Dr Shane Raidal is a senior lecturer at Murdoch University in veterinary pathology with a general interest in avian, fish and reptile diseases and particularly viral diseases of these vertebates.
Birds cannot vomit in the same way as dogs and cats and most people tend to confuse regurgitation with vomiting in birds. So it is important to first establish whether a bird is actually vomiting or regurgitating.
Physiological regurgitation is a common behaviour in many companion birds and is probably best demonstrated by male budgerigars that avidly regurgitate seed to feed their own reflection. When a bird regurgitates it pumps it neck in a way that returns food in the crop to the oral cavity. There is no reverse peristalsis. The action of regurgitation is noticed by most bird owners. Most birds will then chew briefly on the regurgitated material and place it onto a surface such as an ornamental mirror.
Such controlled regurgitation usually does not result in staining of the feathers at the commissures of the beak. However, this often occurs in pathological states, partly as a result of the volume of material being regurgitated and partly due to a lack of fine control.
Vomiting, on the other hand, is usually a rapid flick of the head, which is often not noticed by pet bird owners. The cardinal sign of vomiting in birds is the flicking of small pieces of ingesta around the cage and on top of the birds head (Figure 1). Vomiting often occurs along with regurgitation and is a serious clinical sign.
Figure 1 - This parrot has marked ingesta staining of the feathers around the beak and also flecks of vomitus on the feathers over the crown of its head
History, signalment and clinical examination
If you were presented with a regurgitating or vomiting puppy that had a pot belly, most vets would immediately think of ascarids and reach for the worming syrup. For some reason this logic is sometimes lost when the patient is a bird.
History is important. You need to know the age, breed and source of any new young pet bird. Microscopic examination of a simple wet-mount preparation of freshly collected faeces will quickly demonstrate ascarid eggs in the scenario above, but it is also important to check the nature and consistency of the droppings to assess whether their may be proventricular, ventricular or lower alimentary tract disease.
Bear in mind that anything that disrupts the normal gastric secreting or grinding functions of the proventriculus and ventriculus may lead to a secondary overgrowth of bacteria or fungi in the small and large intestines. Wet-preps of the faeces should be routine in any bird clinical examination but this may provide a diagnosis before you actually examine the animal.
Body muscle condition is also important. A very thin bird does not have acute disease despite what the owners may believe.
Clinical examination of the regurgitating or vomiting bird must include examination of the oral cavity, choana, glottis, tongue and palpation of the crop to check for masses and the volume and nature of crop contents.
In many bird species you can sometimes see the crop contents through the thin skin of the neck. It is also important to notice the colour and nature of the regurgitated material. Green material is an indicator of plant material not bile and the presence of blood-stained fluid, as in other animals, is a poor prognostic sign and an indication of oesophageal or proventricular ulceration.
Diagnostic procedures
Crop wash
Soft rubber gastric tubes or metal crop needles are used routinely to perform crop flushes in birds. It is better to use the latter in parrots and cockatoos, which can easily cut through rubber with their strong cutting beaks.
A small volume of warm saline should be deposited first to facilitate collection of thick contents. Any contents should be examined immediately by wet-mount microscopy to check for motile protozoa such as trichomonads, but Gram and Wright's stained smears are also useful diagnostic steps.
Radiography and endoscopy
Plain lateral and ventrodorsal radiographs can be useful to demonstrate foreign bodies, radiodense material and tumours.
When examining radiographs it is important to consider what anatomical location may be source of dysfunction. The best radiographs are achieved under general anaesthesia using isoflurane, which also permits more detailed examination of the oral cavity and palpation of the crop. This is particularly important if the bird seems otherwise in good body condition, alert and responsive to stimuli because serious systemic disease is less likely.
Endoscopic examination of the oesophagus and crop can also be carried out when indicated. However, good bird radiographs can be taken using physical restraint. Consideration of this is necessary if a barium meal series is to be contemplated.
Obstructions
Foreign bodies are probably most common in nestling and fledgling birds kept on inappropriate substrates such as wood chips or saw dust and in female birds during the breeding season when they might accidentally ingest pieces of wood or stones during attempts to tunnel out a nest hollow.
The clinical signs might be intermittent depending on the size of the object and the nature of the birds diet.
Round objects can often move around in the crop and only occasionally plug the oesophagus at the thoracic inlet.
Most foreign bodies are small enough to be removed orally either with the aid of general anaesthesia, surgical instruments and endoscopy or by palpation.
Ingluvioliths, on the other hand, can be too large to remove through the gape of the upper and lower beaks if they have grown in size over time. A bird may even asphyxiate if it manages to regurgitate a large ingluviolith into its oral cavity. These have to be removed surgically by ingluviotomy.
Extramural obstructions that cause regurgitation are more commonly tumours present in or around the thoracic inlet and hence also cause respiratory signs due to external pressure on the trachea or syrinx. So careful observation and auscultation for respiratory dysfunction and noises is a must in the regurgitating bird. Hyperplastic thyroid or parathyroid glands rarely cause oesophageal obstruction without some effect on respiration.
Figure 2 - Wet-preps of crop wash material containing avian gastric yeasts (arrows). Note the size of adjacent red blood cells and background bacteria
Disease of the upper alimentary tract
Parasitic, fungal, viral and bacterial infections can all cause inflammation of the oral cavity, oesophagus and crop. Avian pox is probably the most common viral cause of pharyngitis and oesophagitis, but lesions in other organs including the skin and respiratory tract are also usually present and are of more importance.
Primary bacterial and fungal infections are relatively rare and are usually secondary to vitamin A deficiency or other organisms or agents that disrupt the normal mucosal defence mechanisms.
Vitamin A deficiency
This results in squamous metaplasia and hyperplasia of epithelial surfaces. Quail and ducks have a high susceptibility. Eclectus parrots also are susceptible, particularly individuals fed a diet of seed (all of which are low in vitamin A). Eclectus parrots are rainforest birds and eat predominantly fruit and vegetables. Thus their natural diet is rich in vitamin A and they probably have a limited functional liver storage capacity for vitamin A. Most other companion birds are desert species, which probably have evolved an efficient hepatic vitamin A storage system to survive long periods when green seed heads and other succulent vegetation, which is rich in vitamin A, is not abundant.
A concurrent deficiency in zinc probably exacerbates vitamin A deficiency because the liver enzyme that liberates stored vitamin A is Zn dependent.
The clinical signs of vitamin A deficiency include corneal cloudiness, a change in voice (due to metaplasia of the syringeal mucosa), dysphagia, swollen sinuses and voluminous and pasty faeces (due to maldigestion).
Multiple swollen or abscessed mucous glands of the oesophagus, pharynx and trachea may be visible at necropsy due to distension with keratinised material. Often there are secondary oesophageal or upper respiratory infections with bacteria of low pathogenicity such as Staphylococcus epidermiditis so don't be surprised if affected birds initially respond to antibiotic treatment.
Initial treatment of vitamin A deficiency must be by injection due to decreased absorption of the vitamin from the intestinal tract.
Trichomoniasis
Trichomonas gallinae is a common protozoan infection of budgerigars, doves, raptors, turkeys, chickens and other birds and is characterised by raised caseous lesions in the oral cavity, pharynx and crop and distal oesophagus. In budgerigars and doves there may also be a focal necrotic hepatitis and or other systemic lesions.
In pigeons and doves the disease is called 'canker' and these birds are the carriers of the organism and up to 50-60 per cent of pigeons and wild doves may shed asymptomatically. The organism is transmitted from asymptomatic parent birds when they regurgitate crop milk for the squabs.
Adult pigeons (and other species) are at risk from stagnant surface water contaminated by pigeons. Raptors can develop the disease after eating infected doves or pigeons.
Affected birds are dysphagic due to large caseous lesions in the oral cavity or oesophagus, which obstruct the lumen. Severely affected birds lose condition. Young budgerigars regurgitate ingested seed in the initial phases and vomit as the condition progresses.
Diagnosis of trichomoniasis is easy by demonstration of large numbers of motile flagellate protozoan (5 x 10µm) in wet specimens from live birds. The organism rotates and spins and progresses forwards by pulsations and flicks of the anterior flagella.
Organisms may not be motile if the bird has been dead for some time (even when you warm the slide). However, they are not as sensitive as spironucleus. Vigorous trichomonads gradually lose motility over four to six hours if the smear is left on the bench at room temperature.
T gallinae can be readily cultured in selective medium. This is the most sensitive method of detecting the organism. Swabs of blood, liver and other tissues can be cultured from post mortem samples. Differentials in pigeons include pox, candidiasis, pigeon herpesvirus infection and capillariasis.
Trichomoniasis in individual pet birds is easily treated with carnidazole (Spartrix 10mg tablets) at a dose rate of 20-30mg/kg (single dose). The drug is safe because it has a high therapeutic margin. Toxicity has not been reported. Adult pigeons are routinely treated with one tablet per bird and squabs with 5mg. Give 2.5mg per budgerigar by crushing the tablet in a small amount of water.
Ronidazole is a similar drug to carnidazole but has better water solubility. Dose rate 6-10mg/kg, orally SID for 6-10 days. Metronidazole (Flagyl S suspension 40mg/ml) is also effective and can be given at a dose of 25-50mg/kg orally for five days or 100mg/L drinking water.
Emtryl (Dimetridazole 100 per cent) was once commonly used at 3g/5L drinking water for seven days (lorikeets and finches 1.5g/L, finches 100 mg/L) but toxicity is common as this drug has a low therapeutic index. It should not be used on hot days, particularly if parents are feeding young. The drugs listed above are much safer and have largely replaced Emtryl.
Trichomonas infection can be prevented and controlled by eliminating known infected birds and all suspect carriers, avoiding overcrowding, revision of water and feed container hygiene and avoiding contact with pigeons and doves.
Figure 3 - Proventricular mucosal thickening consistent with AGY infection in a budgerigar (arrows)
Proventricular and ventricular disease
Parasites
A variety of nematode infections such as acuaria are parasites of the ventriculus and proventriculus particularly in passerine and small psittacine birds. The parasite can be difficult to control because it has an indirect lifecycle involving arthropods as intermediate hosts.
Infection can be missed because the parasite burrows under the koilin lining of the ventriculus. Characteristic embryonated eggs can be identified in the faeces. This also protects the parasite from contact with anthelmintics. Levamisole is the recommended treatment.
Capillaria infections of the mucosa can occur anywhere from the proximal oesophagus, to the large intestine where they often cause considerable damage and inflammation.
Capillaria are a common and significant problem of racing pigeons and other birds. C annulata, C contorta and C obsignata are parasites of the crop and oesophagus of pheasants, quail, ducks and turkeys. Adult capillaria burrow into and beneath the epithelium causing haemorrhage and inflammation. They are small and easily overlooked at necropsy.
The eggs can incite a severe inflammatory reaction and are released when the mucosa sloughs.
Detection of capillaria oocysts in the faeces is best done by repeated faecal wet-preps because excretion of oocysts can be intermittent and they often fail to float on salt solutions. The oocysts have bipolar caps. Adult nematodes may sometimes be seen in faecal wet-preps.
Fenbendazole (10-50mg/kg SID for five days) has been recommended to treat capillariasis but anthelmintics such as this, which are poorly absorbed, may have little effect on adult nematodes because of their protected position beneath the mucosa. Ivermectin 200µg/kg may be more effective.
Cryptosporidiosis
Cryptosporidiosis can be a primary infection of the proventriculus where it causes proventricular dysfunction but it is not an uncommon secondary infection in young psittacine birds with psittacine beak and feather disease. Cryptosporidiosis can be diagnosed by wet-mount examination of the droppings with the addition of a drop of 10 per cent malachite green.
The disease is very difficult to treat but oral paromomycin (100mg/kg SID for five days), enrofloxacin or azithromycin may also be useful.
Avian Gastric Yeast (megabacteriosis)
Avian gastric yeast (AGY) or Megabacteria as they were once named are an unclassified fungal microorganism ranging from 1.5-3.0µm in width to 20-50µm in length (Figure 2). They are a yeast, but the term megabacteria is well established in common use.
AGY are associated with weight-loss in budgerigars and to a lesser extent lovebirds, but have also been found in many other psittacine and passerine birds including ostriches.
The organism inhabits the lumen of the mucosal glands of the proventriculus and can be seen in faeces and or crop washes. Most commonly the disease is a dysbacteriosis rather than an inflammation of the proventriculus. Presumably the clinical signs are related to impaired gastric secretion and dysfunction. The infection is present in wild birds.
Clinical signs of infection include regurgitation, vomiting, yellow pasty droppings, melaena, dehydration and severe weight loss. At necropsy the lesions include yellow-white thickening of the proventricular mucosa caused by dysplastic plaques (Figure 3).
Sometimes acute ulceration of the proventricular-ventricular junction results in haematemesis and in severe case full thickness ulceration results in haemorrhage and localised peritonitis.
The organism cannot be cultured and a diagnosis depends upon examining wet-preparations or Gram-stained smears of faeces or crop washes. Histopathology of the proventricular-ventricular junction is also useful.
AGY infection is difficult to treat because amphotericin B given orally (100mg/kg by gavage BID 10 days) has proven to be the only effective treatment. However, there is some evidence of resistance to this treatment but this may reflect the severity of disease in individual birds rather than drug failure.
The cheaper, oral preparations of this agent (Fungilin, MegabacS ) are become increasingly difficult to source. The IV formulations (administered orally) are very expensive on a flock basis. Itraconazole, fluconazole and ketaconazole are being evaluated as alternatives to amphotericin B.
Candidiasis
Candida albicans is a common cause of disease in ratites, Gouldian finches, psittacine birds (particularly lorikeets and hand-reared nestlings). The oral cavity, crop, proventriculus, ventriculus and occasionally the cloaca are the most commonly affected sites. Many birds of all ages are susceptible, including poultry.
The organism is usually a secondary invader following prolonged antibiotic therapy. However, the disease is common in ratites, psittacine birds and finches, which have no history of antibiotic therapy. C albicans occasionally causes dermatitis or large skin tumours around the head and bones of the head, sometimes in concert with Histoplasma capsulatum.
Birds with candidiasis are often depressed, have ruffled feathers. They continue to eat but fail to thrive. There are whitish ulcers, scabs or plaques at the commisures of the mouth and on the tongue. Ostriches can develop beak deformities.
In ostriches and finches the lesions may be confined to the ventriculus. The crop and proventriculus often have whitish thickened areas of mucosa. Erosions of the koilin lining of the ventriculus and the proventriculus are also commonly seen.
A mucocatarrhal enteritis may be present due to the dysbacteriosis that develops further down the alimentary tract.
Gram-stained impression smears from the oral cavity, crop and faeces are useful for diagnosis as is histopathology and culture of the ventriculus at necropsy.
Nystatin 100,000 units per 30g body weight per os BID until resolution or ketoconazole 4mg/kg BID for 5-10 days are useful treatments.
Chlorhexidine gluconate five per cent solution - dilute 1ml/L DW for five days may be effective for flock treatments. Dactarin gel is useful for oral lesions.
Figure 4 - Radiographic evidence of radiodense metallic material in a cockatoo with suspect heavy metal poisoning. The enhanced cardiac outline (arrow) is not seen in normal radiographs and supports a diagnosis of visceral gout secondary to nephrosis
Figure 4 - Radiographic evidence of radiodense metallic material in a cockatoo with suspect heavy metal poisoning. The enhanced cardiac outline (arrow) is not seen in normal radiographs and supports a diagnosis of visceral gout secondary to nephrosis
Proventricular dilatation disease - macaw wasting disease
Proventricular dilatation disease (PDD) is a common disease of macaws and African grey parrots in North America but has been reported in over 50 other psittacine species. The disease has recently been confirmed in macaws in Australia and similar syndromes do exist in cockatoos.
The cause of PDD is unknown but a viral aetiology is suspected. Both sexes are equally affected. Most birds are mature - more than two years of age.
Clinical signs including depression, weight loss, intermittent or constant regurgitation, passage of undigested seeds in the faeces, lethargy and abdominal enlargement have all been reported.
CNS signs may include ataxia, abnormal head movements, seizures and proprioceptive or motor deficits. Some birds may have CNS disease without clinical signs of intestinal involvement.
Definitive diagnosis can be difficult because survey and contrast radiography are useful diagnostic techniques for confirming a proventricular distension, but these changes are non-specific.
Barium meals are useful for monitoring gastric emptying times. Most of the food should pass through within two hours of administration. Biopsy of crop, proventriculus or ventriculus is required to demonstrate a inflammatory cellular infiltrates resulting in a lymphoplasmacytic ganglioneuritis. A similar lymphoplasmacytic infiltration also occurs throughout the central nervous system.
The prognosis is poor with low morbidity and high mortality. Palliative treatment includes fluid replacement, antiemetics, vitamins and semisolid food. However, recent trials with meloxicam (0.5mg/kg orally BID) and celecoxib (Celebrex) at 10mg/kg orally once daily for up to 12 weeks have been encouraging.
Heavy metal poisoning
Zinc and lead poisoning are common in companion birds and the commonly used terms 'new cage' or 'new wire' syndrome reveal the most common cause.
Most affected birds are depressed, inappetant and have liver and renal involvement. Reddish urates and droppings due to acute haemaglobinuric nephrosis or bright green droppings following acute hepatic toxicity are an indication of heavy metal poisoning. Radiographic evidence (Figure 4) of metallic fragments in the proventriculus or ventriculus along with a rapid response to parenteral fluids and calcium EDTA treatment are diagnostic but blood lead and zinc concentrations can also be measured. Serum lead concentrations of >0.5ppm and zinc concentrations of >2ppm are suggestive of toxicosis.
Rubber stoppers in syringes and on some serum tubes can contain zinc and give a falsely elevated result.
Lower alimentary obstructions
Intestinal parasites are probably the most common cause of lower alimentary tract obstructions, but foreign bodies and phytobezoars are occasionally seen as a cause of regurgitation and vomiting.
Ascarids are common parasites of poultry and captive and wild native birds. The life cycle is direct. Earthworms can act as paratenic hosts for the L2 larvae.
A columbae is commonly found in pigeons but is usually not pathogenic. Ascarids can cause intestinal blockage or rupture in psittacine birds, particularly budgerigars, princess parrots (and other Polytelis spp.), grass parrots, rosellas and Major Mitchell cockatoos.
Occasionally the nematodes migrate through the pancreas and liver and can block the bile duct. The adult nematodes are relatively large (3-5cm long) and are easily detected at post mortem.
Routine faecal flotation is adequate for diagnosis of ascaridiasis because the parasites usually excrete large numbers of oocysts, which float on salt solutions. Most commonly used anthelmintics such as piperazine, fenbendazole and levamisole are effective.
References
1. Klasing K.C. (1999) Avian gastrointestinal anatomy and physiology. Seminars in Avian and Exotic Pet Medicine, 8 (2) 42-50.
2. Rupley A.E. (1999) Diagnostic techniques for gastrointestinal diseases of psittacines. Seminars in Avian and Exotic Pet Medicine, 8 (2) 51-65.
3. Morrisey J.K. (1999) Gastrointestinal diseases of psittacine birds. Seminars in Avian and Exotic Pet Medicine, 8 (2) 66-74.
4. Schmidt R.E. (1999) Pathology of gastrointestinal diseases of psittacine birds. Seminars in Avian and Exotic Pet Medicine, 8 (2) 75-82.
