Clinical Appearance of Avian Viral Disease

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.

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 determine the severity. Birds that 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 or latent infections.

Antemortem diagnosis of polyoma infection involves DNA probes of cloacal/choanal swabs or whole blood.

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.

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 grey 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 lesser degree the epithelium of the feather follicle, beak, and nails are 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 at 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 grey 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 that 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 that 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.

Avian Bornavirus

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, the etiology of which is avian Bornavirus.

Birds with terminal PDD usually present with three characteristic signs: vomiting, weight loss, and passage of undigested food in the droppings. Another form of the disease that often goes undiagnosed is a peripheral weakness manifested by decreased leg strength when perching or unsteadiness when ambulating. Weakness may occur with or without proventricular involvement. Finally, a large percentage of birds may harbor the virus while never showing clinical evidence of its presence.

Necropsy in gastrointestinal cases may reveal 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. Necropsy of other Borna infections may show no gross lesions at necropsy. Suspect submissions should include brain and spinal cord.

Because the epidemiology and pathogenesis of PDD have not been completely proven, hygiene and careful management are the only means of prevention. Most birds showing gastrointestinal signs of this disease die. Rare cases have demonstrated classic signs and survived. Treatment has been directed at feeding highly digestible, low-bulk foods, and controlling secondary infections, dehydration, etc. NSAIDs such as Celebrex may improve the prognosis of affected individuals.

Conclusion

The most important characteristic for a serious avian practitioner to possess 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.