Dr. Gordon Chalmers |
 |
Karl Frank |
It may also be assumed that each of those strains exhibits a different level of virulence. The typical yellow
growths in the mouth, pharynx, and crop as seen on the right are much less frequent than was the case in the past. Although these cheesy masses have
become rare in Europe's racing pigeon scene, the infection trichomoniasis is still regarded there as the largest inhibitor to today's racing pigeon
performance.
The advantage of this system is that even a very low presence of trichomonads can be detected and they can also be tested for antibiotic resistance.Since it is counterproductive to assist in the creation of micro - organisms resistant to available antibiotics, it would be ideal if we could use only
antibiotics to which the organism in question is sensitive to. However, antibiotic sensitivity tests regarding Trichomonas are not readily available in many
locations. The solution is, at least partially, to examine crop smears microscopically not only before treatment but also a couple of days after treatment just
to make sure that the antibiotic used is still effective against the micro - organism in question. A recent study done in the faculty of veterinary medicine in
Barcelona found some Trichomonas organism
resistant to all the nitroimidazole drugs tested. Similar results were obtained by a study done in Utrecht (Netherlands) where it was also found that the dosage commonly recommended for Ronidazole is usually too low and needs to be multiplied many times for the drug to be effective.
The route of infection is usually via contaminated drinking water which may happen in the basket toward the release point of any race. It would just take a
couple of infected birds drinking from the trough and floating some of their protozoan guests into the common drinker. They can multiply relatively fast in
their new host, especially since there is not much competition in a clean bird. Such infection will inevitably lead to reduced performance for which the
bird is often blamed and culled. Some may look at culling for becoming infected with Trichomonas as a tragedy. Any bird can become infected, isn't that
correct?
Very little is known about immunity to trichomoniasis in pigeons (
but please read the very informative article by Dr. Gordon Chalmers further down )
for which reason it may be advisable to have a look at factors affecting Trichomonas infection in humans:
3 microscopically indistinguishable separate species of Trichonomas organisms can establish themselves in humans, the harmless commensals Trichomonas tenax
and Trichonomas hominis as well as Trichonomas vaginalis which can cause a low grade inflammation of the genito - urinary tract in both men and women.
The commensal, Trichonomas tenax, has an incidence of 10-20% in some populations and is transmitted from mouth to mouth. Since it is a harmless
organism it would not be advisable to administer antibiotics just because some keen medical doctor found this organism in a smear of saliva.
The other commensal, Trichomonas hominis, lives in our intestinal tract. It is quite common in the tropics and transmitted by the fecal-oral route.
Trichomonas vaginalis is a common parasite of both males and females. Coitus is the common mode of transmission. The organism is commonly found
in females, surveys indicating from 25-50% of sexually active women being infected; only about 5% of men are infected. Many cases of
trichomoniasis are totally asymptomatic! In fact, asymptomatic cases are the rule in males. The intensity of infection, the ph of vaginal and other
secretions, the physiologic status of the vaginal and other genitourinary tract surfaces, and the accompanying bacterial flora are among the factors
affecting pathogenicity. The organisms cannot survive at the normal vaginal acidity of ph 3.8-4.4.
death of the pigeon without immunity in 14 - 17 days through necrosis of the liver.(University of Massachusetts study)ineffective
against them.The time may have come to look into more natural management practices of many diseases but particularly trichomoniasis. It has been shown by
a number of veterinarians that, try as much as one may, it is not possible to remove the organisms causing canker entirely from the pigeon. There will always
be some left after an antibiotics administration and these will start the cycle anew, multiplying when the growing conditions are favourable for them. Not only
do we run the risk of this organism to develop immunity to our trichomonicidal drugs through repeated dosing but these drugs also have definite toxic effects
on the pigeons we try to protect.
Ad Schaerlaekens wrote an interesting anecdote regarding this very dilemma:
When I read the title of the recent excellent Digest article ("Is There a New Strain of
Canker?" - December 15, 1998) by Dr Kevin Zollars, my first reactions to the question posed
were, "Yes, very likely, and what is more, there are likely more than one new one." I was pleased
when I read the article itself because of the realistic and philosophical points Kevin raised. After it
is read carefully several times, and well absorbed, this article should be placed prominently in the
files of every fancier. It occurred to me then that, as a corollary to this key article, I might present
some background information on strains of Trichomonas gallinae, the cause of canker,
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
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 harbor 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 harbor
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.
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.
During the spring, summer and fall of 1950, there was a major outbreak of canker in
mourning doves across much of the southern USA, with the greatest losses apparently in 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.
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 at the Patuxent Wildlife Research Center, Laurel, Maryland, 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 treated with the old 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.
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 likely North America as well, 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.
Although the subject of under-dosing, especially with Emtryl, is a pet peeve of mine, and I
sound like a broken record on the matter, I think it bears repetition. In my travels, I find that the
dosage of the 40% water-soluble so-called "Canadian" 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 liters). 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 liters) of drinking water
for 5-7 days. For the US gallon (4 liters), 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. As Dr
Zollars pointed out in his article, don't 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 Ridzol for the next one, etc., all at the correct dosage.
Still 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 excellent
articles for the Digest, 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. (Note here that
Dr Zollars has some legitimate concerns about short periods of treatment, etc. -- see pages 32-34
of his article.) 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.
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, 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. 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, along with the recent article
by Dr Zollars, 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 defense 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.
| Sunday January 4, 2004 Robert Lynch Tifton, GA, USA 207.69.75.252 | Another very good article on one of the major problems in racing pigeons. I am a firm believer in building natural immunity and seldom if ever treat my youngbirds during their first 2-3 months or all birds during the winter. However, during the race season I feel it is necessary to treat for canker here in the hot, humid Southeastern US to be competative in both oldbirds and youngbirds. |
| Thursday April 14, 2005 faiz khalid maroc, maroc 81.192.174.233 | thank you for this information about "trichmonose" |
| Thursday April 14, 2005 Jose Castillo Louisville, ky 209.214.169.214 | Thanks for the information |
| Saturday October 1, 2005 Kevin Whittock Huntly, Waikato. New Zealand 222.152.9.84 | Thank you very much for an informative article. Thank goodness for the internet as there is a shortage of literature on racing pigeons in this country |
| Wednesday May 17, 2006 Pablo Lezcano General Pico, La Pampa, Argentina | Thank you for this information. it was very rare to me to take this information... |
| Tuesday June 19, 2007 Emanuel Schembri San Gwann, Malta (europe) 88.203.51.115 | keep up the good site and good information.. I found it very useful.. Emanuel !! |
| Monday July 16, 2007 andrew pace st`venera, malta 88.203.37.199 | wonderful site and instructiv information thanks to youre teaching and knowlage. |
| Wednesday August 29, 2007 saul rincon boulder city, Nevada 207.200.116.67 | you have an wonderful site thankyou for the health tips my birds are now starting to have that extra energy and the offsprings are healthyer than ever wish me luck 2008. |
| Tuesday November 6, 2007 André de Oliveira Vitória, ES-Brasil 201.73.14.232 | thanks for the information |
| Tuesday November 13, 2007 Floyd Revan Sandy Point, St.Kitts 76.76.168.56 | I am happy that information on Tichomonas gallinae was posted. It is very interesting organism that is rarely heard of. The information is important and makes well for research material. |
| Thursday March 6, 2008 Spiros Kalamaras Thessaloniki, Greece 79.130.169.61 | Gentlemen you have amazing information not only about trichomonas gallinae but the entire site is valuable and precious even for the most experienced breeders. Congratulations and keep on going.... |
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