Gordon A Chalmers, DVM
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.
|Last Updated ( Saturday, 31 January 2009 )|