Adding to Graehstone's list of diseases....

[Lisa B]

Aspergillosis: To help you understand

Aspergillosis is the most frequently occurring fungal infection in birds. It occurs in acute and chronic forms. The acute form primarily occurs in young birds and newly imported birds and is the result of exposure to a large number of spores. The chronic form is more likely to occur in older birds that have been in captivity. Aspergillosis spores are widespread in the environment and many birds may carry them in their lungs and air sacks until immunosuppression or stress triggers clinical disease. Aspergillosis has been diagnosed in a variety of captive and free-living species of birds. It is characteristically a disease of captivity and close confinement, particularly when birds are kept in an unclean environment. Aspergillosis is most commonly caused by A. fumigatus, although A. flavus, A. niger, A. nidulans, and A. terreus may cause the disease as well. The fungus is ubiquitous in the environment and flourishes in rotting vegetation and decaying organic material.
The disease is contracted as the result of inhalation of spores. It may also be contracted by oral ingestion, especially if birds are fed moldy seed. The fungus is also capable of penetrating broken skin and egg shells, and so is able to infect a developing embryo.
Susceptibility to aspergillosis is greatly increased in the immunocompromised and malnourished avian patient. Stress pre-existing disease, and the prolonged use of antibiotics and steroids, may further increase a bird's susceptibility.
Contaminated food, water, and nesting material are sources of exposure to spores. In birds, aspergillosis is primarily a disease of the lower respiratory tract. Although the lungs and air sacs are usually involved, the trachea, syrinx, and bronchi may be affected as well. Infection can spread from the respiratory tract to pneumatized bone or enter the peritoneal cavity. Any organ can become infected by the fungus.
In the acute form, anorexia, dyspnea, or sudden death may occur. White, mucoid exudation, marked congestion of the lungs and air sacs, and pneumonic nodules may be present.
In the chronic form, dyspnea, voice change, lethargy, depression, emaciation, polydipsia, and polyuria may occur. Extensive involvement of the respiratory tract can be present before clinical signs are apparent. Ataxia and paralysis occur of the central nervous system is affected.
Aspergillosis is the most frequently occurring fungal infection in birds. All species are susceptible. It may be contracted as the result of inhalation of fungal spores or oral ingestion, especially if birds are fed moldy food or housed on contaminated bedding.Immunocompromised and malnourished birds are most susceptible to the disease.
Diagnosis of aspergillosis can be difficult. A tentative diagnosis may be made of the basis of physical findings, a history of environmental conditions suitable for fungal growth, and recent stress. A hemogram may show a significant leukocytosis (elevated white blood cell count) with a heterophilia early in the disease. As the disease becomes more chronic, a monocytosis, lymphopenia, and non-regenerative anemia develop. An increase in total blood protein with a hyperglobulinemia may develop. Deep tracheal cytology and culture may be performed under anesthesia. A positive culture will usually be present in 18 hours. A single colony growth is considered significant.
Endoscopic examination of the respiratory tract and abdominal cavity will allow cultures to be taken and granulomas (large walled-off areas) visualized.
An indirect ELISA blood test will permit the detection of antibodies, which will be present within a week of exposure to a large number of spores. This test permits detection of a patient early in the course of the disease, before clinical signs become apparent. Antibody titers decline during remission, and thus this test is useful in monitoring a patient's response to treatment. Unfortunately, an infected bird may fail to show a positive titer due to a poor immune state.
Radiographs may be helpful in supporting a diagnosis of aspergillosis. Hyperinflation of air sacs in the lateral and ventraldorsal views is the classic presentation. This occurs as a result of stenosis near the syrinx or mainstem bronchi which results in the trapping of air in the caudal air sacs. Nodular densities may be present in the air sacs and lungs. Loss of definition of air sac lining may occur early in the disease. Asymmetry of the air sacs as a result of air sac collapse, hyperinflation, or filling with necrotic material may be present.
Treatment of aspergillosis involves several objectives:
1. removal of lesions restricting the flow of air through major airways
2. killing and eliminating fungal organisms, and
3. supportive care
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Aspergillosis is the most common fungal infection in birds caused by aspergella fumigates. Although birds are commonly exposed to the spores of this fungus, they develop the disease only under certain conditions. If a bird's immune system is suppressed by a concurrent illness, malnutrition or stress, it may become sick after exposure. Stress-induced Aspergillosis is frequently seen in birds subjected to surgery, reproduction, environmental changes, capture, confinement or shipping.
Aspergella, as well as other fungi, grows readily in damp, dark conditions with poor ventilation. Encrusted fecal matter, damp feed, dirty feeding utensils and food that falls through cage grates all encourage mold growth. Interestingly, we see a high incidence of Aspergillosis in birds in the southwest where the environment is dry and not conducive to fungal replication. The speculation is the low humidity, coupled with the dusty environment, interferes with the normal mucous secretion in the birds' respiratory tracts and predisposes them to mycoses.
Two forms of Aspergillosis are commonly seen in Amazons. The first is an acute generalized form characterized by the fungus in the lower respiratory tree as well as in the intestinal tract and other organs. Patients with this form of Aspergillosis exhibit labored respiration, severe depression and extreme emaciation, and are generally very ill. Unfortunately, the mortality rate is exceptionally high in this form. The second form is called a chronic localized form. This is the most common type of infection seen in Amazons. This chronic Aspergillosis tends to develop localized aspergellomas (pockets of fungal infection). The location will determine the clinical signs. A common place for aspergellomas to localize in Amazons is in the sinus cavity, characterized by intermittent mucoid exudation.
Diagnosis of avian Aspergillosis can be difficult, at best, other than by autopsy. Tentative diagnosis can be made with clinical signs as well as the absence of bacterial infection in moist exudates. A blood test showing an elevation in white blood cell count, mild anemia and an elevation in the monocytes also supports this diagnosis. X-rays should be taken on any suspect patient-many times the radiograph will reveal densities or nodules consistent with aspergellomas. Additionally, your avian veterinarian should take samples and attempt to culture the fungus in specially prepared culture media. Blood should also be submitted for serologic evaluation.
Once a bird is diagnosed as having Aspergillosis, appropriate treatment should be instituted by a qualified avian veterinarian. Each treatment protocol has to be tailored to the individual bird. A prerequisite for success is removing the concurrent immunosuppression that exists. This can be accomplished by management, by treating concurrent maladies and by the judicious use of immunostimulants. Aggressive antifungal treatment is in order, either localized or systemic. Surgery may be necessary with certain localized Aspergellomas, while aggressive nebulization and sinus flushings are warranted in certain other cases. Additionally, a long-term treatment schedule should be instituted.
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http://www.aspergillus.man.ac.uk/
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ASPERGILLOSIS
by Dr. David Phalen A few brief comments on aspergillus. This is a disease that is most likely to occur in birds that are from environments where aspergillosis does not grow well (cool and dry or hot and dry environments). For some reason these birds have a poor ability to fight off this organism. Examples of these birds include sea ducks, ostriches, and penguins. The other predisposing factor is the density of spores. In buildings that are poorly ventillated spore density will increase. Less commonly we see individual animals come down with asper, even though they would not be considered at risk birds. Successful treatment for asper depends on many factors. The location of the infection (nasal passages, trachea, airsacs, lungs), the extent of the disease by the time that it is recognized, and the immune status of the bird that has the infection all are critical factors. Asper grows like mold on bread inside the bird forming colonies on the respiratory surfaces. This elicits a response from the host that causes purulent material to build up around the colonies. The fungus is invasive and in advanced infections will invade into tissues and eventually into a blood vessel. Once a blood vessel is invaded the organism will spread to other organs and block blood vessels. The tissues whose vessels are blocked die. At this point treatment is not likely to be successful. Treatment is also complicated by the fact that asper grows on the surface of airsacs where the blood supply is poor and lots of caseous material builds up in these areas. Therefore, it is difficult to get drugs directly to these locations. Traditional treatment has been with itraconazole given orally. Usually this only has to be given once a day, but we treat until 1 month after the white blood cell count returns to normal, generally about 3 months. In my experience this drug has been very effective. When the organism is in the trachea of the nasal passages, direct application of an antifungal to the lesion has been used in conjunction with systemic treatment. Amphotericin B has been applied directly into the trachea. This drug is caustic and complications from this therapy may occur. Nebulization with clotrimazole has been used in gyrfalcons with asper of the airsacs. I have used clotrimazole as an infusion for a bird with refractory nasal asper. This bird was also on intraconazole. Lamisil is an new drug that Dr. Bob Dahlhausen and others are using. There will be a paper presented at the AAV this year on this product. It may be better or as good as itraconazole. We will have to see.
FUNGAL/YEAST INFECTIONS
Aspergillosis is a fungal infection that is seen in most species of birds. It is considered an opportunistic infection; the infectious organism is wide spread in almost all environments, so all birds are exposed to it; yet, only birds with immunospression or other problems get an active infection since they are normally able to control it. Chronic illness, malnutrition, and inadequate housing BG are all factors in predisposing some birds to an infection. Unfortunately, the structure of the avian respiratory system supplies a perfect incubator for growing a fungus such as aspergillosis-- the airsacs. The airsacs have almost no blood supply, so once aspergillosis gets started in the airsacs, it can continue to grow. There are several situations where the psittacine birds are most likely to be exposed to the greatest risk of aspergillosis. One is with hand-fed chicks where they can aspirate some of the feeding formula into their airsacs, which then acts as a foreign body where the fungus can start to grow. Breeding birds that spend a lot of time in nesting boxes are also at risk since many of the commonly used substrates in nesting boxes offer the perfect medium for growing the fungus which the birds then breathe in within the tight confines of the nest box. Chronic antibiotic therapy that lowers the birds immune system and disrupts the normal microbiological flora of the bird may also allow for a secondary aspergillosis infection. In birds that are identified as being at risk of an infection, a preventative treatment can be started which is very effective at preventing the infection. Basic husbandry and nutrition must be evaluated and problems corrected to also help prevent the disease. Active infections are normally diagnosed via radiographs, endoscopy, and fungal cultures. Many cases are not detected until a necropsy is performed; the birds may have an asymptomatic infection for years. Treatment is difficult and must be done for 6 months or longer to eliminate the infection.
http://numbat.murdoch.edu.au/Anatomy...3.html#RTFToC2
ASPERGILLOSIS
OCCURRENCE All species of birds are susceptible. ETIOLOGY
Aspergillus fumigatus
EPIZOOTIOLOGY
Infection usually occurs after inhalation of large numbers of spores from heavily contaminated feed or litter which overwhelms the resistance of the bird. Aspergillus can penetrate egg shells under ideal conditions and infect the embryo. Such eggs may appear green when candled.
Infected embryos may hatch with well developed lesions.

CLINICAL SIGNS
Dyspnea, gasping, accelerated breathing, diarrhea, anorexia, somnolence, progressive emaciation and increased thirst. If metastasis to the brain has occurred, signs of CNS disturbance
may be seen. If metastasis to the globe has occurred, one or both may have a gray-white opacity.

LESIONS
Yellow or gray nodules and/or plaques in the lungs, air sacs, or trachea; less often in the peritoneal cavity, liver, or at other sites. Mycelial growth with sporulation may be apparent as fuzzy green
material in the air sacs. Yellow or gray metastatic foci may be apparent in the brain, eye,
or at other sites. Infection in the conjunctival sac may result in accumulation of cheesy exudate.
Histopath.: Hyphae within the nodules or plaques.

DIAGNOSIS
Signs & lesions.
Culture. Caution, Aspergillus is a common contaminant.
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Aspergillosis :Description:
Aspergillus - The genus Aspergillus includes a variety of related fungi which cause aspergillosis. An important member of this genera is Aspergillus fumigatus. This fungus produces endotoxins which are generally responsible for the disease known as aspergillosis. Aspergillus species are common in the environment. Spores often become airborne in dry windy weather spreading from one location to another. Spores can enter an individual and develop in the respiratory system, lungs, eyes, and ears. Sick Building Syndrome is a condition caused by continuous fungal growth in areas of buildings and ventilation systems. Growth leads to the release of more spores. This can potentially leads to large scale respiratory infections and distress associated with aspergillosis.

Aspergillosis can be fatal, especially to those with immunodeficiency. This opportunistic pathogen is common among domesticated and cage birds.
*Penicillium notatum and the antibiotic revolution
Not all fungi are problematic, in fact some are vital in fighting numerous bacterial infections. In 1941 Albert Alexander had an infection at the corner of his mouth caused by the bacteria Staphylococci and Streptococci. Over time the infection spread to the rest of his face, eyes, and lungs. At the time, two scientists Howard Florey and Earnest Chain had just begun purifying a substance produced by the fungus Penicillium notatum that killed bacteria and was discovered by Alexander Fleming. Albert Alexander's doctor Charles Fletcher knew that Florey and Chain were looking to test this drug on a human volunteer, and so on February 1941 Albert Alexander became the first human treated with penicillin. Within 24 hours of his initial treatment his temperature dropped, his appetite returned and his infection began to heal.

Transmission: Inhalation of conidia (spores) from contaminated feed, fecal material, and soil. The spores are often present in the environment and healthy unstressed birds are generally resistant to even high levels of spores. However, young and old birds, birds on antibiotics, and those birds whose immune systems are suppressed by surgery, reproduction, environmental changes, capture, shipping, or age are frequently infected.

Aspergillus can also infect the developing embryo by penetrating the egg while the embryo is developing. Infected eggs may develop a slightly greenish tint when candled. Well developed lesions may appear on infected embryos after they hatch.

Symptoms: Symptoms range from respiratory distress, gasping, accelerated breathing, voice changes, abnormal droppings, emaciation, regurgitation, poor appetite, diarrhea, anorexia, gout, increased thirst, nasal discharge, conjunctivitis, dyspnea, neuromuscular disease, somnolence, lesions (yellow or gray nodules and/or plaques in the lungs, air sacs, or trachea; less often in the peritoneal cavity, liver or other sites)
Prevention: Minimize stress and overcrowding. Provide proper ventilation. Reduce contact with mold or spore contaminated nesting materials. Prevent malnutrition with a proper diet. Make sure feed is properly stored and is free of fungal growth. Aspergillus spores may be present in corn and grain products as well as manufactured pellets or extruded food and may develop into fungal growth if conditions are favorable.

Treatment: Antifungal treatment - Amphotericin, Flucytosine, Fluconazole & Itraconazole. Immunostimulants. Surgery may be required with certain localized Aspergillomas

Diagnosis: Tentative diagnosis can be made with clinical signs along with the absence of bacterial infection. A blood test showing an elevation in white blood cell count, mild anemia, and an elevation in the monocytes also supports this diagnosis. X-rays can be taken on any suspect patient. A radiograph can reveal densities or nodules consistent with aspergillomas. Samples of the fungus can also be taken, and cultured in specially prepared culture media. Caution - Apergillus is a common environmental contaminant.
PCR and sequence assays to identify the presence of Aspergillus and identify specific strains.
Sample: When testing individual birds, a cloacal swab and throat culture is recommended. If the sample tests positive and clinical signs are positive, the bird should be placed in quarantine and aggressive treatment should begin immediately.

Environmental testing using swabs of aviaries, countertops, fans, air-filters, nest-boxes etc. is extremely effective in determining the presence of Aspergillus in the environment. Remember Aspergillus is found naturally in certain environments without causing any harm.

Handling: Prior to shipping samples should be stored at 4 C. (refrigerator). Samples must be shipped in a padded envelope or box. Samples may be sent by regular mail, but overnight is recommended.
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Ventilation and the air sacs
Unlike mammals, birds do not possess a muscular diaphragm, and the lungs do not act as a pair of bellows. The design of the avian respiratory system is extraordinarily efficient, so that birds can extract sufficient oxygen for life even while undertaking strenuous exercise at altitudes of up to 7 or even 8 Km.

While the relative weight of the lungs is comparable to that seen in mammals, their relative volume is only one-tenth. This is because air flows through the lungs in a constant one-way stream, unlike mammals and reptiles where there is an inefficient tidal ebb and flow.

In addition the exchange surface (ie distance from air to blood) is much thinner in birds.

A major feature of the respiratory system of birds is pneumatisation of the long bones, the vertebral column and even the skull. These air spaces connect with the air sacs (below).

The air flow is a complex circulation involving pumping action of thin-walled air sacs in the thorax and abdomen. These extend into the long bones: in the 18th century John Hunter showed that birds could still breath with a blocked windpipe provided one of the long bones (he tried both the femur and the humerus) was connected to the outside air. Most of the major bones of the body connect with the air sac system. This gives lightness as well as being a reservoir of oxygen.

The major features of the respiratory system are as follows. See and complete Fig 3.1
The nostrils are generally at the base of the upper mandible. There is no soft palate and both the oropharynx and the choanal opening pass air to the glottis to enter the larynx.

The trachea connects this to the syrinx, the site of vocalization generally at the tracheal bifurcation. This has three potential vibrating surfaces, which explains why birds like Magpies can sing complex harmonies of different pitch simultaneously. Birds vary considerably in the musculature and anatomy of the syrinx and this of course reflects the potential complexity of their vocalisation.

The primary bronchi connect the syrinx to each lung, but the air passes through in the mesobronchi to the abdominal and posterior (caudal) thoracic air sacs. These lie ventro-lateral to the abdominal viscera: between the intestines and the abdominal wall. In addition there are paired anterior air sacs and a single interclavicular air sacarising from the mesobronchi, but there is considerable variation on this basic pattern between species.

From the caudal air sacs the air now flows cranially through the lungs by dorsobronchi and ventrobronchi. These branch out into a complex arrangement of air capillaries or parabronchi. Blood capillaries in the walls of these flow counter to the air stream, allowing for a highly efficient gas exchange.

The stale air then passes to the anterior air sacs and to an unpaired interclavicular air sac, whence it discharges via the trachea.

There is thus a four-beat cycle to respiration:--

(1) First inhalation. Air passes to the posterior air sacs, with expansion of the abdomen.

(2) First exhalation. The abdomen contracts forcing air through the lungs.

(3) Second inhalation. As the abdomen expands again the stale air in the lungs is forced out to the anterior sacs.

(4) Second exhalation. Contraction of the abdomen and anterior sacs drives stale air out of the trachea while fresh air floods into the exchange region. See Fig 3-2 Plan of the air sacs






Fig 3.1 Scheme of air circulation (head to the left) Fig 3-2 Plan of the air sacs






http://www.avianweb.com/sampson.htm

http://www.parrotchronicles.com/marc.../insurance.htm

http://www.parrotsatplay.org/welcome.htm

http://www.parrotsatplay.org/aspergillosis.htm

( I can never figure how to post pics..so if anyone would like them of the figures mentioned above...pm me))

[Kevin]

Good info, but is there a a cliff note version ?

[Lisa B]

no its just a group of articles i complied when my grey was sick..


edited to add:
Aspergillosis antifungal treatments include: Amphotericin, Flucytosine, Fluconazole(Diflucan) & Itraconazole. Immunostimulants. Surgery may be required with certain localized Aspergillomas. Lamisil(terbinafine) and Voriconazole - are showing promise in treating aspergillosis in Greys.(Greys dont handle some meds as well as other species)Ketoconazole was an older antifungal they used to use, but due to its undesirable side-effects , it has been superseded by newer antifungals, such as fluconazole and itraconazole.


Ventilation and the air sacs
Unlike mammals, birds do not possess a muscular diaphragm, and the lungs do not act as a pair of bellows. The design of the avian respiratory system is extraordinarily efficient, so that birds can extract sufficient oxygen for life even while undertaking strenuous exercise at altitudes of up to 7 or even 8 Km.

While the relative weight of the lungs is comparable to that seen in mammals, their relative volume is only one-tenth. This is because air flows through the lungs in a constant one-way stream, unlike mammals and reptiles where there is an inefficient tidal ebb and flow.

In addition the exchange surface (ie distance from air to blood) is much thinner in birds.

A major feature of the respiratory system of birds is pneumatisation of the long bones, the vertebral column and even the skull. These air spaces connect with the air sacs (below).

The air flow is a complex circulation involving pumping action of thin-walled air sacs in the thorax and abdomen. These extend into the long bones: in the 18th century John Hunter showed that birds could still breath with a blocked windpipe provided one of the long bones (he tried both the femur and the humerus) was connected to the outside air. Most of the major bones of the body connect with the air sac system. This gives lightness as well as being a reservoir of oxygen.

The major features of the respiratory system are as follows. See and complete Fig 3.1
The nostrils are generally at the base of the upper mandible. There is no soft palate and both the oropharynx and the choanal opening pass air to the glottis to enter the larynx.

The trachea connects this to the syrinx, the site of vocalization generally at the tracheal bifurcation. This has three potential vibrating surfaces, which explains why birds like Magpies can sing complex harmonies of different pitch simultaneously. Birds vary considerably in the musculature and anatomy of the syrinx and this of course reflects the potential complexity of their vocalisation.

The primary bronchi connect the syrinx to each lung, but the air passes through in the mesobronchi to the abdominal and posterior (caudal) thoracic air sacs. These lie ventro-lateral to the abdominal viscera: between the intestines and the abdominal wall. In addition there are paired anterior air sacs and a single interclavicular air sacarising from the mesobronchi, but there is considerable variation on this basic pattern between species.

From the caudal air sacs the air now flows cranially through the lungs by dorsobronchi and ventrobronchi. These branch out into a complex arrangement of air capillaries or parabronchi. Blood capillaries in the walls of these flow counter to the air stream, allowing for a highly efficient gas exchange.

The stale air then passes to the anterior air sacs and to an unpaired interclavicular air sac, whence it discharges via the trachea.

There is thus a four-beat cycle to respiration:--

(1) First inhalation. Air passes to the posterior air sacs, with expansion of the abdomen.

(2) First exhalation. The abdomen contracts forcing air through the lungs.

(3) Second inhalation. As the abdomen expands again the stale air in the lungs is forced out to the anterior sacs.

(4) Second exhalation. Contraction of the abdomen and anterior sacs drives stale air out of the trachea while fresh air floods into the exchange region. See Fig 3-2 Plan of the air sacs



Fig 3.1 Scheme of air circulation (head to the left)


Fig 3-2 Plan of the air sacs

[Graehstone]

Thanks Lisa!!! I don't know how that one slipped passed me. I know I have the info somewhere, but for the life of me could not find it anymore. I just turned my laptop upside down and shook it a bit but still couldn't find it, I know I have it, but ... (brainfarts)

Hugs and Hickies

[The Outlaw]

Lisa:

Beautifully done. Excellent sources. Compiled in a totally readable format and certainly a terrific source for a compilation of articles discussing all of the aspects of aspergillosis. Thank you very much.

THE OUTLAW

[Lisa B]

Outlaw..I had to do alot of research when my boy was sick to uderstand the Dr's....I saved it to hopefully help someone else if they needed it......