Viral Diseases of Pet Birds

Avian polyomavirus (APV) primarily affects young birds. There are two primary forms of the disease based on species affected: budgerigar fledgling disease and a nonbudgerigar polyoma infection. Both are characterized by peracute to acute death of preweaned neonates. Adult birds typically are resistant to infection; they will seroconvert and shed the virus for up to 90 days, then clear the infection. The incubation period is 7–10 days.

The typical presentation of budgerigar fledging disease is a well-fleshed juvenile, just before fledgling age, with acute onset of lethargy, crop stasis, and death within 24–48 hr. Other clinical signs are cutaneous hemorrhage, abdominal distention, and feather abnormalities. Surviving budgerigars >3 wk old often exhibit feather dystrophy (French molt or feather dusters). In other species of psittacines <4 mo old, the infection is also often fatal. Older nonbudgerigar psittacines may have subclinical disease or hemorrhages and coagulopathies. Prevalence of the virus in adult psittacines, including budgerigars, is thought to be high.

Antemortem diagnosis is accomplished with DNA probes of cloacal swab and blood samples and virus-neutralizing antibody tests of blood samples to identify birds with previous viral exposure. Diagnosis in a flock setting is typically based on clinical signs, signalment, and necropsy findings.

Gross necropsy findings in deceased chicks often include pale skeletal musculature and subcutaneous ecchymotic hemorrhages. The kidneys and liver are enlarged and may be pale, congested, and mottled, or have pinpoint, white foci. Petechial or ecchymotic hemorrhages may also be present on viscera, particularly the heart. The heart is sometimes enlarged and may show hydropericardium. Intranuclear inclusion bodies are often seen in the liver, kidneys, heart, spleen, bone marrow, uropygial gland, skin, feather follicles, etc.

Aviary control methods include avoiding the housing of budgerigars or lovebirds on premises where other species are bred, adhering to standard hygiene procedures, preventing access to the nursery by visitors, and not introducing birds into the aviary without 90 days quarantine and testing. Eliminating APV infection from an infected budgerigar aviary is challenging. First, all breeding must be stopped for 6 mo. The presence of infected neonates, fledglings, and adults propagates the disease. During this time, adult birds are moved to a noninfected area while the entire aviary is disinfected. Nest boxes should be disinfected or discarded and replaced. After 6 mo, adult breeding birds can be returned to a clean aviary and breeding resumed.

Pet store prevention should include separating neonates from different sources, purchasing birds from sources where polyomavirus testing and vaccination are performed, and ideally, not purchasing or selling unweaned birds.

Treatment is supportive care. A vaccine is available. For breeding birds, two doses of the vaccine are administered at a 2-wk interval; this should be done off-season. The manufacturer recommends administration of the first dose when the chick is >35 days old, with a booster vaccination in 2–3 wk.

Psittacine beak and feather disease (PBFD) is caused by a psittacine circovirus. The virus was first recognized in the 1970s in cockatoos with beak and feather lesions. Since then, it has been recognized in most species of parrots and also in Passeriformes and Columbiformes. Infected birds shed virus in their feathers, feather dander, feces, and oral secretions. Transmission occurs by inhalation and/or ingestion of the virus and can occur vertically. The virus is very stable in the environment, so fomites can be a significant source of infection. The name is not as representative of the current typical clinical presentation, which often does not include beak abnormalities and is less likely to have the severe, classic feather abnormalities seen in cockatoos when the disease was first documented. Use of screening PCR tests has greatly decreased the prevalence of the virus in captive bred Cacatua spp. However, disease is still seen in African grey parrots, Eclectus parrots, lovebirds (Agapornis), lorikeets, and other species, but is rare. The natural infection appears to occur primarily in juvenile birds, with few instances of clinical infection seen in birds >3 yr old.

In the classic PBFD infection, the first indication of the presence of disease is a lack of powder down on the beak. The virus causes abnormal formation of growing feathers and immunosuppression. Feathers are pinched or clubbed at their base and may have hemorrhage within the developing shaft. The feathers fall out easily and grow back slowly or not at all. The distribution of affected feathers depends on the age of the bird and the stage of the molt when infected. Pigment loss may occur in colored feathers. The bird may live with these lesions for months to years. As the disease progresses, the immune system is affected, and most birds die of secondary infections. A peracute form of the disease occurs in young birds, which develop enteritis and pneumonia, lose weight, and die. African grey parrots may develop a pancytopenia, because the virus attacks the bone marrow. These birds die suddenly with viral inclusions in the thymus, bursa, and bone marrow.

Diagnosis is based on clinical appearance; results of PCR testing of feces, feather dander, or blood; and biopsy of affected feather follicles showing basophilic intracytoplasmic inclusions. Testing by PCR may detect infection in birds that still appear healthy. These birds may subsequently become ill or may mount an effective response to the virus. Because of the stability of the virus, PCR analysis can also be used for environmental testing. Quarantine and retesting are recommended for PCR-positive, asymptomatic birds. At necropsy, affected birds often have no gross lesions internally, but intranuclear or intracytoplasmic inclusions may be seen histologically in the feathers, bursa, thymus, liver, or other organs.

There is no specific treatment for PBFD, and treatment of infected birds is supportive. The contagious nature of PBFD and its generally terminal outcome in clinically affected birds warrant isolation and eventual euthanasia in most clinical cases. Strict hygiene with attention to dust control, screening protocols including PCR testing of both birds and the environment, and lengthy quarantines are highly recommended in breeding facilities with susceptible species. All new susceptible birds should be tested before introduction to the aviary. In infected breeding colonies, removing all eggs for cleaning and artificial incubation may also be required. Since the development of a PCR-based assay, prevalence of the disease has decreased.

Psittacine herpesvirus is an alpha herpesvirus that is the causative agent of Pacheco’s disease and internal papillomatosis in parrots. Pacheco’s disease causes a viral hepatitis seen predominantly in New World species (Amazon parrots, macaws, and conures). Internal papillomatosis occurs in parrots that have survived Pacheco’s disease. Papillomatosis is most commonly observed in macaws, Amazon parrots, conures, and hawk-headed parrots. Disease is associated with stress, which can cause clinically healthy carriers to shed virus and initiate infection in susceptible birds, as often occurs during introduction of new birds, relocation, or in those with underlying illness or during breeding. It is spread by direct contact, aerosol, or fecal contamination of food or water, with an incubation period of 3–14 days. The outcome of the infection depends on the genotype of the virus, the species of bird infected, and the bird's overall health. Infected birds become chronic carriers and will remain persistently infected and intermittently shed the virus throughout their lives. Old World species are less likely to be either inapparent carriers or clinically susceptible. Patagonian species and some Aratinga spp may be natural hosts in the wild, and some individuals of these species may asymptomatically shed virus when stressed. Other species can also act as carriers.

Terminal signs include acute death in well-fleshed birds and bright yellow urates with scant feces. Other clinical signs are diarrhea, green urates, lethargy, regurgitation, weakness, and depression. Diagnosis in the live bird can be done by DNA probes of combined oral and cloacal swabs or blood samples. Increases in plasma AST activity and marked leukopenia have been reported.

Because of the acute nature of the disease, gross histologic lesions may not be evident. However, most affected birds will have hepatomegaly, splenomegaly, and renomegaly. The liver may be mottled or grossly discolored. Ecchymotic and petechial hemorrhages may be present on the pericardium and within the mesenteric fat. Intranuclear inclusions are seen histologically in the liver, spleen, intestinal epithelium, and pancreas. Primary differential diagnoses for Pacheco's disease include acute salmonellosis, polyomavirus, and psittacine reovirus. Acyclovir (80 mg/kg, tid, or 400 mg/kg in feed) can be used during an outbreak; however, the risk of increased transmission because of handling is great. Autogenous vaccines have been developed during outbreaks and have effectively decreased morbidity and mortality. An inactivated vaccine is available.

The lesions of papillomatosis are predominantly present in the oral and cloacal mucosa but may also be found internally in the intestinal tract, or less commonly, in the conjunctiva or bursa. Owners usually first notice blood from a papilloma in the droppings, and/or the papilloma prolapses through the cloaca. Lesions may be mild or severe (ulcerated and bleeding) and often wax and wane. Ulcerated lesions may need to be cauterized or surgically removed, although they typically recur. Treatment is supportive, such as analgesics, cautery, and antibiotics to prevent secondary infection. Antiherpesviral drugs are not curative and do not appear to impact the course of disease.

Proventricular dilatation disease (PDD), also known as macaw wasting disease, neuropathic ganglioneuritis, lymphoplasmacytic ganglioneuritis, psittacine encephalomyelitis, and most recently avian bornavirus (ABV), was first recognized in the late 1970s in macaws imported into the USA and Germany. The disease primarily affects macaws, conures, and African grey parrots, although all parrots are probably susceptible. The causative agent of this disease is avian bornavirus.

The common presentation of affected birds is chronic weight loss (often following an initial increase in appetite), passage of undigested food (most easily recognized when whole seeds are found in the droppings), and regurgitation. A dilated proventriculus may be seen radiographically. Neurologic signs (convulsions, tremors, weakness, ataxia, blindness) may occur in some species, with or without concurrent GI signs. Clinical signs may be slowly progressive or develop acutely. Outbreaks are sporadic, with a low morbidity and a high mortality.

Before the discovery of ABV as the causative agent of PDD, the only antemortem diagnosis was identification of lymphoplasmacytic infiltrates in the tissues of affected birds, most commonly with a crop biopsy. Histopathologic lesions can be present in the brain, spinal cord, peripheral nerves, nerves of the GI tract, heart, adrenal gland, lungs, and kidneys. Transmission is fecal/oral, and positive results of PCR testing of choanal, cloacal, or fecal swabs confirms the presence of ABV. Serologic assays such as ELISA can also confirm exposure. Although the presence of ABV in the droppings indicates shedding, many birds are positive for ABV with no clinical signs of PDD. If or when these birds may develop disease is unknown.

Because shedding of the virus is intermittent, one negative result of fecal or cloacal PCR testing does not exclude disease. Testing at least three times at weekly intervals, with all three tests being negative, is best before declaring a bird negative for ABV. Differential diagnoses are heavy metal toxicosis, foreign body intestinal obstruction, internal papillomatosis, internal neoplasia, and GI infections (including bacterial and fungal proventricular infections).

Clinicopathologic findings vary, but increased plasma CK activity and mild lymphocytosis, monocytosis, or heterophilia may be seen. Proventricular biopsies in affected birds are prone to dehiscence and are not done routinely. Crop biopsy is a less invasive diagnostic tool and may be useful if the collected sample contains sufficient innervation to be diagnostic; however, a negative crop biopsy does not exclude the presence of PDD.

Treatment for PDD includes providing easily digestible foods and may be aided by administration of an NSAID (eg, meloxicam, celecoxib). Isolation of positive birds is important in disease prevention. Testing by PCR (a minimum of three tests) and separating positive birds from negative birds is a recommended control measure, although the number of false-negative tests (due to intermittent shedding) makes this a long and potentially difficult task. ABV is not a long-lived virus in the environment; therefore, good hygiene and ultraviolet light can help to limit spread of disease in a home or aviary setting.

Poxviruses are large DNA viruses that induce intracytoplasmic, lipophilic inclusion bodies (Bollinger bodies) in the epithelial cells of the integument, respiratory tract, and oral cavity. All birds are considered susceptible to poxvirus infection, but many companion and aviary birds are rarely exposed to a susceptible strain. Because of import restrictions, poxvirus in blue-fronted Amazon parrots is no longer commonly seen. In pet bird practice, veterinarians will generally encounter only canary, lovebird, and pigeon poxviruses and fowlpox (see Fowlpox), which have specific host ranges. Poxviruses are environmentally stable, increasing the likelihood that a viable organism will come into contact with a susceptible host. Poxviruses cannot penetrate intact skin, and a break in the skin or mucous membrane must be present for infection to occur.

Poxvirus infection may cause cutaneous, diphtheritic, or systemic infections based on the strain of virus, route of exposure, affected species, and age and health of the bird. The cutaneous form appears as nodular proliferations or wartlike lesions on the unfeathered skin around the eyes, beak, nares, and legs. The diphtheritic form is characterized by lesions on the mucosa, tongue, pharynx, and larynx. The septicemic form is characterized by a ruffled appearance, depression, cyanosis, anorexia, and wartlike tumors of the skin. The cutaneous form is most commonly seen in psittacines and raptors.

Clinical signs depend on the form of disease, location of the lesions (eye, oral, ear), and overall health of the bird and may include lethargy, respiratory distress, partial blindness, difficulty eating, weight loss, emaciation, and skin lesions. Diagnosis of poxvirus infection is typically confirmed through history, physical examination findings, and histologic findings of Bollinger bodies in affected tissues.

Treatment is usually nonspecific and may include supportive care, fluids, parenteral vitamin A, ophthalmic ointments for eye infections, assisted feedings, and antibiotics to prevent or treat secondary infections. Lesions on the skin may need daily cleaning. Transmission is via insect vectors (mosquito bites) or other entry through breaks in the skin. Therefore, mosquito control and indoor housing are vital to prevent outbreaks. Vaccines for canarypox, fowlpox, and pigeonpox are available but are specific for their host species.

Viscerotropic velogenic Newcastle disease (VVND, see Newcastle Disease and Other Paramyxovirus Infections), caused by a paramyxovirus group 1, affects most avian species and is a significant threat to the poultry industry. Transmission is by respiratory aerosols, fecal contamination of food or water, direct contact with infected birds, and fomites.

Birds may be asymptomatic or die acutely. Clinical signs include depression, anorexia, weight loss, sneezing, nasal discharge, dyspnea, conjunctivitis, bright yellow-green diarrhea, ataxia, head bobbing, and opisthotonos. In prolonged cases, unilateral or bilateral wing and leg paralysis, chorea, torticollis, and dilated pupils also may be seen. Primary differential diagnoses include other paramyxoviruses (non-Newcastle), psittacine proventricular dilatation syndrome, and heavy metal toxicosis. Lesions include hepatomegaly, splenomegaly, petechial or ecchymotic hemorrhages on serosal surfaces of all viscera and air sacs, airsacculitis, and excess straw-colored peritoneal fluid. Diagnosis is traditionally via viral isolation, but agar gel immunodiffusion tests that can be performed on whole blood or serum are available.

Only symptomatic treatment is possible and thus not advised. If suspected, VVND must be reported to appropriate federal and state authorities. Vaccination is prohibited in birds entering the USA, because it does not eliminate the carrier state and hampers viral detection during quarantine.

West Nile virus (WNV) infection is an arthropodborne virus in the genus Flavivirus (family Flaviviridae). WNV was first reported in birds in the USA in August 1999. Many species of birds can be infected, and it has been reported in >320 species of birds. The American crow (Corvus brachyrunchus) and other corvids have suffered particularly high morbidity and mortality. Other affected species include canaries, psittacines, and raptors. Although psittacines appear to be somewhat resistant, the disease has been reported in parakeets, cockatoos, conures, rosellas, caiques, lorikeets, and a King parrot. Affected parrots have been adults housed outdoors with documentation of mosquito populations present. Mosquitoes (Culex spp) are the principal vectors of disease.

Clinical signs include depression, anorexia, weight loss, head tremors, ataxia, blindness, seizures, and death. Juvenile birds are the most commonly affected. Ophthalmologic findings in raptors are anterior uveitis, exudative chorioretinal lesions, and chorioretinal scarring.

Antemortum diagnosis can be difficult. Initial diagnosis may be based on clinical signs, species, and age; however, many diseases may cause similar clinical signs. Serologic tests (serum neutralization) may indicate antibody response to infection. Paired samples submitted 2 wk apart may reveal a rise in antibody levels and give a more definitive diagnosis. Adult birds may have high circulating antibody levels in endemic areas. Diagnosis is often determined at necropsy. The brain and kidney are the preferred tissues to submit for histopathologic examination.

There is no specific treatment for WNV in birds. Some birds may improve with supportive care (fluids, feeding, antibiotics/antifungals as needed) and time. A vaccination protocol using a recombinant vaccine has been successful in some birds. The recommendation is vaccination of captive birds 2–4 wk before mosquito season, with a booster 3 wk after the initial dose.

During the mosquito season, birds should be housed indoors or in completely covered outdoor facilities. Mosquito netting and mosquito traps should be used, and any standing or stagnant water sources eliminated.

Avian influenza is caused by an orthomyxovirus. Because of the zoonotic potential of some strains and the recent discovery of new mutations, this virus may become a more significant pathogen. Both the zoonotic potential and the economic effects on the poultry industry are causes for concern. (Also see Avian Influenza.)