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Gordon A. Chalmers, DVM
gacdvm@telus.net
Lethbridge,
Alberta, Canada.
An Introduction to Gordon Chalmers
I trained in veterinary medicine at the Ontario Veterinary College, University of Toronto, from which I graduated in 1961.
I entered private veterinary practice as an assistant to practitioner for about a year, after which I joined the Alberta gov't
(Dep't of Agriculture) in its veterinary diagnostic service, conducting post mortem examinations on domestic poultry and other
livestock, wildlife, fish and zoo animals....
Later on, I took specialty training in diagnostic pathology at the Western College of Veterinary Medicine, University of Saskatchewan
in western Canada. I returned to the Alberta Dep't of Agriculture, but several years later, I also took another year of training
in diagnostic pathology at the Western College. During my career, I have authored or co-authored about 40 scientific papers
on domestic animals, poultry, aviary birds, wildlife, and yes, even racing pigeons! I have been involved with racing pigeons
for much of my life. I have been without them for only brief periods of time (veterinary education, illness and death of parents)
so they have been pretty much a part of my life for all my years up to the present time. Like many other fanciers, I have
had seasons ranging, in my own terms, from outstanding to mediocre and even very poor.
My most satisfying accomplishments with racing pigeons followed my purchase in 1973 of one outstanding Sion-Stassart-Bastin
stock hen, whose offspring flew extremely well to 560 miles. To date, I have never owned a better pigeon. That stroke of luck,
together with the purchase of the most important book I have ever read to the present time on the natural system, Major Neilson
Hutton's "Pigeon Racing. Win With Olympic", were the keys to the racing successes of my birds for the next 15 or
more years. At present, I fly a team of Janssen, van Loon and Irish Putman crosses.
I race in a small club of 10-12 members, on the north road. Because of the distances between cities, fed or combine racing
just isn't practical or most often, even possible. My present team of birds includes mainly Janssens of several lines, the
older lines of Van Loons, and a few crosses of Irish Putmans - the latter are grand at the distance. I have presented a number
of seminars in the USA and Canada to interested fanciers, on the topics of racing, muscle and fuel requirements, along with
publications on the same topics, plus several on disease updates, in current British, American and Australian racing pigeon
magazines, and the yearbook of the Canadian RP Union.
I am presently retired, but continue to do some consultation work with fish for the Alberta Dep't of Agriculture and private
industry, search out disease information on racing pigeons, along with my current major interest, studies on muscle and fuel
for racing. Finally, I try to share this information with fellow fanciers by writing my findings in articles for racing pigeon
magazines and the yearbook of the Canadian RP Union.
GARLIC:
Some Facts for the Fancier
Gordon A. Chalmers, DVM
Lethbridge, Alberta Email: gacdvm@telus.net
Garlic, whose scientific name is Allium sativum,
is a common plant used worldwide for food. Since ancient times, garlic has been used for a variety of human ailments and problems,
and even magical properties to ward off evil spirits have been attributed to garlic. In fact, it was once considered to be
absolutely essential in warding off vampires! In more modern times, the use of garlic has been a topic of research, especially
in human medicine. Garlic has been reported to have insecticidal, antibacterial, antifungal, and anti-cancer properties, as
well as those of lowering blood sugar and fat levels, and reducing the dangerous plaques that bring about plugging of blood
vessels that lead to heart attacks and strokes in humans. It seems that popular interest is greatest in Germany where garlic
preparations for humans account for the largest sales of all over-the-counter drugs. How garlic affects racing pigeons is
speculative, but here are some general facts gleaned about this plant from a few human medical and nutritional publications.
The
principal, active agent of garlic is allicin, a sulfur-containing compound, which, with its breakdown products, produces the
characteristic odor. The odor is related to the presence of sulfur. When the cloves are crushed, allicin is formed by the
action of enzymes on a pre-existing chemical known as alliin. Other biologically active compounds related to allicin, such
as ajoene, may be extracted from garlic as well. The positive effects of fresh cloves of garlic seem fairly certain, whereas
information for modern commercial preparations in general is not very convincing, to say the least. One reason for the difficulty
of showing the effectiveness of garlic is that many active chemical compounds in the cloves may be lost during processing
--and this is a major problem with commercial products. For example, carefully dried sliced cloves seem to retain their potency,
but extracts or oils prepared by steam distillation or organic solvents may have little activity. Cold-aged extracts have
a reduced odor and may retain more of the activity of garlic. Allicin is known to break down during steam distillation for
the production of the volatile oils used in many garlic preparations. As well, the alliin content of natural garlic can vary
10-fold.
There is also confusion about the issue of "odorless" garlic preparations. Some of them have no aroma, but
neither do they contain any active ingredient. Some active preparations may not have an odor, but if allicin is released when
the product is eaten, there is a very good chance that there will be a detectable aroma -- and it is the aroma that is one
of the problems. Potency of garlic appears to depend on pungency, - that is, odor. Once garlic is dried into odor-free powders
or pills, it loses some of the properties that may make it useful in health!
Distilling all of the information about
garlic to a few simple statements is very difficult to do. However, it seems that, whatever the basis for its use, at the
moment, fresh cloves are the superior source for the important ingredients of garlic. Other commercial preparations such as
powders or oils may or may not be useful, since the processing procedures may dilute or eliminate the effective compounds.
If you have a choice then -- and most of us do -- buy cloves of garlic from your grocery store and prepare fresh solutions
as you need them. Given the "touchy" nature of the important, active compounds in garlic, it seems likely that heating or
boiling crushed cloves above 60oC (140oF) (remember that water boils at 100oC (212oF), likely results in a major loss of key
ingredients. On the basis of this information, it is logical that home preparations of solutions of garlic should not be heated,
in order to retain the important compounds in the soution. Be aware that allicin is readily converted to a more volatile compound
call diallyl disulfide -- which means that its effects can be transient.
Allicin is known to have antibacterial properties
and has been said to be effective in concentrations as low as 1:125,000 (that is, one part allicin to 125,000 parts water).
When compared with penicillin, allicin is said to have an activity that is about 1% of the activity of penicillin. Garlic
inhibits the growth of, or kills, about two dozen kinds of bacteria (including Staphylococcus and Salmonella spp.), and at
least 60 types of fungi and yeasts. Allicin appears to be the major chemical responsible for this effect. So if the aroma
is destroyed by cooking or processing, and allicin is associated with the odor, garlic may lose its ability to fight bacteria,
mold and yeasts.
In one recent study, researchers looked at the ability of garlic to kill the organism causing tuberculosis.
They added an allicin-rich garlic extract to 30 strains of tuberculosis-causing bacteria growing in test tubes. A month later,
the garlic had done critical damage to all 30 cultures. The trace minerals selenium and germanium are two constituents of
Japanese garlic, and these minerals may have some effect by their activity firstly, as antioxidants, that is, substances that
protect cells and tissues from the damaging effects of peroxides in the body.
Secondly they are important in the normal
development of the immune system, and thirdly, they may have good activity as anti-cancer agents. Selenium itself has been
shown to have a broad spectrum of anti-cancer activity in rats, for example.
On the other side of the coin, many cases
of allergic reactions to garlic are known to occur in humans. Reactions such as dermatitis (inflammation of the skin) and
asthma are reported. One investigator found that the maximum tolerable dose of fresh aqueous extract (i.e. extracted into
a water-based solution) in humans to be 25 cc (slightly under one ounce). Amounts greater than this caused severe burning
sensations in the esophagus (gullet) and stomach, as well as vomiting.
Some compounds extracted from garlic are similarly
irritating to tissues in the mouth of humans. A possible benefit of garlic or its compounds may be its ability to increase
mechanisms for eliminating substances such as cancer-producing agents. In some studies, garlic has been shown to have a stimulating
effect on certain enzymes that are known to be effective in removing toxic (poisonous) substances from the body. These substances
can damage body organs, and even lead to cancerous changes, so garlic may well provide some measure of protection.
In
a laboratory study for example, mice were fed diallyl sulfide obtained from garlic, prior to being exposed to a cancer-causing
chemical. Mice fed the garlic-derived compound had 74% fewer cancers of the colon (large intestine) than those that did not
receive the garlic compound. It has also been shown in animals that the sulfide compounds of garlic can inhibit the development
of cancer of the lung, large intestine, and esophagus. Unfortunately, there is no solid evidence that garlic can protect humans
from cancer. This may be because it doesn't protect, or because few good studies have been done in humans.
The question
about whether garlic is good for human hearts can't be answered yet. It is simply too early to tell. However, preliminary
studies in humans and animals suggest that garlic may lower levels of artery-clogging fats such as LDL ("bad") cholesterol,
and raise levels of HDL ("good") cholesterol. In rabbits and rats fed raw garlic or garlic oil, LDL cholesterol levels dropped
and HDL cholesterol levels rose. The catch is that the amounts used were equivalent to 14 to 230 cloves per day for a human!
Obviously it would be very difficult to stand too close to such a person! There may be other positive effects for blood vessels.
Garlic appears to increase the time it takes blood to clot, and may help to dissolve clots that have already formed. Obviously
one bad effect would be the failure to allow the blood to clot in individuals also on other drugs that are used for the same
purpose -- in other words, bleeding could occur when garlic and certain other drugs are used together. Much, much more work
has to be done to evaluate the effect of garlic on human and animal health.
Now what about the use of garlic in racing
pigeons? It is a popular, widely used product, but solid, scientific information on its effects in pigeons seems to be scarce.
Everything from cloves of garlic to powders, pills and oils are available in health food stores, grocery stores and by companies
selling products for pigeons. Are there any real benefits, or are the "benefits" in the eye of the beholder, i.e. the fancier
who uses garlic products? Everyone seems to have an opinion, but are there many facts? Little scientific information for racing
pigeons seems to be readily available, but it should be possible to extrapolate information from work done in humans and laboratory
animals to pigeons.
Firstly (and foremostly), logic based on a number of studies, says that the very best source of
the good effects of garlic is fresh cloves of garlic. Manufacturing procedures in the preparation of garlic powders, liquids
and oils can vary onsiderably, and since important, active compounds in garlic can be lost very easily when garlic is processed
to produce these liquids and powders, etc., it seems best to avoid these products as they may contain few, if any, of the
useful compounds in garlic. Further, it is best to crush cloves of garlic, and add them directly to drinking water for pigeons,
rather than heating or boiling them, to avoid losing a number of key chemicals in the cloves. Remember that heating garlic
cloves above 60oC (140oF) can cause the loss of odor and medicinal properties.
Secondly, garlic may provide a temporary
antibiotic effect on disease-producing bacteria, fungi and yeasts, both in the digestive tract and body tissues, by reducing
their numbers during the period that it is in the drinking water. Thirdly, the trace minerals selenium and germanium present
in garlic may give a boost to the immune system of pigeons, to increase their ability to fight disease-producing organisms
of many kinds. In domestic livestock, selenium is known to be important in the normal development of the immune system while
the animal is growing in the uterus. A deficiency of selenium and Vitamin E has a definite adverse effect, because in such
deficiencies, the development of the immune system is retarded. As a result, the newborn animal or bird may be completely
or severely restricted from protecting itself against invading organisms of all kinds.
Fourthly, although dissolving
blood clots (the cause of heart attacks and strokes in humans) or preventing their formation in the arteries of humans is
important in human medicine, it is known that racing pigeons are highly resistant to the buildup of fatty substances in their
arteries.
In humans, these fatty substances may clog blood vessels or they may induce the formation of a clot at the
point where the vessel is narrowed by the fatty deposits, and result in a heart attack or stroke. In contrast to racing pigeons,
some meat-producing breeds of pigeons are very susceptible to a buildup of fatty substances in their vessels. So garlic might
be of benefit to meat varieties of pigeons, but as racing pigeons are highly resistant to this type of buildup, the benefit
might not be so great in the blood vessels of racing pigeons.
Fifthly, garlic as a de-toxifying agent could have a
role as a "blood purifier" or a "tissue purifier", so to speak -- whatever these phrases may mean, since they can and do cloak
a great deal of the ignorance we all share on this subject. Both are meaningless expressions that really don't explain anything,
but they are used commonly in the mystique of pigeon racing! That aside, there are indications that chemical compounds in
garlic may assist the body to de-toxify, neutralize or eliminate noxious substances. In pigeons, the use of garlic after a
race may assist the so-called "depurative" diets -- whatever that might mean -- in restoring a bird to normal racing condition.
Whether lactic acidosis is a real problem in returned racers is still debatable, in my opinion. Because fat is unquestionably
the major fuel for racing, and because the burning of fat for energy by racing birds is an aerobic process in the body, lactic
acid-- which results when glycogen is used as fuel in an anaerobic process -- should not be produced, at least in any great
amount. Braking and landing at the end of a race are very likely anaerobic processes, but the amount of lactic acid produced
from such rapidly occurring events should be miniscule.
In theory, if it could be shown that birds actually sprint
the last few miles of a race, much as a human marathon runner might sprint the last 100 yards or so, then there could be a
good basis for believing that lactic acid -- one of the so-called "impurities" in the blood -- is produced, and that it needs
to be eliminated. Lactic acid is known to be produced in human distance runners who sprint the last leg of a race. However,
in most cases, usually a 20 minute "cool-down" walk will effectively "burn off" or eliminate the lactic acid from the system.
It is known that pigeons that are not exercised reasonably soon after a long grueling race may develop marked swelling of
the breast muscles that become hard and board-like. The birds become "tied up" and have difficulty flying from the floor to
the lowest perches or nest boxes. Given this knowledge, it is possible, and indeed likely, that lactic acidosis is involved
in such situations and that early workouts after a race would eliminate this problem. It is also possible that the use of
crushed garlic cloves in drinking water at this time might add some extra benefit in allowing the liver and other organs to
metabolize lactic acid and other compounds, and to help restore the birds to normal racing condition. I am aware that there
are certain claims by fanciers about the use of garlic in dealing with problems in the respiratory (breathing) system of pigeons.
Unfortunately, there was just nothing in the literature that was available to me to indicate that garlic was useful in dealing
with the sinuses, trachea (windpipe) or lungs. This is not to say that garlic isn't useful in these organs -- it's just that
I didn't read any reference to the effects of garlic on the respiratory system.
Dosages of garlic for pigeons are
difficult to come by, particularly since there is such variabliity in the amount of the key chemical, alliin, (which is converted
to the active compound allicin), in garlic cloves.
Garlic in racing pigeons remains quite an enigma, and as fanciers,
many of us use it without really knowing why, but our ignorance is shared by many people, including the human and veterinary
medical communities, who have only tantalizing bits of information to suggest that there may be a number of positive effects
from the use of garlic.
Certainly, as indicated earlier in this article, studies in laboratory animals and humans
suggest a number of desirable effects from the use of garlic. Whether these effects apply directly to racing pigeons is just
not known at this time. However, present evidence from human and laboratory animal work, and the empirical experience of many
fanciers, suggest that, when used judiciously, crushed cloves of garlic, used in drinking water, may be a useful product in
the loft throughout the year, but especially during rearing and the racing season. At present, garlic-based oils, powders
and pills are likely much less useful. Possibly newer developments in extracting the active principles of garlic may get around
the present problems associated with current methods. Until these problems are solved, fresh cloves of garlic from the grocery
store are still the best source of the medicinal properties of garlic. I hope that this sketchy outline of the potential value
of garlic, and some of its risks, may stimulate more controlled research on its value (or lack of) in racing pigeons. There
is much to learn! This article merely scratches the surface.
Gordon Chalmers
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.
3) PARATYPHOID. The paratyphoid organism found in pigeons is usually, but not always, Salmonella typhimurium
variety copenhagen. In fact, in the experience of Dr Gerry Dorrenstein of Holland, 94% of the strains of paratyphoid organisms
his group has recovered from pigeons, are variety copenhagen. This variety seems to be almost specific for pigeons, although
occasionally, it has been found to cause disease in chickens. Like other birds and animals, most pigeons exposed to paratyphoid
infection recover completely, either through treatment or natural defensive mechanisms, but as in the case of other species
of birds and animals, the occasional bird is unable to clear the infection, and becomes a permanent carrier. As Dr Dorrenstein
points out, it is still not known just where the paratyphoid organisms hide in the body of a carrier, but he suggests that
this hiding place could be within certain patrolling defensive cells called macrophages where they are protected from the
immune system. (Note: "macro"means "large"; "phage" is from the Greek word "phagein", meaning "to eat"-- hence, these are
large, mobile defensive cells that engulf foreign material, such as invading bacteria, parasites, yeasts etc..) It is obvious
that not all engulfed foreign invaders are killed by these large cells, but in some way, the invaders remain alive and isolated
within the cells that engulfed them, and here they are protected from other defensive mechanisms in the body. As a result,
during periods of stress, the immune system becomes depressed and less vigilant, as a result of which, the paratyphoid organisms
can escape from their hidden locations. Once they have escaped, they begin to multiply and then to be shed in droppings from
which they are readily spread to other susceptible birds in the loft. In my experience, variety copenhagen can be sensitive
to an unusually wide variety of antibiotics, except in cases in which fanciers have misused these products and have induced
antibiotic resistance in these organisms by underdosing the birds in the first place, or by treating for a shorter time than
recommended, or both. For this reason, it is often practical to have laboratory tests run to determine the most suitable antibiotics
to use. Treatment of E. coli and paratyphoid infections is best managed through laboratory assessments of antibiotic-sensitivity
tests to choose the most effective antibiotic or other anti- bacterial product. Given the general misuse of anti-bacterial
products, in some cases these organisms may have developed some level of resistance to antibiotics -- hence the value of laboratory
cultures and antibiotic-sensitivity examinations to ensure use of the most effective product. According to Dr David Marx of
Oklahoma, USA, all of his isolations of paratyphoid organisms from pigeons continue to be sensitive to Baytril (enrofloxacin),
with more than 90% of these isolations also sensitive to Amoxicillin and Cephalexin. By contrast, Dr Paul Miller of Pennsylvania,
USA, reports that his laboratory has isolated some strains of paratyphoid organisms that have developed a great deal of resistance
to antibiotics, and that only Baytril seems to be effective in treating these infections. This information points up, once
again, the value of laboratory cultures and an accompanying antibiotic sensitivity examination. In general, Salmonella
species are notorious for their ability to transfer from one species of animal to another. However, in the case of variety
copenhagen, it seldom ever transfers to other species, and this includes humans. So, in general, the fancier who is experiencing
an outbreak of paratyphoid infection in his birds doesn't have to be overly concerned that he will contract the infection
himself, however individuals whose immune system is weakened or damaged should take extra precautions. However, for the sake
of general safety, fanciers should take normal precautions with sanitation and personal cleanliness while working with an
infected flock. As an advocate of the use of friendly bacteria, also called probiotics, and associated products for a more
natural approach in attempting to prevent E. coli and paratyphoid infections in our birds, I have noted that some commercial
supply houses are offering products containing the sugar lactose to aid in preventing paratyphoid infections in particular.
I certainly support the use of such products and others, in the fight against paratyphoid organisms, but I would offer a few
words of caution on the use of lactose when fanciers are dealing with, or trying to prevent, problems caused by E. coli, and
even paratyphoid. To explain in a bit more detail, friendly bacteria such as those in yogurt or in commercially available
probiotics, usually include Lactobacillus spp., along with certain species of Streptococcus, sometimes called Enterococcus,
etc.. In the USA, commercial products such as PrimaLac and Benebac, among others, are available. No doubt, similar products
are available in other countries around the world as well. Some of these products have been developed specifically for turkeys
as well as for egg-producing and broiler strains of chickens. Dr Gary Davis of North Carolina State University, USA, has done
a great deal of research on the probiotic called PrimaLac in quail, pheasants, domestic ducks, turkeys and laying hens. He
reports that his results have been very positive, with the most significant effects being improvements in livability, egg
size, body weight gains and immunity. The poultry grade of PrimaLac is available from Bob Adams of Star Labs (Email address
: bobadams@siteone.net. Certainly, the best source of these bacteria for pigeons would be those derived from normal,
healthy pigeons, if such products are commercially available. However, PrimaLac seems very promising indeed, especially because
of the range of positive effects found by Dr Davis in several species of birds. It seems likely that pigeons would benefit
similarly -- in fact, a colleague of Dr Davis, Dr Mike Wineland, has been using this probiotic on his own pigeons, and swears
by it. The organisms in all of these products are believed to have at least two mechanisms of operation in the intestines.
Firstly, they can multiply to very high numbers of organisms that form a protective physical barrier that may be up to 12
or more organisms deep, lining the inner surface of the intestines. Secondly, in the low levels of oxygen in which these bacteria
live in the intestines, they produce and release into their environment, lactic acid which of course shifts conditions in
the intestines to the acid side of neutral. (As an aside, it is my understanding that, in some countries such as the USA at
least, two basic kinds of yogurt are available, one a killed product, and the other containing live cultures of bacteria. Obviously,
the product containing live cultures of bacteria is the one to choose. Check the label of the product you buy. As well, remember
that because these products contain live bacteria, you must not combine them with antibiotics or any disinfectant, both of
which will kill the bacteria you want to use in your birds.) Now, E. coli and paratyphoid organisms much prefer to live
and reproduce in slightly alkaline conditions, whereas in a hostile acidic environment, their numbers can drop drastically
(in some studies, up to 97%). In promoting the use of such products, where practical, to reduce the heavy reliance on antibiotics
to solve health problems in pigeons, I have been advocating not only the use of probiotics and a small amount of apple cider
vinegar (5-10 cc per litre, or 2 tablespoons per US gallon [4 litres] of drinking water, as suggested by Dr Colin Walker)
to help acidify intestinal contents, and thereby create conditions that are hostile to the survival of E.coli and paratyphoid
bacteria. While I visited Australia last year, I noted that one Sydney- based company had produced for use in pigeons, a powder
containing a mix of organic acids that also would be ideal for this purpose. I am sure that other equally useful products
exist also. As well, in dealing with paratyphoid infections, I have also suggested the addition of some lactose to the
drinkers, as a source of nutrient for friendly bacteria in their production of lactic acid. Lactose is the chief sugar found
in cow's milk, and is available as whey powder from health food stores, cheese and milk factories, livestock feed companies,
and commercial pigeon supply houses. As noted by Dr Paul Miller, one problem with the use of lactose is that birds lack the
enzyme lactase, and so are unable to break down and utilise the lactose themselves. The presence of this lactose in the intestine
can draw fluids from the bloodstream into the intestine, and may result in diarrhoea and dehydration that can add to that
caused by the concurrent paratyphoid infection. Fortunately, paratyphoid organisms themselves aren't able to ferment lactose
either, which means that they are unable to use this sugar as a nutrient in their life processes. Equally fortunate for us
is the fact that the friendly species of bacteria mentioned earlier certainly will use lactose as a nutrient in their production
of lactic acid. Now here is the fly in the ointment, so to speak. It is important to understand that, although paratyphoid
organisms are unable to ferment lactose, E. coli on the other hand are known to be lactose fermenters, that is, they actually
use lactose as a nutrient in their life processes. For this reason then, it is my opinion that the use of lactose when E.
coli infections are occurring should be avoided because this sugar simply aids these organisms to thrive and multiply in great
numbers. For this reason, I would NOT recommend that lactose be used in drinkers when birds are affected with adenovirus +
E. coli infections, or to help prevent E. coli problems. Yes, use lactose along with probiotics and organic acids, etc., to
help prevent paratyphoid infections, but avoid the use of lactose when you are dealing with or trying to prevent E. coli problems. Summary 1)
To treat ongoing E.coli and paratyphoid infections, use an appropriate antibiotic or other anti-bacterial product, preferably
one selected through antibiotic-sensitivity testing by a laboratory, and at full dosage for the full recommended period of
time. 2) In an attempt to prevent these infections in future, once the original infection has been treated effectively
with the appropriate antibiotic, you can add to the drinking water, probiotics such as yogurt and/or other commercially available
live products, and even apple cider vinegar or other organic acids like citric acid from lemons or commercially available
sources, to help create in the intestines, a physical barrier of friendly bacteria, plus acidic conditions, both of which
are hostile to E. coli and paratyphoid organisms. It is my understanding that, in order it acquire a good, viable population
of friendly bacteria in the digestive system, often takes a number of days. As a result, I usually recommend the use of probiotics
for 7-10 days at a stretch, repeating at intervals, especially throughout the breeding and racing seasons. When attempting
to prevent paratyphoid infections in the first place, or after infected birds have been treated with the correct antibiotic,
at this time, you can add to the drinkers, lactose and apple cider vinegar, or other organic acids. 3) The use of the sugar
lactose will aid friendly bacteria in their own life processes, including the production of lactic acid, in an attempt to
prevent paratyphoid infections. Although it is readily used as a nutrient by friendly bacteria, lactose is NOT fermented by
paratyphoid organisms, so it doesn't aid the growth of these bacteria. For this reason, its use along with friendly bacteria
in probiotics in attempting to prevent paratyphoid infections may be helpful. Lactose should NOT be given either during the
course of E. coli infections, or when attempting to prevent infection by these bacteria, because of the fact that E.coli organisms
actually use lactose in their life processes. There is no point in helping these bacteria to continue causing problems in
our youngsters. Certainly, to try to prevent E. coli problems, use yogurt and/or other sources of friendly bacteria, as well
as products such as apple cider vinegar, etc. to help acidify intestinal contents, but definitely avoid the use of lactose
when E. coli are involved in a disease process. 4) Be aware that the use of lactose in birds may itself cause some diarrhoea
and dehydration.
Gordon Chalmers
"Coccidia
and Racing Performance - A Small Survey"
Gordon A.
Chalmers, DVM Lethbridge, Alberta Email: gacdvm@telus.net
During the summer of 2001,
I received a basic question from the editor of the British Homing World about the amount of actual evidence that exists with
regard to the effects of disease and performance in racing pigeons. In that context, he also asked..... "How much research
has actually been carried out by the veterinary profession on the health of birds in top performing lofts in relation to the
actual performance of individual birds? For example, has much testing been done on pigeons just prior to basketing for a race,
with these results then being studied alongside the actual performance of the birds?"
This was, really, a very interesting,
incisive question, and one for which I am embarrassed to say, I had no ready answer. Accordingly, over the next few weeks,
I contacted quite a number of my veterinary colleagues and some knowledgeable fanciers here in North America, as well as some
in South Africa, Australia, the UK and Europe. The uniform answer to this question was that no one who responded to my inquiry
was aware that the kind of veterinary study mentioned had ever been carried out or published. It would therefore seem that
such a study has yet to be done and published, at least by the veterinary profession. In the light of these questions, I also
mentioned to my veterinary colleagues and the fanciers I contacted, the example of an oocyst count of 96,000 found in one
British fancier's birds after they had flown poorly from a 700-mile race. (Oocysts are the egg-like stage of the coccidial
life cycle found in droppings. They are what fanciers refer to as "cocci counts". To me, at the microscopic level, oocysts
very much resemble hard-boiled eggs that have been cut in cross section or lengthwise, depending on the species of coccidia
involved.) The following information is taken from replies from individuals who responded, and from one published report.
On
the question of coccidia in pigeons, one veterinary reference from Britain (Wallis, AS. 1991. Common conditions of domestic
pigeons. In Practice, pps 96-100) indicated that "a count that was under 3,000 oocysts per gram (opg) of droppings was considered
to be normal, with no expected response to treatment. A count of 3,000-20,000 opg was considered to be moderate, with treatment
often providing a significant improvement in performance. A count of 20,000-50,000 opg was considered to be severe, with improvement
in condition and performance as a response to treatment. A count of greater than 50,000 opg was considered to be very severe,
with marked improvement in the associated clinical picture following treatment. However, Wallis also made the point that counts
greater than 100,000 opg had been seen occasionally, without evidence of any observable abnormality in the birds shedding
these large numbers of oocysts.
On the topic of threadworm (Capillaria sp.) problems, this same reference indicated
that infestations with this species of worm is always considered to be significant. The following findings and interpretations
were presented:
Egg counts up to 1,000 eggs per gram (epg) of droppings were considered to be normal, with little clinical
response to treatment, although eggs were no longer shed in droppings. A count of 1,000-5,000 epg was considered to be severe,
with improved condition and performance to be expected following treatment. A count over 5,000 was considered to be very severe,
with marked improvement following treatment."
Once again, in this same reference, "roundworm eggs were classified in
the same way as those for the threadworm. Disease from roundworms was much less severe than that caused by threadworms, although
heavy infestations often lead to blockage of the intestines and to a chronically enlarged liver which may well have had a
fatal outcome, even though the worms were removed successfully."
Another
prominent, very experienced British veterinarian, Frank DW Harper, commented on coccidia as follows: "
- 1. Is coccidiosis ever a primary
disease in pigeons?
- 2. A high oocyst count (25,000+?)
may well be evidence of heavy infection and therefore a cause of stress, but my perspective is that it is more likely to be
a result of stress (concurrent disease, environment, etc.. Look how the counts vary from section to section [....of the loft].
It is easy to identify from a group of samples, those birds housed in the north-east corner [....of the loft]). Specific treatment
gives a transient improvement at best, but the underlying cause needs to be addressed.
- 3. Given my perspective, I seldom
"treat for cocci", but use the count to monitor the birds. A change in the count is of far greater significance than the actual
figure.
- 4. Although sampling and counting
of [...oocysts in...] individual birds is tedious, it can be of value in predicting performance. Samples from a given bird
will vary through the day, but the overnight sample from a resting bird is of greatest value.
- 5. The "standing count" -- the average
or "normal" in successful lofts -- is usually below 20,000 without treatment. That varies greatly between the individual birds,
but regardless of the actual figure, a rising count usually predicts a fall off in performance (and vice versa). This applies
to the team, but particularly to individuals. Other things being equal,the bird with a count of X thousand, but falling, will
beat a loftmate with the same count, but rising .
- 6. Using these principles, I have
been able to predict the first three home from nine or ten- bird widowhood teams, and have been able to suggest to clients
which birds to pool for the following race, with considerable success....I have never published my data.
- 7. A count of 96,000 after a bad
time at 700 miles? I would regard this as a result, not the cause."
A reply from
Dr GA van Oortmersson, a biologist/racing fancier from Holland reads as follows: "......I was asked to answer your question
about pigeon performance and oocyst counts. I have been asking around whether someone knew anything in this area. The result
however is negative.
The only incidental data which I can recall myself stems from about 20 years ago. Then in my local
club we checked youngsters for oocysts, just to inform and entertain club members. We however did not make real counts. The
pigeons of our champion at the moment (Mister B) contained many, many more oocysts than the pigeons of the rest of the club
members. So Mister B nervously asked what he should do about it. We advised him to do nothing as his birds performed so well!
Next race, his results went down, and he admitted he had given his birds some medicine. This experience is not worth much,
but anyway it tells that the presence of so many oocysts does not inevitably lead to bad results."
A reply from Dr
Ludger Kamphausen of Germany reads, in part, ".....when we have pigeons in our clinic, we investigate their droppings daily.
Sometimes it happens that we can't find anything in these droppings for several days, and suddenly, one pigeon starts excreting
coccidia. This always happens (don't laugh!) on Mondays. It seems that the weekend is a kind of stress for the pigeon because
the rhythm of feeding and cleaning has changed. This stress seems to start the excreting of coccidia. Do you have similar
findings?"
The latter two experiences seem to tie in nicely with the findings reported by Frank Harper of Britain,
ie, that stress can induce increases in "cocci counts", and indeed that these increased counts are the result of stress, rather
than the cause of the problem. Note again the supportive findings of Wallis who indicated that occasionally, counts of over
100,000 opg are seen, with no indication of a health problem in these birds. At this point it should be noted that some veterinary
practitioners don't conduct actual counts, but instead, rely on their years of experience to make practical judgments of low,
moderate or high numbers of the oocysts seen on microscopic examinations of droppings.
So, stressful events like basketing,
handling, mixing with strange birds in a strange environment, shipping, lack of water, liberation, and the physical effects
of the race itself, etc., may well have an influence on the level of shedding, and result in an increased "cocci count". These
stresses cause a release of corticosteroid hormones from the adrenal glands. In turn, these hormones suppress the immune system
and allow the coccidial life cycle to "gear up" again, with the production and release of greater numbers of oocysts in droppings.
In general, it is known that a few coccidia in the intestines of any species cause very little harm, and are useful
in stimulating the immune system to remain alert. The situation resembles a classical stand-off, in which, on one hand, the
coccidia are prevented by an active immune system, from multiplying and causing disease. On the other hand, the immune system
is unable to eliminate them completely, but because of the presence of a few coccidia, the system is kept in a state of readiness.
My concern over time hasn't been the low numbers of coccidia present in the individual bird, but instead, to the potential
for an explosive outbreak of coccidiosis in susceptible birds, especially youngsters, if loft conditions become favorable.
This means conditions such as the presence of persistently wet floor areas from such diverse causes as overflowing drinkers
to a leaky roof during days of rain, etc.. Under such conditions, the oocysts passed in droppings incubate in this cool, damp
environment, and develop in a process called sporulation to become infective. Recently passed oocysts are not infective, but
must go through the sporulation process before they can infect susceptible birds - and this usually means weaned youngsters
in which there can be explosive outbreaks if environmental conditions are favorable for the further development of coccidia
shed in droppings.
These common findings and comments from several sources suggest to me that fanciers who do their
own microscopic examinations of droppings for oocysts may well respond too vigorously to the presence of a few oocysts by
treating quickly to eliminate any hint of this parasite in their birds. A few oocysts in droppings really don't represent
a serious threat to the individual bird, and in fact, they are likely completely innocuous. As pointed out by Frank Harper,
the most significant feature associated with coccidia in his experience, is not the actual "cocci count", but rather, is likely
related to any change, that is, an increase or decrease in the total count. Thus, it would seem that those who rush to treat
when they find a very few oocysts in a sample of droppings are very likely overreacting by a wide margin, and would be better
advised to sit tight and re-examine overnight samples from individual birds on a daily basis to determine whether counts are
either rising or falling, and based on these results, to plan racing/pooling strategies accordingly.
Tying Up
in Racing Pigeons
Gordon A. Chalmers, DVM Lethbridge,
Alberta Email: gacdvm@telus.net
Imagine that near the end of a long, grueling day when
race birds have faced a headwind for much of the day, you have managed to clock two late arrivals, the last one just at dusk.
Both birds are very tired and dehydrated, and have obviously lost some weight. You make sure they have a drink of water and
some light feed before they settle in for the night. The next day, they seem a bit rested but there is no doubt that they
are still tired, so you keep them in the loft for the remainder of the day. After that, because they continue to look and
act tired, they are kept in the loft all the second day as well. When you enter the loft on the third morning, you find both
birds on the floor, and as you approach them, they try to fly. You see that both are now very wobbly and stiff as they try
to lift off the floor. One of them is finally able to fly to a low perch, but the other one remains on the floor with its
wings raised, unable to fly. What is wrong?
Since the birds are so wobbly when they try to fly, one of your first
fears is that they might have paramyxovirus (PMV) infection. After all, you did notice evidence of loose droppings on their
perches the morning after they homed, and now they have trouble flying. You shake your head. How can this be PMV? You vaccinated
all race and stock birds with an approved vaccine twice within five weeks before the birds were paired. In spite of the fact
that the birds look bright, you continue to be concerned about PMV. The rest of the flock looks fine, but since you know that
PMV spreads relatively slowly in an infected loft of birds, you wonder if this is the beginning of a major problem. On the
other hand, could it be paratyphoid infection? The possibility that the birds picked up this organism during shipment, plus
the stress of a tough race, and the presence of loose droppings a couple of days ago, along with wobbly, difficult flight
might mean that paratyphoid organisms entered the bloodstream from the intestines and were spread to a number of tissues,
including the wing joints, and maybe the brain. Wait though all birds were also vaccinated weeks ago against paratyphoid infection.
Besides, these birds, along with the rest of the flock, don't look sick at least, not yet. What is wrong with these two birds?
Very
worried, you decide to take one of the birds and some fresh droppings collected from both birds, to your veterinarian who
is also a member of your Combine. You ask him not to kill the bird if it's possible to avoid it. He agrees, then handles and
examines the bird, draws a small blood sample, swabs its throat, and then cultures and examines the droppings for parasite
eggs and coccidia. You contact him the next day for some early results, and he tells you that, so far, cultures are negative
for paratyphoid organisms, but he needs another day or two to be more certain of today's result. He also tells you that in
the samples of droppings there are a very few coccidia but no worm eggs, and that in the throat swab there are very few canker
organisms. However, his laboratory work on the blood sample shows that the values of two enzymes that are associated with
damaged muscle are elevated, and the value of one enzyme in particular, is very high. One of these enzymes, called aspartate
aminotransferase (ASAT) has a high value of 147 compared with the normal range of 45-123. The reading for the second enzyme,
called creatine phosphokinase (CPK), is very high at 1004 compared with the normal range of 110 - 480. On the basis of the
outward signs in these birds, coupled with the enzyme results and early negative bacteriology, he makes a presumptive diagnosis
of "tying up". What is this disorder?
Tying up is a condition involving the working muscles of an athletic animal after
it has experienced a hard race or competition in which it has overexerted itself. It is seen in horses on the track, in human
athletes, greyhounds and certainly, in pigeons, etc.. One of the worst and most severe expressions of this problem that I
have encountered in my professional experience is called capture myopathy or exertional myopathy (myo=muscle; pathos=suffering;
hence, the word refers to any disease or condition of muscle, in this case, degeneration), a condition which I was able to
study extensively in wildlife at one point in my career. Capture myopathy occurs in various wildlife species, such as those
that are captured either in baited traps or by driving them at high intensity into enclosures, often with ground vehicles
and helicopters. Many more cases of this condition occur when these intense drives are held in hot weather compared with fewer
cases when drives are held in cool weather.
Some of the key clinical signs of capture myopathy include marked muscular
stiffness and associated pain, lethargy, depression, the passage of red or coffee-colored urine, and sudden death if the heart
muscle is affected. The urine is discolored because of extensive damage to the muscle, from which the pigmented, oxygen-carrying,
iron-containing compound called myoglobin (similar to hemoglobin which gives blood its red color) leaks, enters the bloodstream
and is filtered though the kidneys into the urine. At post mortem, significant changes are seen in a number of skeletal muscles,
especially in those of the limbs, but also in the diaphragm and heart. These changes are seen as large, pale yellow or white
streaks in the muscle, and indicate severe degeneration of the affected muscles.
Tying up is a much less severe expression
of the whole process just described, and is characterized by stiffness and reluctance to walk, and in pigeons, inability to
fly or difficulty in flying even to a low perch. Flight at this time is wobbly, and the fancier may well wonder about PMV
or paratyphoid infection, or that the bird has hurt one or both wings. When the bird is held and examined, the breast muscles
are found to be swollen, making the bird feel large in the hand. However, closer attention to the breast muscles reveals that
they are not supple but instead, they are swollen and hard, and to the inexperienced fancier, they may give the false impression
that the bird is still in top physical condition. During handling, the affected bird often appears otherwise bright and normal.
How has this condition occurred?
In my experience, the history given in the first paragraph is characteristic. A bird
arrives home after a tough race, and because he is so tired, the concerned owner feels that he should have a good long rest.
Result: the bird is left in the loft, undisturbed for several days. However, during this enforced period of rest, events are
occurring within the breast muscles to create the clinical signs described previously. You may recall that in the large breast
muscles of the pigeon there are two kinds of muscle fibers, one a narrow-diameter red fiber and the other, a broad-diameter
white fiber. You may also recall too that the red fibers far outnumber the white fibers by about 14 to 1, and that these red
fibers, fueled primarily by fat, are utilized in the presence of oxygen, for prolonged, rapid flight. The lesser numbers of
white fibers in the great breast muscles are able to operate normally and efficiently in anaerobic conditions (an=without;
aerobic= oxygen; hence, these fibers operate effectively in very low levels of oxygen) in which they use glycogen as their
major fuel. Importantly, it is also known that these white fibers are recruited at any time during flight when the rate of
the wing beat, which is usually an average of 5.4 beats per second at cruising speed, is significantly altered, such as in
situations that require dodging or explosive bursts of speed, or for example, if the bird has to pull hard against the wind.
In our original example, since the race was tough, the birds had to pull strongly against the wind, and as a result, there
were significant biochemical changes resulting from the anaerobic use of white fibers in the breast muscles.
Because
the white fibers function in the absence of oxygen or in very low levels of oxygen, one of the biochemical by-products of
their work is lactic acid which can build up in the overworked system. This build up of lactic acid can damage not only internal
organs, but also both types of fibers red and white in the breast muscles where it is first produced. Under these acidic conditions,
the muscle fibers become damaged and they react by swelling to cause the hard, board-like feel noted when affected birds are
handled. The rise in the values of the two serum enzymes mentioned helps to tell the story. Characteristically, CPK values
rise very quickly following injury to muscle, and indicate very recent, on-going damage to the muscle, whereas ASAT values
rise more slowly and indicate earlier damage, in this case, damage that likely began soon after the bird arrived home.
Now,
what about the treatment of birds already affected by the tying up problem? At this somewhat late stage of the condition,
exercise is out of the question for obvious reasons: the bird is too tied up and in pain because of the lactic acidosis that
has caused the damaged muscles to swell. All the fancier can really do at this stage is to wait for the situation to return
to normal, perhaps with the use of light feed such as barley and a little support. In theory, alkaline powders such as baking
powder could neutralize the generalized acidity but there is the risk that overdosing could shift the system from acidic side
to the alkaline side. It would be best to err on the side of caution by relying on rest and time to resolve this problem.
Can
anything be done to prevent the condition in the long run? In my experience, one of the best and most practical preventive
measures by far is unquestionably, exercise. To me, the biggest single contributing factor to the problem after birds return
home is enforced, prolonged rest. Yes, the birds are tired after a hard fly, but I feel very strongly that it is critical
after any race, and definitely after a hard race, to let all race birds out of the loft for light exercise, even for a few
minutes, at the next exercise period that day or certainly, the following day and beyond. The effect of this mild exercise
is to metabolize or "burn off" any build up of lactic acid that has occurred during the race. Note that human sprinters, Thoroughbreds,
greyhounds, etc. all routinely walk for 15-30 minutes after a race, and for the same reason: to metabolize the lactic acid
that has accumulated during the race. For race birds, a few minutes of free exercise not forced exercise each day after a
race is an excellent preventive strategy, even for tired birds. Dimethyl glycine (DMG) known commercially as Spur in North
America, is said to be helpful in preventing lactic acidosis in horses on the track, and may also be similarly helpful in
racing pigeons. As well, in Belgium, carnitine was shown to have some effect in decreasing lactic acid levels in blood. However,
in my experience, light exercise beginning as soon as possible after any race, but especially after a tough one, is a simple
and very practical therapy.
Although the key triggering conditions that set the problem in motion seem to be days of
prolonged rest immediately after a race, especially a long or tough one, there are other management factors that may contribute
to the development of tying up. Vitamin E and the trace mineral selenium are both highly important in the maintenance of normal
muscle structure, and both act to protect muscle fibers against degenerative changes that can occur with intensive work. For
this reason, a water-soluble multivitamin mix containing vitamin E, and to which vitamin C can also be added, one to two days
each week, is very useful on a routine basis throughout the year. Both vitamins C and E are antioxidants that help to prevent
the damaging effects of oxygen in the form of peroxides, in tissues. As well, at all times of the year, fanciers should provide
a loose, wide-ranging mineral mix that also contains selenium, which adds to the protective insurance provided by vitamin
E. Because there is a very fine line indeed between normal and toxic levels of selenium, it is important NOT to add extra
selenium to the mineral mix. Stay with the legal limits of selenium included in the mineral mix you buy.
In my experience,
in selenium-deficient areas, one result of that deficiency in livestock such as cattle and sheep grazing these areas, often
foothills and mountainous terrain, can be sudden death of newborn animals when the heart is severely affected or sudden paralysis
because of degeneration of muscles in the limbs very soon after these young animals become active after delivery. In these
areas of low selenium status, regular supplementation with mineral mixes containing selenium is generally preventive. Why
raise the point about affected calves and lambs in an article on racing pigeons? Well, simply to explain that not only the
forages eaten by livestock, but also the grains grown in these selenium-deficient areas and fed to our birds, are also likely
to be very low in selenium. Thus there is value in the routine use in racing pigeons, of a loose wide-ranging mineral mix
containing legal levels of selenium.
Before closing, I feel that a final couple of explanatory notes might be useful.
Firstly, enzymes, mentioned earlier, are compounds, often proteins, that are capable of producing or accelerating some change
in a specific chemical substance on which they act. Characteristically, the names of enzymes end in "ase". The enzymes ASAT
and CPK are found in normal muscle. If the muscle is damaged, as it was in this case, these enzymes leak out of the muscle
and circulate in the bloodstream where their levels can be measured and interpreted. In order to function properly, enzymes
often require a helper chemical known as a co-enzyme. It is in the role of co-enzymes that many of the B vitamins function
most effectively.
Secondly, the enzyme values reported here were taken from an actual case of tying up in one of two
racing pigeons (affected at different times) from the same loft. I am grateful to my veterinary colleague Dr Paul Miller (PA
Veterinary Laboratory, Harrisburg, PA) who asked me to comment on this case at the time it occurred, for his courtesy in allowing
me touse these values in this otherwise fictional account of tying up.
Canker: Strains of the Causative Organism
Part 1:
An article that I read recently asked if there was a new strain of canker,
and it reminded me that there are indeed strains of the canker-causing organism. Canker is the name of the disease caused
by the tiny parasite called Trichomonas gallinae. It occurred to me then that, as a reply to the question asked by this article,
I might present some background information on strains of Trichomonas gallinae, and their importance to all of us.
I have drawn the information in this article from a number of important
old and some fairly current scientific papers selected from my files. Incidentally, in the following material, when I refer
to the canker organism, I will likely use the terms "Trichomonas gallinae, T. gallinae (the latter is simply a shortened form
of the full scientific name), trichomonad, trichomonas and canker organisms" interchangeably -- all mean the same thing.
Infection by this organism was first identified in Europe in 1878 by
a researcher named Rivolta. Many years later in the USA, a scientist named Robert Stabler, conducting research in the state
of Colorado, pioneered extensive work on the organism in pigeons -- in fact in 1938, he gave the organism its scientific name,
Trichomonas gallinae.
In a 1948 publication on the subject, he noted that not all pigeons that
harbour the organism die of the infection, or even have internal changes to indicate the presence of this organism. As well,
he found that youngsters from some parents in a loft nearly always died of canker in a few days or weeks after hatching, whereas
certain other parents, although infected, raised healthy youngsters indefinitely.
Obviously these facts gave rise to the idea that there were strains with
differing abilities to cause disease, a suggestion that had also been proposed by other scientists who had worked on canker
in pigeons.
To test this idea, Dr Stabler then set up an experiment in which he used
canker organisms that he arbitrarily designated as "strains" (see explanation in the next paragraph), from five different
sources: Strain 1 from an infected wild youngster, Strain 2 from a healthy adult King, Strain 3 from a healthy adult Carneaux,
Strain 4 from an adult racing pigeon that had a history of transmitting lethal canker to his youngsters and to at least three
successive hens, and Strain 5 from the mouth of a peregrine falcon that had died with severe canker of the mouth.
(Note that canker caused by T. gallinae occurs in birds of prey in which
it is called "frounce". Broadly related organisms in this group also cause infections, variously, in the reproductive systems
of humans, cattle, and sheep, and in the digestive tracts of domestic chickens and turkeys. I have also seen it in devastating
outbreak form in small aviary finches in which the disease very much resembled that seen in the oral cavity of young pigeons.)
Dr Stabler defined "strain" as the particular canker organisms removed
from the mouth of an individual bird, even though he recognized the possibility that any given bird might harbour more than
one strain. The results he obtained seemed to justify the use of the organisms from a particular bird as "a strain", at least
in terms of their ability to cause disease. He maintained the five individual strains mentioned previously by inoculating
them by eyedropper into the mouths of clean pigeons, and took great care to be sure that the different strains weren't accidentally
mixed. The clean pigeons he infected with these five strains came from his own loft of racing pigeons that he knew were free
of canker-causing organisms.
In the first experiment, he used 25 of his own young birds, aged 6 weeks,
5 1/2 weeks, 5 1/2 months, 7 months, and 9 months, with five birds in each group. One bird in each age group was inoculated
by mouth with Strain 1, one in each group received Strain 2, and so on. Results showed that the Strains 1, 4, and 5 caused
severe signs of disease that ended in the death of all except two youngsters, a 7 and a 9-month-old bird infected with the
Strain 4. These two birds had severe canker for over a week, but they recovered. Strains 2 and 3 either didn't produce signs
of disease in the youngsters they infected, or the infection was very slight and lasted only 2-4 days.
Part 2:
In follow-up work, Dr Stabler showed that Strain 1 (which became known
in trichomonad circles as his famous "Jones' Barn" strain) obtained from the wild youngster with canker, was the most deadly
of the five strains, killing 12 of 13 birds inoculated with it in an average of 10.6 days. Over all, he was able to show that,
of 119 pigeons infected successively with this potent strain, 114 (95.8%) died in 4 to 18 days. In later work, he showed that
Strain 1 was deadly even if only one organism was placed in the mouths of susceptible pigeons. Obviously, this single organism
multiplied rapidly into the thousands or more to cause serious illness.
These results showed that there was a marked difference in the ability
of these five different strains of T. gallinae to cause disease in pigeons. These strains varied from those that caused little
or no disease to those that caused high losses. Obviously, there were also strains that were intermediate in their ability
to cause canker, since they were able to cause serious illness from which most birds eventually recovered.
In important later studies, Dr Stabler was able to show that mild strains
of the canker organism were able to protect birds against more deadly strains, a finding that continues to have practical
application today. To confirm these results, he first gave eight of his own trichomonas-free youngsters the relatively potent
Strain 5 obtained from the peregrine falcon. All developed severe canker of the mouth, six birds recovered and two died.
Fifty-four days after the initial infection with Strain 5, the six survivors
were given the very deadly Strain 1. None of them developed evidence of disease during the following month. These six birds
were then killed and examined at post mortem. There was evidence of scarring of the liver of three birds, findings that suggested
infection from the previous dose of organisms. The other three birds were almost completely free of signs of infection. The
only significant finding in these birds was the loss of the palatal fringe on the roof of the mouth. (Dr Stabler believed
that, in every case examined, this change was highly characteristic of evidence that the canker organism was the cause.)
He then repeated this experiment with eight more clean youngsters that
were first given the mild Strain 3 from the adult Carneaux. Only two youngsters developed a mild form of the disease. About
a month later, all eight birds were given the deadly Strain 1. In the next three weeks, only two of the eight birds developed
signs of canker. One had a mild form of the disease, and the other had a severe form from which it eventually recovered.
Post mortem examinations of these eight birds determined that tissues
of seven birds were completely normal, and that the bird that developed severe canker had severe changes of canker in the
liver. At the same time, as a control, Dr Stabler inoculated 13 youngsters from his own loft of trichomonas-free birds with
deadly Strain 1; 12 of the 13 birds died. Thus, these experiments demonstrated that infection by a mild strain of T. gallinae
conferred protection against a more deadly strain of the organism. However, the duration of that immunity wasn't determined
at that time.
Part 3:
During the spring, summer and fall of 1950, there was a major outbreak
of canker in wild mourning doves across much of the southern USA, with the greatest losses apparently in the state of Alabama
where it was estimated that deaths might well run into the thousands in that state. Dr Stabler obtained strains of trichomonads
from several sources of these doves to see if the organisms from these doves could cause illness in pigeons.
He inoculated 50,000-100,000 organisms from different doves, into each
of five pigeons from his clean colony. For comparison, he inoculated only 3,000-10,000 organisms of his deadly Jones' Barn
strain into another five clean pigeons, all of which subsequently died of canker of the liver. The most deadly of the strains
from the doves came from a bird collected in Alabama, and like the Jones' barn strain, this one proved to be equally deadly,
killing all but one of the pigeons inoculated with it. The other four strains obtained from the doves proved to be relatively
mild when inoculated into pigeons, as most of these pigeons survived the infection.
The next question to resolve was this: would pigeons that survived the
infections with mild strains obtained from doves, be able to withstand infection by the deadly Jones' barn strain? To test
this idea, Dr Stabler inoculated all of these survivors with the Jones' barn strain. The result was that all birds inoculated
with the Jones' barn strain survived, findings that indicated good protection following infection with strains from the doves.
Did the fact that these birds survived mean that 1) the strains derived from doves had killed off the deadly Jones' barn strain,
or 2) was the Jones' barn strain still present in these surviving birds, and if so, was it now altered so that it was now
a mild strain, or 3) was the Jones' barn strain as powerful as ever for clean birds, but unable to cause illness in protected
birds??
To test these ideas, Dr Stabler collected canker organisms from birds
that had a combination of a mild strain and the deadly Jones' barn strain, and inoculated these organisms into clean pigeons.
The results were variable, as some of the newly infected clean birds had only mild changes of canker, whereas other birds
either died of severe canker, or almost died. These results indicated that the deadly Jones' barn strain continued to be present,
and equally important, was as potent as ever. Over all, of 13 birds infected, six died outright, one barely survived, and
six had mild cases of canker. Incidentally, Dr Stabler reported that the Jones' barn strain typically caused the most severe
disease in the liver of infected birds, whereas milder strains produced only oral infections.
Although the procedure isn't too practical for us as pigeon fanciers,
Dr Richard Kocan, working in the USA, found that blood plasma from pigeons infected with even a mild strain of T. gallinae
could protect other pigeons infected with a deadly strain of the organism. Much more practically, Dr Kocan was also able to
demonstrate that previously infected pigeons that had been treated with the formerly used anti-canker drug Enheptin, were
free of the organism for as long as 16 months, yet remained immune to infection when they were inoculated with deadly strains.
On this point, some of his other work showed that 172 of 313 wild pigeons
and 54 of 66 mourning doves (all of the mourning doves captured were completely free of the canker organism) -- all trapped
in his area, were resistant to the deadly Jones' barn strain. His conclusions: recovery from an infection with T. gallinae,
even when the birds eventually completely eliminate the organism from their systems, results in long-term immunity to this
parasite -- a fact that is of great importance to us as pigeon fanciers, one that we can use to advantage, especially in these
days of apparent resistance by this organism to some of our modern, previously useful drugs.
Part 4:
The subject of drug resistance by the canker organism to modern drugs
is also of major current importance to us. Almost 10 years ago, in 1990, Drs Lumeij and Zwijnenberg of Utrecht University,
Holland, demonstrated the fact that canker organisms recovered from a large flock of pigeons in that country, were uniformly
resistant to all of our commonly used modern drugs -- Emtryl, Ridzol, Spartrix and Flagyl. On the basis of that information,
it seems likely that canker organisms in many other untested flocks of pigeons in Holland and indeed throughout Europe, and
other countries, could have been similarly resistant at that time, likely, as these researchers pointed out, because of the
common practice among fanciers, of continually under-dosing birds with these drugs.
On the subject of under-dosing, especially with Emtryl, I find in my
travels in the USA and Canada, that the dosage of the 40% water-soluble Emtryl, as
recommended by several pigeon supply houses in North America is far below
that recommended for pigeons by the producer of the drug. (At one time, this company sold small 3-gram packets of Emtryl,
the exact dosage for one Imperial gallon - 4.55 litres). The fact that Emtryl is being recommended today at much lower dosages
could certainly contribute to the problem of drug resistance mentioned in the previous paragraph, and may be a developing
problem with major far-reaching consequences for us.
I would remind fanciers that the correct dosage of Emtryl for
pigeons, as recommended by the company, is 3 grams (or one level teaspoon) per imperial gallon (4.55 litres) of drinking water
for 5-7 days. For the smaller US gallon (4 litres), this is about 3/4 teaspoon per gallon for the same treatment period.
To avoid the problems of toxicity if birds drink excessive amounts of
water especially during hot weather, try an Australian method that I know works well. Make up the correct dosage of Emtryl
and place it in front of the birds at, say, the evening feeding for a couple of hours or so. After this time, throw out the
medicated water and replace it with fresh water until the next evening. Repeat the correct dosage for a couple of hours or
so each evening for a total of 5-7 days. This method insures firstly, that birds receive the correct therapeutic dose each
day for the treatment period, and secondly, that problems with toxicity can be largely avoided. It is important not to treat
with Emtryl or other drugs of the same family during the pairing up period, because there is some suggestion that the drug
can interfere with fertility. It is also 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 another appropriate for the next one, etc., all at the correct dosage.
On the subject of canker and treatments, some fanciers subscribe to the
idea that if it's not broken, don't fix it. Dr Colin Walker, the Australian veterinarian who has written many excellent articles
for racing pigeon magazines, seems to accept this idea. In one of his books, he states that drugs alone will never control
a canker problem. He feels that it is important to allow developing youngsters enough exposure to the organism that they can
develop natural resistance -- my idea for many years as well, based on the work of Dr Stabler.
Dr Walker expands on this idea by stating that if birds in the stock
loft (and presumably their youngsters) did not develop canker the previous year, no treatment is needed this year. However,
if canker did occur in stock birds and their youngsters last year, birds should be treated this year with a suitable drug
prior to mating, and for two days every week after that.
Further, he suggests co-ordinating these two-day treatments
with the hatching period when trichomonad shedding is the highest. If the occasional youngster still develops canker, he recommends
treating the parents and both youngsters in the nest with Spartrix or Flagyl for three days. (Incidentally, some veterinary
writers in the USA have some legitimate concerns about short periods of treatment because of the risks of resistance by the
canker organism to these drugs.) Dr walker also recommends avoiding the treatment of breeding pairs whose
youngsters don't develop canker, so that there is no interference in
the development of natural resistance, an idea that makes a great deal of sense to me.
Part 5:
Speaking of natural resistance, I recall that when I worked in New Zealand
during the early 1980s, a medical doctor there raced pigeons, but apparently didn't treat his birds for any disease. Instead
he preferred to rely on the development of natural resistance to any virus, bacteria or parasite his birds might encounter.
For the past several years, I haven't used preventive canker treatments
on any of my old or young birds, and touch wood(!), so far there hasn't been a detectable problem. It is probable that the
natural resistance developed in these birds by repeated exposure to the strains of canker organisms that very likely reside
in my birds has (to date) been holding the disease at bay.
Based on information from Dr David Marx, one of the top pigeon veterinarians
in the USA, I have also been examining the mouths of my birds during the racing season for evidence of reddening and excess
stringy mucus, findings that could suggest multiplication of canker organisms and increased irritation of the oral cavity
during this stressful time.
So far, on the basis of finding clean, pink throats, I haven't felt a need to treat preventively
during the racing season, although it is possible that deeper areas such as the crop, which I didn't examine, may have been
affected. I acknowledge the possibility, however, that if I had treated periodically for canker in spite of these normal findings,
some racing performances might have improved. As far as canker is concerned, the idea "if it's not broken, don't fix it" seems
to be working in my loft. If things change for the worst, I am ready to treat if I have to.
I hope that this look at the historical background of strains may stimulate
thought on this subject among fanciers. As the risk of drug resistance by canker organisms (and other agents as well) increases
steadily, I hope that fanciers may be better able to assess the facts surrounding natural immunity, and to use these facts
to their advantage by recognizing the biological benefits of using any mild strains of canker organisms that reside in their
birds as a major defence against deadly strains.
In saying this, I also recognize the need to treat birds when or if the
disease occurs. A combination of judicious treatment when necessary, plus strategies to allow for the development of natural
resistance may well be the best approach. I also hope that information on the correct dosage of Emtryl -- and by extension,
other drugs as well -- may help to reverse the trend of vastly underdosing our birds with these products.
Australia is fortunate to have veterinary specialists such as Drs Walker
and Marshall, to name two individuals, for practical guidance on these subjects.
Gordon A Chalmers, DVM,
Considering the movement and trade in pigeons
over the world, fanciers should not be surprised when a variety of diseases occur in our pigeons over a period of time. In
most cases, there is a triad of circumstances consisting of: 1) the resistance (or lack of) of the pigeon, 2) the presence
of the bacterium, virus or parasite, plus 3) the environmental or stressful conditions that permit the particular disease
to occur. It is the interaction of these three factors in any bird or amimal that determines whether disease will occur. Note
that infection itself by a given disease-causing agent does not necessarily mean the existence of overt disease. For example,
the presence of a few coccidia in the intestines of resistant pigeons tends to maintain a very high level of immunity to that
type of coccidia. This situation is most certainly infection of tissues of the intestines. However, coccidiosis, the disease,
is not present. In this case, there is a good balance between the presence of a few coccidia and the immune system of the
bird which is able to control the numbers of coccidia quite well. However, frank disease may occur if circumstances tip
the balance in favor of the coccidia. For example, persistently wet floors during a rainy period, or overflowing waterers
that keep the floor constantly wet, can change the balance. In this situation of cool, damp conditions that are ideal for
coccidia and other parasites, those coccidia shed in droppings are now able to develop further to a stage that makes them
infective and therefore, potentially dangerous. Very quickly, under these wet conditions, many thousands of infective forms
of the coccidia can develop on the floor. Birds picking around the floor can swallow many of these infective stages, and as
a result, there may be an overwhelming challenge to the immune system as numerous coccidia invade cells of the inner surface
of the intestines, and the birds develop signs of the disease coccidiosis. Youngsters represent an age class that is particularly
vulnerable because these birds have not yet had an opportunity to develop good immunity through exposure to low numbers of
coccidia in the environment. Instead, they are now faced with a massive, overwhelming challenge, and the result can be a severe
outbreak of coccidiosis. Other organisms, notably the bacteria, but also the viruses, chlamydia, etc., often operate in
the same way, taking a biological advantage when environmental circumstances are favorable and there is a concurrent relaxing
or failure of defence mechanisms in the birds. Salmonella spp. (also called paratyphoid organisms), and also E. coli, are
bacteria that represent other examples of the same situation. In pigeons, the most common Salmonella sp. is Salmonella
typhimurium variety copenhagen, although several other strains of salmonella organisms can certainly be involved in producing
disease in pigeons. Variety copenhagen seems to have a close and even specific relationship with pigeons. If there is any
good news (or maybe more correctly, less bad news!) about salmonella infections, some of it is associated with variety copenhagen
. Firstly, this strain is often highly sensitive to a very wide range of antibiotics and other anti-bacterial drugs. Secondly,
this strain seldom ever causes infection in humans. This is a significant point because the major importance of most strains
of Salmonella sp. is their known capacity to leap species barriers and infect quite a number of classes of birds and animals,
including humans. In general, Salmonella typhimurium variety copenhagen seems to be most associated with pigeons, even though
at times, it is able to infect other species such as chickens. Problems with Salmonella sp. and E. coli infections in pigeons
are most common in younger birds. Adult birds often don't have signs of infection, but in some instances, they too can become
infected and develop overt signs of disease. Youngsters with salmonellosis develop diarrhea that is often green. This occurs
because the intestines are empty of food, and only bile-stained fluids pass through as droppings. Later, in a more chronic
stage that occurs after these bacteria invade the bloodstream, they can then move into and infect joints which become inflamed,
swell and result in nodular lumps on wing or leg joints. A number of antibiotics and other anti-bacterial products can
be used in treatment, with varying degrees of success. Part of the reason for this fact is that, although most infected birds
(or any animal, bird or human) infected with a Salmonella sp., completely eliminate the infection, the occasional bird or
animal will remain a permanent carrier of the organism -- and this is the catch. Such carriers are generally very healthy,
with no visible indication that they harbor the organism, but they continue to be a ready source of Salmonella sp. organisms
for other birds in the loft. In many species, these bacteria likely hide in the gall bladder, but as pigeons don't have a
gall bladder, the organisms likely live in the bile ducts of the liver. If conditions are ripe, and carrier birds become
stressed from feeding, weaning, racing, etc., such birds can begin to shed greater numbers of these bacteria from the bile
ducts into the intestines, and from there they are passed in droppings into the environment. If susceptible birds, including
youngsters in particular become exposed, they can develop serious disease after swallowing numbers of these bacteria. Stress
produces chemical and cellular changes that decrease the ability of the body to defend itself against infection. Opportunistic
organisms such as Salmonella sp., among others, take advantage of the situation and begin to multiply and produce thousands,
and likely millions more organisms that are shed in droppings to contaminate the local environment from which they are picked
up and swallowed. As mentioned earlier, antibiotic treatment can be highly successful in many birds, but the very real
possibility that a carrier bird may exist in the loft after the infection has gone through many or all birds, poses a continuing
threat to the health of the entire loft. The use of sodium acid sulfate as a loft dressing on floors, perches and nestboxes
is a chemical approach that has merit because it creates an acidic environment that a number of disease-producing organisms,
especially intestinal bacteria, find too hostile for survival. As fanciers, we can use this information to our own advantage.
E. coli and Salmonella sp. bacteria much prefer to live in an alkaline environment, so it is obvious that the use of lime
as floor, perch and nestbox dressings should be avoided when infections caused by Salmonella sp. and E. coli occur. As
well as the use of antibiotics, there are other management approaches to prevention and treatment as well. In 1973, a man
named Esko Nurmi in Finland developed a procedure in which he fed to normal, day-old chicks, litter and droppings from salmonella-free,
clean, healthy flocks of chickens. 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 colonized 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 colonized 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 10-12 bacteria deep. These protective bacteria actually bind to specific sites on the inner
surface of the intestine, and by this means, prevent the attachment of Salmonella sp. on 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, that is, without oxygen), ie, they are able to live and reproduce in an environment
in which levels of oxygen are very 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 the bacteria into the surrounding environment of the intestine,
creates a shift from a normally alkaline state to a more acidic condition in the intestine.
The importance of this fact is that, as mentioned
previously, many disease-producing bacteria like Salmonella sp. and E. coli, for example, like to live in a slightly alkaline
environment 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 Streptococcus, among others. Dr Kevin Zollars has mentioned this point more than once in his informative articles
in the Digest. The Lactobacillus sp. bacteria not only multiply and colonize 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 trials 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 with the use of Lactobacillus sp.. A few basic products incorporating these ideas of using "good"
bacteria to combat Salmonella sp. infections are being 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. Thirdly, there are 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. All of these products are given to birds by mouth,
often through feed or drinking water. (The advertising columns of racing pigeon magazines offer similar products for use in
drinking water. No doubt, many are good products, but in the past, I have cultured at least one widely touted, advertised
product and found very few bacteria present.) In the poultry industry, these bacterial products are being 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. 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. 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. 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, than they are against Salmonella spp., for example. Yet another class of probiotics are the organic
acids, that include lactic, formic, and propionic acids, that are being added to feed and water for poultry, to produce the
same effect, ie, acidification of intestinal contents to increase resistance to disease-producing bacteria in the intestine. Even
given some of the limitations of these different products, it is known that methods that will 1) effectively "block out" disease-causing
bacteria, and 2) create an acidic condition in the intestines of birds will help to eliminate or markedly reduce the numbers
of a variety of disease-producing bacteria. (Unfortunately, they don't have any effect on coccidia or worms.) Two small examples
from my own limited experience: A pigeon fancier who had a number of undetermined losses associated with diarrhea in nestlings,
decided to try this non-antibiotic approach. He obtained a package of yogurt starter, mixed it with warm milk, incubated it
in a warm place to allow the bacteria in the starter to multiply, and added it to a mixture of small grains and rolled oats,
to produce a somewhat crumbly, semi-dry mash that he placed in a feeder on the floor. His old birds took to this mixture avidly
while they were feeding youngsters. The result was that no more youngsters were lost, and the health of remaining birds improved
markedly. In another example, a fancier was having problems with the intestinal infection called ulcerative enteritis (caused
by the bacterial organism called Clostridium colinum) in youngsters aged 12-20 days, the age that seems to be most critical
for the occurrence of this bacteria-caused disease. Some youngsters in the first round had been affected and he decided to
try to prevent it in the second round. He mixed plain yogurt with enough warm water to make a thin milkshake-like solution,
stirred it to remove any lumps, and gave it by feeding tube to 10-11 day-old youngsters in the nest, before there was any
sign of disease. This was done twice and sometimes three times a day for 4-5 days. Result: no evidence of ulcerative enteritis
in any of these youngsters. Both of these cases definitely don't represent solid scientific proof of the effectiveness
of this type of product because no group of youngsters was left untreated for comparison. However, there were very strong
indications from these limited trials that there may be a great deal of merit in this approach to prevent some bacteria-caused
infections of the intestines -- in spite of studies that showed very little positive effect in eliminating or reducing the
numbers of Salmonella sp. by the use of cultures of Lactobacillus sp. alone. What are some other stressful situations that
could lend themselves to this application? One of the most obvious times occurs when youngsters are weaned, when stresses
are very high: they have been separated from their nestbox and close parental care, they are now in strange, unfamiliar surroundings,
and they may be frightened, tired, hungry and thirsty. If the weather is also bad, add another stress to the list. Possibly
just before weaning and through the first 2-3 days after weaning, the addition of yogurt or yogurt starter slurry in a mash
feed or in drinking water might be enough to load the crop and intestines of these youngsters with a formidable barrier of
protective lactobacilli and streptococci. Practically speaking, it would seem best to try mass treatment of the entire
flock, and to use most of these procedures at regular feeding times, so that parents will eat fresh crumbly mash or drink
fresh water containing these "good" bacteria, which are then fed immediately to youngsters in the nest. Weaning youngsters
onto such a mash, or providing water containing these bacteria after weaning would also be practical. I have found that a
tablespoonful of plain yogurt added to a gallon of drinking water seems to be very helpful. When first used, large amounts
of yogurt may cause birds to back away from the drinker, but if smaller amounts, say a quarter to half teaspoonful, are used
for a few days, birds become used to the taste. Two other critical times during which these preparations could be useful
are just before shipping birds -- old or young -- to a race, and/or just after the birds return from a race. If birds are
sent racing with a protective wall of "good" bacteria lining the crop and intestines, this procedure could this be effective
in preventing establishment of colonies of disease-producing strains of Salmonella sp. and E. coli picked up in shipping baskets.
Work with poultry has demonstrated a definite
decrease in numbers of Salmonella sp. in these birds if "good" bacteria are allowed to become established in the intestines
before there is any exposure to salmonella organisms. Logically then, the most opportune time to use these methods is a day
or two before birds enter the shipping baskets to be certain that the intestines are well colonized by "good" bacteria beforehand.
A similar process used right after birds return from a race also might help to prevent infection at this stressful time. Another
point is that if returning racers bring with them Salmonella sp. or disease-causing strains of E. coli, the use of these products
both before and after the race might also protect stock birds, racers and youngsters that remained at home. Exhausted, flown-down
birds that return days or weeks late, possibly injured, from tosses or races, would seem to be ideal candidates for this type
of therapy, given the high level of stress they have been and are under. These methods would be equally useful in all new
birds acquired locally or from Europe, etc.. Birds, especially youngsters, that are ill from other infections such as circovirus
infections, canker or coccidiosis, could be highly susceptible to intestinal infections, and might benefit considerably from
a treatment of "good" bacteria at this time. Note again: It is highly important that you don't mix antibiotics in the water
if you also plan to add "good" bacteria. The antibiotics will kill these bacteria in the same way that they kill disease-causing
bacteria. If antibiotics are judged to be necessary, use them first for the required number of days, and then add "good" bacteria
to fresh water after the antibiotic treatment has been completed. Two additional approaches with a similar objective are
used today in the poultry industry, with special emphasis on eliminating Salmonella sp. from breeder flocks, and even broiler
flocks. One of these procedures is to add the sugar lactose to pelleted rations or to drinking water at the level of about
5%. A good practical source of lactose is whey powder (it is about 70% lactose), available at feed companies, milk and cheese
factories, and food stores, and can be added to drinking water. The principle is this. When whey is swallowed, the lactose
present is converted by "good" bacteria in the crop and intestines into lactic acid, which, in turn, shifts conditions to
the acid side of neutral, and provides the same kind of control over disease-causing bacteria in the intestines. The other
modern approach uses combinations of the organic acids, lactic, formic and propionic -- mentioned earlier in this article
-- which do the same thing, ie, acidify intestinal contents to create a hostile environment for disease-causing bacteria.
These products are available for use in pelleted feeds, as well as for drinking water for poultry, and could easily be adapted
for use in pigeons, especially the water formulation. Check with your local co-op or feed company for these products, often
called "acid packs". Directions for use are given on the container or package. Pigeons are not poultry, so why use methods
developed for the poultry industry? Well, as I see it, there is just no point in letting good scientific information from
one species go to waste, when there could be direct application of the same principles in another species -- in this case,
racing pigeons. Sometimes it seems that there is a real scarcity of good scientific information on racing pigeons, particularly
because of the great secrecy that abounds in the sport, and until we become more open as racing pigeon sportsmen and women,
we have to be able to borrow useful information and ideas from other domestic species, and adapt them for use in pigeon racing. From
the foregoing information, it is obvious that, not only is one of these procedures valuable and practical, but also, combinations
of these approaches just add more arrows to your bow, so to speak. So, the addition of Lactobacillus and Streptococcus spp.
cultures from yogurt or similar products (friendly bacteri) to feed or water can easily be combined with the addition of organic
acids and/or lactose, to insure that intestinal contents become acidic, and therefore, protective against serious disease-causing
bacteria such as Salmonella, E. coli, and Clostridium spp. of bacteria, among others. A major point about the use of "good"
bacteria, lactose, and organic acids, singly or in combination, is that by these means, we should be able to begin the process
of halting the uncontrolled, cavalier use of cocktails of antibiotics and other anti-bacterial drugs so much in use --and
abuse-- not only by fanciers, but also by many segments of our livestock industries. I sense that too many of us are using
too many drugs too often, and obviously, unnecessarily in some cases. It is better to have a plan to try to manage and out-manoever
disease problems rather than relying primarily on antibiotic treatments. We can take the approach of medicating with antibiotics
only when necessary, and then use management strategies that could include those outlined in this article, among others, to
stay ahead of disease, or to say it another more positive way, to promote good health.
Gordon Chalmers
West Nile Virus and Pigeons
Adenoviral, E. coli and Paratyphoid Infections in Pigeons
Avian Influenza (Bird Flu) and Pigeons
Bacterial Infections of the Intestines of Pigeons
Coccidia and Racing Performance
Garlic: some facts for the fancier
Health care regime
Listing of some drugs commonly used in pigeons
"Moving the Zoo" the Implications for Racing
"Pigeon Breeders" Lung
Probiotics, Prebiotics and Immunostimulants
Streptococcus bovis Infection in Pigeons
Tying Up in Racing Pigeons
Avian Influenza - Update Winter 2005

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