Avian Diseases

[Lisa B]

I am going to do a sticky of all the Disease info I can find that have to do with our parrots. I urge you to read through it, or print it out for future use.
We can never gather too much info, that will help our babies. They are depending on us. Its up to US to keep them safe. As I find more info, I will pasted it here, and then delete any nonsence I wrote to just keep it informational .


Psittacine Beak and Feather Disease (PBFD)

by : Dr. Branson Ritchie D.V.M.,Ph.D

PBFD is caused by a virus which infects and kills the cells of the feather and beak. The virus also impairs the immune system. Consequently many diseased birds succumb to bacterial and other infections. Psittacine Beak and Feather Disease (PBFD) is a devastating viral disease that has first been noticed in cockatoos, but has since been diagnosed in many species of birds, specifically in African Greys, budgies, cockatoos, Eclectus parrots, lovebirds, macaws, and Rosellas.
Symptoms / Disease Progression

PBFD should be considered in any psittacine bird that displays progressive feather loss or abnormal feathers. Most birds which succumb to PBFD are less than 2 years of age. However, all age groups should be considered susceptible to circovirus infection.

Young birds are affected by an acute form of PBFD, which occurs during their first feather formation, after replacement of down feathers. The developing feathers often fracture, bleed or fall out. Young birds may die following a short period of anorexia (loss of appetite), depression and diarrhea, with very little feather abnormality.

Older birds are thought to develop a chronic form in which dystrophic feathers stop growing shortly after emerging from the follicles. The feathers become increasingly abnormal with each successive molt. Contour feathers are usually affected early, while primary feathers are affected later in the disease. Contour feathers often are lost over most of the body. New feathers may have retained feather sheaths, blood within the shafts, are curled and deformed, or are short and clubbed. The beak may also be involved in the disease process. It may change from a dull black to a glossy appearance. It may grow abnormally long and develop splits and cracks which break and peel. Bacteria and fungi often invade the abnormal beak, causing further destruction and necrosis (death) of the tissues. The abnormal beaks often make it difficult for the bird to eat as it may be very painful.

Spontaneous recovery from acute PBFD can occur in many species. However, the majority of chronically affected birds do not recover from the disease.

Transmission:

PBFD is spread by inhalation or ingestion of virus particles. Feather dust has been found to contain a large amount of virus. The virus has also been found in crop secretions and in fecal material. The virus may also be ingested as a result of preening. The incubation period of variable among species and the age at which the bird is exposed. Again, neonates and young birds are most susceptible, while adult birds over two years of age are thought to be at less risk.

It is possible for a bird to undergo a transient subclinical infection. This means that the bird's immune system is able to eliminate the virus. This is why it is recommended that a normal appearing bird who tests positive be retested 90 days later. If the bird has eliminated the virus it will test negative. If it remains positive, it should be considered latently infected and should be expected to break out with clinical disease in the future.

This is considered a fatal disease, and there is no cure, or treatment known.

A pet bird with PBFD can live a long life, if it is in a stress-free environment. It would never have contact with other birds since it is capable of spreading the virus.

Diagnosis / Testing:

Whole, anticoagulated blood should be submitted from a bird without feather abnormalities, while both blood and several abnormal feathers should be submitted from a clinically abnormal bird. A test was developed by Dr. Brandon Ritchie, and is run by Avian Research Associates Laboratory.

Interpreting the Results of the Psittacine Beak and Feather DNA probe test.

A. If Bird Has Dystrophic, Necrotic Feathers and you Test Blood for PBFD Virus using DNA probes:*


1. If Positive: Suggests Active Infection

Management: : If bird is from a breeding aviary: Bird should be removed and all areas that could be contaminated with feather dust from the infected bird should be repeatedly cleaned. If companion bird: Bird should not be exposed to other birds outside of the household and you should be aware that the virus can be transported to other locations on your clothes or in your hair. Be courteous of other birds and do not expose them. It should be noted that, occasionally, some PBFD infected Psittaciformes of South American descent have spontaneously recovered from the disease.


2. If Negative: A feather biopsy (including the feather follicle) should be submitted for histopathologic examination.

B. If Bird's Feathers are Normal and you Test Blood for PBFD Virus using DNA probes:*


1. If Positive: Indicates that the bird has been exposed to PBFD virus and that the virus is present in the blood. The bird must be retested in 90 days. If the bird is negative when retested, it indicates that the virus was not detected in the blood cells. If the bird is still positive, it indicates that the bird is either clinically infected or that the bird is being repeatedly exposed to the virus. It should be noted that most birds that are exposed to the PBFD virus develop a transient viremia followed by an appropriate immune response that results in the bird clearing the infection.


2. If Negative: Indicates that PBFD virus was not detected in the blood.

*Testing available from:
INFECTIOUS DISEASES LABORATORY DEPARTMENT OF MEDICAL MICROBIOLOGY COLLEGE OF VETERINARY MEDICINE UNIVERSITY OF GEORGIA ATHENS, GA 30602-7386

For questions, please call: 706-542-5812

Branson W. Ritchie, D.V.M., Ph.D.
College of Veterinary Medicine
Small Animal Dept.
Athens, GA 30602

[Lisa B]

Aspergillosis
Compiled by Lisa Bono

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
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
Aspergillosis is 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.

[Lisa B]

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.

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.
__________________________________________________ _____________
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
__________________

[Lisa B]

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.
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
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

[Lisa B]

Most birds have 9 air sacs:
one interclavicular sac
two cervical sacs
two anterior thoracic sacs
two posterior thoracic sacs
two abdominal sacs
Functionally, these 9 air sacs can be divided into anterior sacs (interclavicular, cervicals, & anterior thoracics) & posterior sacs (posterior thoracics & abdominals). Air sacs have very thin walls with few blood vessels. So, they do not play a direct role in gas exchange. Rather, they act as a 'bellows' to ventilate the lungs (Powell 2000).

http://i40.photobucket.com/albums/e217/LisaB1005/cartoons/airsacs_12-2.gif


Air sacs and axial pneumatization in an extant avian. The body of bird in left lateral view, showing the cervical (C), interclavicular (I), anterior thoracic (AT), posterior thoracic (PT), and abdominal (AB) air sacs. The hatched area shows the volume change during exhalation. The cervical and anterior thoracic vertebrae are pneumatized by diverticula of the cervical air sacs. The posterior thoracic vertebrae and synsacrum are pneumatized by the abdominal air sacs in most taxa. Diverticula of the abdominal air sacs usually invade the vertebral column at several points. Diverticula often unite when they come into contact, producing a system of continuous vertebral airways extending from the third cervical vertebra to the end of the synsacrum. Modified from Duncker 1971
http://i40.photobucket.com/albums/e217/LisaB1005/cartoons/airsacs5-2.gif

[Lisa B]

PDD

a site devoted just to PDD, by the Avian Health Network

http://stoppdd.com/problem/pdd_faq.html

[Lisa B]

Avian Viruses...
What They Are and How They Cause Disease

Understanding what viruses are and how they function will help individuals develop a perspective of how viruses can affect birds.Viruses are the most basic of all organisms. They contain only nucleic acid (DNA or RNA) and a protein coat cover. Some more complex viruses are enclosed in a protective envelope derived from the infected cells own cell membrane. Viruses require the help of other cells to reproduce. Bacteria, fungi, chlamydia are more complex and have a nuclear body (DNA or RNA) and cytoplasm that contain components that convert nutrients into energy to drive the functions of the cell. These organisms can reproduce on their own. The nucleus of a cell can be viewed as the control center and the cytoplasm the factory. Viruses have a control center but no cytoplasm therefore a virus is dependent on the cell it infects to provide the factory it needs to produce energy or reproduce itself. Viruses are very small. For example, it would take 21,517 Psittacine Beak and Feather Disease (PBFD) viral particles to cover the tip of a needle. These tiny particles can survive in the environment for months to years and can be spread to other birds in a home or aviary via contaminated fingernails, skin, hair, jewelry, cloths, food bowls, perches etc.

The general steps in viral reproduction are:
Attachment of virus to a receptor on the bird’s cell
Penetration into the interior of the bird’s cell
Uncoating or removal of the protein coat releasing the viral nucleic acid into the infected cell
Transcription/translation of the virus’ nucleic acid, resulting in the infected cell producing new copies of the viral protein coat and nucleic acid
Assembly of protein coat and nucleic acid into a new viral particle
Release of the new viral particle from the cell.
The protein coat has binding sites that recognize receptors on the cells of susceptible bird species. A bird is considered susceptible to a viral infection if a receptor on its cell allows the virus to attach. If this receptor is not present then the bird will not be infected even if it has been exposed to the virus. For example, a duck may not be susceptible to a parrot virus or vice versa but an Amazon parrot would be susceptible to a Macaw virus. Disinfectants work by destroying these sites on the virus thus preventing the virus from initially binding to the cell.

A virus infection can cause disease in a bird in several ways:
The virus can directly induce lesions in an organ by causing the rupture of infected cells
The virus may stimulate the bird’s immune response, which then destroys the virus-infected cells
The virus may damage the bird’s cells causing them to become neoplastic (cancer).
The virus may establish itself in the bird such that the infected bird becomes a persistently infected carrier of the virus.
Viruses may damage host cells in several ways:
The virus uses the cell’s metabolic functions exclusively for the virus therefore the host cell starves.
The virus produces products that are toxic to the cell.
The virus ruptures the cell membrane thus destroying the cell.
The virus alters the cell wall causing the cell to loose vital fluid and die.
The virus may change the DNA of the cell causing it to become cancerous.
The result of exposure to a virus depends on the age, species and condition of the bird and the characteristics of the particular virus. A healthy bird that is exposed to a virus to which it is susceptible can become infected. The infected bird may remain clinically normal or it can become obviously diseased. If the bird remains clinically normal and develops a subclinical infection, it may destroy the virus and be protected from future infections, or it may remain persistently infected (carrier state). Likewise, a clinically infected bird (showing obvious signs of disease) may mount an effective immunologic response to destroy the virus and develop protection from future infections, or it may recover from the disease and remain persistently infected (a carrier) or it may die. Young birds are more susceptible to viral infections because their immune system is not fully developed likewise very old birds are more susceptible due to an age related decrease in immune system function. Birds are most resistant to disease during their reproductively active years. If all other factors are equal, a healthy bird exposed to a small number of viral particles is less likely to become ill than the same bird exposed to a large number of particles. Maintaining numerous birds in close proximity will increase the likelihood that a virus can be transmitted from bird to bird. Depending on the type of infection, birds may or may not produce antibodies. Antibodies produced in response to viral infection help clear the infection and protect the body from future infections.

Potential methods of viral transmission in birds:
Preening
Rubbing
Inhalation of aerosols
coitus (mating)
insect or animal bites
contamination of egg
ingestion of contaminated feces
contact with contaminated fomites
ingestion of contaminated food or water
ingestion by neonates of regurgitated food from infected parent
fighting related injuries
insects-mechanical vector/biologic vector
from infected hen to egg in utero (while egg is in the reproductive tract)
contamination of egg by infected hen immediately after laying
Diagnosing Viral Infections
Diseases are frequently caused by the interaction of more than one type of infectious agent, including bacteria, fungi, viruses and parasites. A virus may cause damage to a bird allowing other pathogens (particularly bacteria and fungi) to colonize damaged tissues. The bird may clear the viral infection that initiated the disease process, and it is a bacteria or fungi that is detected on diagnostic testing of the ill bird. In these cases, the virus is referred to as the PRIMARY infection and the bacteria is referred to as the SECONDARY infection. Therefore, many birds that are diagnosed with bacterial/fungal infections may have initially had a viral infection.

Clinical abnormalities, necropsy findings and microscopic abnormalities may suggest that a bird was infected by a virus; however, clinical signs or lesions that absolutely confirm that a particular type of viral infection occurred are rare. A thorough necropsy with collection of necessary diagnostic samples should be performed on any bird that dies. Diagnostic samples may include portions of tissues placed in formalin for microscopic evaluation, samples of blood for bacterial or viral isolation and swabs or samples of abnormal tissues for viral, bacterial or fungal isolation.

Preventing Viral Infections
The goal of maintaining any bird in captivity is to insure that it is in the best possible condition. Few effective vaccines exist against the viruses that infect companion and aviary birds. Careless exposure of a single bird within a flock can result in viral outbreak that may affect the entire flock.

Ways to prevent spread of virus:
Use clean, disinfected feeding utensil for each bird
Quarantine all new birds minimum 30 days if captive bred; 90 days for all others
Isolated any sick birds ASAP
Do not allow fecal contamination of food/water bowels
Disinfect food/water bowls daily
Disinfect cage area as often as possible
Limit outside visitation of aviary
Use disinfectant foot baths on entry/exit from aviary
Veterinary evaluation of sick birds
Necropsy examination of dead birds - Place bird in refrigerator as soon after death as possible - DO NOT FREEZE REMAINS - this damages tissues making microscopic evaluation difficult.
Limit exposure to noxious fumes esp. cigarette smoke.
Provide nutritionally, complete diet.
Relatively stress free environment
>Do not overcrowd
Do not mix babies from different nests/parents
Wash hands between handling birds
Eliminate vermin
Maintain good air circulation
Reduce fecal and food accumulations
Cleaning and Disinfection
Viruses are susceptible to inactivation when they are outside the bird’s body. The destruction or removal of the virus from the bird’s environment is one of the best methods for control of viral transmission. This can be achieved by a combination of:

Washing - to remove viral particles from the environment
Painting - permanently fixes virus to the surface
Disinfection - destroys the receptors that allow a virus to bind to a cell or destroys the viral nucleic acid
The presence of soil, feces, food, blood, mucous, or bedding material can interfere with the disinfection process in two ways: it can inactivate the disinfectant or it can prevent the disinfectant from contacting the virus. The contact time between virus and disinfectant is also important to allow complete inactivation.

[Lisa B]

Common Disinfectants
Chlorinated compounds - widely available, inexpensive, low residual toxicity. In general a 1:32 dilution (1/2 cup bleach per gallon water) is sufficient. These compounds are rapidly inactivated by organic material and sunlight, require frequent mixing-every few hours-to maintain an active solution. The solutions and fumes they produce can be irritating to skin, eyes and respiratory tract therefore should only be used in well ventilated areas.
Chlorine dioxide - similar to bleach and in some studies may be superior to bleach but is rapidly inactivated by organic material and sunlight.
Chlorhexidine gluconate - relitively non-toxic to skin, often used to cleanse wounds, non-corrosive and good activity against many bacteria, yeast (Candida) and some enveloped viruses, however, should not be considered a reliable viricide. Inactive in presence of organic material and limited stability.
Glutaraldehyde - rapidly inactivate many bacteria (including mycobacteria-avian tuberculosis), viruses and chlamydia, active in presence of organic debris, and stable as working solution from 2-4 weeks. These compounds are infrequently used because of widespread side effects of irritation to skin, respiratory tract and eyes especially following long term exposure.
Iodines - used for cleaning wounds and skin and is effective against many bacteria (not Pseudomonas), some viruses and fungi. Rapidly inactivated by organic material.
Phenols - inactivate many bacteria (including mycobacteria and Pseudomonas), fungi and some viruses, inexpensive but are irritating to skin, eyes and respiratory tract, toxic to cats and reptiles.
Quaternary Ammonium Compounds - inexpensive, relatively safe, and inactivate many bacteria, some viruses and chlamydia. May be inactivated by organic debris, and are ineffective against spores, mycobacteria, fungi, nonenveloped viruses and Pseudomonas. Hard to rinse from some surfaces and leave a slimy residue. Not recommended for use on objects that would be in direct contact with birds i.e. feeding utensils, food or water bowls.
Wood tar distillates - low toxicity but poor disinfectant.
Alcohols - 70% ethyl alcohol inactivates many bacteria and viruses but require minimum of 20 minutes contact time. Dissolve plastics, glues, and rubber.
Vaccines
Few vaccines have been developed and tested for use in companion and aviary birds. When a bird recovers from a viral infection, it does so because its immune system produces specific antibodies and specialized immune system cells that react to the surface proteins that compose a virus’ coat or envelope. Vaccination is intended to induce a similar immune response. Depending on the particular virus, a vaccine may initiate an immune response that will prevent the virus from infecting the bird or it may allow a bird to be infected but produce a minor, rather than a severe, disease. In either case, the bird should develop an active immune response following vaccination. Over time, the response will decrease and administration of a booster vaccination will be necessary. Vaccines may fail to produce effective immune response if the vaccinate bird is immunocompromised, already infected, or undergoing immunosuppressive therapy (steroids, some antibiotics). Any vaccine may be expected to cause an inappropriate reaction in a certain percentage of birds. These reactions can vary in severity from a sore/scab at injection site to lethargy or rarely death.

Definitions:
Infection - process of a virus entering a bird’s cell and reproducing
Disease - abnormal changes that occur in the bird’s cells as a result of infection. The severity of the disease that occurs depends on the bird’s age, nutritional status, stress level and environmental conditions.
Carrier state - a subcliniclly infected bird that shows no outward signs of virus infection but can spread the virus to other birds.
Types of Infection:
Subclinical - No signs of disease. Immune system controls infection and birds develop antibodies.
Peracute - Very rapid progression of disease. Infected birds recover or die within hours to days of infection. Recovered birds usually develop antibodies.
Acute - Rapid progression of disease. Infected birds recover or die within days to weeks after infection. Recovered birds usually develop antibodies.
Persistent - Chronic, Latent, or Slow
Chronic - Long-term infection with persistent shedding of virus. May persist for months to years. Birds may or may not develop antibodies.
Latent - Long-term infection with intermittent shedding of virus. May persist for months to years. Birds may or may not develop antibodies. No disease or shedding of virus during dormant state. Birds shed virus and may develop disease when virus is activated.
Slow - Progressive disease over months to years eventually causing the death of the bird. Virus reproduces over a long time period. No signs of disease early on.
Fomite - Inanimate object responsible for spread of disease i.e. cage toy, cleaning utensils, feeding syringes, clothing, human skin.
Biologic vector - living organism that becomes infected with virus from bird then carries that virus to another bird i.e. Western Equine Encephalitis infects mosquito when mosquito bites horse then infects bird when same infected mosquito bites a bird.
Mechanical vector - living organism that spreads virus by carrying it on its body from one bird to another i.e. poxvirus infections
Disinfectant - will destroy many disease causing organisms on the surface of inanimate objects. Some organisms and heat-resistant spores may be resistant.
Sterilant - will destroy all microbial organisms including heat resistant spores. Achieved by autoclaving, boiling or exposure to toxic chemicals.
Germicide - Kills a specific group of organisms when used as directed.
Sanitizer - reduces surface microorganisms to an acceptable level on inanimate objects.
Antiseptic - reduces surface microorganisms to an acceptable level on skin.
Active compound and trade names of common disinfectants.

ACTIVE COMPOUND PRODUCTS
Chlorinated compounds bleach, Clorox, Purex
Chlorine dioxide Dent-A-Gene
Chlorhexidine gluconates Hibitane, Hibistat, Nolvasan, Virosan
Glutaraldehydes Banacide, Cidex, Cybact, MC-25, Sporocide, Sonacide, Sterol, Wavecide
Iodine Betadyne, Scrubodyne, Povidone, Prepodyne, Virac, Wescodyne
Phenols Avinol-3, LPH, Lysol, Matar, Amerse, One Stroke, Environ, O-Syl, Staphene
Quaternary Ammonium A-33, Baraquat, Cetylcide, Floquat, Hitor, Merquat, Omega, Parvasol, Quintacide, Roccal, Zepharin
Wood tar distillates Hexol, Pine-Sol


From: Ritchie, WR. Avian Viruses: Function and Control. Wingers Publishing, INC. Lake Worth, Florida, 1995.
The majority of information in this article was obtained from Ritchie, WR. Avian Viruses: Function and Control. Wingers Publishing, INC. Lake Worth, Florida, 1995.

[Lisa B]

West Nile Virus
by Lisa Bono


Dr Ritchies lecture this question was addressed. He feels that the benefits of sunshine out weigh the risks about West Nile, and The Bird Flu. The Bird Flu is not here yet...and has mostly affected poultry and water fowl.
West Nile, he suggest late morning, early afternoon for your birds to be out. That is the time there are less mosquitoes.



Bald Eagles were one of the first species effected by WNV. Crows/Raptors/water fowl are more susseptable to death from WNV.
Condors were the first to be vaccinated before the virus jumped over the Rocky Mountains. It was a success!
It was introduced into the US in the 1990, by a house sparrow from Europe, and the virus is HUMAN MADE. (not sure what the meaning was behind that because I had to get up when he explained)
African species of parrots are tolerant of the disease, and will most likly not die.
South Pacific and New World Parrots are more likely to die if infected with WNV.
WNV is shed in bird droppings and transmitted through blood.
Best to avoid outside birds, and dont let them eat from any feeder/dish your bird might eat from.

VIRUS' HATE SUNSHINE AND HEAT.

[Lisa B]

Avian Polyomavirus
Vaccinated birds SHOULD NOT be housed with VACCINATED birds.
Eclectus parrots and Caiques NEVER outgrow the risk of Polyoma, while other species are most affected under the age of 2 years old.


http://www.oldworldaviaries.com/text/miscellaneous/polyoma.htm

[Lisa B]

Baterial Infections & Mega Bacteria/Megabacteriosis

http://www.avianweb.com/bacterialinfection.html

[Lisa B]

PAPILLOMATOSIS DISEASE
by Linda Pesek DVM, Diplomate ABVP (Avian)


Papillomatosis refers to pink, proliferative, vascular wart-like or cauliflower-like growths of epithelium. Papillomas may occur singularly or in clusters. Although they may occur in the oral cavity, crop, esophagus, proventriculus, ventriculus, cloaca, respiratory tract and conjunctiva, the most common locations are the oral cavity and cloaca. Thought to be of viral etiology and infectious, spread is probably through preening and other close contact between birds.
The highest incidence of papillomatosis occurs in central and south american psittacines - especially greenwing macaws (cloacal), blue and gold macaws (oral), as well as in amazons, conures and hawk headed parrots (cloacal).

The signs exhibited depend upon where the papillomas occur. Oral lesions may cause wheezing, difficulty swallowing and open mouth breathing. Papillomas in the glottis may cause suffocation if they obstruct the airway. Papillomas in the gastro-intestinal tract may cause vomiting, loss of appetite and wasting. Cloacal papillomas may be initially mistaken for a prolapse. They may be seen protruding from the vent when the bird becomes stressed or during elimination. Straining, blood in the droppings, passing gas and an abnormal odor to the droppings occur. The lesions often spread throughout the cloaca and may become so extensive they cannot be retracted back up into the vent.

Infertility may occur due to mechanical obstruction or ascending infection. Although birds may live for years with papillomatosis, the long term prognosis is guarded. A waxing and waning course often occurs, with signs subsiding for a while. Over time, however, the lesious progress. Papillomatosis has been accociated with bile duct and pancreatic duct in amazon parrots.

Diagnosis is by physical examination, contrast radiographs and fluoroscopy.

A number of treatment modalities have been tried which include surgical resection, cryosurgery, chemical cautery, autogenous vaccination, and laser. Laser surgery seems to offer the best results.

All new birds of susceptible species should be thoroughly examined to identify those with oral or cloacal papillomas. Infected birds should not be housed with non-infected birds.

Papillomatosis in unable to be cured. Palliation can be done to make affected birds more comfortable, but it is often a progressive, debilitating disease.

This disease can mimic other diseases such as foreign bodies, bacterial and fungal infections, lead poisoning and PDD.

[Lisa B]

Psittacosis
: The enigmatic disease
by Darrel K. Styles, DVM
(Editors note: More accurate tests for psittacosis have been developed since this article was written. And, the genus Chlamydia has been separated into two genera.)

Psittacosis or parrot fever is caused by the bacterium Chlamydia psittaci. This is one of the oldest known diseases of our domestic birds and still causes significant physical and economic loss to aviculturists.

Several species of Chlamydia exist: C. trachomatis, which is a venereal disease of humans that causes pelvic inflammatory disorder in women and is the leading cause of infectious blindness in the world; C. pneumoniae, which is a primary human respiratory pathogen; and C. psittaci, which is an extremely cosmopolitan organism infecting a wide variety of animals including all species of birds, mammals including humans, and even reptiles! This highly nonselective nature is what makes psittacosis such a unique disease and an important zoonotic infection (a disease transferred from animals to humans). We will limit our discussion of C. psittaci to how it can affect our collections and even ourselves.

Chlamydia psittaci is a bacterium, contrary to popular literature you may have read that asserts it is a virus. However, it is a highly specialized bacterium in that, like a virus, it is an obligate intracellular parasite, meaning that it must have an animal host cell in order to grow and reproduce.

For this reason, we cannot culture psittacosis organisms on conventional bacterial media like we would E. coli. Conventional media contains only nutrients and a gel matrix for support. C. psittaci requires cells to grow. Cell culture is a more expensive and complex method of propagating the bacteria, but is the only means available.

The bacteria go through a highly complex method of reproduction and growth which is beyond the scope of this article. Suffice it to say that it results in cell death and may even kill the host.

C. psittaci is easily and casually transmitted by means of secretions, both in the stool and in respiratory secretions where the infection is airborne. Therefore, it is not easily confined like other bacteria.

The organisms survive outside their host in a specialized form called an elementary body. These elementary bodies hold the bacteria in stasis until they either find their way into a host or die. Elementary bodies can persist in the environment for a long period of time, especially when encased in organic material such a feces, but will eventually succumb to desiccation (drying out).

Psittacosis manifests itself differently in each different animal. Even different species of parrots show different signs when infected. For example, when the birds become infected they may immediately begin to show signs. Or the infection may become occult, and the birds can latently hold the disease for long periods of time, even years.

If the birds do become ill, we first typically see the bird display sick bird syndrome. This may quickly be followed by loose lime-green to yellowish stool. What is happening to cause this change in stool appearance? The organism is attacking the liver. The liver becomes somewhat dysfunctional, which causes certain blood pigments to be spilled into the urine. This causes the entire stool to be discolored, and increased urine output causes the loose nature. A component of diarrhea also is included, which further complicates matters.

This scenario is typically observed in Amazon parrots. However, macaws may show strictly respiratory signs. It is hard to say whether this is a function of species or the strain of Chlamydia infecting the bird. Nevertheless, if the infection goes untreated, death or at least severe liver damage often ensues.

The latent nature of psittacosis makes it another candidate for time bombs in our collections. We do not fully understand how this organism can lie dormant for weeks to years without causing disease, and then have a stressful event precipitate an outbreak. The bacteria probably reside in the liver waiting for an opportunity to strike. This occult behavior makes it very hard for us to detect carriers in our flocks or in newly purchased acquisitions.

The lack of reliable testing methods is another difficulty. Chlamydia may be intermittently shed in low numbers making it a difficult disease to detect. I have even heard of an instance where the organism was dormant for up to 5 years in a solitary pet Amazon who succumbed to the disease for no apparent reason. So, this bacterium can cause no illness for a long period of time, then suddenly strike.

Diagnosis and detection is a real problem! Several commercially available tests are on the market. Some of these tests have fair-to-good reliability and some, in my opinion, are not very useful. Many vets use the Kodak sure-cell test kit, which is designed for human C. trachomatis but will react to C. psittaci. This test is particularly useful in that it can be done in the office and is fairly reliable. However, the test typically cannot detect carriers because the organisms must be shed in sufficient quantities for the test to detect them, and carriers typically do not shed sufficient quantities.

Another test, latex agglutination, detects antibodies to psittacosis. But this test has mixed results and will not detect carriers. Other commercially available tests exist, which I cannot mention by name, but give very high degrees of false positive results in my experience. These tests cannot be relied upon, and I do not recommend their use. “Gold standard” tests rely upon culturing the organisms, but unfortunately are only done at the university level.

The oldest means of diagnosis is intuition. Vets experienced in seeing birds with psittacosis will usually be able to diagnosis many cases by the clinical data and patient presentation. In any event, therapy must start immediately and often on a presumptive basis until all the results are in. Fortunately, psittacosis can be treated if the disease is diagnosed early and treated properly. However, treatment is a nightmare for patient and doctor.

Psittacosis is a reportable disease in some states, which means diagnosis requires reporting to a local or state health authority. Therefore, its treatment is mandated by certain federal regulations, sort of. By this I mean that the USDA determined totally empirically that the treatment period for psittacosis must be at least 45 days. This pulled-out-of-the-hat number probably comes from quarantine days, where it took at least 30–45 days to get the results of the Newcastle disease test back from the federal testing labs. The USDA was not really concerned about psittacosis but wanted to ensure that exotic Newcastle disease did not enter the country, because it could devastate the poultry industry. However, to “protect” the public the USDA did require that quarantined birds be treated with tetracycline-treated feed for the duration of the quarantine.

Well, the birds just hate the taste of that medication. Often the station owners just would not put the medicine into the food. Otherwise they would sustain losses due to birds not eating bitter feed. At any rate, most veterinarians comply with these loose guidelines to stay out of malpractice suits and recommend a 45-day treatment period. This makes it stressful for both the bird and the aviculturist, because it is the bird owner who must conduct the bulk of the therapy unless he can afford a very expensive vet bill. Many other vets and I believe that the treatment period is probably less, maybe 10-14 days with the newer long-acting tetracyclines. But we are compelled by federal precedent to recommend the longer period.

Most vets treat with some form of tetracyclines. There are many types, all of which are effective. Some newer drugs are being used in human venereal infections that are effective after only a few doses. These hold great promise for the aviculturist if certain clinical trials now in progress prove effective.

If we are treating a solitary bird or only a few, some people elect to use an oral suspension called doxycycline. This drug is long acting and highly effective against psittacosis. But, it is difficult to get therapeutic doses down the unwilling patient. The drug has a sticky consistency with a raspberry color, which serves to stain both bird and owner in the battle. If the bird does not take the syrup willingly, it can be dangerous to try to force it down once to twice a day depending on the species.

The other option is medicating the birds in their feed. This is the only viable alternative for flock medication and can be conducted in two ways, either feed the drug as a food bolus or pill or purchase pelleted medicated feeds, which are commercially available from a variety of dealers. One can also concoct a homemade mash and incorporate the drug.

However, often birds will refuse the pellets or mash and the aviculturist must battle to get the drug in somehow. Once the treatment is finished, the bedraggled birds must again be treated for the ensuing yeast infections which result because of wiping out the normal bacterial flora.

[Lisa B]

Aviculturists must be vigilant during the treatment period to make sure birds are eating and not losing too much weight. So, as you can see, medication for psittacosis is an arduous undertaking not without risk. (Ed: I know of one story of small birds starving to death. Although they were ravenous and acting like they were eating the tetracycline-impregnated food, they were actually refusing it while they frantically picked through the food to find something palatable.)

Injectable forms of long acting tetracyclines are used by Canadian and European aviculturists, but they are not available in this country. However, newer drugs offer the hope that we can reduce the duration and frequency of therapy. Even in a very sick bird, if we can initiate tetracycline and supportive therapy early enough, the bird can be returned to virtually a normal state in 48-72 hours, so the drugs are quite effective.

Once the treatment is completed, you have hopefully eliminated the organism and the carrier state. But there is no guarantee. And, because the birds have been infected once does not mean that they cannot be reinfected. Immunity is short lived, probably on the order of 3 months. I had a blue-and-gold macaw that I treated who came back to me 6 months later reinfected. It seems pigeons were daily visitors to his cage and probably served as the vectors.

Also, you can get Parrot Fever. I speak from experience because I have had it twice. If it is not treated effectively, or if exposure is prolonged, it can cause heart problems later in life, due to infection of the heart valves. The symptoms include malaise, joint pain, and fever--like a bad case of the flu only worse. Tetracycline therapy makes you feel much better in about 12 hours. However, it appears large doses are required to infect us. I got my cases after treating large outbreaks in collections or pet shops where the birds were filling the air with psittacosis.

You must be vigilant. Because you own birds, if you experience these symptoms, advise your doctor that you may have been exposed so he can do suitable diagnostics and begin treatment. And you should know that this can be a very serious infection in immuno-compromised individuals and the very young and very old. So don’t treat psittacosis lightly.

Some states even require a quarantine if a large outbreak is detected, which can lead to the closing of pet shops. I recommend to my clients that they close their collections and not sell or accept birds during the treatment period to help eliminate liability. Retesting for effective treatment is always a good idea.

To summarize, hopefully you can detect the organism during the stressful quarantine period. But be aware that it may slip into your collections even born by wild birds. If psittacosis is diagnosed, work with your veterinarian to design a suitable treatment regimen and be aware of its human infective potential.

[Lisa B]

Pacheco's Disease
by Linda Pesek, DVM
Westbury Animal Hospital
319 Union Avenue
Westbury, NY
516-333-1123

Pacheco's disease is caused by a herpes virus. This disease is dreaded by aviculturalists because it is very devastating and often fatal. It was first recognized in Brazil when birds started dying several days after becoming ill.

Different strains of herpes virus are believed to exist. A variety of birds may be infected, such as chickens, ducks, pigeons and psittaformes. Psittaciformes are most susceptible to the virus. Macaws, Amazons, African greys, cockatoos, budgies, cockatiels and conures are some of the species that can be infected. Patagonian and Nanday conures are frequently asymptomatic carriers. Any bird that survives an outbreak should be considered a "latent" carrier of the virus.

Infected birds may die suddenly or show nonspecific signs such as lethargy, anorexia, ruffled feathers, sinusitis and intermittent diarrhea. Urates may become green, indicating that liver damage has occurred.

The first sign of a problem often occurs when a seemingly "healthy" carrier bird is introduced into a collection and birds start to die suddenly. Any type of stress (e.g., breeding) can activate the virus and result in its being shed in large numbers in the feces. The incubation period is thought to be as short as several days in some of the smaller parrots.

The biggest problem is that there is no good antemortem test that can be used to detect the virus in a live, "healthy" carrier bird. Diagnosis is usually made on postmortem with virus isolation and characteristic histopathology changes. If an outbreak occurs, some people suggest using the human herpes medication Zovirax (registered trademark for acyclovir), given by gavage. Vaccination in the face of an outbreak is considered by some to be controversial, since handling may help spread the virus.

A vaccination using killed vaccine is available and can be given in a series of two injections, 4-8 weeks apart. Some species, such as cockatoos, have had vaccination reactions. Only birds with high risk of exposure, such as pet store birds, should be vaccinated.

Prevention is the best way to avoid an outbreak. Strict quarantine measures should be carried out. Some advise not to mix conures with Amazons, since conures can be asymptomatic carriers and serve as a source of infection for susceptible birds.