Two types of disease commonly associated with Herpes virus occur in pigeons. One, pigeon Herpes encephalomyelitis virus, affects the brain and causes lack of coordination and paralysis. This disease is comparatively rare. The other, inclusion body hepatitis, primarily affects the liver. It occurs in pigeons world wide. There are several different strains.
These strains may also cross-infect other species, including budgies, and, interestingly, even falcons. Native raptors around the world are susceptible to infection with pigeon Herpes virus and the so-called falcon and owl Herpes viruses are actually pigeon Herpes virus. Wild feral pigeons are thought to be a reservoir of infection for racing pigeons. In one Australian survey three feral flocks in Melbourne and three feral flocks in Sydney were tested for Herpes virus by doing a DNA test on swabs collected from the oral cavity.
All flocks were infected with Herpes virus.
Clinical course
When introduced into a flock, Herpes virus can kill young and adults by causing varying degrees of hepatitis (liver inflammation) enteritis (bowel inflammation) pancreatitis (pancreatic inflammation) ingluvitis (inflammation of the crop wall) and stomatitis (inflammation of the lining of the mouth). Infected birds shed the virus in saliva, nasal discharge, droppings and crop milk.
These strains may also cross-infect other species, including budgies, and, interestingly, even falcons. Native raptors around the world are susceptible to infection with pigeon Herpes virus and the so-called falcon and owl Herpes viruses are actually pigeon Herpes virus. Wild feral pigeons are thought to be a reservoir of infection for racing pigeons. In one Australian survey three feral flocks in Melbourne and three feral flocks in Sydney were tested for Herpes virus by doing a DNA test on swabs collected from the oral cavity.
All flocks were infected with Herpes virus.
Clinical course
When introduced into a flock, Herpes virus can kill young and adults by causing varying degrees of hepatitis (liver inflammation) enteritis (bowel inflammation) pancreatitis (pancreatic inflammation) ingluvitis (inflammation of the crop wall) and stomatitis (inflammation of the lining of the mouth). Infected birds shed the virus in saliva, nasal discharge, droppings and crop milk.
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Obviously unwell youngsters, which were subsequently
diagnosed with Herpes virus infection. |
Transmission can occur through contact with contaminated food or water as well as through direct contact between birds. Youngsters between four and 16 weeks of age are most susceptible to developing clinical disease, but birds of any age can catch the disease, particularly if they are run down. When the disease enters a loft, typically 50% of the birds become unwell with 10–15% of these birds dying. Those that survive are immune to subsequent disease but are carriers and, if bred, from will pass the virus on to their young.
Herpes virus is a DNA virus. This means that when birds become infected, the virus’s DNA is actually incorporated into the genome of the pigeon. Birds are therefore infected for life (as they say for humans ‘True love comes and goes but Herpes lasts forever.’). Young birds infected by parents that are carriers will not, however, develop disease, possibly because of the passive transfer of immunity. The virus, however, becomes enzootic (that is, a permanent resident) in the flock but clinically inapparent unless the birds become immunosuppressed (run down), when an outbreak of disease can occur.
Herpes virus is reasonably stable in the environment, being able to survive at 56C for up to 30 minutes. The virus has an incubation period of five to ten days. Clinical signs of the disease vary enormously because the virus can affect multiple sites throughout the body and affect each of these to an extent that varies from one bird to another. Thus the disease mimics signs seen in other more common diseases such as canker, Chlamydia, Circo virus and Salmonella.
Herpes virus is a DNA virus. This means that when birds become infected, the virus’s DNA is actually incorporated into the genome of the pigeon. Birds are therefore infected for life (as they say for humans ‘True love comes and goes but Herpes lasts forever.’). Young birds infected by parents that are carriers will not, however, develop disease, possibly because of the passive transfer of immunity. The virus, however, becomes enzootic (that is, a permanent resident) in the flock but clinically inapparent unless the birds become immunosuppressed (run down), when an outbreak of disease can occur.
Herpes virus is reasonably stable in the environment, being able to survive at 56C for up to 30 minutes. The virus has an incubation period of five to ten days. Clinical signs of the disease vary enormously because the virus can affect multiple sites throughout the body and affect each of these to an extent that varies from one bird to another. Thus the disease mimics signs seen in other more common diseases such as canker, Chlamydia, Circo virus and Salmonella.
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Autopsy specimen – a pigeon with a Herpes virus hepatitis. The liver is swollen and has an unusually dark colour. Herpes virus causes inflammation of the bile ducts that drain bile from the liver. The bile ducts become swollen and narrowed, causing the deep green bile to accumulate in the liver and give it the darker colour. Pigeons have two lobes in their liver, the left and right. In this photo, bile stasis has become so advanced that the green bile can be seen accumulating below the liver capsule in the left lobe (the top lobe in this photo). This photo was taken about ten minutes after the pigeon died of Herpes virus. |
In individual birds, Herpes virus can infect one or all of the following sites:
• the liver, leading to weight loss, poor appetite and green diarrhoea
• the bowel, leading to dehydration, weight loss and diarrhoea
• the crop, leading to delayed crop emptying and vomiting
• the throat, causing mucus production and the appearance of small pale spots in the pharyneal tonsil of the palate
• the trachea, leading to shortness of breath and coughing
• the nerves of the neck, wings and legs, leading to lameness and wobbly S-shaped necks
• the skin.
Severity of infection varies from one bird to another, so that some become acutely sick and may die within 24 hours without living long enough to lose condition. Others may be unwell for extended periods and then die or, alternatively, make a full recovery, while others still may just appear a bit quiet for a few days.
In summary:
1. When the virus is introduced into a flock many birds will show a variety of symptoms and a significant number will die.
2. Survivors are immune to subsequent disease but carry the virus in their system and, if bred from, will pass it to
their young.
3. Young birds infected by parents are carriers of the virus but do not develop disease.
4. The virus, however, becomes established in the loft but its presence is not apparent unless the birds become run
down.
5. Feral pigeons and birds from infected lofts are the usual source of infection.
Diagnosis
Typically, it is the flock picture rather than the signs exhibited by a single bird that arouses suspicions that the birds are infected with Herpes virus. Usually several birds are affected at any one time, showing a variety of signs as listed above, with the more affected birds typically being fluffed up, reluctant to move, underweight and with green diarrhoea. If Herpes virus is suspected, usually routine tests on the droppings and throat swabs are done initially to rule out other problems. Sometimes results here are suggestive; for example, the throat mucus may contain a lot of bacteria and white blood cells. A gross autopsy usually reveals grey-green localised ulcers on the lining of the upper airway, throat, crop and intestine. The air sacs, liver, and abdomen generally and, less commonly, the kidney, pancreas and spleen may be inflamed. For definitive diagnosis, however, tissue samples collected from a freshly dead bird (less than four hours) can be examined microscopically by an avian pathologist. The virus is visible with special stains under high magnification as either red or blue inclusion bodies within the nuclei of infected cells. A PCR test that checks for herpes virus DNA is now also available.
Fanciers should be careful when introducing birds from a loft with a history of disease. If Herpes has been diagnosed or is suspected, a Herpes PCR test on a throat swab should be done before introducing a bird.
How to manage an outbreak
The first thing to do in the face of an outbreak is to establish an accurate diagnosis. Herpes virus should be suspected with any disease problem that mainly affects youngsters that have moulted fewer than three flights and that start to show a variety of signs as described, with some dying. As these unwell birds are an ongoing source of infection, they should be immediately isolated, in order to minimise the exposure of other birds and so avoid fresh cases. Of these unwell birds, one or preferably two should be selected for submission to an avian vet for diagnostic purposes.
No drug is available to routinely treat the disease on a flock basis. Attention must therefore focus on controlling further spread of the virus and ensuring that the pigeons’ immune systems are maximally functional by providing ongoing good care and controlling any concurrent disease. This not only enables them to resist infection but also minimises the effect of the virus if they do, in fact, become infected. This involves four steps:
1. Identify and correct any predisposing stress-based loft factors and provide ongoing good care - No overcrowding,
good hygiene, free access to good quality grain and grit, no forced flying, provision of vitamin and
mineral supplements;
2. Control of concurrent diseases - A health profile is essential to identify concurrent diseases, in particular parasites,
so that these in turn can be treated, to prevent them prolonging the birds’ recovery. Both American and
Australian avian veterinarians have noted that recurring canker is common in flocks with endemic Herpes virus.
3. Minimize exposure to the virus by further birds - This is achieved by removing unwell birds and the maintenance
of hygienic conditions.
4. Probiotic use - One of the ways Herpes virus enters the body is through the digestive tract. The maintenance
of a healthy bowel population of bacteria will help birds resist the disease. Similarly, in unwell birds, the normal
bowel bacteria are disrupted. Keeping this population as normal as possible helps speed recovery. I usually recommend
that an initial course of 5 - 7 days of an avian probiotic (eg ‘Probac’) be given, followed by a minimum
of 2 - 3 days weekly until birds stop becoming unwell.
These measures may appear inadequate to fanciers dealing with an outbreak of Herpes virus in their birds. This is a nasty disease and at times it is frustrating that more cannot be done.
Other species of Herpes virus infect other birds, and for some of these a vaccine is available. Different Herpes viruses cause Infectious Laryngo Tracheitis and Mareks disease in chickens and Pacheco’s disease in parrots. Vaccine use here, however, is not without its problems, as the vaccine occasionally causes severe side effects and sometimes fails to give immunity. At present, no vaccine is available for use in pigeons.
A drug, Acyclovir, has been shown to be effective in treating some strains of Herpes virus. It is expensive and not always available, but has been given to individual birds (assuming a weight of 500g) as a water-soluble powder at the dose of 40mg directly into the crop three times daily. The same powder can be added to the food at doses as high as 2.5g/kg of feed. This drug can have severe side-effects, particularly involving the kidneys, and its use is far from routine. However, it may have a role in saving individual birds of particular value.
The author would like to thank Dr David Phalen of Sydney University for his assistance and technical advice with this section.
• the liver, leading to weight loss, poor appetite and green diarrhoea
• the bowel, leading to dehydration, weight loss and diarrhoea
• the crop, leading to delayed crop emptying and vomiting
• the throat, causing mucus production and the appearance of small pale spots in the pharyneal tonsil of the palate
• the trachea, leading to shortness of breath and coughing
• the nerves of the neck, wings and legs, leading to lameness and wobbly S-shaped necks
• the skin.
Severity of infection varies from one bird to another, so that some become acutely sick and may die within 24 hours without living long enough to lose condition. Others may be unwell for extended periods and then die or, alternatively, make a full recovery, while others still may just appear a bit quiet for a few days.
In summary:
1. When the virus is introduced into a flock many birds will show a variety of symptoms and a significant number will die.
2. Survivors are immune to subsequent disease but carry the virus in their system and, if bred from, will pass it to
their young.
3. Young birds infected by parents are carriers of the virus but do not develop disease.
4. The virus, however, becomes established in the loft but its presence is not apparent unless the birds become run
down.
5. Feral pigeons and birds from infected lofts are the usual source of infection.
Diagnosis
Typically, it is the flock picture rather than the signs exhibited by a single bird that arouses suspicions that the birds are infected with Herpes virus. Usually several birds are affected at any one time, showing a variety of signs as listed above, with the more affected birds typically being fluffed up, reluctant to move, underweight and with green diarrhoea. If Herpes virus is suspected, usually routine tests on the droppings and throat swabs are done initially to rule out other problems. Sometimes results here are suggestive; for example, the throat mucus may contain a lot of bacteria and white blood cells. A gross autopsy usually reveals grey-green localised ulcers on the lining of the upper airway, throat, crop and intestine. The air sacs, liver, and abdomen generally and, less commonly, the kidney, pancreas and spleen may be inflamed. For definitive diagnosis, however, tissue samples collected from a freshly dead bird (less than four hours) can be examined microscopically by an avian pathologist. The virus is visible with special stains under high magnification as either red or blue inclusion bodies within the nuclei of infected cells. A PCR test that checks for herpes virus DNA is now also available.
Fanciers should be careful when introducing birds from a loft with a history of disease. If Herpes has been diagnosed or is suspected, a Herpes PCR test on a throat swab should be done before introducing a bird.
How to manage an outbreak
The first thing to do in the face of an outbreak is to establish an accurate diagnosis. Herpes virus should be suspected with any disease problem that mainly affects youngsters that have moulted fewer than three flights and that start to show a variety of signs as described, with some dying. As these unwell birds are an ongoing source of infection, they should be immediately isolated, in order to minimise the exposure of other birds and so avoid fresh cases. Of these unwell birds, one or preferably two should be selected for submission to an avian vet for diagnostic purposes.
No drug is available to routinely treat the disease on a flock basis. Attention must therefore focus on controlling further spread of the virus and ensuring that the pigeons’ immune systems are maximally functional by providing ongoing good care and controlling any concurrent disease. This not only enables them to resist infection but also minimises the effect of the virus if they do, in fact, become infected. This involves four steps:
1. Identify and correct any predisposing stress-based loft factors and provide ongoing good care - No overcrowding,
good hygiene, free access to good quality grain and grit, no forced flying, provision of vitamin and
mineral supplements;
2. Control of concurrent diseases - A health profile is essential to identify concurrent diseases, in particular parasites,
so that these in turn can be treated, to prevent them prolonging the birds’ recovery. Both American and
Australian avian veterinarians have noted that recurring canker is common in flocks with endemic Herpes virus.
3. Minimize exposure to the virus by further birds - This is achieved by removing unwell birds and the maintenance
of hygienic conditions.
4. Probiotic use - One of the ways Herpes virus enters the body is through the digestive tract. The maintenance
of a healthy bowel population of bacteria will help birds resist the disease. Similarly, in unwell birds, the normal
bowel bacteria are disrupted. Keeping this population as normal as possible helps speed recovery. I usually recommend
that an initial course of 5 - 7 days of an avian probiotic (eg ‘Probac’) be given, followed by a minimum
of 2 - 3 days weekly until birds stop becoming unwell.
These measures may appear inadequate to fanciers dealing with an outbreak of Herpes virus in their birds. This is a nasty disease and at times it is frustrating that more cannot be done.
Other species of Herpes virus infect other birds, and for some of these a vaccine is available. Different Herpes viruses cause Infectious Laryngo Tracheitis and Mareks disease in chickens and Pacheco’s disease in parrots. Vaccine use here, however, is not without its problems, as the vaccine occasionally causes severe side effects and sometimes fails to give immunity. At present, no vaccine is available for use in pigeons.
A drug, Acyclovir, has been shown to be effective in treating some strains of Herpes virus. It is expensive and not always available, but has been given to individual birds (assuming a weight of 500g) as a water-soluble powder at the dose of 40mg directly into the crop three times daily. The same powder can be added to the food at doses as high as 2.5g/kg of feed. This drug can have severe side-effects, particularly involving the kidneys, and its use is far from routine. However, it may have a role in saving individual birds of particular value.
The author would like to thank Dr David Phalen of Sydney University for his assistance and technical advice with this section.