The following article is based on the disease section of a two-part illustrated seminar presented by the author to fanciers in the Gippsland, Melbourne and Adelaide areas in October, 2000. The other section of the seminar dealt with muscle and fuel, the details of which can be found in several recent past issues of the ARPJ. Ed

1. Canker

Canker is caused by a small, one-celled, microscopic parasite called Trichomonas gallinae. The same organism causes a disease called frounce in birds of prey. In pigeons, there are strains of this organism that range from very mild, relatively innocent types through to those that are very deadly.

Canker is probably most important in young birds, but it can also be a serious threat to old birds as well. The commonest form of the disease in youngsters is a yellowish lump in the mouth or throat area (Figure 1). It may also affect lower areas such as the crop or liver where it would not be visible to naked eye inspection. "Going light" is one of the first signs of illness if there is no visible change in the mouth or throat, although canker is definitely not the only cause of "going light".

 

The disease may affect the liver severely, especially when one of the more deadly strains is involved (Figure 2). Here, "going light" may be the first sign of illness. Another important sign when the liver is severely involved is a puffiness in the abdomen, which can be detected by examination of the area between the keel and the vent bones. Occasionally, the mouth and the whites of the eyes may have a yellow discolouration in this situation. It is common for involvement of the liver to occur in youngsters in the period soon after weaning when stresses are very high. At that time, depending on the strain of organism involved, one or more youngsters in a group of recently weaned birds may be affected. They go off feed, are listless and sit in a hunched posture with feathers ruffled.

A commonly used drug in treatment is Emtryl, even though in Europe, strains of the organism are developing resistance to this drug, likely through misuse of the drug, ie, underdosing. This product is usually purchased as a 40% water-soluble powder that is added to the drinking water at the rate of 1 level teaspoon (3 grams) per Imperial gallon (4.55 litres). Birds should be treated for a minimum of 5 days, and not longer than 7 days. Don't buy the feed-grade formulation of Emtryl.

One problem is that Emtryl can be poisonous. Commonly, birds are overdosed during hot weather or when they are raising youngsters, or both, because of their greater need for more water. In my experience, this tends to happen when fanciers leave Emtryl-treated water before the birds 24 hours a day in hot weather. One of the dramatic side effects is to see Emtryl-poisoned pigeons flopping upside down on the floor of the loft, with the remainder of the birds in the loft terrified by this aberrant behaviour. Other, more subtle nervous signs of poisoning can be detected by the observant fancier. If these signs occur, simply remove the treated water and replace it with fresh, clean water, and affected birds will often recover in a day or so.

Fanciers may attempt to compensate during hot weather by cutting the dosage. However, such an approach (as well as putting Emtryl on the end of a toothpick and dropping it into the mouth of a bird -- avoid this procedure) opens the door widely to the development of resistance by the canker organism, and since there seem to be fewer and fewer effective anti-canker products on the market, it is important not to squander perhaps one of the few remaining arrows in our quiver, so to speak.

Luckily, there is a practical solution that should avoid both lower dosages and the possibility of resistance. The practical answer is one that was proposed several years ago by an Australian biologist. Having tried it many times, I am convinced that it works, and works well. Here is what the Aussie report recommended.

At the evening feeding, make up the correct dosage of Emtryl in the drinking water, that is, one level teaspoon of Emtryl per imperial gallon. The Aussie who proposed this method recommended that treated water be placed in the loft and left for a couple of hours or so, after which, the medicated water is thrown out and replaced with fresh untreated water for the next 24 hours. At this time, on the next evening, water containing the same correct dosage is placed in the loft and left for two hours or so, then replaced with fresh water until the next evening. This process is repeated each evening for a total of 5-7 days. This practical answer has two major advantages. Firstly, the birds receive the correct therapeutic dosage of Emtryl for the required number of days. Secondly, the problem with poisoning seems to be largely avoided.

I have often modified this procedure in my own loft by leaving the treated water in the loft over night, and haven't had any problem even with small youngsters in the nest. Note that the company producing Emtryl recommends avoiding treatment if the adults are feeding small youngsters. Caution: if the weather is extremely hot as it can be at times in Australia, I would suggest that, to be more certain of avoiding a poisoning situation, I would follow the Aussie recommendations and remove the treated water each evening after two hours or so, and replace it with fresh clean water until the next evening. Note that the dosage mentioned here is the one recommended for pigeons by the producer of Emtryl. The information presented here simply follows company recommendations for the use of Emtryl to treat or prevent canker in pigeons.

Sometimes during the racing season, performances will fall off and birds are no longer at the top of the sheet, even though they continue to look good. One possibility is that during the stresses of racing, the immune system of the birds is weakened, and canker organisms have begun to multiply. If you examine the mouths of these birds, you may see marked reddening of the tissues and excess stringy, even dirty, mucus in the back of the throat. It is possible that canker organisms have begun to multiply into the many hundreds of thousands to cause irritation of the throat. To protect the throat from the irritation and to soothe the surface, glands in the area pour out a thick mat of protective mucus. When swabs of this mucus are examined under a microscope, the material is seen to be teeming with many tumbling, wriggling canker organisms.

For those who like to medicate against these canker organisms for one or two days at the beginning of the week, every 2-3 weeks during the racing season, it would seem advisable to use the correct dosage, that is, at the rate of 1 level teaspoon per gallon of water. Like others, I have some concerns about these short one or two-day treatments, because of the strong possibility of resistance developing in the organism as a result of the short treatment period. However, to treat for a full five days could throw the birds completely off form, so the short term treatment period may well be the lesser of two evils. For example, if your race finishes on Saturday, you may want to treat Sunday and Monday, or Monday and Tuesday, but no later. The company producing Emtryl also recommends that you do not inhale the dust, and if you get any of the powder on your hands, wash it off immediately.

Ronidazole is another product that can be used effectively in pigeons in the treatment or prevention of canker, and at least one formulation of the product is available in Australia as Turbisole. Ronidazole is reported to be far superior to any other drug in the USA. It seems to be less toxic and more effective than other comparable drugs in the treatment or prevention of canker. Spartrix and Flagyl are two other drugs that seem to be useful treatments.

It is likely a good idea to change drugs each time you feel birds need to be treated, say, Emtryl for one 5-7 day treatment period, and Ronadizole, for the next one, etc.. This procedure may help to avoid the development of resistance to these drugs by the canker organism -- and all drugs have to be used at the correct dosage.

One of the great problems faced by fanciers everywhere is resistance of the canker organism to a variety of treatments available to us. This problem has developed because fanciers routinely underdose their birds (witness the use of Emtryl or similar drugs on the end of a toothpick, or rubbing a canker lesion with a solution of an anti-canker drug). The answer lies in treating with the correct dosage of drug for the required number of days.

Another important issue is the matter of the resistance of pigeons to the canker organism. To begin this subject, it is a well-established fact that mild strains of the canker organism will protect birds against a deadly strain, an important point that we can use to advantage in the loft. This fact was established about 50 years ago by Dr Robert Stabler who worked with the canker organism in Colorado, USA. He worked with several strains of the organism, including a very deadly strain that he called his "Jones' barn strain", obtained from a wild youngster. He passed this organism by eyedropper to 119 successive, clean pigeons; so potent was this strain that 114 of the 119 birds infected with it, died of canker. Dr Stabler found that the transfer of even one organism of the Jones' barn strain to clean pigeons was capable of causing death. Obviously, the single organism multiplied rapidly to very large numbers (hundreds of thousands) in the mouth and crop of infected pigeons. Even so, mild strains of the organism were able to protect birds against this deadly strain. In general, if you haven't had a canker problem in old birds or their youngsters, especially for a few years, it is possible that there is sufficient resistance in your birds to protect them against more deadly strains. If it's not broken, don't fix it! Fortunately for Aussie fanciers, Colin Walker has published some good practical advice on criteria for dealing with canker in the loft - see his books on health.

2. Paratyphoid Infection

In pigeons, this bacterial disease is caused most commonly by Salmonella typhimurium variety copenhagen, but other species of S. typhimurium

can also cause infection in pigeons. If there is any good news about variety copenhagen, it is that, firstly, it seems to be virtually confined to pigeons, although there have been occasional outbreaks of this type in chickens. Secondly, although Salmonella spp. very often readily cross from one species to another (witness the ongoing concerns about the spread of this infection from food-producing animals and birds -- notably chickens -- to humans), variety copenhagen very rarely infects humans. Thirdly, unless antibiotics have been underdosed in a loft consistently, copenhagen is often highly susceptible to a wide range of antibiotics.

One of the best if not the actual best is Baytril (enrofloxacin). The second best product is either Cephalexin or Amoxicillin. Treat for a minimum of 10 days with any of these products, and at the same time, it often helps to vaccinate during treatment. Avoid training for at least a week during these treatment periods, and don't race your birds while they are infected. It is immoral and very unsportsmanlike to transmit his infection to your competitors.

Paratyphoid disease is usually spread in the droppings of actively infected pigeons or in the droppings of birds that are silent carriers of the infection. It can also be spread through the egg as a result of infection of the ovary of the hen. Rats and mice are obvious culprits in the spread of some types of paratyphoid. According to Dr David Marx, USA, it is a rare loft that doesn't have infected birds, a finding that may surprise many scrupulously clean fanciers who consider their lofts to be paratyphoid-free. It is a common finding that newly introduced, healthy looking birds may be a source of this infection -- which is why wild pigeons or strays from another loft should not be allowed into your loft. Naturally, it is always possible that your own race birds may have been exposed to one or more paratyphoid-infected birds during shipping, so racing is always a risk, not only for paratyphoid infections, but others as well -- E. coli, coccidiosis, paramyxovirus, etc..

Outbreaks are common during the breeding season, especially later on in the season after the parents have had to rear several rounds of youngsters on their own. In this situation, they are severely stressed, and their resistance is down. At this time there has also been quite a drain on the immune system of the parents, because their bodies attempt to include protective substances (antibodies) in the yolk of the eggs and in crop milk. This process results in lowered antibodies in the parents, and they become very susceptible to infections such as paratyphoid.

According to Dr Marx, classical paratyphoid is common in breeding cocks which can become sick and die very quickly -- the bird is fine one day and dead the next. Hens can become sick in the same way, but this form is more common in cocks. In hens, paratyphoid is a more chronic disease in which the affected hens often have severe weight loss ("going light"), sticky droppings containing a lot of mucus, swollen wing joints ("wing boil") and affected livers. Another clue to paratyphoid is eggs that turn black and appear rotten. Such eggs were once fertile, began to develop, and then the embryo died of the infection. (If eggs are infertile in the first place, they stay clear for the whole incubation period.) The organisms can contaminate the surface of the egg as it is laid, or it can be incorporated in the egg as it was being formed in an infected ovary (same with E. coli infections). Another key characteristic of paratyphoid infection is youngsters that begin to hatch but die in the shell. Diarrhoea, dehydration and death in 7-10 day-old youngsters in the nest can occur. Often, only one of the two will get sick and die.

Sore joints in the legs and wings, with or without swelling of these joints, can occur, especially in hens. Characteristically, the elbow joint is often affected, producing the "wing boil" mentioned earlier. Tilted heads and twisted necks as the result of infection of the brain can occur in paratyphoid infections, but are more commonly associated with paramyxovirus infections. Both paratyphoid and paramyxovirus infections can cause birds to pass a lot of fluids. In paratyphoid infections, the fluid is from a true diarrhoea because it comes from the intestines and contains a lot of mucus, possibly some small gas bubbles, and even blood, and may have a detectable odour. In paramyxovirus infection, much of the so-called diarrhoea is actually clear fluid coming from the kidneys which are often severely affected by the virus, and as a result, are unable to perform their natural function of concentrating urine. There is often a pool of fluid from the kidneys, in the centre of which is a small "snake" of normal droppings from the intestines.

Whenever you are faced with an outbreak of paratyphoid infection in your birds, the first thing to avoid is the use of lime or any other alkaline substance on floors or perches. Reason: paratyphoid bacteria (and E. coli, among others) like alkaline conditions which actually favour their multiplication, something you want to avoid at all costs. Floor dressings such as sodium acid bisulphite create acidic conditions that these bacteria find hostile for their reproduction. To prevent transmission through drinking water contaminated by droppings, you can add a teaspoon of household chlorine bleach (sodium hypochlorite) to a gallon of water to kill the bacteria. For other purposes, some fanciers like to use cider vinegar in drinking water, which effectively produce an acidic environment that is also unfriendly to paratyphoid organisms.

Another approach is to make use of "friendly" bacteria. There are commercial products available for pigeons, as well as capsules of these bacteria for human use. One inexpensive source of these friendly bacteria is plain yogurt, but you must buy the product that contains live cultures of bacteria (it's my understanding that yogurt containing either live or killed bacteria are available in Australia - buy the one containing live cultures of bacteria). This approach of using "friendly" bacteria is based on research conducted by a scientist named Esko Nurmi in 1973. Working in Finland, this man developed a procedure in which he fed litter and droppings from salmonella-free, clean, healthy flocks of chickens, to normal, day-old chicks. Afterward, he found that these chicks were resistant to a challenge dose of salmonella organisms given to them by mouth. The principle behind this process is that "good" bacteria in the droppings of clean flocks of birds colonised the intestines of these chicks and simply overwhelmed sites of invasion by salmonella organisms. The same principle applies when a broody chicken scratches in the soil and calls her chicks to pick in that area. The intestines of these chicks are colonised very quickly with masses of "good" bacteria picked up in the soil at this time. In other words, this defence network competes with and excludes disease-producing bacteria -- hence the expression competitive exclusion.

The means by which this protection against salmonella and other disease-producing bacterial organisms is accomplished are not completely understood. However, there are two known mechanisms that operate to protect birds against disease when the principle of competitive exclusion is applied. Firstly, the "good" bacteria in the normal droppings seem to form within the intestine, a physical barrier that may be as much as 10-12 bacteria deep. These protective bacteria actually bind to specific sites on the inner surface of the intestine, and by this means, prevent contact by Salmonella sp. with the inner surface of the intestine, and so, prevent these disease-producers from breaching the wall of the intestine and entering the bloodstream.

The second process that occurs is an actual chemical alteration in the intestine. The "good" bacteria in clean droppings are anaerobic species (an = without; aerobic = oxygen), ie, they are able to live and reproduce in an environment in which levels of oxygen are low. In such a situation, the life processes of these bacteria are completed in an anaerobic state. In such an anaerobic environment, these organisms produce and excrete lactic acid as one of the by-products of their life processes. In turn, the lactic acid that is excreted by these bacteria into the surrounding environment of the intestine, creates a shift from a normally alkaline state to a more acidic, hostile condition in the intestine.

The importance of this fact needs to be re-iterated: many disease-producing bacteria like Salmonella sp. and E. coli, for example, like to live in a slightly alkaline environment -- such as the intestines -- where they can reproduce well. In an acidic environment, they are prevented from reproducing, and their numbers drop dramatically, in some cases by 97% or more. One of the many "good" bacteria present is the Lactobacillus sp. that we also find in yogurt and similar products used for human food.

Other "good" bacteria that are also present in yogurt include two species of lactic acid-producing Streptococcus, among others. The Lactobacillus sp. bacteria not only colonise the intestines, but they also attach to the wall of the crop, and are mixed with food that has just been eaten. As the food moves into the proventriculus and gizzard, and then into the intestine, the "good" Lactobacillus sp. bacteria move mechanically with it and multiply in the intestine. However, scientific information obtained from experiments using several pure cultures of Lactobacillus sp. in chickens showed that this organism alone was not capable of conferring on chickens, the desired resistance to Salmonella spp.. Additional methods had to be incorporated along with the use of Lactobacillus sp..

A few basic products incorporating these ideas of using "good" bacteria to combat Salmonella sp. infections have been examined in the poultry industry. One of these products is called "an unidentified culture". In this situation, intestinal contents from chickens known to be salmonella-free are incubated in a warm, anaerobic environment. The bacteria that are grown in this way are not specifically identified, but this culture is then fed to the birds. The second of these products is called "a defined culture", meaning that specifically identified bacteria from a culture of intestinal contents of normal chickens are included in a mix of bacteria that may contain up to 50 different species of bacteria.

There are also products called "probiotics" which are cultures of only a very few kinds of bacteria, ie, for example, the kinds that are found in yogurt. One such starter product for preparing yogurt at home contains a Lactobacillus sp., as well as two identified species of Streptococcus. One species of Streptococcus, that produced lactic acid, for example, was found to inhibit the growth of 75-85% of disease-producing strains of E. coli, but only 45% of livestock varieties of Salmonella spp..

In poultry, only the "unidentified culture" appears to be effective against salmonella organisms. "Defined cultures" and "probiotics" are more effective against disease-producing strains of E. coli, for example.

A fairly recent development is a mix of 29 bacterial types that is sprayed on newly hatched chicks. The birds pick at their down and of course, swallow the bacteria sprayed on them. These bacteria reproduce in the intestines and block the attachment of Salmonella spp.. It is possible that this spray could be helpful in pigeons as well.

In the poultry industry, these types of products have been used in at least three situations:

1. They are given to day-old chicks to allow the rapid colonization of the intestine with "good" bacteria which protect against infection by Salmonella sp..

2. In mature breeder chickens, these products are used if there has been an outbreak of salmonella infection. Birds are first treated with an appropriate antibiotic, after which they are given the "unidentified culture" to prevent re-infection.

3. At times of stress, these products are given to increase the numbers of "good" bacteria that, in turn, will increase the acidity of the intestines, and thereby decrease the risk of an outbreak of intestinal disease.

For pigeons, you can buy commercial products that contain "friendly" bacteria said to be derived from pigeons, or you can use common yogurt that contains friendly bacteria.

These products are alive, ie, they contain live bacteria, and in order to be useful, the bacteria have to remain alive. So, exposure to sunlight or heat during periods of storage will adversely affect these cultures. They must not be mixed in water that contains chlorine, iodine or other disinfectants, simply because these chemicals will kill the desirable bacteria in the culture. Similarly, they can't be used when there are antibiotics in the water, for the same reason.

To further assist the "friendly" bacteria, you can add some whey (from a milk or cheese-producing company) to the drinking water. Whey contains the sugar lactose which these bacteria use a source of food, and from which they produce lactic acid to acidify the intestines. The additional use of acidifying substances like cider vinegar was mentioned earlier.

On an equally practical level, some fanciers feed their birds, especially youngsters, right on the floor of the loft, so that they pick up cultures of normal "friendly" bacteria from their own environment. A similar approach would be to sprinkle fresh droppings from old birds that are known to be clean, on the floor of the young bird loft. There are obvious risks to these procedures, especially if the weather is damp and the floor tends to stay wet: in the dampness, worm eggs and coccidia are able to reach a stage of development that allows them to infect the youngsters. Disease-producing bacteria, including E. coli and paratyphoid organisms, can also begin to multiply in the billions in damp conditions and become a threat to the youngsters.

3. Respiratory Disease.

Respiratory diseases, including one-eyed colds in pigeons, are associated with various bacteria, Mycoplasma spp., Chlamydia spp., and viruses, including herpesvirus. Other important factor in the development of respiratory disease is poor ventilation, and by extension, crowding. Never mind the "overcrowding" we read so much about all the time. Do those who talk so constantly about overcrowding mean that if overcrowding is very bad, crowding is better or just a little less bad?? Avoid crowding, and NEVER allow overcrowding!! The stresses and social tensions associated with crowding, plus the reduced amount of oxygen available to birds in a poorly ventilated loft, can set up birds for any number of diseases and problems, including fly-aways. The old saying that there should be a perch for every bird, but there should not be a bird for every perch, is well worth heeding.

Respiratory signs can vary from a very slight "teary" appearance of the eyes to marked inflammation and fluid discharge from the eyes, accompanied by sneezing, head-shaking, a rattling sound in the trachea (windpipe), dirty, greasy cere, the discharge of mucus from the nostrils ("snots"), and excess mucus in the throat. In these cases birds don't tolerate exercise very well, and may actually refuse to fly. Be aware that birds with excess stringy, even dirty mucus in the mouth and throat may not have respiratory disease at all, but instead may be affected by increasing numbers of canker organisms that irritate the tissues and result in an outpouring of protective mucus. In such cases, swabs of the mucus will likely reveal the presence of many canker organisms.

Viruses (eg., herpes) that may be involved in respiratory disease problems aren't affected by antibiotics, so the use of these products is to treat the chlamydia, mycoplasma and bacteria that may be contributing to the problem. A combination of a full dose of a tetracycline-based antibiotic such as Terramycin (oxytetracycline), plus a full dose of Tylan in drinking water is an excellent treatment for respiratory disease. A veterinary friend who is also an excellent fancier, finds that Aureomycin (chlortetracycline) plus Tylan together seem to be an even better treatment. A recommendation for Aureomycin and Terramycin is 4 1/2 level teaspoons of the regular strength products (or 2 1/2 level teaspoons of the concentrated products) per 4.55 litres for 7-14 days. When combined with Tylan (tylosin) at 1800 - 3600 mg per 4.55 litres of water for 7-14 days, these drugs are a powerful treatment against respiratory disease.

Doxycycline, another powerful drug in the same family as Terramycin and Aureomycin (the three of them are called tetracyclines), is also highly effective -- if you can get it. When using any member of the tetracycline group, you should ideally remove the grit and oyster shell, because the calcium in grit and oyster shell ties up these antibiotics and prevents the birds from making good use of them.

Combined with these treatments is the absolute necessity to improve the ventilation and reduce the crowding and social tensions that contribute a significant component to the whole disease process. Treatment alone is just not enough.

4. Worms.

There are two major species of worms that cause problems in pigeons: roundworms (Ascaridia spp.) and threadworms or hairworms (Capillaria spp.). Roundworms live free in the intestines, whereas threadworms bury their heads into the wall of the intestine.

i) Roundworms -- these worms are fairly large, and measure 1 1/2 to 2" or more in length. They are believed to compete with the pigeon for nutrients in the intestines, so in heavy infestations, roundworms can be another cause of "going light" because they absorb nutrients that the pigeon needs. In light infestations, these worms tend to gather in the upper part of the intestines, close to the proventriculus and gizzard. In heavy infestations they spread out along the entire intestinal tract and may even be found in the droppings. In large numbers roundworms can effectively block the intestines, and food has a very difficult time passing through.

Female roundworms lay many thousands of eggs regularly, so it doesn't take long for the loft to become heavily contaminated. Soon after they are passed in droppings, eggs aren't able to cause infection in pigeons, even if they are picked up from the floor and swallowed. The eggs need time -- about 2 weeks -- in damp, cool conditions for a young worm to develop. At this stage, if droppings containing eggs have contaminated feed or grit, or if birds are just picking on the floor and swallow eggs, the young worm hatches in the intestines, and over time, becomes an adult -- and the cycle repeats. If loft conditions are too dry, the thick wall of the eggs protects them from dehydration, and they remain dormant until conditions for development are more favourable. They can live in this way for years if necessary.

The only truly effective way to break the cycle after you have eliminated the adults from the intestines is to clean the loft thoroughly, and then burn all floor surfaces with a controlled flame - used very, very carefully (!!), to prevent a fire. Hot lye (1 small can of Gillett's lye to 5 gallons of very hot water) also works but there is always the risk of alkali burns to yourself or your birds when lye is used. If you use lye, you have to wear protective goggles or a plastic face shield, plus a rubber apron and gloves. All surfaces that the lye has touched have to be well flushed with clean water after the lye has had a chance to act, so that birds are not burned after they are returned to the loft.

Treatments include the old drug piperazine, but it is only 60-80% effective in killing worms in the intestines. According to Dr Marx, Tramisol, Ivomec and Telmintic are still 80-90% effective, even though worm resistance to Ivomec is developing.

ii) Threadworms (Hairworms) -- these worms are very small (up to 1/4 " long) and very thin, so seeing them in the intestines is very difficult, and requires special techniques. Because these worms bury their heads right into the wall of the intestines, they cause tissue damage and irritation that can result in haemorrhage, diarrhoea and loss of weight. Like roundworm eggs, those of the threadworm are not infective when they are passed in droppings, but need about a week in damp, cool conditions for the development of a young worm. Piperazine and Tramisol aren't effective against these worms. The best drugs continue to be Ivomec and Telmintic.

5. Coccidiosis

Coccidiosis is mainly an important infection of youngsters after weaning, likely because their immune system is not yet as fully developed as it will be later. Like worm eggs, the coccidial form (called an oöcyst) that is passed in droppings isn't yet at an infective stage, and requires, cool, damp conditions for development to the infective stage. Depending on the species of coccidia, microscopically, an oöcyst looks very much like a boiled egg cut in half or lengthwise. Under ideal conditions for the species of coccidia involved, the oöcyst undergoes what is called sporulation, to produce, depending on the species of coccidia involved, 4 or 8 banana-shaped structures called merozoites.

If a pigeon picks up a sporulated oöcyst and swallows it, within the intestines, these 4 or 8 structures break out and each one enters a cell where it divides to produce more merozoites, that in turn, break out of the cell and enter more cells. This process of repeatedly entering and breaking out of cells causes in the intestines, a great deal of damage and irritation that results in diarrhoea. At some point, the process just described changes a bit, and the result now is the production of many oöcysts that break out of cells and pass out with the droppings, ready to start the whole cycle again.

In the past, the common treatment of coccidiosis was the use of sulpha drugs, notably Sulmet. One of our modern drugs, also a sulpha-based product, is Vetisulid (sodium sulphachlorpyridazine) which is useful against coccidia and bacterial infections as well. One of the best modern drugs to use is Amprol (Amprolium). Another very effective drug is Baycox. After using Amprol (not while you are using it), give your birds a day or two of a multi-vitamin mix in the drinking water.

6. E. coli Infections

E. coli (short for Escherichia coli) is a very common bacterial organism in the intestines of humans, birds and animals and can be cultured from droppings almost all the time. For this reason, the isolation of this bacterium from a sample of droppings sent to a laboratory should not be surprising. If a culture of droppings reveals many E. coli, it is possible that these increased numbers may signify a problem. If the sample was fresh and held chilled until it reached the laboratory, high numbers of organisms are likely meaningful, especially if there was a related history of illness in the birds the sample came from. However, a high count may mean little if the sample wasn't refrigerated right after collection and wasn't sent chilled to the laboratory. Under conditions of little or no refrigeration, bacteria begin to multiply in the warmth, and can create a false picture of events happening in the birds. So don't read a lot into culture results that show high numbers of E.coli, unless you can eliminate warm shipping conditions, and can tie these high numbers to an illness that is compatible with E. coli infection.

If a post mortem examination and culture of a number of organs from sick birds reveals a high number of E. coli in these organs, these E. coli are likely to be significant in terms of the illness occurring in the birds. Also, if sick birds are vomiting, have mucoid diarrhoea that has an odd odour, such findings are highly suggestive of a significant E. coli problem. E. coli can complicate other diseases by moving in as secondary invaders, a common finding in adenoviral and other infections, for example. Sometimes pathogenic (ie, disease-producing) strains can invade the bloodstream and, like the paratyphoid organism, can result in infections in joints, testes and ovary (which can produce dead-in-shell embryos -- black eggs), "going light", sudden death in youngsters or old birds, etc..

Some of the more useful treatments of E. coli infections include Baytril, amoxicillin, cephalexin, and trimethoprim/sulpha. Vetisulid seems to be much less useful than it used to be, likely because of overuse.

7. Paramyxovirus Infection

This infection is caused by paramyxovirus-1 (PMV-1), an agent that is very closely related to the virus that causes Newcastle disease in chickens -- both are PMV-1 agents. The virus in pigeons is a genetic variant of the virus in chickens. The disease in pigeons seems to have begun in North Africa from which it spread to Mediterranean countries, Europe, the UK, and finally North America. These countries have lived with this disease for several years, and the likelihood is that it isn't going to go away any time soon. It seems to me that it is only a matter of time before this virus reaches the shores of Australia where it will demonstrate its devastating effects in exposed, susceptible pigeons - unless proactive, preventive steps are taken.

Infection with paramyxovirus (PMV) in pigeons often manifests itself in two forms. One of these is the nervous form in which the virus has invaded the central nervous system (brain and spinal cord). The signs of this form of the infection include staggering as though birds are drunk, tremors, a twisted neck with the beak pointing to the ceiling, or paralysis of legs or wings. Fortunately, a number of infected birds will recover if they are able to eat and drink. Some recovered birds may have residual signs of the infection, especially in a mild form of the disease.

The other expression of paramyxovirus infection is the kidney form in which a great deal of fluid is passed through the kidneys. This occurs because the virus causes severe damage to the kidneys and prevents them from concentrating the urine. The result is that the floor of the loft may be awash in fluid. This is not true diarrhoea, because the bulk of the fluid passed is from the kidneys, not from the intestines. Characteristically, a large volume of fluid is passed, with a "snake" of droppings from the intestines in the middle.

PMV infection tends to spread relatively slowly through a loft, a fact that can allow a fancier to act quickly to vaccinate all birds and stop the disease in its tracks. An example. When the some fanciers in western Canada experienced outbreaks of PMV, they immediately vaccinated their birds. Several months later, I spoke personally to some of the fanciers involved in these outbreaks and learned that spread of the disease in their lofts came to a halt within a relatively short time after vaccination, and they haven't had any more problem with PMV. Hence, my belief in vaccinating birds in the face of an outbreak.

Recently, I heard one Aussie fancier say that any bird of his that becomes "crook" is immediately killed. However, this policy won't work when a fancier is faced with PMV infection - more infections will just occur and more "crook" birds will occur - unless the fancier vaccinates in the early stages of the infection. I realise that currently the Australian government will not allow the vaccination of pigeons against PMV - either in imported birds, or those already living in the country. Such a policy, however well informed and well intended, definitely leaves Australian fanciers with a highly suceptible, very vulnerable population of birds that are just ripe to succumb to this infection when it occurs - as I feel it will, inevitably.

Consider this. Because birds imported to Australia are not allowed to be vaccinated against PMV infection, it is entirely possible - and eventually probable - that one or more of these non vaccinated birds will have been exposed to the virus in its country of origin prior to shipment, and is incubating the infection on route to Australia. Because of the long incubation period of this disease (incubation period is the time interval between initial infection and appearance of signs of a disease), such a bird could be released from a quarantine facility, soon after which it develops signs of the disease, and begins to spread virus to other susceptible pigeons. This isn't fantasy, as such a problem actually occurred in Canada, so it is a very real possibility that a similar situation could occur in Australia.

To those who might say that I am scare-mongering, I would reply that I am simply facing reality, having had experience with PMV infection in Canada. The only sure way I know to prevent PMV infection in susceptible pigeons is to take a proactive stance (rather than a too-late reactive stance), and vaccinate them with an appropriate, approved, killed vaccine. Given the large numbers of highly susceptible pigeons in Australia, I would say that infection with this virus is likely have devastating effects on these populations. (As well, in Australia there are many beautiful species of indigenous pigeons and doves that are very likely to be as highly susceptible to this virus as domestic pigeons.) Vaccination of domestic pigeons in Australia seems to me to be a practical answer to the impending dilemma of PMV infection in these susceptible birds. For these reasons, I would urge fanciers and their national organisations to contact their MPs and the federal Minister of Agriculture to request that Australian fanciers be given the right to provide protection for their birds through vaccination against this infection (proactive measures), and to require that imported pigeons be appropriately vaccinated against PMV infection well in advance of shipment.

Note: If vaccination is allowed, avoid the use of the live, water-based LaSota-type vaccines used in domestic poultry as protection against Newcastle disease. They are virtually useless in protecting pigeons against PMV infection and for this reason, they are a complete waste of time and money. You may find that some money-hungry individual will try to convince you that this vaccine is the answer, but don't fall for his arguments.

8. Avian influenza is another viral disease of poultry, and is one that can cause devastating losses in infected domestic chickens. It has caused interruption or cancellation of racing schedules in the USA, because of the fear by federal and state officials that racing and other pigeons could be a source of virus to major poultry operations. However, I mention this disease only because scientific facts show that these fears are groundless.

Several scientific studies (including at least one in this decade) conducted over several years by respected scientists in the USA and Canada have shown that pigeons are not infected by this virus (not even by the North American strains that are most deadly to poultry), that they don't carry it, and that they don't transmit it to domestic poultry. On the other hand, wild waterfowl are intimately associated with a number of strains of the influenza virus, and are likely the major source of virus for the poultry industry. If Australian state or federal authorities are interested, I have a good list of scientific references that show that pigeons are not affected by this virus. I would be more than happy to provide titles and sources of these references for these individuals.

9. Pigeon Pox

This is another viral disease that has posed some problems for fanciers over the years, especially in the summer time when flies and mosquitoes are abundant. The characteristics of the disease are wart-like growths on the side of the beak, nostrils, ceres around the eye and beak, feet and skin (dry pox). Occasionally, it will cause problems inside the mouth (wet pox) and may be confused with canker in this location.

The disease is readily preventable by proper vaccination, which should be done several weeks before training and racing begin. As the vaccine is alive, the idea is to pull a few feathers, usually from the area of the outer thigh, and with the use of the stiff brush provided, rub the brush that has been dipped in vaccine, into the exposed feather follicles. Avoid using the skin of the breast as a vaccination site to prevent any damage to the underlying muscles of flight. If there has been a "take", the early signs are swelling of the empty follicles at the vaccination site, followed in a few days by scabbing of the area. If scabbing doesn't occur, the birds haven't been vaccinated. It is a good idea to examine birds 7-10 days after vaccination to insure that there has been a "take". Vaccination in the face of an outbreak can be effective.

In North America in the past few years, there have been a number of reports from fanciers that in birds apparently vaccinated correctly, there has been no evidence of good immunity. The reasons can be varied. Some suggestions have included: 1) the idea that in the pigeon pox virus, there has been a mutation to a more pathogenic strain, 2) that there has been improper vaccination technique, 3) that there has been improper handling of the vaccine during transport or after it is in use, 4) that a number of outbreaks were related to use of a European vaccine (blue vaccine) that gave no indication of a "take", 5) that some vaccines may have been ineffective, or only minimally effective in producing a "take". On this point, one producer of vaccines has assumed this to be the problem with their vaccine, and have undertaken to examine all of their procedures on the production line to determine if there was a "weak link" in production. They too have wondered about a mutation in the wild virus to produce a strain that vaccines can't currently protect against.

There is no practical treatment of pox. The old treatment of using flowers of sulphur in the grit container is just not effective. The use of iodine on the pox lesions themselves could help to prevent spread of the virus to other birds, but these pox lesions will take just as long to resolve whether you use iodine or nothing at all.

If birds in your loft are infected with pox, DON'T enter your birds in club training tosses, or in club or combine races. Be a responsible flyer. DON'T infect birds in the lofts of other flyers. Keep your infected birds at home, even birds that aren't showing signs of the disease.

10. Adenovirus

In 1995 a new, fatal disease of racing pigeons was described in Belgium. It began in October, 1992 and was characterised by sudden death in pigeons of all ages (note!). There were very few clinical signs in affected birds prior to death -- occasionally, there was fluid, yellow diarrhoea and vomiting. However, the main sign was sudden death which occurred within 24 hours of the onset of illness, with none of the obviously sick birds surviving longer than 48 hours. Antibiotic treatment had no effect on the outcome of this disease. Losses in individual lofts was variable but usually amounted to 30%.

At post mortem examination of these birds, veterinarians found that about 15% had a yellow, pale, swollen liver that exhibited a red sheen as the most characteristic change. Microscopic examination of these livers revealed widespread localized or more diffuse areas of death of this tissue. As well, there were characteristic structures called inclusion bodies in the nuclei of affected liver cells.

Investigation of the field situation showed that, although this illness occurred initially in one age group in 65% of affected lofts, in about 70% of the cases, the disease finally spread to all ages of birds in these lofts. Losses of birds in affected lofts were usually about 30%, but in some cases, reached 100%. The investigators were astounded that in lofts in which these acute deaths occurred, pigeons that did not die remained completely normal, with no sign of clinical illness. Even youngsters in the nest grew normally if they were able to feed themselves or were raised by other pigeons, after their parents had died.

Special examinations of the livers of affected birds by means of an electron microscope determined that the cause was likely an adenovirus (pronounced ADD-enovirus).

The disease reported this year from Belgium is the second known adenovirus-caused condition to affect pigeons. The first one (called Type I) was discovered in 1976, and was associated with disease in young pigeons during the first half of the year, with peak frequency in June. Clinically, in this type, there is watery diarrhoea and weight loss. Intestinal bacteria called E. coli often complicate this adenoviral infection, and results in a more severe diarrhoea, as well as vomiting and occasionally, death. This adenovirus-E. coli combined disease is usually successfully treated with appropriate antibiotics which deal with the E. coli infection. In birds that die from this combined disease, the liver often appears grossly normal, or only mildly affected.

However, microscopically, there are characteristic inclusion bodies of adenoviral infection in cells of the liver (Figure 3 .) Extensive death of liver is not seen in this condition. Gross evidence of enteritis (inflammation of the intestines) is usually present.

By contrast, the adenoviral disease described in Belgium in 1995 (called Type II), causes extensive destruction of the liver, and sudden death of affected birds within 48 hours of the onset of illness. All ages of birds are affected in Type II.

If a number of young birds begin to vomit and have diarrhoea, and are off colour, it would be fair to consider this adenoviral-E.coli combined disease as a good possibility. Further examinations of dead birds by your veterinarian and diagnostic laboratory will help to confirm the diagnosis, and will likely result in a better approach to antibiotic therapy

For some time now, different strains of circoviruses have been known to cause disease in chickens and in psittacine birds (eg., parrots, budgerigars, cockatiels). Since 1986, a third strain of circovirus has been suspected to have caused illness in pigeons, first in Canada, then in Australia in 1989, and in the USA in 1990, where sporadic cases have occurred in

pigeons since that time (Figure4 .)

How are circoviral infections in pigeons recognised? The short answer is -- with difficulty. If case histories of affected birds are examined, it is seen that a wide variety of clinical signs may occur in different birds. For example, the first case in the USA involved a flock of 50 racing pigeons in which 3 to 5 young birds were affected each week. Signs included loss of appetite and dullness, with death occurring in 3-4 days. In another flock, affected birds had diarrhoea, dullness, rapid loss of weight, inability to fly, and death.

In other cases, affected birds developed (variously) breathing difficulties, loss of weight, emaciation, nasal discharge, and pox-like changes on the beak. Affected young pigeons in western Canada developed olive green to chocolate brown, messy gelatinous droppings, weight loss and death in several days. Given all of these different findings, it is difficult to find common patterns of disease as a basis for suspecting a circoviral infection. However, the occurrence of of one or more diseases in young pigeons may well provide the first tell-tale clues that circovirus is active in your birds.

Like many other infections, circovirus infections seem to be most important in young pigeons. Information from the veterinary literature on this subject indicates that infected birds ranged in age from six weeks to one year. Presumably, older birds have an age-related resistance, or have developed solid immunity as the result of earlier infections. In one case that I investigated, only four of 42 young birds died -- yet other birds of similar age in that loft did not develop signs of disease and remained completely healthy, even though there was direct daily contact between sick and normal birds. Both first and second round pigeons were affected.

The main problem with circovirus infections in pigeons and other affected species, seems to be a primary result of their ability to cause massive destruction of cells that direct and co-

ordinate body defences against a variety of other diseases. This is an important point. If body defences are severely weakened or even destroyed by these viruses, it is in the very nature of other disease-producing agents -- viruses, bacteria, moulds, and parasites such as the canker organism -- to take advantage of this weakened situation, and to begin to invade where defences are weakest.

To illustrate this important point, case studies of this disease indicated that pigeons infected by circoviruses had a variety of other infections as well -- for example, those caused by Chlamydia sp. (the cause of a condition called variously, chlamydiosis, or psittacosis when it occurs in psittacine birds, and ornithosis when it occurs in other classes of birds, etc.),

canker organisms, adenovirus, paramyxovirus, poxvirus, herpesvirus, moulds, as well as infections caused by E. coli and Salmonella (paratyphoid) species of bacteria. This wide range of secondary and tertiary infections in pigeons known to be infected by circovirus points up the highly important role of this viral agent firstly in destroying defensive cells in the body, and secondly, in allowing a wide variety of other disease-producing agents to invade the tissues.

It is quite possible, and indeed likely, that as circoviruses spread among our birds, we will see more outbreaks of other diseases, and these happenings may be our first clue that circoviruses are operating in our flocks. Spread of this virus -- and many other types of viruses of course -- is virtually an iron-clad guarantee because of the nature of our sport. Contact in pigeon trailers and transporters, at shows, sales, the introduction of new birds to our lofts, etc., are all excellent means of spreading a variety of infectious disease-causing agents, including circoviruses.

Is there any way at present to prevent circoviral infections in our birds? The practical answer seems to be no, simply because of what we do in the sport -- train and race our

birds together, and exchange or purchase birds from a variety of sources within and outside our own areas. Given these circumstances, we likely have to accept the inevitability of circoviral infections in our birds, much as we have had to with paramyxovirus, herpesvirus and adenovirus infections.

We can hope that early exposure of our birds to this agent will immunise them sufficiently to prevent serious problems with the secondary diseases that may well herald the existence of circoviral infections in our birds in the first place. We can also act vigourously and quickly to obtain veterinary diagnoses and information on treatment of these other conditions -- especially canker, and E. coli and Salmonella sp. infections when they occur. If you submit sick birds to your veterinarian or veterinary diagnostic laboratory, and you have had one or more recent outbreaks of the same or different diseases, especially in young birds, be sure to ask the staff to undertake a microscopic (histological) examination of a variety of tissues, including the very important spleen and bursa of Fabricius, as well as other lymphoid tissues, to search for "footprints" of circoviral infection.

It is in these tissues that this virus causes the most serious changes, and it is here that evidence of circoviral infection can best be demonstrated. The disease produces characteristic "inclusion bodies" (clusters of millions of viral particles) in infected cells of the organs just mentioned. These inclusions, which appear to contain large aggregations of viral particles, have a blue-black grape-cluster appearance when tissues are stained with the commonly used H and E stain (Figure 1). Your veterinarian or laboratory personnel will understand the term "H and E". Electron microscopic examination of these inclusion bodies will further reveal the characteristic appearance of the viral particles they contain.

Circoviral infections are not likely to disappear in the near future, and as the virus spreads, there will likely be more cases of the secondary diseases mentioned earlier to indicate that

circovirus is active in a number of lofts. Forewarned is forearmed. We can help our own situations by getting accurate veterinary and laboratory diagnoses of circoviral infections and the diseases that follow it. Vigourous and rapid treatment of these secondary diseases are likely to be our main defence against losses triggered by infection with circovirus.

Even now, this infection may be much more widespread among our birds than we realise, firstly, simply because of the widespread bird-to-bird and loft-to-loft contact among racing

pigeons, and secondly, because of the number and variety of outbreaks of other infectious diseases that occur in many flocks. In other words, we may have many more outbreaks of diseases such as paratyphoid, canker, adenoviral disease etc. among pigeons because of the masked or hidden activity of circoviruses.

Most viral diseases in themselves are simply not treatable, and it certainly seems that circoviral infections will fall into the same category. Treating the secondary and tertiary bacterial and parasitic diseases unleashed by the circoviral damage to the immune system is about all that can be accomplished at the moment. Even so, treating the current disease condition, whether it is canker, paratyphoid or E. coli infections etc., is a highly important approach, to allow birds to survive long enough for the damaged immune system to repair or partially repair itself.