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Clinical Appearance of Avian Viral Disease

Don J. Harris, DVM
Avian & Exotic Animal Medical Center
Miami, FL

Viral disease in avian species is much more significant than once believed. In the early days of avian medicine, bacteria were cited as the primary causes of avian illness. It was eventually recognized that bacterial disease in birds is often secondary to malnutrition, stress, or other predisposing factors. In recent years, it has become obvious that viruses are extremely prevalent and significantly pathogenic in certain avian populations.

A practitioner is constantly faced with the challenge of trying to determine the etiology of a clinical presentation. While almost no illness can be diagnosed based on clinical signs, certain diseases provide visual cues that should lead a practitioner to suspect a viral etiology. Never should the possibility of a viral etiology be dismissed; too much is at stake in a facility where others could be exposed to potentially fatal disease. Advance warning of the presence of a certain viral disease however allow action to be taken which more directly and efficiently allows an illness to be characterized and appropriately treated.

Papovaviruses: Polyoma

Polyomavirus is currently one of the most threatening of all avian pediatric diseases. It appears in two primary forms based on affected species: Budgerigar Fledgling Disease and non-budgerigar Psittacine polyoma infections. Both presentations affect neonates most severely and are characterized by peracute to acute death in pre-weaning babies. Prominent feather signs and carrier states that commonly occur in budgies are rare in other psittacines.

Budgerigar Fledgling Disease may appear as sudden death or death following a brief illness with depression, cutaneous hemorrhage, feather abnormalities, and abdominal distention. If babies are infected later than a few weeks of age, they may exhibit feather dystrophy. "French Molt" is a mild to fatal condition of budgies in which the majority of flight and contour feathers are markedly dystrophic. Polyomavirus is one cause of this condition. While individual birds may clear themselves of the infection, the virus may circulate through the flock causing the flock itself to act as a carrier.

In all other psittacines Polyomavirus generally produces either rapid terminal illness or transient inapparent infection. Again, the age at which the bird is infected determines how it is affected. The younger the host, the more serious and rapid the disease.

In non-budgerigar psittacines less than 16 weeks of age the infection is usually fatal. Birds 3 to 6 weeks old may die without clinical signs. Those 5 to 16 weeks old often display sudden widespread ecchymosis visible in random patterns throughout subcutaneous regions. Most often the hemorrhage is seen along the ventral aspect of the neck where normal feeding reflexes cause rupture of the fragile vasculature. Bleeding may be observed in the absence of other clinical signs although some degree of depression, anorexia, crop slowing, regurgitation, etc. usually occurs. The vast majority of babies that die of polyoma do so at fledging, the period when flight feathers have matured and contours are emerging.

Young birds between the ages of 16 and 21 weeks of age demonstrate variable response to polyoma infection. Anything from subtle feather dystrophy to fatalities with characteristic signs may be observed. The maturity and condition of the immune system probably determines the severity. Birds which are malnourished or weakened by other ailments are more likely to fall victim to the serious effects of the virus. Once birds exceed five months of age most will experience a brief viremia with or without obvious signs and fully recover from the infection. In fact, evidence indicates that there are far more subclinical adult infections than fatal neonatal ones. Unlike budgies, the carrier state in other psittacines is undetermined. No doubt, non-budgie psittacines can transmit the virus, but it is unclear whether these are transient versus latent infections.

Necropsy of deceased babies usually reveals random areas of profound hemorrhage, usually in the subcutaneous spaces. Musculature and internal organs may be extremely pale due to exsanguination. Other findings include hepatomegaly, pericardial effusion, splenomegaly, and ascites. Diagnosis is confirmed through a DNA probe of affected tissues. Histopathology may reveal hepatic necrosis with karyomegaly and intranuclear inclusion bodies in the liver and spleen. The bursa of Fabricius may be depleted of lymphocytes. Vascular necrosis in many areas explains the hemorrhage and transudation.

Treatment of affected patients is purely supportive. Survival once hemorrhage is visible is unknown. Prevention depends on minimizing exposure and vaccination. Babies older than 3 weeks of age may be vaccinated every two weeks until they are 9 weeks old. Protection is significant after 7 weeks of age. Those vaccinated after that period require one initial vaccination and one booster at 2 weeks. Vaccination of adult birds is controversial but undoubtedly would help prevent circulation of the virus through a susceptible flock.

Papovaviruses: Papilloma

Papillomaviruses have been identified in many mammalian species as causes of isolated epidermal masses. The common wart in humans is a typical example of the well defined pedunculated growth that occurs. In avian species papillomaviruses have been confirmed as the cause of epidermal growths only in small passerines (canaries & finches) and African Gray parrot. These growths appear as small fleshy pedunculated masses originating primarily from featherless areas such as the feet of face. Their clinical significance depends on mechanical effects.


The most common association of papillomavirus with disease in pet birds involves "papillomatosis", granulamatous masses that develop in the cloaca, choana, oropharynx and to a lessor degree other areas of the gastrointestinal tract. Fact is, papillomavirus has never been identified in these lesions. In fact, no virus or any other infectious agent has ever been identified as the cause of this syndrome. Although some evidence supports an infectious etiology, other situations produce conflicting evidence. For example, the introduction of an affected bird in certain populations has resulted in increased prevalence of the disease in that population, while in other situations the mates of affected birds have remained unaffected.

The clinical significance of papillomatosis depends in part on the location of the lesion. Large granulomas in the cloaca may reduce breeding potential although in one aviary the highest production came from the isolated papilloma colony. Secondary bacterial infections are common in protruding inflamed tissue. Aside from the mechanical effects, papillomatosis has been suspected to be related to the development of bile duct carcinomas. Also, some association has been suggested with the Herpes virus of Pacheco's Parrot Disease.

Because an agent has not been identified, means of control are not established. Flock closure has not prevented the disease from occurring. At this point, isolation of affected individuals is recommended. Pronounced lesions may be excised and recurrence is variable.

Psittacine Circovirus

For many years the cause of Psittacine Beak and Feather Disease (PBFD) was unknown. The suspected etiologies included autoimmune disease, endocrine disorders, infectious agents, etc. Ultimately a virus was discovered representing the smallest class of viruses known to infect animals. These viruses are currently classified as Circoviridae.

The primary site of viral replication in the avian host is epithelial cells. As with polyoma, the severity of disease depends on the species of bird involved and the age at which he is infected. Birds more than a few months old do not develop clinical disease but rather experience a transient viremia, then clear the infection. In some species, especially juvenile African Gray Parrots, the virus may cause fatal peracute disease attacking primarily the thymus and cloacal bursa with no epithelial component. Typically however the epithelium of growing feathers and to a lessor degree the epithelium of the feather follicle, beak, and nails is affected. Clinical signs are entirely related to the age of exposure and the extent of epithelial damage. The hallmark of PBFD is the occurrence of deformed, stunted feathers many of which are strangulated at the base and fall out prematurely. The percent of plumage affected depends on what stage of molt the bird is in at the time of infection. Baby birds producing their first growth of plumage may show no normal feathering while an older bird already beyond the juvenile molt may demonstrate scattered feather dystrophy. Evidence indicates that birds of any age showing clinical signs were in fact infected a very young age. Incubation is minimally 4 weeks but may be as long as months to years. Onset of clinical signs correlates to the onset of significant molting.

A variation of PBFD is the peracute illness seen frequently in African Gray Parrots, among others. It is characterized by sudden depression and anorexia with death occurring within one to five days after onset. These birds demonstrate profound anemia with variable leukopenia. Although birds have been known to survive this form of the disease, it is usually fatal. One survivor confirmed by DNA probe demonstrated a PCV of 4 at the peak of illness.

Diagnosis of PBFD is accomplished with a DNA probe of blood or epithelium. Histopathology of developing feather shafts or follicles demonstrates both intranuclear and intracellular inclusion bodies. It is imperative that diagnosis be confirmed; birds have been euthanized which ultimately proved to have disease not related to psittacine circovirus. Also, asymptomatic adults testing positive to the DNA probe but showing no clinical signs may mount an effective immune response to the virus and entirely clear the infection. Euthanasia of these patients is not warranted, but strict quarantine is.

Control of PBFD centers around eliminating clinically affected individuals which are the sources of infection for susceptible individuals. A vaccine does not currently exist so preventing spread of the disease is the only means of control. Clinically normal individuals which test positive should be isolated until a subsequent test is negative. Those testing positive and demonstrating typical feather signs are unlikely to recover and euthanasia may be warranted. No successful therapy exists and these individuals shed inconceivably high numbers of viral particles posing tremendous threats to susceptible babies.


Poxviruses are the largest and most diverse group of viruses known to infect avian species. Unlike some of the other viruses, poxviruses are highly host specific and severity of infection is highly dependent on the species of both host and virus involved.

Pox infections occur in three forms which are represented by particular species in the pet bird population. The cutaneous form consists of discreet 2-4mm crusts that appear on the eyelids and feet and is frequently seen in lovebirds. The diphtheritic form is characterized by ulceration and the formation of pseudomembranes in the oral cavity and upper airways, a common finding in Amazon Parrots especially when importation was practiced. Canaries commonly suffer from the worst form, a fatal septicemia.

Transmission of avian poxviruses is highly dependent on precipitating factors. The virus can be destructive once introduced into the host but it is unable to penetrate intact epithelium. In order for the virus to gain entry there must occur a break in the epithelium such as a wound or insect bite. As such, mosquitoes pose a serious threat in transmitting the disease.

The severity of illness depends on the manifestation of disease and the degree of secondary problems. The cutaneous form is rarely fatal unless it produces a viremia. The diphtheritic form may result in fatalities due to oropharyngeal discomfort and inability to eat leading to starvation. Viremia produces hepatic necrosis, myocarditis, pneumonia, air sacculitis and peritonitis.

Diagnosis is accomplished by visualizing the pathognomonic "Bollinger" inclusion bodies via histopathology. Vaccination is available for some species but is not commonly practiced. Minimizing exposure to mosquitoes and avoiding other causes of epidermal disruption greatly reduces incidence. Treatment is directed at secondary problems.


The viral infection most frightening to many aviculturists is "Pacheco's Parrot Disease", or avian herpesvirus. Pacheco's disease has been known to kill as many as 7000 psittacines in one outbreak. Its ability to strike quickly and with little or no warning and its relative disregard for age or species has caused many an aviculturist to awake to large numbers of dead specimens.

Herpesviruses are one of the most ubiquitous viruses in nature. In most cases in the animal kingdom, the viruses exist in a latent stage shedding periodically with few or no clinical signs. In psittacines it is believed that there are pathogenic and non-pathogenic strains. At the very least, the virus may remain dormant for an extended period of time surfacing during periods of stress. Historically, Patagonian and Nanday conures are accused of being the primary carriers of this disease, but almost any psittacine is capable of surviving an outbreak and becoming a permanent carrier.

Clinical signs of a Pacheco's outbreak often don't exist. When they do they are extremely brief, vague, and consist simply of listlessness, depression, anorexia, and yellowing of the urate portion of the droppings. The sudden appearance of yellow urates with death occurring in less than 24 hours should send chills down the spine of any aviculturist. The vast majority of outbreaks witnessed by the author have begun this way. In contrast to traditional beliefs, most of these outbreaks have lasted 3 - 7 days and resulted in no more than 20% of the flock being lost. Reports of outbreaks support the variability of expression. Flock losses range from one bird to 100% of the colony.

Transmission of herpesviruses is typically through close contact. Husbandry and hygiene may have an influence on spread of the disease. Outbreaks may follow the introduction of a carrier into a flock although most arise somewhat spontaneously or after periods of increased stress. Virulent strains of the virus produce death in 3 - 10 days after introduction. Any bird that survives infection is believed to become a carrier. The virus which infects psittacines does not affect non-psittacines. Not all psittacines develop disease when infected. Some acquire the infection in the absence of clinical signs and become carriers.

Diagnosis is based on clinical features and necropsy samples. Deceased birds display an enlarged yellowish-brown liver, splenomegaly, and vascular congestion in almost any organ. Histopathology demonstrates necrosis, congestion, and hemorrhage within the liver, spleen, and kidney. Intranuclear inclusions may be demonstrated in the above organs as well as the pancreas and esophagus. Although the inclusions are suggestive they are not pathognomonic for Pacheco's disease. Confirmation is achieved with electron microscopy, cell culture, Antigen detection, or DNA probe.

Of all the viral diseases, Pacheco's is the one which responds to some degree to antiviral therapy. Acyclovir has been used effectively in outbreaks to reduce the duration and severity of the disease in the flock. The greatest benefit is obtained in birds not yet showing clinical signs. Those already showing clinical are not likely to survive even with treatment.

Prevention depends on vaccination and avoiding exposure, but neither is foolproof. There is no way to guarantee that a carrier does not exist within an aviary. Colonies which have been closed for four years have broken with Pacheco's. A vaccine is available which affords some protection, but it is likely that serotypes exist apart from that included in the vaccine and therefore not affected by it. The best means of preventing large losses from Pacheco's is to practice good avicultural hygiene. Birds in a collection should always be handled in a manner which minimizes the spread of any agent from bird to bird.


In the early 1970's The USDA imposed restrictions on the importation of exotic birds. Paramyxoviruses are a large and very diverse group of viruses, one of which causes spectacular losses in domestic poultry flocks. This virus, paromyxovirus type 1 (PMV-1), is not endemic in the United States but was known to have been introduced via birds imported for the pet trade. Even though legal importation is essentially non-existent, smuggling still creates the possibility of an epidemic in domestic poultry populations. Other paramyxoviruses exist in avian populations in this country, but none present the threat that PMV-1 does. PMV-2 and PMV-3 cause variable illness, if any, in some passerines and psittacines.

Paramyxovirus type 1 is more easily recognized by the familiar name of "Newcastle Disease". Four classifications of disease exist based severity of illness. In order of increasing severity they are lentogenic, mesogenic, velogenic, and viscerotrophic velogenic. It is the latter which destroys poultry flocks. Poultry display acute diarrhea, respiratory distress, and neurologic signs with death occurring within a few hours. Psittacines infections are usually less severe and appear as conjunctivitis, rhinitis, diarrhea, depression, torticolis, tremors, paralysis, and seizures. Often the clinical signs may escape detection or be inapparent.

Transmission occurs via virus laden secretions which can be passed directly or indirectly. The virus survives well outside the host making insects, pests, and man possible vectors. Incubation period is 3 to 28 days. Birds with inapparent infections or those recovered from illness may shed virus for as long as one year. The virus is zoonotic and can cause vague illness with conjunctivitis in man.

Gross lesions vary from none to cardiomegaly, splenomegaly, hemorrhage, pulmonary and tracheal congestion, and edema of the respiratory and gastrointestinal systems. Microscopic lesions reflect hemorrhage, edema and necrosis of the described systems as well as the brain. Intranuclear or intracytoplasmic inclusion bodies are rare and found in the brain. Diagnosis is confirmed with virus isolation, paired serum samples, or electron microscopy.  

Control of paromyxovirus in poultry is through vaccination, but this vaccine may be fatal in psittacines.

PMV-2 and especially PMV-3 are the paramyxoviruses endemic to avicultural populations in the U.S. PMV-2 causes mild to no illness in passerines but more serious disease in psittacines. Illness is nonspecific and includes tracheitis, pneumonia and enteritis. PMV-3 causes vague illness in psittacines and is common in grass parakeets. Diagnosis is as for PMV-1.


Blue and Gold Macaws were the first species reported to suffer from a disease in which the proventriculus became paralyzed and dilated resulting in wasting away and death of the bird. Thus "Blue and Gold Wasting Disease" eventually acquired the names Psittacine Wasting Syndrome, Proventricular Dilatation Syndrome, Neuropathic Gastric Dilatation, Splanchnic Neuropathy, and others. "Proventricular Dilatation Disease" (PDD) is the term currently employed at the University of Georgia where the disease is being researched.

Although a virus has been isolated which is believed to be the causative agent, its identity has not been clearly established. The disease may appear sporadically or as an epidemic lasting several months. Necropsy reveals a proventriculus enlarged to the capacity of the abdomen and thin-walled enough for ingesta to be seen through the proventricular wall. Pathology of deceased individuals demonstrates an accumulation of lymphocytes and plasma cells in the gastrointestinal tract, spinal cord, and brain.

Birds with PDD usually present with three characteristic signs: vomiting, weight loss, and passage of undigested food in the droppings. Another form of the disease which often goes undiagnosed is a peripheral weakness evidenced by decreased strength of perching or unsteadiness when ambulating. Weakness may occur with or without proventricular involvement.

Because the cause of PDD has not been proven, hygiene and careful management is the only means of prevention. Most if not all birds showing proventricular signs die. Rare cases have demonstrated classic signs and survived, but PDD was not confirmed. Treatment has been directed at feeding highly digestible, low bulk foods, and controlling secondary infections, dehydration, etc.


The most important characteristic for a serious avian practitioner to posses is open-mindedness. Most of the viral diseases described here were defined only after years of clinical encounters in which the etiology remained unidentified. It is likely that in the future new viruses will be discovered amidst problems being experienced today.

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