The infection with the fungus Aspergillus sp. is a common cause of respiratory disease in birds such as parrots, raptors and aquatic species. The fungus is ubiquitous in the environment and infection occurs by inhalation of spores from the environment, but it is not a contagious disease. Environments with decomposing vegetable material or damp litter, or those with faecal and urine contamination provide ideal conditions for fungal proliferation. In addition, lack of ventilation and immune suppression facilitate infection. Some species are particularly predisposed, such as Pionus parrots, gyrfalcons, goshawks, snowy owls, golden eagles and aquatic species. The disease can be caused by inhalation of small numbers of spores over a prolonged period of time or by inhalation of a large quantity of spores acutely. 

Aspergillosis is commonly a chronic disease with the formation of granulomas in the respiratory system, particularly lungs and air sacs. Clinical signs include weight loss, voice changes and dyspnoea. Development of granulomas in the syrinx may produce acute dyspnoea and should be treated as an emergency. Diagnosis can be made based on clinical signs, blood results (increase in globulins, leucocytosis with monocytosis and heterophilia, toxic heterophils, non-regenerative anaemia) or detection of antibodies or antigen in blood. Radiography is usually non-diagnostic until the disease is very advanced. Endoscopy is the best diagnostic technique, and allows direct visualization of lesions and collection of biopsies for histopathology and culture; in addition, it allows for granuloma removal and intralesional treatment with antifungals. If endoscopic equipment is not available, referring the case should be considered. 

Treatment of aspergillosis may be rewarding depending on the case. Very advanced cases or those cases in very nervous/stressful animals are usually unresponsive to treatment. The acute presentation of a bird with a syringeal granuloma carries a better prognosis if the granuloma is removed via tracheal endoscopy (with a previous placement of an air sac tube). Tame psittacines and raptors respond in an acceptable way to medical treatment. During endoscopy, large granulomas should be removed if possible, and amphotericin B can be instilled into the lesions. Surgery to remove large granulomas may also be indicated. An intravenous injection of amphotericin B before the animal wakes up from anaesthesia should be followed by long-term medical treatment (at least 1-2 months) with oral and nebulised antifungals. Response to treatment should be assessed with endoscopy. 

Candidiasis 

The yeast Candida albicans is a normal part of the avian gastrointestinal flora. Disease is seen with the indiscriminate or prolonged use of antibiotics or in young birds with poorly developed immune systems. Hand-reared birds fed improperly prepared rearing formulas are also at risk. The crop is the main site of infection. Clinical signs include regurgitation and vomiting, a distended, slow emptying crop, beak necrosis and white/cream plaques in the oral cavity. Rarely the infection will spread systemically. The diagnosis is by cytology or culture of lesions. Treatment is by the direct application of nystatin, which is only active in the gastrointestinal tract (its antifungal effect is by direct contact with the fungus/yeast). 

Avian Gastric Yeast 

Previously known as megabacteria, Macrorhabdus ornithogaster morphologically resemble large Gram positive rods. They require microaerophilic conditions for growth. The disease is most often seen in canaries, finches, budgerigars, lovebirds, cockatiels, small parrots and occasionally in larger psittacines. Megabacteria cause proventricular and ventricular disease. Clinical signs include wasting, lethargy and passage of undigested food. Radiography may show proventricular dilatation. Necropsy lesions include proventricular ulceration and dilatation. Diagnosis is by demonstration of large quantities of organisms on Gram stain or wet mounts. Macrorhabdus ornithogaster is a long, straight, narrow rod that is 3 to 4 μm wide and 20 to 80 μm long. It will occasionally branch, but this is rare. The infection responds to treatment with oral amphotericin B or sodium benzoate (an antifungal preservative for food). This is a very common problem in wasting canaries and budgerigars. 

Avian chlamydiosis 

Chlamydia psittaci is an obligate intracellular bacterium that produces mostly respiratory and liver disease in parrots and other birds. Avian chlamydiosis is a zoonosis and can produce serious disease in humans. It is shed in body secretions (faecal, nasal and ocular fluids) and can survive in the environment for several weeks. 

Clinical signs seen include conjunctivitis, nasal discharge, ocular swelling, sneezing, lethargy, ruffled feathers, weight loss, inappetence and bright green urates. Asymptomatic carriers are common, particularly cockatiels, budgerigars and pigeons. The severity of clinical signs depends on the virulence of the strain, the species of bird affected and the immunocompetence of the bird. Diagnosis is better done by combining a serologic test with a PCR from a choanal-faecal swab. For the detection of carriers, a PCR from faeces collected over 3-5 days is indicated, as shedding may be intermittent. Similar to aspergillosis, bloodwork may demonstrate leucocytosis, monocytosis, heterophilia with toxic changes and increases in globulins. In addition, the liver is commonly affected and increases of AST and bile acids are common. Radiography may show signs of hepatosplenomegaly and air sacculitis. Endoscopic examination will allow a direct evaluation of these organs and the collection of biopsies for histopathology or PCR. 

Avian chlamydiosis treatment 

Treatment of birds generally involves doxycycline for 4-6 weeks either once a week by injection or once/twice a day orally. Injections produce significant tissue necrosis, but it is the best method to treat birds that will not take oral medications. Different protocols of doxycycline in drinking water or in food have been tried with success. Fluoroquinolones have some activity against Chlamydia, but they are not as good as doxycycline to eliminate infection. Azithromycin is also effective. All infected birds will require isolation, and those critically ill will need supportive care as well. Follow-up testing 2-3 weeks after treatment is required to confirm elimination. Infection does not provide immunity against future infections. 

Psittacine beak and feather disease (PBFD) 

It is caused by a circovirus, which are viruses that can remain stable in the environment for prolonged periods of time. The virus is shed in feather dander and faeces and is transmitted by inhalation or ingestion. Vertical transmission is also possible. The virus favours rapidly dividing cells and the clinical signs are related to its effects on dividing tissues and the targeted systems are the epithelial cells, the gastrointestinal tract and the immune system. Birds that are exposed to the virus can develop a wide variety of clinical signs and have a varying incubation period. 

In the classical chronic form birds develop feather loss and feather deformity as the most common clinical signs. Feathers grow abnormally, are dysplastic with retained sheaths, haemorrhage can occur within the pulp cavity, feather shafts can fracture and eventually complete feather loss can occur. The condition worsens with each new moult. There can also be oral ulceration and hyperkeratosis, overgrowth or fracture of the beak. Some texts report the beak as being shiny or glossy as there is no powder down. Secondary infections are common as the disease produces marked immune suppression. The disease is always fatal, but death can occur years after the initiation of clinical signs. 

The acute form affects young birds during first feather formation and is characterised by depression +/- diarrhoea followed by the rapid development of dystrophic feathers. These birds usually have severe anaemia and leucopaenia, particularly grey parrots. Change of the colour of the feathers can occur in some animals, and sudden death is also possible. 

can carry PBFD and juveniles can exhibit normal feathering except for complete absence of primary and secondary flight feathers (‘French moult’ or runners) or become severely alopecic. Mild cases survive and can regrow feathers at the first moult (12 weeks old). The same signs occur with polyomavirus infection in budgerigars, although PBFD is reported to be far more common. Polyoma is more likely to lead to nestling death with leucopaenia, anaemia and widespread haemorrhages. 

The diagnosis of PBFD infection is based on a PCR to detect the genetic material of the virus. Ideally, samples should be taken from abnormal feathers, although blood samples are also good. Severe leucopaenia can produce false-negative results in the PCR. Histopathology of the abnormal feathers can also yield a diagnosis. If the bird has died, the most important organs to be collected are the bursa of Fabricius, and also liver, spleen and skin with abnormal feathers. The infection produces basophillc intracytoplasmic inclusions and lymphoid depletion. Any suspect carcases should be kept frozen as a PCR can be performed on frozen tissue. 

Positive birds that are healthy should be quarantined and re-tested in 90 days to see if they have cleared the virus. There is no specific treatment for the infection, although avian interferon has shown promising results (but it is not commercially available). Control is by proper quarantine and disinfection of the premises. All birds should be screened before entering a collection. Birds should be contained in separate air spaces to limit disease transmission. Other circoviruses can be found producing disease in young canaries and pigeons, with similar problems of immune suppression. 

Pox viruses  

can also lead to skin disease. The virus is environmentally resistant and excreted in saliva, nasal and lacrimal secretions, and sometimes faeces. Transmission is via mosquitos (mechanical vector), direct contact, fomites, inhalation, ingestion, and wounds. Infection can be seen in lovebirds, canaries, pigeons, New World parrots and raptors, but it is more common in wild birds. Birds that recover do not carry the virus. There are three forms:

- cutaneous (dry pox - causes nodular lesions and scabs on the face)
- diptheritic (wet pox – lesions on mucous membranes and respiratory disease)
- septicaemic (common in passerines -rapidly fatal causing pneumonia with or without diptheritic enteritis).

Diagnosis by clinical signs, history of exposure, biopsy/cytology (eosinophilic cytoplasmic inclusion bodies Bollinger bodies in epithelial cells are found). It is believed that ectoparasites are linked to disease leading to skin trauma and allowing entry of the virus. 

Proventricular dilatation disease (PDD) 

Caused by Avian Bornavirus (ABV). Histologically, the disease is characterised by a lymphoplasmacytic ganglioneuritis in the nerves of the gastrointestinal tract, particularly the ventriculus and proventriculus. Lesions can also be found in other organs, most importantly the brain. The nerve lesion produces dilatation of the GI tract and increase in the gastrointestinal transit time. The proventriculus becomes dilated, sometimes also the ventriculus and the intestines, and the bird starts with a symptomatology of weight loss, abnormal faeces, undigested seeds on faeces and lethargy. Neurological signs can also occur.

The disease is more common in large psittacines. Incubation periods can vary between 2 weeks and a maximum of 4 months. The disease is more common in adult birds and in large psittacines (˃ 300 grams). Vertical transmission can occur. Infection is by contact with faeces, secretions or feather powder. Chronic, low-level mortality is more common than outbreaks.

Proventricular dilatation disease (PDD) 

Caused by Avian Bornavirus (ABV). Histologically, the disease is characterised by a lymphoplasmacytic ganglioneuritis in the nerves of the gastrointestinal tract, particularly the ventriculus and proventriculus. Lesions can also be found in other organs, most importantly the brain. The nerve lesion produces dilatation of the GI tract and increase in the gastrointestinal transit time. The proventriculus becomes dilated, sometimes also the ventriculus and the intestines, and the bird starts with a symptomatology of weight loss, abnormal faeces, undigested seeds on faeces and lethargy. Neurological signs can also occur.

The disease is more common in large psittacines. Incubation periods can vary between 2 weeks and a maximum of 4 months. The disease is more common in adult birds and in large psittacines (˃ 300 grams). Vertical transmission can occur. Infection is by contact with faeces, secretions or feather powder. Chronic, low-level mortality is more common than outbreaks.

Diagnosis should start with a good history (animals kept alone as pets for years are unlikely to develop a viral disease). The disease is more common in collection of parrots. Radiographs can demonstrate dilatation of the proventriculus as the most common finding, and contrast radiographs can show increase in GI transit time. A definitive diagnosis is made by combining serology and a PCR from faeces +/- crop swab. Animals with clinical disease usually are very positive to PCR and have a very high level of antibodies. 

The disease is always fatal and there is not treatment to target the virus, although supportive treatment may be indicated in some cases. Prevention is by screening birds before entering a collection and disinfection of premises that have held infected birds, although the virus is not very stable in the environment.