Update on Proventricular Dilatation Disease and Bornavirus
Probably one of the most frightening and frustrating disease of parrot species is proventricular dilatation disease (or ‘PDD’). The disease goes by many names such as macaw wasting syndrome, myenteric ganglioneuritis, proventricular dilatation syndrome and more.
The bottom line is that the disease is characterized by a specific inflammatory pattern found around nerves that causes the target organ to fail. If the affected nerves supply the proventiculus (stomach), food passes undigested and the bird wastes away and starves to death. If nerves in the brain are affected, the bird may suffer from seizures and strange neurological abnormalities. If the nerves to the eyes are affected, the bird can become blind. Wherever nerves can be found, they can be affected by this disease. An affected bird may show only gastrointestinal or neurologic signs in addition to a combination of both.
Left untreated, the disease is often progressive until the bird succumbs. Even if treated (usually with anti-inflammatories and autoimmune type drugs), some birds may have progressive disease or stable but persistent clinical signs.
While the disease has been studied for over two decades, it has only been since 2008 that avian bornavirus infection has been linked to PDD. With the recent discovery of the avian bornavirus relationship to PDD, we have learned a lot (and created more questions).
Bornavirus is a RNA type virus and has previously been reported to cause, or is associated with, disease in rats, horses, primates, chickens, pigs, humans and now parrots and finches. Avian bornavirus, as opposed to borna disease virus recognized in other animals, is now confirmed as at least one cause of PDD in parrots. It is speculated, but not proven, that avian bornavirus triggers an autoimmune reaction whereby the bird’s immune system attacks it’s own nervous tissue.
At this time, there appear to be seven avian bornavirus genotypes that affect parrots species differently. While most infections are of one genotype, recent research supports multiple genotype infection is possible. To make things more confusing, there is also a passeriforme bornavirus (and 3 distinct canary bornavirus genotypes) and a waterbird bornavirus. Unless the ‘bornavirus’ test defines which genotype, all one can say is that ‘the bird is positive for avian bornavirus’. More on testing below.
The general incidence of avian bornavirus infections in parrot populations is relatively high. One study in which researchers screened 1400 birds found that 22.8% were positive for avian bornavirus. Other estimates conducted non-scientifically at veterinary hospitals suggest up to 1/3 of pet parrots are positive for avian bornavirus. At this point, no studies have clarified the incidence of each genotype within general parrot populations.
Until a recent presentation given in 2013, avian bornavirus infection and PDD were considered diseases of captive parrots. Research by Enderlain, et al showed that 33% of tested free-ranging parrots (84 birds total, 7 different species) from Brazil were positive for avian bornavirus on PCR. Members from all species, both sexes and different ages were positive. Twenty two percent had specific anti-avian bornavirus antibodies (only genotype IV found in this group- see more on genotypes below). Finally, 11 birds had histologic lesions consistent with PDD (of these, only 4 were avian bornavirus positive via PCR). It is important to note that this information has not gone through peer review (and should not be used for reference material) but will hopefully be published soon. This is the first time that we have support that both avian bornavirus and PDD are present in wild parrots and has implications as to the origins of the virus and disease. As a note, avian bornaviruses have been found in free ranging Canada geese, North American Gulls and other non-parrot birds.
Transmission of avian bornavirus in parrots has been proven in the lab (by injecting virus directly into a bird’s bloodstream, brain, oral/nasal tissue, etc) but has not been completely worked out in a natural setting. Recent research has even shown that developing embryos can carry the virus in multiple tissues supporting ‘vertical’ transmission (from mother to egg). Collectively, these studies support a fecal-oral transmission. However, with so many tissues potentially infected with virus, other means of viral shedding (not just through the droppings) are possible. Additionally, infected hens may pass the virus to their young.
The true means of transmission is still not clear. While we know that bornavirus can be readily found in the crop and feces of infected birds, how it gets into susceptible birds and causes infection is not clear. Lab induced oral and nasal infection has not been successful in infecting susceptible birds. Recent research published at a European conference in 2015 suggests that the infected hen passes the virus on the eggshell (not necessarily in the developing embryo). Additionally, cleaning the eggshell and pulling the egg for artificial incubation may break the cycle.
Birds may become bornavirus positive in as little as 6 days after exposure. Shedding of the virus (through feces) may occur in as little as 18 days after infection. This supports the assumption that transmission occurs at least through a fecal-oral route.
Testing is generally directed at identifying the presence of the virus and/or antibodies against the virus. Getting a positive avian bornavirus test (general PCR that checks for the presence of the virus) only means the bird is infected and not necessarily diseased. Again, this test generally does not give genotype information but rather infection with a member of the avian bornavirus family. This type of test is more commonly performed and commercially available in the US. Getting a positive antibody titer implies the bird’s immune system has recognized the infection and is attempting to fight the virus. This type of test is more typically performed in research situations but can be found commercially outside of the US.
While it might seem intuitive that birds with high levels of antibodies against the virus could be protected against disease development, recent research suggests otherwise. In fact, one study showed that parrots positive for the virus and with high antibody levels were at greatest risk of developing PDD (compared to those with low antibody titers).
We still don’t understand the factors that lead to infection with avian bornavirus and the development of disease. It has long been suspected that birds housed in a closed building (as opposed to free standing cages outside) are at greatest risk of infection. While this has not been proven scientifically, it seems logical since aerosolized fecal matter has the greatest chance to be inhaled by a naïve bird when sharing the same airspace with infected individuals. African grey with neuro PDD
Genotype of the avian bornavirus appears to be one major factor in PDD devlopment. For example, we know that genotype II can cause disease more rapidly and severely in cockatiels than infection with genotype IV. Also the presence of serum (blood test) antigangliosides antibodies (recognized autoimmune markers that seem to be correlated with nerve fiber injury) has been associated with the development of PDD in some parrots. This s not a commercially available test at this time. And, of course, some birds confirmed with PDD also test negative for serum antiganglioside antibodies (just to make things a little more confusing).
Diagnosis of PDD can only definitively be made by identifying the classic lesions in affected nerve tissue. This of course means biopsying affected nerve tissue! Because the lesions can be randomly scattered or inaccessible (the brain and spinal cord) on a live bird, we are not always able to get a definitive diagnosis. Our next best option is a presumptive diagnosis based on clinical signs (consistent with PDD) and supportive blood tests (positive avian bornavirus PCR and/or anti-viral antibodies). As a note of caution, PDD clinical signs can mimic many diseases and a positive avian bornavirus blood test does NOT equal PDD!!!
Treatment options are limited generally to anti-inflammatories. Only a few different drugs have been trialed to treat parrots with PDD.
A recent (2013, non-peer reviewed) publication from Rossi, et al suggested that a combination of Mycobacterium tuberculosis extracts and a specific non-steroidal anti-inflammatory drug can be used to suppress nerve inflammation and clinical signs associated with PDD in parrots. The treatment protocol is under patent protection and is still being investigated but may, in the near future, offer a more targeted treatment option for birds affected with PDD.
At this time, non-steroidal anti-inflammatories along with general nutritional support and management of secondary diseases appear to be our most readily available options.
What does this all mean???
- Avian bornavirus has been confirmed to cause PDD in parrots and both the virus and disease can be found in captive and wild populations.
- There are seven genotypes of avian bornavirus, all of which likely have different infective and disease causing capabilities. Other genotypes of avian bornavirus can infect non-parrot birds.
- An infected bird may shed virus through multiple routes, thereby infecting the environment and other birds, long before it shows any clinical signs (if ever).
- General avian bornavirus (PCR) testing at least determines which birds carry the virus and can be used to isolate infected from non-infected birds.
- Diagnosis of PDD is still frustrating and challenging, but at least the identification of avian bornavirus and newly available tests can help.
- Treatment options are generally limited to supportive care and anti-inflammatories.
- Talk with you avian veterinarian about the latest options for preventing, diagnosing and treating PDD as our understanding of this disease is changing rapidly!
M. Scott Echols, DVM, Dipl ABVP (Avian Practice)
Kindly reviewed by:
Prof. Dr. Michael Lierz, MRCVS, DZooMed, DipECZM (WHM), DipECPVS
Giessen University, School of Veterinary Medicine