Adenoviral, E. coli and Paratyphoid Infections in Pigeons
The occurrence of adenovirus and its combination with the bacterial organism E.coli (the shortened form of its longer scientific name, Escherichia coli) has been causing grief to fanciers in many parts of the world today, especially in youngsters as they begin mixing with those from other lofts during the racing season. This is a highly stressful time for these birds, and because their immune system is often not completely developed at this stage of their lives, they are susceptible to any number of infectious agents. As well, in response to the stresses imposed by crowding, training and racing, etc., their adrenal glands, located just ahead of the kidneys, right under the vertebral column, release corticosteroids into the circulating bloodstream. These steroids depress the ability of the incompletely developed immune system to respond effectively to invading agents such as bacteria, viruses and parasites. One unhappy consequence of this depressed situation may be infection with adenovirus and a disease-producing strain of E. coli, which together, can bring about signs of illness characterised by vomiting and diarrhoea (Young Bird Sickness). Vomiting may be difficult to evaluate since it can occur during the night, and by dawn, other youngsters in the loft may have eaten the disgorged grains. In other instances, digestion is slowed and affected youngsters may retain feed in their crop ("holding their corn").
The following section is a brief summary of some aspects of these infections.
1) ADENOVIRUS. In Europe, two different adenoviral infections are known to occur in pigeons, and are designated Types I and II. Type I was discovered in 1976, and occurred in young pigeons during the first half of the year, with a peak frequency in June. The major sign of
this adenoviral disease was watery diarrhoea. E.coli often complicated this disease, and resulted in a more severe diarrhoea, as well as vomiting and occasionally, death. Treatment with appropriate antibiotics was often successful. At post mortem of affected birds, there was evidence of enteritis (inflammation of the intestines), and the liver was often normal or only mildly abnormal. However, microscopically in the liver, there were characteristic changes that indicated adenoviral infection. Type I adenoviral infection seems likely to be the disease that affects many young birds over the world today.
Type II adenoviral infection occurred in Belgium in 1992, and was characterised by sudden death in pigeons of all ages. There were very few clinical signs in affected birds prior to death. Occasionally, there was fluid, yellow diarrhoea and vomiting. However, the major sign was sudden death within 24 hours of the onset of illness, with none of the obviously sick birds surviving longer than 48 hours. Antibiotics had no effect on the outcome of this disease. In individual lofts, losses were variable, and usually amounted to 30%, but in some cases reached 100%. At post mortem, affected birds had a pale, yellow, swollen liver that had a characteristic red sheen. Microscopically, there was massive destruction of the liver, along with typical changes indicative of adenoviral infection. Although this infection began by affecting one age group in a loft, in 70% of cases, the disease eventually spread to all age groups. To the surprise of investigators, in lofts in which these acute deaths occurred, pigeons that did not die remained completely normal. Even youngsters in the nest grew normally after their parents died of this infection, if they were able to feed themselves or were raised by other pairs. Whether Type II infection has yet occurred in other areas of the world is not known to me.
In my experience with other species of domestic birds and animals, adenoviral infections usually occur when immune function is depressed. For example, in young, growing broiler chickens, infection with a virus known as the agent of Infectious Bursal Disease severely damages the immune system, thus allowing for the invasion of another virus, this one an adenovirus, that causes a disease known as Inclusion Body Hepatitis. Fortunately, a vaccine developed against the Bursal Disease virus has been effective in preventing Inclusion Body Hepatitis. In another example, some Arabian foals are born with an inherited condition known as Combined Immunodeficiency Disorder in which the immune system is severely underdeveloped. Massive adenoviral infection, especially a pneumonia, is often associated with the death of these foals.
In pigeons, I continue to wonder about the largely hidden effects of circovirus infection which, like the AIDS virus in humans, causes severe damage to the immune system, and thereby, acts as a "trigger" that sets in motion, the further destructive effects of adenoviral and E. coli infections. Circoviral infection in pigeons could have an effect similar to that of the virus of Infectious Bursal Disease in chickens, ie severe damage to the immune system followed by invasion of the adenovirus and E.coli. One of the characteristic "footprints" of circoviral infection is an upsurge in outbreaks of other conditions - canker, coccidiosis, paratyphoid, etc., so it would be reasonable to include adenoviral -E. coli infections in that list of possibilities..
Treating adenoviral infections is difficult, if not impossible. Unlike bacteria, viruses are not susceptible to antibiotics. However, in recent months, the use of elderberry juice in treating affected youngsters, has been touted as a method of dealing with this infection. Although I am not certain of any scientific basis for this claim, it may be worth examining.
At least one adenoviral vaccine has been offered for sale in Europe and North America. One prominent veterinary friend whom I contacted about this vaccine observed that the results of vaccination in his area were mixed, likely because many fanciers didn't follow through with the required second (booster) vaccination, which, by extension, likely didn't allow for the development of a sufficiently high level of immunity to protect exposed birds.
Perhaps the only practical approach is planned exposure to the virus, which could be accomplished through early mixing of young birds from different lofts in say, club training tosses, etc., well before the racing season, to allow them to go through the infection and develop protective immunity that would carry them though the race season. The use of the dewormer known as levamisole has been shown to stimulate the immune system, and according to Dr John Kazmierczak of New Jersey, USA, a dosage of 50 mg per 4 litres of drinking water once a week, may be helpful. Also, the use of a multivitamin mix containing vitamins C and E in the drinkers once or twice a week is practical and provides additional support to the immune system. A wide-ranging loose mineral mix containing the trace mineral selenium, which is important in the normal development of the immune system, should be available free-choice all year long.
2) E. COLI. Broadly speaking, E. coli are usually innocent, normal inhabitants of the intestines of many species, including humans. However, like other creatures, E. coli organisms exist in Nature as a number of strains that range from the most innocent through to the most deadly. Some dangerous strains of E. coli in the intestines may cause disease by their production of potent toxins (poisons) that are absorbed through the intestinal wall into the bloodstream, from which their far-reaching effects in many tissues throughout the body are manifested. I suspect that the E. coli strains that are part of the adenoviral-E.coli problem in youngsters these days are toxin-producing strains. Still other dangerous strains of E. coli are able to breach the intestinal wall, enter the bloodstream where they multiply (called "septicaemia") and are distributed to a variety of tissues to produce signs of illness. Some joint, brain and ovarian infections, etc. in pigeons are caused by these tissue-invasive strains of E. coli. Like other creatures, humans are not exempt from the effects of dangerous strains of E. coli. Improperly cooked hamburgers containing a hazardous strain of E. coli have caused serious illness and death in humans. Last year, in Walkerton, Ontario, Canada, seven people died and many more individuals in the town became seriously ill after they were exposed to a deadly toxin- producing strain of E.coli identified as 0157 that contaminated municipal drinking water.
Some strains of E.coli recovered from sick domestic birds and animals may be specifically identified by the use of specialised laboratory techniques, such as those that identified the aforementioned strain of E. coli in humans as 0157. In other examples, young pigs with diarrhoea may have a strain of E. coli identified in part, as K88, and young calves with a similar problem may be affected by a strain identified in part, as K99. However, I am not aware if these or related procedures have been used commonly to identify disease-producing strains of E. coli in pigeons.
In pigeons, as in many other species, the mere finding of E. coli organisms in a sample of droppings cultured in a laboratory does not necessarily mean that they are the cause of a problem. They could be completely innocent. For example, if samples of droppings are collected several hours after they have been passed, and if these samples have not been refrigerated during shipment to the laboratory, E. coli organisms that are present in these droppings can multiply during transit and, on culture, result in large numbers that may give the false impression that they are the cause of the problem. However, if freshly passed samples of droppings are collected quickly, refrigerated immediately, and kept refrigerated on route to the laboratory, there is a greater chance that large numbers of organisms cultured from these droppings may well be significant, especially if those large numbers can be tied to the problem being experienced in the birds. If a pure culture of E. coli organisms is recovered from a variety of tissues (heart blood, liver, kidney, etc.) from a freshly killed sick bird, there is a strong likelihood that they are the cause of that particular problem. Fanciers should ask for and expect an interpretation of the laboratory findings of E. coli (or any other significant organism cultured) found in submitted samples. However, if the fancier hasn't properly collected, refrigerated and shipped specimens to the laboratory, it becomes very difficult for laboratory staff to provide useful interpretations of their findings. An advance phone call to the laboratory for instructions on collecting, handling and shipping samples of droppings or other specimens, is a always good idea.
The occurrence of adenovirus and its combination with the bacterial organism E.coli (the shortened form of its longer scientific name, Escherichia coli) has been causing grief to fanciers in many parts of the world today, especially in youngsters as they begin mixing with those from other lofts during the racing season. This is a highly stressful time for these birds, and because their immune system is often not completely developed at this stage of their lives, they are susceptible to any number of infectious agents. As well, in response to the stresses imposed by crowding, training and racing, etc., their adrenal glands, located just ahead of the kidneys, right under the vertebral column, release corticosteroids into the circulating bloodstream. These steroids depress the ability of the incompletely developed immune system to respond effectively to invading agents such as bacteria, viruses and parasites. One unhappy consequence of this depressed situation may be infection with adenovirus and a disease-producing strain of E. coli, which together, can bring about signs of illness characterised by vomiting and diarrhoea (Young Bird Sickness). Vomiting may be difficult to evaluate since it can occur during the night, and by dawn, other youngsters in the loft may have eaten the disgorged grains. In other instances, digestion is slowed and affected youngsters may retain feed in their crop ("holding their corn").
The following section is a brief summary of some aspects of these infections.
1) ADENOVIRUS. In Europe, two different adenoviral infections are known to occur in pigeons, and are designated Types I and II. Type I was discovered in 1976, and occurred in young pigeons during the first half of the year, with a peak frequency in June. The major sign of
this adenoviral disease was watery diarrhoea. E.coli often complicated this disease, and resulted in a more severe diarrhoea, as well as vomiting and occasionally, death. Treatment with appropriate antibiotics was often successful. At post mortem of affected birds, there was evidence of enteritis (inflammation of the intestines), and the liver was often normal or only mildly abnormal. However, microscopically in the liver, there were characteristic changes that indicated adenoviral infection. Type I adenoviral infection seems likely to be the disease that affects many young birds over the world today.
Type II adenoviral infection occurred in Belgium in 1992, and was characterised by sudden death in pigeons of all ages. There were very few clinical signs in affected birds prior to death. Occasionally, there was fluid, yellow diarrhoea and vomiting. However, the major sign was sudden death within 24 hours of the onset of illness, with none of the obviously sick birds surviving longer than 48 hours. Antibiotics had no effect on the outcome of this disease. In individual lofts, losses were variable, and usually amounted to 30%, but in some cases reached 100%. At post mortem, affected birds had a pale, yellow, swollen liver that had a characteristic red sheen. Microscopically, there was massive destruction of the liver, along with typical changes indicative of adenoviral infection. Although this infection began by affecting one age group in a loft, in 70% of cases, the disease eventually spread to all age groups. To the surprise of investigators, in lofts in which these acute deaths occurred, pigeons that did not die remained completely normal. Even youngsters in the nest grew normally after their parents died of this infection, if they were able to feed themselves or were raised by other pairs. Whether Type II infection has yet occurred in other areas of the world is not known to me.
In my experience with other species of domestic birds and animals, adenoviral infections usually occur when immune function is depressed. For example, in young, growing broiler chickens, infection with a virus known as the agent of Infectious Bursal Disease severely damages the immune system, thus allowing for the invasion of another virus, this one an adenovirus, that causes a disease known as Inclusion Body Hepatitis. Fortunately, a vaccine developed against the Bursal Disease virus has been effective in preventing Inclusion Body Hepatitis. In another example, some Arabian foals are born with an inherited condition known as Combined Immunodeficiency Disorder in which the immune system is severely underdeveloped. Massive adenoviral infection, especially a pneumonia, is often associated with the death of these foals.
In pigeons, I continue to wonder about the largely hidden effects of circovirus infection which, like the AIDS virus in humans, causes severe damage to the immune system, and thereby, acts as a "trigger" that sets in motion, the further destructive effects of adenoviral and E. coli infections. Circoviral infection in pigeons could have an effect similar to that of the virus of Infectious Bursal Disease in chickens, ie severe damage to the immune system followed by invasion of the adenovirus and E.coli. One of the characteristic "footprints" of circoviral infection is an upsurge in outbreaks of other conditions - canker, coccidiosis, paratyphoid, etc., so it would be reasonable to include adenoviral -E. coli infections in that list of possibilities..
Treating adenoviral infections is difficult, if not impossible. Unlike bacteria, viruses are not susceptible to antibiotics. However, in recent months, the use of elderberry juice in treating affected youngsters, has been touted as a method of dealing with this infection. Although I am not certain of any scientific basis for this claim, it may be worth examining.
At least one adenoviral vaccine has been offered for sale in Europe and North America. One prominent veterinary friend whom I contacted about this vaccine observed that the results of vaccination in his area were mixed, likely because many fanciers didn't follow through with the required second (booster) vaccination, which, by extension, likely didn't allow for the development of a sufficiently high level of immunity to protect exposed birds.
Perhaps the only practical approach is planned exposure to the virus, which could be accomplished through early mixing of young birds from different lofts in say, club training tosses, etc., well before the racing season, to allow them to go through the infection and develop protective immunity that would carry them though the race season. The use of the dewormer known as levamisole has been shown to stimulate the immune system, and according to Dr John Kazmierczak of New Jersey, USA, a dosage of 50 mg per 4 litres of drinking water once a week, may be helpful. Also, the use of a multivitamin mix containing vitamins C and E in the drinkers once or twice a week is practical and provides additional support to the immune system. A wide-ranging loose mineral mix containing the trace mineral selenium, which is important in the normal development of the immune system, should be available free-choice all year long.
2) E. COLI. Broadly speaking, E. coli are usually innocent, normal inhabitants of the intestines of many species, including humans. However, like other creatures, E. coli organisms exist in Nature as a number of strains that range from the most innocent through to the most deadly. Some dangerous strains of E. coli in the intestines may cause disease by their production of potent toxins (poisons) that are absorbed through the intestinal wall into the bloodstream, from which their far-reaching effects in many tissues throughout the body are manifested. I suspect that the E. coli strains that are part of the adenoviral-E.coli problem in youngsters these days are toxin-producing strains. Still other dangerous strains of E. coli are able to breach the intestinal wall, enter the bloodstream where they multiply (called "septicaemia") and are distributed to a variety of tissues to produce signs of illness. Some joint, brain and ovarian infections, etc. in pigeons are caused by these tissue-invasive strains of E. coli. Like other creatures, humans are not exempt from the effects of dangerous strains of E. coli. Improperly cooked hamburgers containing a hazardous strain of E. coli have caused serious illness and death in humans. Last year, in Walkerton, Ontario, Canada, seven people died and many more individuals in the town became seriously ill after they were exposed to a deadly toxin- producing strain of E.coli identified as 0157 that contaminated municipal drinking water.
Some strains of E.coli recovered from sick domestic birds and animals may be specifically identified by the use of specialised laboratory techniques, such as those that identified the aforementioned strain of E. coli in humans as 0157. In other examples, young pigs with diarrhoea may have a strain of E. coli identified in part, as K88, and young calves with a similar problem may be affected by a strain identified in part, as K99. However, I am not aware if these or related procedures have been used commonly to identify disease-producing strains of E. coli in pigeons.
In pigeons, as in many other species, the mere finding of E. coli organisms in a sample of droppings cultured in a laboratory does not necessarily mean that they are the cause of a problem. They could be completely innocent. For example, if samples of droppings are collected several hours after they have been passed, and if these samples have not been refrigerated during shipment to the laboratory, E. coli organisms that are present in these droppings can multiply during transit and, on culture, result in large numbers that may give the false impression that they are the cause of the problem. However, if freshly passed samples of droppings are collected quickly, refrigerated immediately, and kept refrigerated on route to the laboratory, there is a greater chance that large numbers of organisms cultured from these droppings may well be significant, especially if those large numbers can be tied to the problem being experienced in the birds. If a pure culture of E. coli organisms is recovered from a variety of tissues (heart blood, liver, kidney, etc.) from a freshly killed sick bird, there is a strong likelihood that they are the cause of that particular problem. Fanciers should ask for and expect an interpretation of the laboratory findings of E. coli (or any other significant organism cultured) found in submitted samples. However, if the fancier hasn't properly collected, refrigerated and shipped specimens to the laboratory, it becomes very difficult for laboratory staff to provide useful interpretations of their findings. An advance phone call to the laboratory for instructions on collecting, handling and shipping samples of droppings or other specimens, is a always good idea.