Pigeonbasics Forum: DETAILED THREAD ON CANKER TRICHOMONIASIS - Pigeonbasics Forum

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Posted 5 October 2009 - 15:33 PM

Trichomoniasis is an infrctious protozoal disease of many species of birds with a special prevalence for doves and pigeons.

It is caused by a unicelluar flagellate, Trichomonas columbae, has a world-wide distribution and is familular to all fanciers who have been in the sport for some time. Significant in the racing of pigeons, it presents as an acute disease with a high mortality amoungst younger stock or as an erosion disease with a chronic course, in older racers.


Canker in pigeons i cause by an infection with Trichomonas cilumbae, a motile protozoal organism with four flagellae at the anterior end, which give the organism motility and enhance it's microscopic visibility. Trichomonas occur in and is pathogenic to many animal species, in particular the doves, falcons and hawks. (Raptors become infected after feeding on infected pidgeons and odves). Other relatives of the parasite are found naturally in many species of birds (ducks, turkeys, owls, hawks, grouse, coots, cormorants etc), without apparent harm to the host. Pathogenic species e.g. T. foetus and T. vaginalis inhavit the general tract of bovine and primate speices and can be difficult to eradicate. According to Whitney, Five strains of the parasite have been ifentified in pigeons, with three occuring to any great extent. We see three distinct forms of the disease but whether these are caused by different individual strains, has yet to be determined.


It appears as if pigeons are natural hosts to trichomonas with almost every pigeon hosting the organism in the crop and gulley. Premunity exisits in adult birds but its duration and effectivness is stress-related.
Transmission of the disease occurs when pigeon are billing and feeding young. Stabler demonstrated that newly-hatches squabs are infected at their first feed. Drinking from a communal water bowl spreads the infection between adult birds in the loft.
The disease is more prevalent during the summer months and we see a marked reduction in the inceidence of acute cases in winter. This is probably related to better survival of the organism outside the body of its host when outside tempretures are closer to normal body temprature. At temperatures of 25c and above, moist grains have maintained viable T.gallinae for atleast 13 days.

Trichomonas will survive for one whole day in water at 25c

Clinical Signs and Pathogenesis

Signs of infection appear a week after introduction of the organism. One of three forms can occur.

1. Classical (acute) form.

This form of the disease usually occurs in youngsters, from babies in the nest until 2-3 months after weaning. The birds are obviously sick, with ruffled feathers, loose watery droppings, loss of weight, excessive thirst and decreased appetite. They are apathetic, lose interest in their surroundings and may be picked up without moving. When this stage is reached mortalities must be expected. Such babies probably never would have developed into strong racers should they have survived and it is better to cull them at this stage


Upon examination the bird will usualy have yellow cheesy growths in the throat, adherent to the muscosa. Many stages of severity occur. We see one or two match-head size lesions, indicating a more resistant bird to one with large cheesy lumps, nearly filliwing the throat and mouth and hindering eatting. The growths may encroach upon the epiglottis, causing respiratory distress. From the throat, infection may spill over into the upper airways and spread to the internal organs, especially the liver and heart.
A less prevalent form occurs in nestlings where the navel is affected. infection spreads rapidly from the enlarged navel area to the abdomen and the liver. The abdomen appears pendulous, swollen and soft and the baby rapidly loses weight and dies. Severe liver damage occurs and though treatment might save it's life, a healthy robust bird cannot be produced; culling is preferable.

2. Obstructive Form.

I have categorized this form only because the predilection site of the parasite leads to a distinct disease syndrome. It is probably caused by a sigular strain of T. columbae, not occuring commonly. The morbidity in a flock is high, in the region of 60 to 70 percent, with a 100 percent mortality.


Birds of all ages affected, even though they are initially in good conditionand the occurrence of outbreaks is not related to stress levels. Initially, the pigeons appearto eat and drink normally but gradually lose condition. Some birds may vomit. At a more advanced stage, the pigeons are unable to swallow their food, stand very upright with heads high, necks stretched and make repeated efforts at swallowing. (Their posture has been likened to that of a penguin). Their crops are full of water but the pigeons gradually become more and more dehydrated. lose weight and die. Numerous trichomonads are seen on microscopic examination of a throat swab.


The typical yellow caseous lesions of trichomoniasis are found in the short area of distal oesophagus, between the crop and the proventriculus. This section lies in the throat inlet, which is narrow and serves as entrance for the gullet and trachea to the inside of the body. The organisms attack the oesphaageal epithelium here and produce the typical cheesy growths which enlrage, invade the surrounding tissues and occlude the thoracic inlet. Total obstruction to the passage of food and water follows, with stravation, dehydration and death.

Usually no other signs of trichomoniasis are seen. In a few cases the pressur is more sever on the trachea causing marked respitatory distress with a drooping tail, heaving sternum and open mouth breathing. Death quickly ensues.
Similar invasive yellow grothers have been seen in the throat, mouth area (palate, side of the mouth etc) and sinuses, causing the deaths of large numbers of free-living wild doves. It is a highly contagious, fatal infection and its locality is very specific, not occuring elsewhere in the body. More recently a similar infection appearing in adult racing pigeons but in sporadic instances. It is thought that a specific strain is responsible for the symptoms.

3. Subclinical form.

All the bird that are carried of trichomonads and are not showing signs of the disease, are grouped here. They have had the disease clinically and revovered or may never have shown a sign of ill health. (it is contentious whether they ought to be known as carriers of the infection or as birds with a premunity. They are not carriers in the sense that we normally undertsnad the term.) i do not believe as a truly symbiotic relationship can exisit between a racing pigeon and trichomonad parasites. For a pigeon to be able to perform regulart at it's best, it must have NO parasites. Health alone is not sufficient - it must posses super health. Any evidence of meaningful numbers of trichomonads found in the throat of a pigeon involved in racing, is detrimental to its chance of being successful.

Within the concept of subclinical infection many stages are seen.
The most severe usually have one of two yellow lesions in the back of the throat, but show no sign of ill-health. Others may demonstrate numerous white spots, pinhead in size, on the curtain in the back of the throat. These spots are of no consequence at this stage as they are possibly healed, calcified lesions of a previous attack of canker. (There is still some doubt as to etiology of these spots; signs of herpesvirus infection, abscesses caused by E. coli, calcoliths in salivary glands etc., have all been popular as cayses.) The spots are seen most often in yearling pigeons and generally diappear after a few month. If the bird no longer harbous trichomonas the spots, which do not respond to treatment, do not interfere with racing.
Some birds have lost a section of the curtain from a previous epsode of crop canker. This will not affect their racing provided there are no active trichomonads
The largest group of birds are those that have never shown any obvious sign of infection, yet upon microscopic examination are found to harbour many organisms. These are the carried, Regarded as healthy by many fanciers but who consist of the real problem, by reducing the performance of a race team and being a constant source of weak and sickly babies in a breeding loft. At best they reproduce the carrier state in their offspring, who perpetuate their poor racing performance. Any 'Better' breeding stock, introduced from another loft, is soon reduced to the standard of the old stock as infection spreads and their offspring sugger the same fate as that of their predecessors.

Virulence and Immunity.

At present there is no explination for the divergence of virulces seen in the various strains of T.columbae. Neither are there satisfactory explinations for the mechanism of premunity nor for the factors which reduce that permunity and cause the typical lessions to appear.

We know that;

1. Different strains, varying in virulence, exist.
2. Cross-immunity exists between virulent and avirulent strains.
3. A birth that has survived has been immunixed by exposure, reains it's immunity for over one year.
4. When immune birds are subjected to challenge by a virulent strain they can become carriers of the virulent strain and transmit it to other birds.

I have gone into some detail above, so that the reader may understand why it is desirable that every racing bird is treated. Because premunity exisits in explosed, revovered birds, they can become carriers of a virulent strain. If at some stage, due to stress factors of racing or breeding, the premunity breaks down, these bird would be susceptible immediatly to the birulent strain, which they are carrying with them. At any time they are able to pass o this virulent strain to a non-immune loftmate, or to their own progeny.
Trichomonisis is ubiquitous and i believe that breeding stock need not be kept sterile of the germ but be allowed to build up a mild trichomonad population. Continued carful monitoring and treatment at the first sign of the disease, allows youngsters to build some premunity before they are transfered to the main loft. In this race loft, particularly during the racing season, all birds must be streile of trichomonads as far as possible.


The obviously sick, acutely-affected youngster with yellow growths choking his throat, is parctically self-disgnostic. Confirmation of disease is obained by squashing a little of the inspissated pus from the edge of the lesion, mixing it with a few drops of water on a glass slide and microscopically demonstrating thousands of trichomonads. Internal forms of trichomoniasis can only be disgnosed on autospy.
The subclinical form is easily demonstrated. A cotton bud is moistened and a throat and crop swab is taken. (if a cotton bud is too short to reach into thee crop, a home-made swab, made from a splintered tongue depressor and cotton wool, serves equally well.) With an assistant holding the pigeon, the examiner holds the bird's head, streches the neck and opened the mouth with one hand. With the other hand he introduces the cotton bud into the pigeons throat and down into the crop, where it it is movedup and down five or six times, in order to collect mucus. The cotton bud is now squeezed out over a glass slide and a drop of the liquid is examined under a microscope at medium (100 X) magnification.
Once warmed by the microscope light source, the trichomonads appear mobile and jiggle together in small clumped groups, or if in single state, they move briskly in small haphazard circles or spin dizzily. It is essential that atleast 5-10% of the birds per loft are examined, because it not infrequently happens that 2 or 3 birds are negative with the fourth or fifth strongly poritive. Only one strongly positive bird out of the five examined, is needed to recommend treatment for the whole group. Re-examination, two weeks following treatment, is recommended.

Differential Diagnosis.

Canker must be distinguished from two other disease conditions:

1. Diphtheroid pox.

Position. The yellow pox lessions in the mouth and throat may resemble crop canker but the lesions of pox, resulting when birds have fought, are usually more in the front, middle and side of the mouth. Canker is seen further back in the throat.

Adhesiveness. Pox lesions are well attached to the underlying mucosa and have a good blood supply, bleeding profusely of forceibly removed, whereas canker growths are fairly loose and do not bleed much if removed.

Other signs. The pigeon with distheroid poc, or its loftmates, will usually have other external pox lesions.

Microscopical. The pigeon with pox may test negatively for the presence of trichomonads, the canker bird will always be positive. Be aware that some birds have both pox and canker.

2. Pigeon Herpes Virus. (PHV)

Differentiation from canker may be difficult, especially where both conditions occur together.

Pathogenicity. PHV is the more pathogenic condition. Affected bird are extremely dull and listless and appear to be sleepy, oblivious to their enviroment.

Adhesiveness. PHV does not cause distinct lumps of pus, but tends to coat the mouth and throat with a purulent exudate which is non-adherent to the mucosa. Lessions of PHV emit a rotten stench.

Response to treatment. Birds affected by PHV do not respond to treatment.

Confirmation. Virus isolation is the only method of confirming an herpes virus outbreak. Finding intranulear inclustions in the liver is strongly suggestive.


Flock treatment

Spin-offs from the pig and poultry industies gave us first 2-amino-5-nitrothiazole (Enheptin, Entramin, Tricoxine etc.), and later dimetridazole (Emtryl, Dovatric etc.). Metronidazole (Flagyl, Meditrich, Carnidazole (Spartix)  and ronidazole (Ridsol S, Tricho-plus) are now added to the list and have wider spectrum of safety. Newer german-made progucts like Gamba-Metro are also safe and effective. Though most remedies are excellent and can be used with success, in all cases control checks must be done two weeks later to the test efficacy treatment.

individual treatment. Valuable pigeons can be treated singly by first gently removing as many lesions from the mouth and throat as possible, after which a concentrated solution of dimtridazole (Emtryl) or 2% iodine solution is brushed onto the affected parts. Metronidazole, in pill form, may be given instead of the dimtridazole and antibiotic injection is always included to treat secondary ingections. It is debatable whether a pigeon that suffers clinically from trichomoniasis is worth keeping. Current thought is that it must be immunodeficient and that it could pass on its weak resistance to its offspring.

Flock treatment by dosing each individual pigeon with a pill is safe and very effective. The method is often adopted for pigeons that are being prepared for a special race. Carnidazole (Spartrix), Dimetridazole (Dovatric), Metridazole (Flagyl, Meditrich), Gamba-tabs and Gambamix-Trio are just some of the excellent products avaliable.
Early in 2003 a new formulation, reportedly excellent against trichomoniasis, was developed in Norway. According to reports, BERIMAX forte, a plant extract, was able to clear a pigeon of trichomonas germs within a short time. We await further trials and the release of a product that promises to be a good alternative treatment.


Control of the disease and prevention of acute outbreaks, must resolve around:

1. Regular treatment.
2. No breeding during high summer in hot moist climates.
3. Careful attention to hygeine - especially reguarding regular cleaning and disinfection pf water thrghs, clean fresh water and never allowing food to become soiled.
4. Careful surveillance of the number of pigeons kept per unit of loft space. Overpopulation, especially in summer, can lead to explosive outbreaks of the disease. (Maximum number is two pigeons per cubic metre.)
                                         WRITTEN (COPIED) BY BRUCE
                                         IDEA BY BLAZ UNCLE GARY C
               copped from the great book by dr wim peters FIT TO WIN
1st fed eatbourne 9th nat 1st fed ypres 18th nat1st fed marlborough 19th nat 1st fed ypres 8th nat 1st fed maidstone 16th nat 1st fed yb open newark 1st fed yb nat

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