INFECTION VERSUS DISEASE

It has become evident that infection and disease are not synonymous. Many birds are infected by the virus but only a certain, and sometimes small, percentage of these birds will develop disease.6,7,30,44,48 Whether disease will develop is dependent on the species of bird infected, the age of the bird infected, whether that bird is also infected with the PBFDV, and other factors that remain unclear. Birds that are infected and do not develop disease still have virus replication within their bodies and shed virus in their droppings for a period of time.6,7,30,44,48 The length of time that virus shedding occurs, again, depends on the age the bird at the time of infection and the species of the bird.6,7,48

INFECTION IN BUDGERIGARS

As previously mentioned, in the United States, the English variety of budgerigar appears to have some resistence to APV infection.44 The most devastating outbreaks of disease occur in large commercial aviaries of the American variety of budgerigar where birds are bred in rooms containing tens or hundreds of free-flighted birds. Both nestling and adult budgerigars are susceptible to infection. Death, however, is confined to young birds between the ages of 10 and 25 days. The nestling mortality (death) rate is often high and may approach 100% when the virus is first introduced to an aviary. If there is no intervention, in subsequent breeding seasons mortality rates will decline but production will always remain depressed.34,37,38

Birds that survive infection may have abnormal feathering or appear completely healthy.18,32,38 Survivors shed virus in their droppings and probably their skin and feather dander for up to 6 months after infection.38 Virus shedding stops with the onset of sexual maturity or during the first breeding cycle. The infection cycle is then maintained through the shedding of virus by nestlings and young adult birds. Thus, birds are exposed to the virus immediately after hatch and have virus circulating in their blood by the time they are 7 to 10 days old.37 Fledglings and young adult birds are also important sources of virus exposure for other birds when they are taken to bird shows, bird marts, and sold to pet stores.

It has been suggested that egg transmission of APV occurs in the budgerigar.10,56 This conclusion is based on 2 observations. First, intra nuclear inclusion bodies where reported in day-old nestlings suggesting that these birds had virus growing in them before they hatched.2 Secondly, in a clinical trial, eggs were removed from a flock of budgerigars experiencing an outbreak of disease and placed under the hens of a clean flock. The young from these eggs subsequently developed disease. This author's experience, however, does not support this conclusion. I have not seen inclusion bodies in birds less than a week old. Also, there is another interpretation for the results of the clinical trial. If the transferred eggs were contaminated with virus, then the chicks could have been exposed at hatch. Additionally, budgerigar hens eat the egg shells. Thus they could have become infected and then passed the infection onto their young. In a paper I presented in Utrect, The Netherlands, I found very low concentrations of APV DNA in some embryos and very young nestling budgerigars.37 This data has also been used to suggest that egg transmission occurs.56 These birds never developed disease and subsequently, I found that one of the reagents used in this work was contaminated with viral DNA. Therefore, at this point in my understanding of APV disease in the budgerigar and other species, I feel that there is only very limited and circumstantial evidence that egg transmission occurs.

Dr. Branson Ritchie, citing my data, has stated that budgerigars are the only bird that is continuously infected with APV and remain sources of virus for life.56 In justifying this conclusion Dr. Ritchie cites one of my publications,38 but ignores another.42 In the first publication,38 I found that virus DNA could be detected in tissues of budgerigars at least to the age of 4 years. Virus concentrations were highest in 6 month old birds, but diminished in birds breeding for 4 months and were even lower in birds continuously breeding for 17 months. Although virus DNA was found in birds of all ages, it was not clear that the older experienced breeding birds were actually shedding virus. In my second study,42 I took older breeding birds that we new had been infected with virus and rested them from breeding for 7 months. These birds were then allowed to breed and their young were monitored for signs of infection and the development of antibody to the virus (an indication of infection). None of the 107 young birds produced by these previously infected budgerigars developed disease. Therefore, we must conclude that older experienced budgerigar breeders are not sources of virus infection and even if small concentrations of virus DNA can be found in their bodies, they do not actively shed the virus.

INFECTION IN NON-BUDGERIGAR PARROTS

Susceptible birds infected with APV infection will die. Rarely, a susceptible bird will have transient signs and survive.5 In birds resistant to disease, infection is unapparent. In these birds, viral DNA can be first detected in blood after which it is detected in the cloaca.7,8,48 Cloacal samples may intermittently be negative, but generally the blood will remain positive.7,8,48 When the bird is about to stop shedding, the blood will become negative and within a week or two, cloacal swabs will also become negative.48 The length of time that birds are blood and cloacal positive is dependent on the species of bird and the age that it was infected. It appears, for the most part, that the older the bird is at the time of infection, the shorter the duration of shedding.7,8,48

Conures: Many, possibly most, conure nestlings exposed to APV at six weeks of age or younger will develop disease and die. In birds older than six weeks, APV causes an unapparent infection (Fig. 1). In conures, unapparent infections are best detected by examining the blood for virus DNA. Virus shedding can be expected for 4 to 8 weeks in most birds, but up to 16 weeks in the rare individual.7,8

Macaws: Macaws are susceptible to APV infection and disease up to approximately 14 weeks of age, after which infection is unapparent. Peak mortality in macaws occurs from 4 to 8 weeks of age (Fig. 1). Unapparently infected birds will become blood positive and cloaca positive. In a recently completed study, 2 blue and gold nestlings that survived infection shed virus 14 weeks. Two fledgling red-fronted macaws shed virus for 10 weeks. Adult blue and gold macaws and hyacinth macaws shed for 6 weeks or less. The nestling birds became blood negative first, then negative on the cloacal swab.48

Eclectus parrots: Infection of otherwise healthy nestling eclectus parrots will cause their death if they are less than 14 weeks old (Table 1). Specific studies on the length of virus shedding in these birds have not been done.39

Cockatoos: As a general statement, cockatoos of any age are highly susceptible to infection with APV, but are extremely resistant to disease. Healthy adult cockatoos are not expected to ever develop APV disease and the same is true for nestling cockatoos under most circumstances. In a recent study, it was found that citron-crested and umbrella cockatoo nestlings exposed to the virus at less than 3 weeks of age developed abnormal feathers. These birds showed transient signs of a systemic illness, then recovered with supportive care. Older birds and other cockatoo species remained healthy, although nearly all of them became infected.48 Virus shedding, as determined by cloacal swab, lasted 8 to 10 weeks. Virus could be detected in the blood consistently until just before shedding stopped. In this group of birds, cloacal swabs were not consistently positive and several birds that were originally cloacal positive became negative and then positive again.48

I have documented 2 cases of APV disease in nestling cockatoos that resulted in their deaths. Both birds were also infected with the PBFDV.47