacine papovavirus present in affected birds, appeared to be related to the polyomavirus subgroup of the papovaviruses. They also concluded that fledglings from seronegative parents should not be introduced into a nursery with chicks from seropositive parents. Also in the same year Pass and Perry from the School of Veterinary Studies, Murdoch University, Murdoch, Western Australia, described a disease called Psittacine beak and feather disease [21]. The disease is characterized by loss of feathers, abnormally shaped feathers and overgrowth and irregularity of the surface of the beak. The disease was seen in Sulphur-crested Cockatoos, Lovebirds, Budgerigars and Galahs. During their investigations they found viral particles 17 to 22 nm in diameter who could be identified in a later state as the picorna virus which is not a member of the Papova virus family.

In 1985 Pass published a papova-like virus infection of Lovebirds [22]. The article was published in the Australian Veterinary Journal and contained information about similarities to papovavirus infections of psittacine birds described elswhere.

Krautwald and Kaleta (1984) investigated 250 budgerigars obtained from 45 different breeders. Approximately 50 birds came from breeders who never had F.M. in their aviaries [14]. It was observed that birds who never had any problems with F.M. were very easy to infect for lack of sufficient antibodies. In the German Cancer Research Center of the University of Giessen, Lehn and Müller (1986) cloned and characterized for the first time a virus isolated from fledgling budgerigars, designated BFDV [16]. A relationship to the polyomavirus subgroup was already recognized and suggested by previous investigators, but it was now confirmed by this investigation. Their experiments showed that BFDV is related to but not identical to the other polyomaviruses. Until now, polyomaviruses had been isolated only from a variety of mammalian species including man; in contrast, BFDV represents the first avian member of this subgroup. Lehn and Müller found strong evidence that BFDV is associated with French Moult.

In 1986 Müller and Nitschke from the Institute for Virology, University of Giessen, Germany, investigated a virus isolated from fledgling budgerigars suffering from F.M. Results obtained by their investigation led to the conclusion that the virus isolated warrant the classification as a polyoma-like virus [20].

David Graham and Bruce Calnek reported in Avian Diseases (1987), a papovavirus infection in 44 parrots of at least 18 species exclusive of the budgerigar [10]. They compared this infection to a generalized virus infection of young budgerigars which had been recognized in the United States, Canada, Italy, Hungary, Japan, and the Federal Republic of Germany. A papovavirus infection was confirmed in 27 of the birds by using antibody tests.

In the Journal of Veterinary Medicine (1989), Krautwald, Müller and Kaleta from the Institute of Poultry Diseases and Institute of Virology, University of Giessen, Germany, examined 298 budgerigars from 49 different flocks in order to obtain some insight into the aetiology of FM and BFD [15]. The difference between birds infected with FM and birds infected with BFD is that FM birds mostly survive and BFD infected birds die when 2-to-3-weeks old. Mortality rates even reached up to 100% in several flocks. However, surviving budgerigars showed disorders of feathers, similar to those of birds with FM; these birds remained less developed, and many of them were unable to fly (runners). The structural and physicochemical properties of viruses isolated from budgerigars with BFD and from several budgerigars with FM described by Krautwald and coworkers and their results published in a previous paper (1984) confirm the recently published classification of BFDV as a member of the polyomavirus group (Lehn and Müller,1986; Müller and Nitzschke,1986). They proposed to place this virus into a distinct subgroup within the polyomavirus family.

Regine Stoll and coworkers (1993) studied molecular and biological characteristics of avian polyomaviruses from different species of birds including chickens and a parrot [24]. The chicken polyomavirus is called BFDV-2 and the parrot polyomavirus is called BFDV-3. The non-mammalian polyomavirus isolated from Budgerigars is now called BFDV-1 virus. They consider Budgerigar Fledgeling Disease virus (BFDV) to represent the first avian virus being recognized as a member of the polyomavirus genus in the family papovaviridae (Müller & Nitschke, 1986;Lehn & Müller,1986). They also consider French moult of Budgerigars to be a milder and more protracted form of a BFDV infection resulting in chronic feathering disorders (Krautwald,1989). It is proposed that the avian polyomaviruses should be placed in a distinct subgroup within the polyomavirus genus of the family Papovaviridae and the designation Avipolyomavirus is suggested (Stoll,1993).

The aetiology of French Moult has been very well investigated throughout the years. It appeared to be a contageous viral disease caused by a member of the papovaviridae family and is designated now as the avipolyomavirus. This mammalian virus was obviously able to adapt, replicate and survive in psittacine birds because of its unique properties (Griffin,1983) [11]. Two forms of the disease have been recognized in Budgerigars; the most severe form (BFD) causing mortality rates up to 100% in budgerigar fledgelings and a mild form called French Moult causing feather disturbances resulting in birds called "runners". If an outbreak of the disease occurs, precausions should be taken to prevent the virus from spreading throughout the aviary (Baker,1990) [1]. Adult birds probably spread the disease through feather dust and droppings. Runners spread the virus through feather dander, feather dust and droppings. The infection is egg-transmitted for eggs from pairs producing affected young will also give diseased birds when fostered by pairs whose own youngsters are normal. The use of an effective disinfectant such as Vircon S is recommanded. If the disease is present in your aviary, do not sell or exhibit birds because if you do so, you will spread the disease to other fanciers.

AnaPatricia García, Kenneth S. Latimer, W. L. Steffens, and Branson W. Ritchie

College of Veterinary Medicine, The University of Georgia, Athens, Georgia 30602.

Abstract. An adult female Budgerigar was presented with dyspnea and abdominal distention. After a few days of supportive treatment the bird died and a necropsy was performed. A large, cystic, perihepatic mass was present. Microscopically, this mass was composed of multifocal to coalescing aggregates of proliferating heterophils. The neoplastic cell population showed maturation from the blast stage to differentiated granulocytes. Electron microscopy demonstrated that the granulocytic cells belonged to the heterophilic lineage. The final diagnosis was granulocytic sarcoma.

Key Words: Avian, Budgerigar, Melopsittacus undulatus, Chloroma, Granulocytic sarcoma, Heterophil, Myelocytoma, Myeloblastoma

Granulocytic leukemia is the neoplastic proliferation of granulocytes originating in the bone marrow. Infrequently, granulocytic leukemia in mammals is associated with the formation of sarcomatous tissue masses called chloromas.¹ These neoplastic tissue masses usually arise in visceral organs. They are characterized by a green color that is imparted by myeloperoxidase in the specific (azurophilic) granules of neutrophils. Similar hematopoietic neoplasms in birds are known by the synonyms granulocytic sarcoma, myelocytoma, or myeloblastoma. These neoplasms are associated with the proliferation of heterophils and their precursors, which lack myeloperoxidase. Granulocytic sarcoma is relatively common in domestic fowls but is rare in exotic birds.^1-3 The purpose of this case report is to describe a granulocytic sarcoma in a Budgerigar.

An adult female Budgerigar (Melopsittacus undulatus) was presented to the University of Georgia Veterinary Medical Teaching Hospital with abdominal distention and dyspnea. The bird died a few days after admission despite supportive treatment. Necropsy examination of the animal revealed a large, cystic, perihepatic mass.

Microscopically, the mass was composed of multifocal to coalescing aggregates of proliferating granulocytes (Fig. 1). This cell population showed maturation from myeloblasts to more differentiated granulocytes (Fig. 2). Cytoplasmic granules appeared red and slightly elongate, suggesting heterophilc cell lineage. The neoplasm also contained numerous variably sized and shaped vascular spaces. More normal sections of liver contained scattered foci of extramedullary heterophil production, often centered around blood vessels beneath the hepatic capsule.


Fig. 1. Budgerigar, granulocytic sarcoma, H&E stain. Perihepatic mass appears hypercellular.	Fig. 2. Budgerigar, granulocytic sarcoma, H&E stain. More differentiated cells contain red cytoplasmic granules.

Electron microscopy of ultrathin sections of the mass revealed two types of neoplastic cells. The first cell type consisted of large, round blasts with a thin rim of cytoplasm containing occasional granules. The second cell type appeared smaller, round , and more differentiated. These cells had more aggregated chromatin within cell nuclei and more abundant cytoplasm containing membrane-bound granules (Fig. 3). The cytoplasmic granules were round in cross section and elongated in longitudinal section. Some of the granules were more electron dense than others and occasionally appeared to have a lighter central core (Fig. 4). These ultrastructural characteristics were typical of heterophilic lineage. The definitive diagnosis in this Budgerigar was perihepatic granulocytic sarcoma.


Fig. 3. Budgerigar, granulocytic sarcoma, electron micrograph. Heterophil granules are round in cross section and elongate in oblique or longitudinal section. Notice variation in granule radiodensity.	Fig. 4. Budgerigar, granulocytic sarcoma, electron micrograph. More radiodense heterophil granules occasionally have a lighter central core. Radiolucent granules also are present.

Neoplasia is a frequent cause of death in pet Budgerigars (Melopsittacus undulatus), affecting more than 15% of birds that are examined at necropsy.¹ The most common neoplasms in Budgerigars are carcinomas of the kidney, ovary, and testis. In contrast, hematopoietic neoplasms are rare in Budgerigars. Carcinomas of the genitourinary tract and fibrosarcomas in chickens are part of a spectrum of neoplasms that may be caused by infectious type C retroviruses (avian leukosis/sarcoma viruses). In addition, two similar forms of hematopoietic neoplasia (designated myelocytomatosis and myeloblastosis) have been observed in chickens. These neoplastic diseases are associated with avian myeloblastosis virus and often result in hepatomegaly and splenomegaly from neoplastic cell infiltration.¹ Furthermore, myelocytomatosis is associated with the formation of neoplasms on the surface of bones with intimate contact to the periosteum. These neoplasms consist of compact masses of uniform myelocytes. In contrast, myeloblastosis affects most parenchymatous organs and is characterized by massive intravascular and extravascular accumulations of myeloblasts with a variable proportion of more differentiated myelocytes.²

The avian leukosis/sarcoma viruses are closely related and, depending on their genetic makeup, cause a variety of neoplasms with short to long latencies. Some viral strains such as avian myeloblastosis virus, avian erythroblastosis virus, and the sarcoma viruses contain specific viral oncogenes that cause rapid neoplastic transformation of target cells with subsequent tumor development within a few days or weeks. These avian leukosis/sarcoma viruses of chickens have been divided into six subgroups (A, B, C, D, E and J) on the basis of their host range in chicken embryo fibroblasts of different genetic types, interference patterns with members of the same and different viral groups, and type of viral envelope antigens. Viruses of subgroup A and B occur as common exogenous viruses in the field. In contrast, viruses of subgroups C and D rarely have been associated with field disease in chickens. The subgroup E viruses include the ubiquitous endogenous leukosis viruses of low pathogenicity.² Subgroup J viruses have been isolated from meat-type chickens and are associated with an increased incidence of myelocytomatosis.^2,3

In chickens and other animals harboring infectious retroviruses, the virus particles can be detected readily by electron microscopic examination of normal or neoplastic tissues. However, electron microscopic search for retroviral particles
in budgerigar neoplasms has been unrewarding.⁴ Using immunodiagnostic techniques, avian leukosis viral antigens have been detected in sera from tumor-bearing Budgerigars using an enzyme-linked immunosorbant (ELISA) assay.⁵ In addition, renal tumor tissues from Budgerigars were positive for the RAV -2 strain of avian leukosis virus using dot-blot analysis and Southern blot hybridization. These data suggest that avian retroviruses may be implicated as etiologic agents of certain neoplasms in Budgerigars. In the Budgerigar of this report, we did not observed viral particles in granulocytic sarcoma tissue prepared for electron microscopic examination. Further analysis of neoplastic tissue will be required to confirm or refute the presence of retroviruses in this neoplasm.

Granulocytic sarcoma (chloroma, myelocytomatosis, myeloblastic sarcoma, myelocytic sarcoma) has been reported in four Budgerigars and a White-tailed Black Cockatoo (Calyptorhynchus funereus latirostris).⁶ The histologic differential diagnosis for these lesions also includes osseous metaplasia, extramedullary hematopoiesis, myelolipoma, and hemangiolipoma.⁷ Osseous metaplasia is recognized by the presence of osteoid and spicules of mineralized bone associated with the hematopoietic cells. Extramedullary hematopoiesis occurs with some frequency in birds and may be observed in diverse locations including the spleen, liver, kidney, adrenal gland, gastrointestinal tract, heart, and dura mater. Histologically, extramedullary hematopoiesis is associated with the production of mature leukocytes, erythrocytes, and/or thrombocytes in any combination. Hematopoietic cell proliferation is unaccompanied by sarcomatous tissue masses. Myelolipoma consists of the coproduction of hematopoietic cells and lipocytes. These masses are observed most commonly in the subcutis and liver, but also may be observed within the thoracoabdominal cavity.^7,8 Hemangiolipoma consists of adipose tissue and a vasoformative component similar to hemangioma. The diagnosis of granulocytic sarcoma is based upon the presence of a sarcomatous tissue mass composed of proliferating myeloblasts that show little differentiation to mature granulocytes.

Diarrhoea in Budgerigars
An Approach to Treatment

Dr John R Baker

Diarrhoea, otherwise known as scour, wet vent or, is a common complaint affecting either an individual bird or the whole stud. Diarrhoea varies widely in appearance from normal colour but soft or runny, to odd colours, mostly grey or grey-green. If dark, bottle-green, soft droppings are being produced, this indicates that the bird is not eating but there is probably nothing wrong with the bird's digestive system. If the black part off the dropping is normal but the white part is soft or fluid, this indicates kidney problems which are not covered by this article. As described elsewhere, the causes of diarrhoea are many and varied, and some of these are amenable to treatment and others are not. The aim of this article is to give fanciers some help in the treatment of affected birds always remembering however, that the best person to advise on treatment is a veterinary surgeon with an interest in cage bird diseases.

The first thing to do, once you have spotted that you have a bird with diarrhoea, is to catch it and have a close look at it to check if there are any other symptoms. Is there any matting of the feathers on the head indicating that the bird is vomiting as well? Look at the bird's beak and eyes - do they look normal? If not, it may well not be a digestive problem. Gently feel the bird behind the keel bone (sometimes known as the breast bone which can be felt as a hard line along the lower side of the birds chest) - is it pot-bellied or can you feel a swelling which should not be there? This could indicate cancer which your veterinary surgeon might consider attempting to operate on. If you notice these or any other symptoms, consult your veterinary surgeon as soon as possible. For the purposes of this article we will assume, apart from the diarrhoea, there is nothing else to be found other than the bird being fluffed up and perhaps not eating.

Having examined the bird it should not be put back in the flight where it might spread it's disease to other birds, but put it in a cage on its own or with other similarly affected birds. The next thing to do is to decide how the bird is. Is it bright and alert and looking around at its new surroundings, or is it ill, as indicated by it being dull, listless, fluffed up and sitting on the floor of the cage?

If the bird is obviously ill, treatment is urgently required otherwise the bird will die. The first thing it needs is warmth and it should be put somewhere where the temperature is about 80 Fahrenheit. Ideally, this should be in a proper hospital cage, but the use of a show cage in the airing cupboard is quite a good idea if you don't have a proper hospital cage. It will also need fluid; about a teaspoonful (6ml) a day divided into 5 or 6 doses and also containing a readily digested source of energy.

If you make up a solution of 2 heaped teaspoonfuls of glucose to 3 pints of water this will supply both requirements. This should be given warm and directly into the crop with a dosing tube, (available from good pet shops) which all fanciers should have in stock and know how to use. If you have not used one before ask a local experienced fancier or your veterinary surgeon how it is done. If the bird does not respond to this treatment within a day or two the outlook is not good and it should be seen by your veterinary surgeon.

If the bird shows little or no sign of illness, except for the diarrhoea, and is eating and drinking, there is a possibility that some change in management may have upset its insides. Has it recently been purchased, been to a show, been introduced to a strange group of birds, had its diet or water changed, or been given large amounts of green food? If any of these has happened the chances are that the bird will get over its problem in a day or two. Most of the birds we receive at the University for examination have diarrhoea for the first day but nearly always get over it quickly without treatment. If the problem persists, put the bird back on its old diet and/or water or take it out of the strange group and see if this does the trick. Another not uncommon cause of diarrhoea is stress; some birds can not cope on their own and some can not cope with being mixed with others and, in both these situations there can be an intestinal upset. If you find, for example, that each time you put a specific bird in a flight it gets diarrhoea, this will be one of these stress susceptible birds which are upset by being in the flight. Remember that the large, bulky, wet droppings produced by breeding hens are quite normal and should not be confused with diarrhoea.

If there has been no change in the way you look after the birds and there is a problem with diarrhoea then you will have to start to think about some form of treatment. The first point to make about this is that the last thing you should use are antibiotics. Don't dash for the yellow powder that most fanciers seem to have. The reasons for this are first, that only very rarely is diarrhoea due to specific disease causing bacteria which are the only thing which antibiotics will cure and second, the more you use antibiotics the more likely they are to lose their effectiveness. Antibiotics do have an important role to play in bird medicine but they are not the first drug of choice for the treatment of most cases of diarrhoea. The way to treat the bird is what is termed symptomatically that is, treating the symptoms rather than a specific disease. What we need is something which will calm the gut, and two things which are good for this are cold strong tea - about a teaspoonful - and kaolin (pure kaolin from the chemists, don't use preparations for treating humans which have other things added) about 1 or 2 drops. These should be given directly into the birds beak or better still with a dosing tube.

If the diarrhoea persists other treatments may be tried. The work we have done at the University suggests that quite a number of cases of diarrhoea are due to a disturbance in the types and numbers of bacteria in the gut, without a specific disease causing germ being present. It is necessary in these cases to re-establish the normal germs. There are two ways of doing this, one way is to collect some normal droppings from healthy birds, make these into a slurry with a few drops of water and, with a dosing tube put this into the birds crop. Obviously there is the risk of spreading disease if this is done and a better approach is to use a probiotic. These are available from the pet shop under a wide variety of trade names. One that is normally available is called "Revive" but there are a number of others which are equally good, on the market. Probiotics are cultures of harmless germs which are normally present in the birds intestines and the idea is to swamp any germs which might be causing the problem and re-establish the normal ones and hopefully, cure the disease. They can also be used to establish germs in the intestines when they have been lost for some reason. Some of these come with their own dosing tube holding the right amount and with others the instructions on the bottle should be followed

If none of these methods work now is the time to try antibiotics if you have some in stock. If not, contact your veterinary surgeon and show him the bird and he will probably prescribe them. If the antibiotics don't cure the problem contact your veterinary surgeon and ask him to arrange for samples of droppings to be sent off to a laboratory for examination so that the specific cause of the problem can be identified and the correct treatment given.

Megabacteria are associated with disease and death in Budgerigars and a range of other birds. They inhabit the proventriculus or true stomach where they cause changes in the structure and function of the organ. The proventriculus becomes dilated and the wall thickened; the production of digestive juices is impaired; excess mucus is produced and there may be ulceration at each junction of the proventriculus and gizzard. The disease is extremely common in exhibition Budgerigars in the UK and is the major cause of illness and death in these birds.

It was believed that apparently healthy birds could carry this infection and live in balance with it, and that these birds were responsible for spreading the infection from stud to stud as birds were bought, sold and exhibited. Some vets, and others, believe that megabacteria are normal inhabitants of the bird's stomach, and that some other disease is responsible for the changes in the proventriculus which allows the number of megabacteria to increase. No proof of this has ever been produced so work was carried out to establish whether carriers existed or not. Was megabacteria after all, simply a normal inhabitant of the proventriculus? It was also hoped that it would be possible to demonstrate the role of megabacteria in causing proventricular disease.

As part of the Budgerigar Society diagnostic service, dead Budgerigars are examined post-mortem. In 160 birds received over the last few months, particular attention has been paid to the proventriculus, and this organ has been examined for megabacteria regardless of the cause of death. The results were as in the table below.

As only one-third of the birds with normal proventriculi have megabacteria in the organ, the bacteria cannot be considered to be a normal inhabitant of this part of the Budgerigar. However, in most other diseases where clinically normal carriers are present, they form a lower percentage of the population than this. A possible reason for the high prevalence of clinically normal carriers, is the very high prevalence of the clinical disease which results in large numbers of healthy birds being exposed to the infection and becoming unwell or carriers of the infection.

The birds with megabacteria infection of an abnormal proventriculus showed changes, such as an excess of mucus in the organ or a minor degree of dilation, thickening of the wall, and ulceration at the junction of the gizzard and proventriculus. Many of these birds had been clinically ill but, in some of the cases of birds with minor lesions, the birds had died of other causes. While nearly all cases of abnormal proventriculi were due to megabacteria infection, a few were not. In this survey six birds had abnormal proventriculi due to:

This is a copy of the notes that Dr Baker sends out after carrying out post-mortem examinations.

Megabacteriosis is an infection of the stomach which interferes with the proper digestion of the food, and in the long term, the affected birds die of starvation. Some of the affected birds show retching or vomiting and some have diarrhoea. Occasionally birds die rapidly from this disease, and in these cases there has been the formation of an ulcers in the stomachs and the birds can bleed to death internally from these.

There appear to be different strains of this bacteria, some of which cause relatively rapid death, while others cause mild symptoms which can last for a long periods, months, and occasionally years, before the condition becomes serious.

Once this infection gets into a stud, you must expect occasional birds to go down with this disease. This is particularly prone to occur when the birds are subjected to stress, for example, when they are put down to breed, taken to shows or moved to a new owner's premises.

There is a drug which will eliminate the megabacteria from the birds, but only rather more than half the birds get better because, in some birds, the damage to the stomach is so severe that it never heals. To be effective it is essential to treat birds early on in the disease. It may be worth getting some of the drug to try treatment of any other birds which go down with weight-loss and the symptoms described above. The drug is amphotericin B which is sold under the trade name of Fungilin Suspension (manufactured by E R Squibb and Sons Ltd). Birds should be given 0.1 ml of this preparation into the beak, or preferably by crop tube, twice a day for at least 10 days. It is very important that there is no break in the treatment and that the doses are given at 12-hour intervals. I regret that it is not possible for me to treat affected birds here. You will be able to obtain the drug through your local veterinary surgeon; you may have to show him this letter and some of the birds before he will let you have it.

You may have read in the fancy press that the condition can be treated with various acids; I have tried a number of these completely without success

Unless you are prepared to dose all the birds as detailed above, there is no way of eradicating the infection from a stud with drugs available here. The Australians do have a drug which can be given in the drinking water to eliminate this infection, but unfortunately, it is not available in the UK. The immunity to this infection is weak, so that if treated birds are exposed to the infection again, for example at a show, or if an infected bird is bought and added to the stud, they are very likely to catch it and the disease may reappear.

While I have use amphotericin B in a very large number of birds without ill effect I am required to tell you that the product is not licensed for use in birds. This means that if some adverse reaction occurs you will have no claim on the manufacturers, the veterinary surgeon prescribing the product, nor myself.

The research project into budgerigar ailments, sponsored by the Lancashire, Cheshire and North Wales including the Isle of Man Budgerigar Society, was started in 1984 and lasted for 8 years. From 1992 there will be some change of emphasis so this seems a good time to look back at what has been achieved.

The project starts each year in February and prior to this discussions are held to decide the topic for the year. The aim is to pick a topic of interest to the fancy, which stands a reasonable chance of being completed in the year, and taking into account the limited time that I can devote to research and the constraints imposed by the finance available. The latter two are particularly important and mean that a number of topics of great interest to the fancy, such as French moult, cannot be investigated.

The topic chosen for 1984-5 was 'going light.' Many diseases of cage birds make them lose weight and 'go light.'

1985-6 was the year of vomiting budgies. Birds actually being sick or or trying to vomit were noticed by a number of fanciers as being a common problem.

After this success with a disease at the top end of the digestive system, in 1986-7 attention was turned to the other end to look at why some birds developed diarrhoea.

In 1987/88 attention was turned to reproduction and in particular why exhibition budgies had (and still have) such an abysmal breeding record when compared with almost all other breeds of cage birds and poultry.

In 1988-89 it was decided to find out exactly what the causes of death of exhibition budgerigars are.

I had noticed when talking to fanciers that many used a great variety of mineral and vitamin supplements and it was not unusual for 2, 3, or even more of these to be used in one stud.

In 1990-1 it was decided that we would investigate the condition of clagged vents in which large amounts of droppings accumulate around the vent.

The last project, undertaken in 1991-2, was an investigation of eye problems in budgerigars.

Also in 1990-91 the University purchased some very expensive equipment for doing blood chemistry on the normal domestic species that we deal with and this had the capability to do chemistry on minute amounts of blood. This equipment was used to find out the normal levels of a number of substances in normal budgerigar blood and, following this, to use it as a method for locating the problem in sick birds. It has proved its worth in the diagnosis of liver and kidney diseases and also in cases of diabetes.

Due to the lack of support by the fancy for the last 2 projects, and also as we could not think of projects which would appeal and be practical for 1992-3 at least we were offering a free treatment and advisory service to members of the LCNWBS; other fanciers are to use this service but a charge was made for any work done.

While the above describes briefly some of the "official" projects, a lot of other work has also been carried out. Quite early on in the project it became clear that there was a need for a diagnostic service using samples, live birds or post-mortem examinations and at least as much time has been spent on this as on the "official" research. Many interesting diseases have been seen and even now new ones are cropping up. Small projects have been carried out on three of the most serious diseases; psittacosis, budgerigar fledgling disease and megabacteriosis.

In brief psittacosis is treatable and there is certainly no need for fanciers to put down infected studs. The other two diseases are not currently treatable but we now know enough about them to advise as to what to do and what to expect.

There have been other benefits to come out of the project. The first of these is that the veterinary students at Liverpool University now get some lectures on budgerigar diseases and a certain amount of hands-on experience. Second we are now able to offer to veterinary surgeons in practice, an advisory service for budgerigar problems and this is quite popular. Third, it became obvious very early in project that fanciers were having difficulty in locating vets with experience of cage birds and their diseases. As a result of this a list was drawn up of vets working in this field, and it has proved very popular indeed and has now been amalgamated with one produced by a commercial company (Vetrepharm) so that fanciers should always be able to find somebody in their area who can assist with problems.

Last but not least there is no point in doing this type of research and clinical work unless the findings are made available to the fancy and I am most grateful to Cage and Aviary Birds, The Budgerigar and the News Report of the LCNWBS for publishing articles based on the work I have done; articles are also published in various veterinary magazines from time to time to keep the profession aware of what has been going on.

While the "official" projects have been stopped, for a year in the first instance, I do very much hope that the mutual assistance which has been of such benefit to all parties, the fancy, the research committee, and myself will continue and flourish for many years to come.

Budgies and cockatiels are the most common pet birds seen in practice. It is important to understand the most commonly encountered diseases and conditions of these popular little birds, in order to be able to properly diagnose and treat them. When dealing with the owners of budgies and cockatiels, do not underestimate their attachment to these little birds. Offer them the same diagnostics and level of care that you would the owner of a macaw or Amazon parrot. To many budgie and 'tiel owners, their birds are true members of the family and they are willing to have any necessary diagnostics performed, and have any required treatments administered. Do not compromise the quality of care offered to the smaller birds.

The budgerigar, Melopsittacus undulatus, is a fascinating little psittacine with well-deserved popularity due to its small size and big personality. The budgie is the best known of all parrots, and has found its way to virtually every country in the world. It may be considered a domesticated parrot, as it has bred prolifically in captivity since the mid 1800s. While sexual maturity usually occurs at approximately six months of age, researchers have shown that young male budgies may produce spermatozoa within 60 days of leaving the nest. This rapid sexual development is a physiological adaptation to an arid environment and enables very young birds to reproduce quickly when conditions are propitious.

Most parrots are taken out of the nest as babies to be hand fed to make them more tame, however, budgies are usually left with the parents until after they are fledged. Baby budgies tame down very quickly and make devoted, wonderful companions.

Budgies are about seven inches in length and weigh between 26-30 grams. English budgies are slightly larger and weigh proportionally more. The average life span is between six and ten years, and the maximum recorded life span is 18 years. Budgerigars are native to Australia, and tend to live in large flocks, although they may also be found in small parties. In their native habitat, they feed on seeds procured on or near the ground, and the important food items are seeds of native grasses. Crop contents studied included grass seeds and a few seeds of Portulaca oleracea. Budgies have been described as extremely nomadic in Australia and they can be found inhabiting timber bordering watercourses, sparsely timbered grasslands, dry scrublands and open plains. It is very important to note that wild budgies are very active birds, flying great distances to visit waterholes and seeding grasses. They fly from tree to tree and scurry through the grass searching for seeds. Many problems with captive budgies can be directly attributed to the sedentary lifestyle of the pet caged budgie, when its activity level is compared to that of a wild budgie.

Male budgies can be excellent mimics and can develop huge vocabularies. Hens may whistle and can learn a few words, but they are not nearly as loquacious as males. Budgies are dimorphic. Adult males of most colors, except albino and the very pale pastels, develop a blue cere. Hens have a lilac or tan cere that turns brownish upon maturity.

Cockatiels are usually taken from the nest when they are two to three weeks of age for hand-feeding. Any of the commercially available hand-feeding formulas are fine to use. Cockatiels are usually 12.5 inches in length, and weight between 75-125 grams. Larger boned show cockatiels may weigh 10-15 grams more. Feel the pectoral muscles, if they bulge away from the center keel bone, then the bird is probably overweight. Sexual maturity may occur as early as six months of age, and up to 12 months. The recorded maximum life span is 32 years, but on the average, a cockatiel will live for 15-20 years in captivity, given proper conditions.

Cockatiels are dimorphic once they have molted out the baby feathers. This molt usually occurs at about six months of age. Adult grey males have bright yellow facial feathers and bright orange cheek patches. Adult grey hens have dull facial feathers. With the color mutations, adult males have solid primary remiges and retrices. Hens will have yellow dots on the remiges, stripes of yellow on the retrices. These marks are subtle. Males are great mimics, and can whistle tunes and talk very well. Hens will vocalize, and can whistle a bit, but most won't talk.

Budgies and cockatiels consume a primarily seed diet in the wild, and they do seem to thrive on a seed-based diet. However, pellets, sprouted seeds, fresh fruits, vegetables, pasta, whole wheat bread and healthy table foods are sound additions to the budgie diet. A budgie that eats just seeds should have access to a cuttlebone or mineral block, and should receive supplemental vitamins (but NOT in the drinking water) as directed by your avian veterinarian. Some budgies and cockatiels are extremely resistant to dietary changes.

It should be noted that it can be dangerous to try and convert any bird to a different diet without first ascertaining that it is healthy. Dietary conversion in a sub-clinically ill bird can precipitate a health crisis. Always evaluate a bird's health before to attempting to change a budgie's or cockatiel's diet to make sure that is healthy enough to withstand the stress of changing the diet.

Budgies, and to a lesser extent, cockatiels, are very prone to obesity and the problems related to being overweight. The obese budgie or cockatiel may develop lipomas, which are benign (non-malignant) fatty tumors. These may be found over the crop area, the chest or the abdomen, most commonly. In other cases, the bird may develop generalized lipomatosis, which is a layer of fat over the entire surface of the body under the skin. Xanthomas, yellow fatty tumors, may also occur. Surgery may be necessary, especially if the skin over the tumor ulcerates, but often, the tumor will recur, unless changes are made in the diet and activity level.

Obese birds usually have some degree of liver problems. When fat is deposited in the liver, normal liver cells are replaced with fat and over time, if enough normal liver tissue is destroyed, it can no longer function properly. Birds with fatty liver syndrome (also called hepatic lipidosis) will suffer from some degree of liver dysfunction and may bleed excessively, as the liver is responsible for providing clotting factors in the blood. Hepatic lipidosis is very serious and can be fatal. Prolonged liver damage may result in the liver becoming fibrotic eventually, leading to cirrhosis of the liver. Hepatic lipidosis can have multiple causes, and may have a genetic predisposition. Birds on an all-seed diet with restricted exercise are prime candidates for hepatic lipidosis. Thyroid dysfunction may result in obesity. Toxins such as aflatoxins can result in fatty changes in the liver. Steroid administration (from topical ointments or hormone injections with methylprogesterone, for example) can cause a bird to gain excessive weight.

Budgies and cockatiels with liver disease may have overgrown toenails and beaks. The best indicator for liver disease in birds is the bile acids blood test. To definitively diagnose liver disease, a liver biopsy should be performed. However, in many cases, a bird with advanced liver disease cannot withstand the stress of a surgical procedure and may have problems with the blood not clotting, so surgery may not be recommended or possible.

While I do not condone allowing any pet bird free-flight in the home due to the risk of injury or escape, it must be remembered that budgies and cockatiels are naturally very busy birds, so the largest cage that is practical should be purchased. They should have toys, swings, ladders and playgyms, and owners should encourage their birds to play and exercise frequently to prevent obesity.

Obese birds, and those with lipomas, should be offered a diet lower in fat. Each case should be discussed individually with your avian veterinarian. As guidelines, I usually recommend decreasing regular seed mix and increasing millet, since millet is lower in fat than the other seeds. Sprouted seed is healthier, and should be offered daily. I also recommend offering pasta and whole wheat bread, plenty of fresh veggies and fruit, and some table foods (without butter, margarine or other added fats). Increasing the activity level of obese birds should be undertaken.

It should be noted that feeding greens, fruit and vegetables does NOT cause diarrhea, as is often quoted in budgie books. Consuming foods with more water in them will cause increased urination, and not diarrhea. Feeding vegetables and some fruits is recommended and bird owners should not be put off by printed misinformation that discourages them from feeding those healthy foods.

Iodine deficiency in the diet may result in thyroid dysplasia in budgies, although this is not as common as it used to be. This occurs in birds that consume an all-seed diet that is deficient in iodine. Birds with thyroid dysplasia present with respiratory signs from the enlarged thyroid glands pressing on the trachea and syrinx. Some develop a characteristic squeak when they breathe. This is treated by prescribing an iodine supplement. Injectable iodine: 20% sodium iodine in saline for injection, 0.01 ml/budgie once, IM. Oral: Make stock solution of 2 ml Lugol's iodine in 30 ml water. Mix one drop of stock solution in 250 ml drinking water. Use daily for treatment, 2-3 times per week for prevention.

Cockatiels should probably not receive a 100% pelleted diet. Cockatiels that have been on a pelleted diet for years have developed renal disease. For this reason, I recommend not feeding more than 50% pellets, some seed, and a good portion of the diet should be table foods, fruits, veggies, pasta, whole wheat bread, and other nutritious items. Avocado, chocolate and onions should not be fed, due to potential toxicosis problems.

Budgies with a crusty cere, feet and vent are usually infested with the Knemidokoptes mite. Most budgies with this condition are young (usually less than one year of age). These mites do not cause pruritis (itchiness), and cause a honeycomb type appearance to the skin and cere, upon close examination. Scrapings of the lesions or examination of the crusts in oil under the microscope will show the mites. The treatment of choice is ivermectin based upon careful dose calculation Dosage: 0.2 mg/kg PO, repeat in 10-14 day intervals until signs decrease. Although they do not appear to be very contagious, it is recommended that all birds kept in the same cage also be treated with ivermectin, either orally or topically. As with demodectic mange in dogs, this mite appears to be related to the immune status of the bird, and often the offspring of infested birds will develop Knemidokoptes, as well. Treatment should be repeated at two-week intervals until the bird is clinically normal. Long term infestation may result in permanently deformed beaks, which will require periodic shaping by an avian vet with a grinding tool and emery board. Mites do not live off the bird, so treating the cage is not necessary, but is recommended. Mites that occur in older birds usually indicate some underlying medical problem, such as hepatic lipidosis, diabetes mellitus or even tumors. Mites occasionally occur in other species of birds, rarely cockatiels.

Red mites can occur in budgies and cockatiels. These mites are very contagious between birds of different species, and they suck blood. They are visible to the naked eye as tiny specks of red pepper. Red mites (Dermanyssus species) remain off the bird and climb on the host to take a blood meal. They can make the infested birds very nervous and irritated. They sometimes bite people when birds are absent. In addition to treating the birds with red mites, the entire cage and bird area must be thoroughly disinfected to prevent reinfestation. Treatment with oral ivermectin and topical 5% carbaryl, repeated weekly, is usually effective. I saw one case involving a military macaw that had a severe infestation with red mites, and the poor baby bird had multiple feather cysts caused by the damage from the mites.

Feather mites can occur on budgies, and two species have been described to infest budgies. These mites, however, are not commonly encountered. Feather and quill mites can be found (rarely) on cockatiel feathers (usually primary and secondary remiges). Many budgie and 'tiel owners believe that they must use some sort of protection against mites, which can be hung on the outside of the cage, but these are ineffective and potentially dangerous, as the fumes can cause liver damage and perhaps cancer if inhaled for a long period of time. Mite protectors usually have mothballs (paradichlorobenzene) as the active ingredient. If a budgie does not have mites, a mite protector is not necessary to prevent infestation. If a budgie does have an external parasite, it is best to seek the expert advice of an avian veterinarian who can diagnose the exact problem and prescribe the correct medication to treat it at the proper intervals.

Giardia and ascarids (roundworms) frequently occur in budgies and cockatiels. (Don't forget, I practice in Florida, the land of bugs and parasites!) It is important to realize that birds need not be kept in walk-in aviaries (with access to the ground), nor do they have to be housed in sub-standard conditions to harbor these parasites. I have found that ivermectin is not the most effective dewormer for ascarids. Pyrantel pamoate is a better choice. Trichomonads occasionally occur in budgies and cockatiels, as well, and this parasite is most often diagnosed from a swab taken from the oral cavity or crop.

I recommend that avian vets routinely deworm a pet bird at least once or twice, during routine first examination, with a very safe medication, even if fecal parasite examinations are negative. This is because the gastrointestinal tract transit time is so fast in birds that worm eggs do not concentrate in the fecals (as they do in dogs and cats), and it is not only possible, but likely, to miss roundworms on a fecal exam. I have performed countless second opinions on small birds with GI problems that have had negative tests for worms, yet, when I dewormed them, they passed roundworms! If a bird passes roundworms, it should be periodically dewormed for the rest of its life, as the worms may form cysts in the tissues that are released from time to time, resulting in additional worms setting up housekeeping in the intestines.

Note: fenbendazole can cause fatal hepatopathies, and should not be used in pet birds routinely, also causes feather abnormalities if administered when bird is molting

Giardia, a one-celled protozoal intestinal parasite is often difficult to diagnose in birds. Wet mounts of fresh droppings may sometimes show the protozoa. However, other tests may be necessary to diagnose Giardia. An ELISA (enzyme-linked immunoassay) test on the droppings may be performed. One lab has had great success in diagnosing Giardia (and other parasites) by having the vet place feces in 5% formalin (not the usual 10% used to preserve tissues for histopathology) which prevents damage to the fragile Giardia cysts, and then the droppings are examined with special stains and microscopes.

The lab I recommend is:
Parasitology Research Lab, LLC
P.O. Box 10/357
Neosho, MO USA 64850-0357
Phone/fax: 417-451-0201
Call to set up an account and get fee schedule.

Treatment of Giardia can be problematic, and most available drugs only kill Giardia in a low percentage of birds. Metronidazole works in about 30-40% of cases. However, it has poor palatability, as well. Ronidazole or dimetronidazole are more effective. Fenbendazole may work well, however, due to potential hepatic toxicosis, this should be avoided. One way to prevent reinfestation is by having a bird use a water bottle in place of the more common water bowl.

While budgies and cockatiels are very hardy little birds, bacterial infections are commonly encountered. Most occur in birds that have a water bowl or cup and not a water bottle. Even the most diligent owner cannot prevent fecal and food contamination of water in an open vessel, which will rapidly grow bacteria. Budgies and 'tiels are very smart little birds and most will rapidly adapt to using a water bottle.

Even though budgies and 'tiels are very small birds, it is possible to run complete blood counts and blood chemistry panels on them. The complete blood count is probably the most important single test that can be run on a bird, as it helps the avian vet determine if a bird has a bacterial, fungal or viral infection, and it shows if a bird is anemic, dehydrated or suffering from a myriad of problems. Bacterial culture of the eye, respiratory tract, choanal slit, crop, cloaca or lesion may help diagnose bacterial problems. Fungal cultures may be helpful. A Gram's stain may help screen birds for potential problems, however, it is only useful as a screening test, and not as a true diagnostic test in most cases. Usually, a healthy bird will have predominately Gram positive cocci and rods. Gram negative rods are not normally found in high percentages in most birds. An abnormal Gram's stain should be followed up by appropriate culturing. Candida may be picked up on Gram's stain, as well, but some foods add brewer's yeast to the diet, which may show up on the Gram's stain. If yeast is causing problems, it may be budding or have pseudohyphae. When in doubt, ask for a fungal culture, which will differentiate between brewer's yeast and potentially pathogenic Candida.

Yeast infections with Candida can occur, especially in birds that don't get enough vitamin A in the diet. Many bacterial and yeast infections in budgies and cockatiels occur as a result of owners allowing birds to eat out of their mouths, or if they allow a bird to have contact with human saliva. Our mouths contain many microbes that can cause disease in birds, and contact with the human mouth should be strictly prohibited.

A controversial disease in budgies is called megabacteria. These large bacteria can be found in the proventriculus (and sometimes the crop or other portions of the GI tract) of both healthy and ill birds. It can be difficult to diagnose in live birds. Some researchers believe that megabacteria are normal inhabitants of the GI tract and others feel that this organism is responsible for causing disease in budgies. This can also occur in other birds, including cockatiels.

The bacteria responsible for causing tuberculosis, Mycobacterium, may cause disease in budgies and 'tiels. One screening test is called an acid-fast stain, and the organism may also be grown on culture, but a special lab and special techniques must be used to culture it. Often, birds with TB will have an elevated white blood cell count.

A primitive bacterium is responsible for causing the disease known as chlamydiosis (also caused psittacosis or parrot fever). This organism may cause respiratory disease in budgies and cockatiels, and is contagious to other birds through infected droppings, and infected secretions. It may also affect the liver and GI tract. Budgies and 'tiels can be carriers of chlamydiosis, and may not show clinical signs. Chlamydiosis is fairly common in budgies and cockatiels, and it should be noted that testing is not always accurate in the live bird. DNA PCR testing is helpful in procuring a diagnosis and the white blood cell count may be mildly elevated, or it may remain normal. Chlamydia is very host-adapted to cockatiels and diagnosis is very problematic in the live bird.

Due to potential legal problems, every cockatiel owner should be advised about the zoonotic potential of chlamydiosis. I give every 'tiel owner a hand-out (purchased from the AAV publications office). If an owner declines testing, be sure to note that in the chart.

AAV Publications office address:
Kathy Lyon
Publications Coordinator
P.O.Box 210732
Bedford, TX USA 76095
PH: 817-428-7900
e-mail: AAVPubs@aol.com

AAV Central Office:
Adina Rae Freedman, CAE
Executive Director
P.O.Box 811720
Boca Raton, FL USA
PH: 561-393-8901
e-mail: AAVCtrlofc@aol.com
Website: www.aav.org/aav

Another disease that may present with similar clinical signs is mycoplasmosis. Both chlamydia and mycoplasma may be treated with doxycycline or enrofloxacin. Enrofloxacin dosage: 7.5-20 mg/kg q12 hrs. For flock treatment: water-soluble doxycycline is available from Global Pigeon Supply, phone: 912-356-1320.

Budgies are often implicated in outbreaks of polyomavirus infection. This virus can cause budgie fledgling disease. French moult, a slow, debilitating disease of budgies may be caused by polyomavirus or psittacine beak and feather disease virus (PBFD). A vaccine against polyomavirus is available to protect non-budgerigar psittacines, and a vaccine for budgies is under investigation. Cockatiels may also suffer from polyoma viral infections. Budgies and cockatiels may also be affected by other types of viruses, including Proventricular Dilatation Disease, PDD.

Budgies are determinate layers, meaning that a hen will lay a predetermined number of eggs per cycle, usually four, six or rarely eight. This is in contrast to cockatiels, called indeterminate layers. A cockatiel hen will continue to lay eggs to replace those lost from her clutch. So, if an owner takes the eggs away from a hen as she lays them, she may lay so many eggs (the record in my practice is 27!) that she becomes depleted of her nutrients, which can be life-threatening. However, the budgie will usually cease laying once her clutch is complete, even if the eggs are taken away from her. This is why so many more cockatiels end up with egg-related problems when compared to budgies.

Hypocalcemia can be treated with vitamin D3 injection, injectable calcium (Calphosan: calcium gluconate 50 mg/ml and calcium lactate 50 mg/ml, IM, 5-10 mg/kg q12 hr PRN. Make sure bird is well-hydrated when giving injectable calcium. I usually dilute 50:50 with sterile saline for IM injections). Neocalglucon in the drinking water can be administered in the drinking water, 1 ml per ounce (30 ml) drinking water.

Male budgies of many colors, excluding some of the pale colors, will develop a blue cere as they mature. The hen will develop a tan or brown cere upon maturity. Some hens will develop brown hypertrophy of the cere, a thickening of the cere that is considered normal, however, for cosmetic reasons, an avian veterinarian can carefully peel off the excessive growth. If the cere color of a mature male budgie changes from blue to brown, this is often an indication of a tumor of the testicle.

Occasionally, a hen may have difficulties in laying an egg. This is termed dystocia, and it may have many causes, including not enough calcium in the diet resulting in a soft-shelled egg, a weak or infected oviduct, malnutrition, a damaged or small pelvis, a malformed egg, poor muscle tone and body condition of the hen or tumors. Supplying the hen with heat and humidity may help her pass the egg, however, dystocia can rapidly become an emergency, requiring immediate veterinary care. Applying mineral oil or water-soluble jelly to the vent is not likely to be effective, unless the egg is clearly visible just inside the vent. Many egg-bound hens are dehydrated, so the first treatment an avian vet will perform is usually the administration of fluids. Radiographs (x-rays) may be helpful in confirming dystocia. An injection of calcium may help the hen by allowing the oviduct to contract more strongly. An injection of vitamin D helps calcium absorption. If fluids, the vitamin injection and the injectable calcium, in addition to heat and humidity don't facilitate passage of the egg, a prostaglandin gel (Prepodil gel) may be applied inside the vent, as long as the egg can physically pass. The prostaglandin gel works along the natural pathways, and is a much better drug to use in place of oxytocin, which is the drug that was classically used to cause contractions of the oviduct (and is used in mammals). Extreme care must be taken by any female personnel dealing with this gel, as it can cause serious problems with the female reproductive tract. Occasionally, a hernia may be associated with egg-binding.

Budgies often suffer from a myriad of tumors as they age. Budgies that develop a limp or weakness of one leg often have a tumor pressing on the sciatic nerve, causing the leg problem. The tumor may be of the kidney, gonad or adrenal gland. Other tumors may occur in almost any organ. Cockatiels can also develop malignancies as they age. Fibromas and fibrosarcomas are the most commonly seen in my practice.

Hypothyroidism, although not well-described, may occur in budgies. Diabetes mellitus, also quite rare, occurs in budgies, as well. Tumors of the adrenal or pituitary gland have occurred. Cockatiels, especially, fat, female and four, may develop diabetes mellitus. In birds, diabetes is due to an overproduction of glucagon, as opposed to a lack of insulin in mammals.

Gout is quite common in budgies. It may be a result of kidney disease or it may be primary in origin. If urates are deposited in the joints, this is called articular gout. This is a very painful condition and treatment is usually unrewarding. Visceral gout, where urates are deposited on the surface of organs, such as the heart and liver, is usually diagnosed at necropsy. Gout also occurs in cockatiels, and is usually secondary to renal disease.

Budgies and cockatiels, being the inquisitive little birds that they are, may get underfoot, and may be injured by being stepped on, closed in a door, etc. Fractures of the wing or leg frequently occur, and can be usually simply treated by using a tape splint. Bird bones heal quite rapidly, so splints won't need to be kept on as long as one would for a dog or cat.

Budgies and cockatiels may get a concussion from flying into a window or mirror, or injuries may occur by an encounter with a ceiling fan. This is clinically called "shredded tweet."

A budgie may regurgitate to a favorite toy, mirror or its favorite person. This is a normal behavior. This must be differentiated from regurgitation resulting from disease. Cockatiels may also regurgitate to a favorite person or toy, but not as commonly as in budgies.

Budgies and cockatiels are wonderful little birds with great ability to mimic speech. They can be loving companions. Veterinary care is important for them, and just because they are small birds, their preventative medical care should not be neglected. Avian veterinarians are able to provide the same quality of care for a budgie as for a macaw. Always offer the budgie and 'tiel owner the same diagnostic plan that you would for the owner of a larger bird. With proper care and diet, the budgie and cockatiel can live a long, healthy life.

Osteopetrosis

Osteopetrosis is a rare disease of mammals and birds. The name means "stone bones" suggesting that the bones are even harder than normal although this is not always the case. While the disease has been diagnosed in various types of domestic poultry there appear to be no reports of it in cage birds.

The four budgerigars in which the disease was seen all belonged to the same fancier, and were from two clutches which also included some normal chicks. The condition was first noted when the birds left the nest boxes but may have been present before this.

The affected birds had difficulty in moving about but this varied in severity from bird to bird; one could only get about at all by hooking its beak into roughness on the cage floor, while another stood in a slightly crouching position, but could walk and fly, at least as far as the nearest perch. The birds had normal appetites and were in good bodily condition. Once the condition was diagnosed in the most severely affected bird the others were put down and two of the four bodies were examined post-mortem.

The post-mortem examination showed that some of the bones were thickened, especially the tibia (drumstick). Three of the bones of the wing, (humerus, radius and ulna), the ribs and the bones of the shoulders, (the wish-bone, shoulder blade and the coracoid). Not all of these bones were affected in individual birds; the one which could stand had unaffected leg bones. Diseased bones were swollen along their shafts to two or three times the normal diameter by a layer of new soft bone laid down on outside of the original shaft of the bone, which still persisted.

In addition there was new bone completely filling the marrow cavities of the affected bones. As seen in the budgerigars the affected bones were soft. In most species the new bone eventually becomes very hard and stone-like but these birds were not allowed to live long enough to see if this would happen. The bones not affected by this disease were a little soft and more easily broken than normal, possibly because of an insufficient intake of calcium for the formation of both the normal and the diseased bone. The muscles of the legs were very small although otherwise normal, and this, possibly coupled with pain, was the explanation for the birds' inability to stand properly. The small size of the muscles meant that the legs were not noticeably swollen. The wing muscles were unaffected, possibly because the underlying breast bone was normal.

In other animals there are two causes of this disease. In most mammals it is inherited; when two animals which are unaffected carriers of the disease mate, a proportion of their offspring will inherit two of the recessive genes and will go down with the disease. In domestic poultry the disease is caused by a virus which means that the conditon is infectious; however, it seems very probable that only the young chicks are susceptible to infection. When the disease in was studied many years ago, in order to get experimental cases young chicks had to be exposed to the virus at not more than a few days old but the disease did not develop for a few weeks after birds were infected.

In the cases reported here, it is not known if the disease was the inherited form or the infectious form; the parents could have been carriers of either the defective genes or the virus. However the chance of mating two sets of different males and females all of which carried the defective gene seems somewhat remote so that the infectious theory seems more probable. The fancier concerned also kept poultry and while he had not recognised the infection in them it is possible that one or more of them were carriers, and the fancier transferred the infection into the budgerigar stud; this does, however, remain unproven.

The recognition of new diseases, albeit rare ones, is one of the valuable outcomes of the veterinary service offered to members of the Budgerigar Society, as the more diseases are recognised the better will be our understanding of the causes of illness in these birds. While the poultry were not proven to be the the source of the illness this disease outbreak does suggest that totally dis-similar birds can have the same diseases - there are other diseases of poultry which can and do spread to budgerigars.

Over the past few years fanciers have increasingly reported feather abnormalities in their exhibition type budgerigars. In particular, they have noticed a tendency for birds to lose their tail feathers which then fail to regrow ("tail-less wonders"). Reports of similar abnormalities in larger members of the parrot family increased at the same time.

In view of these reports, discussions took place between the Budgerigar Society Lancashire, Cheshire & North Wales BS and myself. It was decided that the two societies would fund work on feather diseases to be carried out at the University of Liverpool. Their financial support is acknowledged with thanks. The work was begun on 1 July 1993 and concluded on 30 June 1995.

We are grateful to members of the fancy for the supply of birds and feathers together with related information. Birds and other samples were received from all areas ranging from the Isle of Wight to Glasgow and from Cornwall to Norfolk, though the majority came from Lancashire, Merseyside, Cheshire and North Wales. The total number of birds and feather samples received was 198.

A technical version of this report will be produced and submitted to the veterinary press, making the results available to veterinary surgeons. They will then know which diseases commonly occur and will be able to advise clients with feather problems in their birds.

The diseases and other abnormalities found in the survey are summarized in Table 1 (at the bottom of this page). Also in the table are figures from the other comparable work found in the literature. This was a survey of biopsies (small pieces of tissues taken from live animals) from a variety of psittacines with feather disease, which were examined microscopically. The work was carried out in America (Schmidt 1987). It will be noted from the table that the diseases found in the American survey were of a limited nature.

Only some of these were seen in my survey but at a different prevalence. The exception was psittacine beak and feather disease, where the incidence was equivalent in both surveys. In the Schmidt survey the causes of the diseases were not investigated, nor was there any attempt to correlate certain diseases with feather type. Caution is required when interpreting the figures in Table 1. The figures are correct for the birds we received, but some fanciers supplied large numbers of birds with the same condition and this has skewed the results. This was particularly true in the case of psittacine beak and feather disease, where two breeders supplied over half the affected budgerigars. With pulpitis, the same tended to occur, though to a lesser extent. Conversely, many fanciers did not submit birds with French moult as this disease was specifically excluded from the project. For these reasons the figures in the table give only a rough guide to the prevalence of these conditions in the overall budgerigar fancy.

It will be noted from Table 1 that there was an average of 1.48 conditions per bird. Most of these were cases of mite infestation and damage in birds with other feather disorders. In other cases two apparently unrelated feather conditions occurred in individual birds.

Before considering the results in detail it may be useful to define a few terms.

These are a type of germ which lives and breeds inside the cells of animals. They are capable of living outside the animal but will not multiply in this situation. As far as birds are concerned no treatment for viral diseases is available.

These are much bigger than viruses and usually live between the cells of the infected animal and multiply both within the animal and outside. They can usually be killed by antibiotics.

This is a disease which the bird has from the time it hatches, although occasionally the symptoms may not show for months or even years. Such diseases may or may not be inherited.

This is a disease which is passed from parent to offspring via the animal's genes. Depending on the mode of the inheritance the parents may, or may not show evidence of the disease.

This is transmission of a disease from parent to offspring by contact or via the egg. Such diseases are not inherited although they may appear so.

This is transmission of a disease to other in-contact birds but excludes parent to offspring transmission.

A small pocket-like depression of the skin from which the feather grows and by which it is attached to the bird before a moult.

The branches coming from the feather shaft and forming the bulk of the feathers.

These branch off from the barbs and have small hooks on them (barbicels) which lock together the barbs and thus the feather.

The part of the report which follows details the findings in each condition or groups of conditions and gives an indication of the cause and treatment when this is known.

It came as a considerable surprise that this topped the list of diseases occurring in 21.2% of all the birds submitted, because in the first year no cases were seen at all. One possible explanation is that the disease has only recently been introduced into the exhibition budgerigar and only became widespread in the last year or so.

The disease is caused by a virus. Infected birds may be symptomless carriers although no such cases were found in the survey. This was to be expected as only sick birds were seen. Fanciers were unlikely to send in a symptomless bird for examination. There appeared to be two manifestations of the condition depending on the age of the bird. In budgerigars less than 6 months old the feathering was poor with extensive bald or semi-bald areas on the body and legs, loss of most or all of the large wing and tail feathers, and loss also of some of the smaller feathers in these sites. The remaining feathers tended to be of poor quality and sometimes misshapen. Young affected birds tended to be small for their age. In older birds the contour feathers were usually unaffected, but all, or some of the primaries, secondaries and large tail feathers were missing. Regardless of age of the bird the head and upper neck was spared. In no cases was the beak abnormal. Affected birds seemed lively and active and no bird died from the condition, although such birds were kept at the university, only a few months at most.The disease is transmitted to other birds on the premises both horizontally and vertically, although transmission tends to be relatively slow. There is no treatment for the disease, nor are there any preventative treatments in the UK. Measures such as cleanliness, the testing of new arrivals and the isolation of affected birds, will reduce the rate of the spread of the disease. An experimental vaccine has been shown to be effective in the USA. Should fanciers or societies wish to support further research into this disease I can provide a contact name in America.

This is an inflammation of the pulp of the growing feathers, especially the large ones of the wing and tail. Such diseased feathers may break off or be shed prematurely. Once shed the feather may not regrow. A significant proportion of the birds submitted with this disease had been sent in as "tail-less wonders". Pulpitis is believed to be a major cause of this condition. The cause of pulpitis is usually a bacterial infection,predominately Staphylococci or Streptococci although about 15% of cases are probably of viral origin. These germs are thought to live on the bird's skin but only cause problems when they invade the growing feathers. There is a strong correlation between this condition and markedly buff, suggesting there may be something inherent in buff feathers which makes them susceptible to this condition. There is also some evidence of vertical transmission.

While in theory, prolonged antibiotic treatment might cure the condition when a bacteria is the cause, this has not been tried. Repeated bathing of the birds in Virkon S seems to cure about 40% of cases. A few appear to recover spontaneously. At the present time there appears no way of predicting which birds will respond to treatment and which will not.

Feather mites of a variety of species are very common on budgerigars, but are not usually seen by the fancier as they are mostly very small. They are visible only under microscope. They also tend to live deep in the feathers close to the skin. In the majority of birds they cause no problems at all. Occasionally mites can cause feather disease in a number of different ways. There were feather abnormalities in all the cases of mites listed in the table. Firstly, in heavy mite infestations these active parasites caused irritation. This in turn led the birds to scratch and bite their plumage, leading to tatty feathers, or feathers which had been bitten off at various positions along the shaft. As mites prefer to live on a bird's rump, the tail feathers are frequently the most affected. Secondly, some species of mite will eat small segments of the growing feathers, so when they are fully formed a small part of the feather is seen to be missing. These are most obvious on the large wing and tail feathers, although the contour feathers can be affected at times. The third way mites can affect the feathers is by invading the follicles, which results in the growth of a distorted feather. Only the follicles of the large feathers of the wing or tail seem big enough for the parasite to enter, and usually only one or two feathers are affected. These are frequently very short or horn-like.

The diagnosis of this condition depends first on finding the mites. However, as these parasites are so common, one has to eliminate the causes of the feather disease before a diagnosis of the mites can be made. Treatment with any of the proprietary anti-mite drugs is effective.

It had not been anticipated that this condition would be such a common cause of feather abnormalities. The other unexpected feature of this condition was, that in the vast majority of the cases, the cyst or cysts had not been spotted by the fanciers. The birds had been sent to me because they had feathers which would not regrow.

Almost all the feather cysts occurred on the outer parts of the wing or the tail, although some were seen on the necks of birds. The cysts were of three types, the first and most common for 70% of the cases, was roughly spherical, up to 1.25cm (just over half an inch) in diameter. Cysts of this type were either very hard or slightly soft, depending on the thickness of the fibrous capsule. This capsule surrounded a core of yellow cheesy material, and the distorted remains of one or more feathers.

The second type was very similar to the first, but the surrounding skin was inflamed and thickened. As most of the lesions had not been noticed by the fanciers it was not possible to establish whether the damage to the skin came before or after the development of the cyst.

The third type was only seen on wings and accounted for fewer than 10% of cases seen. These were multiple and long and narrow in shape, lying side by side with one cyst corresponding to the follicle of one primary feather. They contained cheesy material as in the other cysts but in a proportion, a very short malformed feather was protruding from the tip of the cyst.

There was a very strong correlation between the first two types of cysts and marked buffness. Birds with this type of inherited plumage have a strong tendency to develop cysts. Unfortunately fancier's records were insufficiently detailed to show if cysts themselves are inherited, as is the case with the equivalent condition in canaries (lumps).

Research suggests buff feathering is linked to feather problems. There is no treatment for this condition other than surgical removal and it must be borne in mind that the birds will never regrow the feathers. It is probably not advisable to breed from birds with feather cysts or from their close relatives.

Under this category we will look also at the absence of barbs and barbules, poorly formed barbs or barbules, and improperly shed sheaths. Stress marks are lines on the feathers where the barbules have not formed. Sometimes there is a line of weakness in the shaft at the same level, and the feather may break off at this point. If the barb and barbules are absent from a section of the feather, or if they are poorly formed, the feather does not hold together, giving the bird a tatty appearance. Improperly shed sheaths is a condition when the feather sheath is not shed in the usual way and instead persists over a greater part of the feather than is normal.

Occasionally, fully-formed feathers are totally enclosed in their sheath. In all three conditions the abnormality is most easily seen in the large wing and tail feathers.

In all these conditions, the changes seen in the feathers usually indicate something wrong in the bird's system in general. This needs to be attended to rather than concentrating on the feathers. With stress marks, the disturbance is general short lived, a matter of a few days to a week or thereabouts. The other conditions are associated with longer periods of illness, which can be quite mild, periods of stress or poor diet. When one or two birds in a flight are affected, this does not mean that the overall diet is unsatisfactory. Some budgerigars are very pernickety feeders and while different foods need to be supplied, it does not mean every bird will eat all of them. Provided the underlying problem is identified and corrected, the birds will almost certainly grow a set of normal feathers at the next moult.

This well known condition in which the feathers of the affected birds grow continually is noted very shortly after the birds begin to feather up. Such birds usually die at 6 to 8 weeks of age. the budgerigar that we had for a long time eventually died at 2 years. It grew contour feathers up to 24cm (9.5 in) long.

Some, and probably all, cases of this disease have a genetic inherited basis. There is a strong correlation between affected birds and buff feathering. A paper by Kevin Eatwell in Budgerigar World said that unaffected siblings of feather dusters are excessively buff and therefore may be retained for breeding. My view is this is not advisable.

The 8 conditions described above were responsible for two-thirds of the cases seen. The other 29 diseases accounted for the remaining third. These will form the second part of this report.

Respiratory Disease in Budgerigars:
an Approach to Treatment

Dr John R Baker

Respiratory disease in budgerigars is relatively common and, while in some circumstances death is so rapid that no treatment can be given, in other cases birds can be affected for long periods and eventually recover. The purpose of this article is to describe the types of symptoms that may be seen in birds with diseases of the respiratory system and to detail the steps that owners can take to help to nurse the affected birds back to health. Reaching the exact diagnosis is sometimes difficult and a veterinary surgeon experienced in cage bird medicine should always be consulted before a course of treatment is used. While the use of terramycin, which most fanciers seem to have, may produce a cure in odd cases, getting a proper diagnosis and having the proper treatment is much more likely to result in a cure.

The birds respiratory system extends from the nostrils (the small holes at the top of the beak) right through the bird to near the vent. Not only do they have nostrils, a windpipe and lungs like mammals but in addition, they have a series of structures called air sacs which sprout out of the lungs. These air sacs are like small balloons which go around the other internal organs and even extend into the bones of the wing. The intimate association of the air sacs with the intestines means that diseases of the intestines may also affect the respiratory system and conversely, respiratory disease can affect the intestines producing diarrhoea.

There may be a discharge from the nostrils, this can be either watery or thick and it frequently dries on the beak and the feathers around the cere. The nostrils may become blocked with this discharge, either at opening or internally, and occasionally odd objects breathed in causing blockage; I have seen a budgerigar with a millet seed stuck up its nose. As in humans, there are a number of sinuses (air spaces opening off the nose) and these can become affected causing swelling around the head and this can spread to affect the eyes which become inflamed with a discharge matting the feathers and sometimes sticking the eyelids together.

Sometimes birds sneeze, and this again can suggest respiratory disease; they may also cough. Affected birds can make other noises, there may be wheezing, there may be loss of voice or a change in the pitch of the song if the bird's voice box is affected. Birds with breathing difficulties may make clicking noises and this is often associated with the beak pointing upwards which straightens the trachea and can ease breathing slightly. If the bird is having difficulty in breathing, the most obvious sign is tail bobbing. The tail goes up and down in time with the bird's breathing. If the bird is really having difficulty in getting enough air into the system, it makes it almost impossible for the bird fly, climb or even perch and the rocking as it breaths may make it fall off the perch. The bird will usually feel ill at this stage and may just sit quietly in a corner with its feathers ruffled up. As death approaches the feet and beak may go blue.

If presented with a bird with these symptoms what can the owner do as first aid and how can the bird be nursed when a course of treatment has been started? First of all minimise stress. When a bird is stressed its need for oxygen increases and if bird is having difficulty in breathing, added stress may make the difference between life and death. As in most conditions prompt treatment gives a much better chance of recovery than will be the case if treatment is delayed, so contact a veterinary surgeon in your area who has experience in the treatment of cage birds or at least ask the advice of an experienced fancier. In this context, it should be stressed that if your vet has prescribed a course of treatment the full course must be given. The bird may rapidly improve and the temptation is to stop treatment. If you do this the bird may well relapse and you will be back to square one again. Affected birds should be isolated from the rest of the stock as many respiratory diseases are highly infectious and are spread through the air. Isolation in this case means completely separate from the rest of the birds in a different room; just putting the diseased bird in a show cage in the bird room is not isolation. If you have a bird in isolation for whatever reason, always see to the healthy birds first as in this way you are less likely to spread the infection about. Where is a temptation to look at the diseased bird first when you work in the aviary 'just to see how it is', this temptation must be resisted.

Once a course of treatment has been started the bird will need nursing care to aid its recovery. First of all the bird must be kept warm at about 80°F or 27 C. This will not only keep the bird more comfortable but will reduce the energy requirement and thus the amount the bird needs to breath. The lighting should be subdued as this appears to reduce stress and the bird is likely to be more relaxed in semi-darkness. Do not turn the light off altogether this will stop the bird eating and drinking.

If the bird is having difficulty breathing, the perches should be lowered, which makes it easier for the bird to get back on the perch where it will feel better than if it is forced to sit on the floor. Lowering the perches also means that should the bird fall off it has less far to drop and is less likely to injure itself. Make sure that food and water are within easy reach. Discharge from the nostrils or eyes can be cleaned away with moistened cotton wool and the same technique can be used to open the eyes if the lids are gummed together. If hard material is seen in the nostrils a needle can be carefully used to dislodge it.

Many birds that die when they are diseased, die not of the disease directly, but of either dehydration or starvation. A useful guide to see if these are taking place is to weigh the bird at regular intervals and I would suggest that scales to weigh birds would be worthwhile investment. If weight loss is occurring or if the bird is seen not to be eating or drinking, the first thing to do is to get some fluid in by crop tube. Budgerigars have very variable water intakes, but 5ml per day in three or four doses will be satisfactory. The addition of glucose to the water at two teaspoonfuls to the pint will supply some energy as well. If the bird has to be dosed by tube for some time, fruit varieties of baby food, diluted enough to get it down the tube, are recommended by some authorities and this will provide both energy and fluid.

The last point that must be mentioned is that a number of bird respiratory diseases can be caught by humans, and the most important of these is psittacosis. Should you have sick birds and you get flu like symptoms with a high temperature, aching joints and a cough, it is important that you contact the doctor and tell him that you have a sick bird and that you might have psittacosis. This is important because if caught early it is easily treated but if left for some time it can become serious and is occasionally fatal.

During the first year of the diagnostic service offered to members of the Budgerigar Society and members of the area societies, common diseases, such as pneumonia and megabacteria, were frequently seen. However, two conditions were found which I had not seen before, and which had not been previously reported by other people studying diseases of Budgerigars or other cage birds. Although rare so far, I will discuss these briefly as it should be of interest. Both diseases were seen in the birds of one fancier and both birds also had megabacteria.

The first case was one of stones, which had formed in the crop in much the same way that stones can form in humans in the kidney or gall bladder. The affected budgerigar had two stones in it's crop They were hard, roughly eggshaped and measured 1.1 and 1.2 centimetres in length and were off-white in colour. In this particular bird they were causing no trouble, except that they took up space in the crop so the bird could not eat as much as normal when feeding. In other birds smaller stones could potentially move into the lower part of the gullet leading from the crop to the stomach and become stuck, leading to a rapidly fatal blockage. Stones as large as these could be felt in the crop, could be seen using an endoscope or diagnosed using X-rays; the only treatment would be surgical removal. Why the stones formed is not known.

The second case was a bird which was losing weight and which had diarrhoea. Megabacteria was diagnosed and treated but the symptoms persisted and the bird eventually died. Post-mortem showed that the internal damage due to the megabacteriosis was quite severe, but that the symptoms, at least in part, were due to the presence of an egg in the abdominal cavity. The egg was collapsed. It was causing a partial obstruction of the intestines so that the bird's weight loss was partly due to interference with digestion. The question arises how a fullsized egg, complete with a thin shell, could get out of the oviduct (where the white and shell are added to the yolk) into the body cavity.

There appear to be only two possible routes. First the egg could have passed back up the oviduct and out the top end where there is an opening, so that the yolk can get into the oviduct from the ovary. The argument against this is that the oviduct is relatively narrow at the top, and an egg going back up would be a tight fit. The second possibility is that the oviduct burst and the egg fell out. As the oviduct is relatively free of bacteria this would not immediately cause problems. As the bird was not in laying condition, the oviduct was small and this type of damage could not be detected. This rare condition could only be diagnosed using X-rays or viewing the body cavity with an endoscope. The only treatment would be surgical removal of the egg. As it seems possible that this condition might recur, the oviduct might also need to be removed to prevent this happening again. Such radical surgery would render the Budgerigar sterile. Note that this case is different from so called "internal layers" in which only the yolk goes into the body cavity. The yolks fall from the ovary but miss the opening at the top end of the oviduct.

Vaccination to control polyomavirus in budgerigars

Branson W. Ritchie, DVM, PhD, Kenneth S. Latimer, DVM, PhD,
Denise Pesti, MS, Raymond Campagnoli, MS, Phil D. Lukert, DVM, PhD
Psittacine Disease Research Group
University of Georgia, College of Veterinary Medicine
Athens, GA 30602

Reprinted in part from Avian Viruses: Function and Control Wingers Publishing, Lake Worth, FL, 1995.

Budgerigar fledgling disease (BFD), caused by an avian polyomavirus, was first noted as a clinical syndrome in 1976 and was first reported as a disease affecting budgerigars in the United States and Canada in 1981.1 Since its initial recognition as an etiologic agent of disease in psittacine birds, polyomavirus has spread throughout aviaries and the pet trade to a point where it is a leading cause of death in psittacine birds. 2 While avian polyomavirus has been shown to be distributed world-wide, there are some apparent regional differences in the clinical changes associated with infections in budgerigars. 3-7 1,8 9,10 11 12,13 14-16 For example, in Europe a more chronic form of the disease is common in budgerigars, while in the United States and Canada an acute form of disease with high mortality is typical.

Unlike most members of the Papovaviridae family which have a restricted host range, avian polyomaviruses appear to infect a wide variety of Psittaciformes (parrots), Passeriformes (weaver finches, canaries) and gallinaceous birds (chickens and turkeys). 17 Polyomaviruses from budgerigars have been confirmed to be antigenically related to some virus isolates from finches and antigenically and genomically related to the polyomavirus isolated from non budgerigar psittacine birds. 4,18-21 DNA probes have been developed to detect specific segments of the nucleic acid found in the avian polyomavirus. These DNA probes, designed from polyomavirus recovered from budgerigars, will detect the virus in excretions, secretions and infected tissues of non budgerigar psittacine birds. 6,22,23 The genome of the polyomaviruses isolated from budgerigars, a blue and gold macaw and a chicken house have been shown to be closely related. Because of these similarities, it has been suggested that avian strains of polyomavirus be placed in the subgenus Avipolyomaviurs. 13

The type of clinical disease induced by polyomavirus in budgerigars seems to be influenced by the age and condition of a budgerigar when it is exposed to the virus. Budgerigar neonates from infected flocks may develop normally for 10 to 15 days and then die suddenly without premonitory signs. 24 Other infected hatchings may develop clinical signs, including abdominal distention, hemorrhage under the skin and reduced formation of down and contour feathers. Some infected budgerigars have been reported to develop neurologic signs characterized by ataxia (incoordination) and tremors of the head and neck several days before dying. 1,9,24-27 Infected budgerigars that die shortly after hatching routinely develop more severe and widespread lesions than do birds in which the morbid state is more prolonged. The mortality rate associated with naturally acquired avian polyomavirus infections in young budgerigars may range from 25% to 100%, depending on the age of the birds. Older birds are considered relatively resistant to disease, while at the peak of viral activity, up to 100% of exposed budgerigars less than 15 days of age may die. The mortality rate reported for older (greater than 3 weeks of age) juveniles ranges from 30% to 80%.I,8,9,24-29

Although mortality rates vary with the age of the exposed birds, polyomavirus infections in young budgerigars usually are rapidly fatal once clinical signs develop. In most aviary outbreaks, the incidence of clinically recognized disease will progressively increase during a period of several months, with peak virus activity occurring during the most active portion of the breeding season. 25 In one particularly aggressive outbreak of avian polyomavirus, 90% of young budgerigars were affected within a 2-to 3-week period.8

Reports vary on the effect of avian polyomavirus on egg and embryonic development. In one budgerigar aviary, polyomavirus was thought to have caused an 80% to 90% decrease in egg hatchability at the same time that hatchling mortality increased from 10% to 60%.8 In another study, there was no apparent increase in embryonic mortality in eggs from budgerigar hens that were considered persistently infected with avian polyomavirus. Additionally, many of the chicks from these hens were found to be infected, but remained asymptomatic. 30 Findings from the first report would suggest that avian polyomavirus can cause embryonic deaths and decreased hatchability, while findings from the second study would suggest that avian polyomavirus infections do not cause problems in embryonic development. It is possible that both findings are correct and the effect of the virus may depend on as yet unidentified factors. Like mammals, budgerigars that recover from polyomavirus infections are thought to remain persistently infected.30-32 Evidence suggests that these persistently infected budgerigars are responsible for the spread of this virus through budgerigar flocks and within the avicultural industry.

1,21,31,14 Stress associated with changes in weather, diet, breeding or concomitant disease may cause persistently infected budgerigars to shed virus resulting in outbreaks of disease. In polyomavirus outbreaks at 23 different budgerigar aviaries, the onset of disease could be traced to the addition of new, clinically normal breeders. 1,25

Polyomavirus inclusion bodies frequently can be detected in feathers, feather follicles, spleen, liver and Kidney from persistently infected, clinically normal adult budgerigars. 25,26 Viral inclusion bodies are common in the renal tubular epithelium. Persistence of virus in the kidneys of budgerigars, with subsequent excretion in the urine, has been proposed as a method of virus transmission. 1,26,29,33,35 Viral nucleic acid has been detected in the excrement, feathers and oral mucosa of clinically normal budgerigars. 36

The incidence of polyomavirus activity in budgerigars is high. In one study, virus was demonstrated by histology and virus isolation from all of 10 budgerigars with clinical signs of avian polyomavirus and from 5 of 10 (50%) clinically healthy budgerigars. 26 In another study, 4 of 7 (57%) nestling budgerigars had microscopic changes suggestive of avian polyomavirus, while all of 7 nestlings had viral nucleic acid in their tissues. 30 Polyomavirus nucleic acid was demonstrated in the serum of 9 of 12 (75%) 9-to 13-day-old budgerigars from a flock in which virus activity was considered enzootic. 34 The possibility that up to, 100% of the budgerigars in some flocks could be infected with avian polyomavirus was first discussed in 1984.25 This has been confirmed in subsequent studies using viral-specific DNA probes. In one study involving a flock of budgerigars with a history of repeated polyomavirus-induced disease, all of 40 clinically normal budgerigars had polyomavirus nucleic acid in their tissues. Virus-neutralizing antibodies to avian polyomavirus were detected in all 144 of another group of budgerigars. 30 Experimental data and observations with the natural disease suggest that polyomavirus transmission in budgerigars may occur by both horizontal and vertical routes, that is, both among members of a flock and between generations from parent to offspring. 1,5,27,28,30 Experimentally infected 3-to 10-day-old budgerigar neonates died 11 days after being given BFD virus intramuscularly. 37 When 25-day-old budgerigars were exposed intranasally to virus collected from the skin of diseased birds, they developed microscopic lesions characteristic of a polyomavirus infection but remained clinically normal. 1,25 These findings suggest that inhalation of aerosolized virus could be a natural route through which polyomavirus enters a susceptible bird. In one trial, young seronegative budgerigars seroconverted within 16 days after being placed in the same enclosure with seropositive birds.

Seronegative budgerigars also seroconverted when they were placed in enclosures adjacent to those containing seropositive birds. These finding suggest that direct and indirect transmission of polyomavirus can occur. 27

Unvaccinated susceptible psittacine birds may be exposed to polyomavirus through exposure to virus-contaminated feces, feather dust, urates and respiratory secretions. 17,25 Until polyomavirus can be controlled in budgerigars through a widespread vaccination program, it should be considered dangerous to house budgerigars in the same air space with unvaccinated non budgerigar psittacine birds. The potential for intraspecies transmission of polyomavirus may be a particular problem for pet retailers that maintain both budgerigars and non budgerigar psittacine birds. In one environmental study, it was found that polyomavirus nucleic acid could be detected using DNA amplification and detection techniques in all of 5 samples collected from 3 different pet shops which housed budgerigars. (Dr. Nancy Jaax, personal communication) Budgerigars should be considered the primary reservoir of polyomavirus. 'The potential for budgerigars to continue to spread this environmentally stable virus among unvaccinated psittacine birds is cause for action.

Controlling Polyomavirus in Budgerigars

It has been suggested that polyomavirus disease-free budgerigar nestlings can be produced by interrupting the breeding cycle, removing all but the older breeding birds and disinfecting the aviary. 8 Breeding cycle manipulation was used to control polyomavirus infections in budgerigars, after hatchability of fertile eggs dropped from 80% to 90% at the same time that hatching mortality increased from 10% to 60% in an aviary experiencing an avian polyomavirus outbreak. By interrupting the breeding cycle for 7 months and thoroughly cleaning the aviary with bleach, return to 80% hatchability and a cessation of hatching deaths was achieved when breeding resumed. However, in other affected aviaries, mortalities and disease have continued when breeding was resumed following a rest period. 8 In another study, it was demonstrated that older breeding budgerigars shed fewer virus particles and less frequently than young adults. 30,32 Any attempt to manage polyomavirus through manipulation of the breeding cycle has the inherent problem that persistently infected budgerigars, and thus a future source for virus shedding, remain in the flock.

In budgerigars, which are known to develop persistent polyomavirus infections, the detection of polyomavirus-neutralizing antibodies can be used to screen for infected budgerigars which should be considered a risk for transmitting the virus. 34,38 Testing budgerigars for the presence of virus-neutralizing antibodies and culling positive birds has been suggested as a method to establish flocks of polyomavirus-free budgerigars. 33,36 Additionally, depopulation of budgerigar aviaries experiencing outbreaks, followed by restocking with seronegative birds has been suggested as a method of controlling enzootic infections in this species. 8,33,36 The practical problem with using this testing strategy for controlling polyomavirus is that once a seronegative flock of budgerigars has been established, the flock would then be highly suceptible (theoretically 100% susceptible) to polyomavirus infection if the virus were inadvertently introduced to the aviary. However, by using a serologic assay to establish "polyomavirus-free" budgerigars followed by vaccination to protect the budgerigars from subsequent infection, it should be possible to prevent polyomavirus-induced disease in the budgerigar aviary and reduce the role that budgerigars play as a reservoir for polyomavirus in the pet trade.

In non budgerigar psittacine birds, polyomavirus can be controlled using an inactivated avian polyomavirus vaccine. 3944 Controlling polyomavirus infections in budgerigars presents a different set of problems. A budgerigar infected with polyomavirus is considered to be infected for life and can shed the virus for long periods of time. This high prevalence of polyomavirus in budgerigars, and the fact that an infected budgerigar continues to shed for extended periods, renders vaccination alone of questionable value in controlling the virus in a budgerigar flock. Additionally, the cost of the inactivated vaccine makes it difficult to economically justify in commercial budgerigar flocks. None-the-less, it is important for the avicultural industry to control polyomavirus in budgerigars because this group of birds is serving as a reservoir for the virus. For the past year, we have been evaluating an economically feasible testing and vaccination program to control polyomavirus in budgerigars. We are currently testing this program in flocks of budgerigars and our data is encouraging.

This vaccine* was developed by identifying a virus isolate which, when administered intramuscularly, will cause an immune response without inducing virus shedding or detectable persistence of the virus. In one safety and immunogenicity trial, 4 recently weaned budgerigars with no detectable polyomavirus-neutralizing antibodies were injected intramuscularly with the experimental vaccine. Another budgerigar that was housed in the same enclosure with these vaccinates served as a contact control. None of the vaccinates had any clinically recognizable adverse reactions following vaccination.

The experimental vaccine designed for use in budgerigars was found to stimulate an immune response in birds inoculated intramuscularly but not in birds inoculated by the combined intraoral, intranasal and intraocular routes. A group of 5 recently weaned budgerigars that were negative for polyomavirus-neutralizing antibodies was used in this safety and immunogenicity trial. Two birds (#6 and #7) were inoculated by the combined intraoral, intranasal and intraocular routes with experimental vaccine. Three birds (#8, #9 and #10) were injected with the same suspension intramuscularly. Serum was collected from each bird on day 0, 10 and 20. None of the vaccinates had any clinically recognizable adverse reactions.

The results of this study indicated that the experimental budgerigar polyomavirus vaccine induced a detectable virus-neutralizing antibody response when injected intramuscularly (considered an unnatural route of exposure) but not in the birds inoculated by the combined intraoral, intranasal and intraocular routes (considered a natural route of exposure). This finding suggests that the polyomavirus contained in the experimental vaccine has been sufficiently altered to prevent it from inducing an infection when a bird is exposed by a natural route. In an additional safety and immunogenicity trail, 7 mature budgerigars were inoculated intramuscularly with the experimental budgerigar polyomavirus vaccine. Two birds were housed in the same enclosure with the vaccinates and served as contact controls. Serum was tested for virus-neutralizing antibodies on day 0 (which was also the day of vaccination) and approximately 1 month later. None of the vaccinates had any clinically recognizable adverse reactions.

These safety and immunogenicity trials suggest that the experimental budgerigar vaccine will induce an immune response, as detected by a significant increase in virus-neutralizing antibodies, when injected intramuscularly and that vaccinates do not shed a sufficient quantity of viable virus to be a risk for infecting birds with which they are in direct contact. It is anticipated that the ongoing studies which are necessary to obtain USDA registration of this vaccine will further confirm its safety and immunogenicity in budgerigars.

I had noticed when talking to fanciers that many used a great variety of mineral and vitamin supplements and it was not unusual for 2, 3 or even more of these to be used in one stud. This led to concern that there was the distinct possibility of birds being poisoned; indeed vitamin A poisoning was diagnosed in a stud of birds at about this time.

It was decided to investigate this in 1989-90. The work which was done indicated that vitamin A poisoning was a distinct possibility if certain of the commercial supplements were mixed. On the other hand vitamin D3 poisoning, while it was produced experimentally, was unlikely to occur in fanciers' birds.

This work also indicated the minimum levels of these vitamins and from this point of view all the commercial available supplements were satisfactory. The moral of this work was that fanciers should use only one of these supplements and that the manufacturer's instruction should be followed.

1985-6 was the year of vomiting budgies. Birds actually being sick or or trying to vomit were noticed by a number of fanciers as being a common problem. As with 'going light' the fancy came up trumps and provided large numbers of birds for post-mortem investigation. This showed that affected birds had a disease of the oesophagus (gullet) and crop which were inflamed and partly obstructed and that this was producing the symptoms.

After a number of false leads this disease was found to be due to a minute parasite called Trichomonas gallinae. A number of treatments were already available for this condition in pigeons and one of these in particular (Emtryl soluble) was adapted to budgerigars and was shown to be highly effective in curing this condition and eliminating the disease from studs.

The only major problem was that some fanciers would just not believe that the minute amount of the drug needed was enough and as a result they massively overdosed. More than one fancier almost wiped out their entire stud due to the toxic effects of very large doses. The moral of this is always use in accordance with the vet's instructions or follow the manufacturer's information to the letter.

DISEASES TRANSMITTED TO EGGS

Diarrhoea in Budgerigars An Approach to Treatment

Dr John R Baker

Osteopetrosis

Respiratory Disease in Budgerigars: an Approach to Treatment

Dr John R Baker

Vaccination to control polyomavirus in budgerigars

Controlling Polyomavirus in Budgerigars

Diarrhoea in Budgerigars
An Approach to Treatment

Respiratory Disease in Budgerigars:
an Approach to Treatment