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PicturesTop of page
IdentityTop of page
Preferred Scientific Name
- avian trichomoniasis
International Common Names
- English: avian trichomonosis; canker; frounce; roup; Tichomonas gallinae infection in birds; trichomoniasis, trichomonas gallinae, tetratrichomonas gallinarum, in birds; trichomonosis, avian; Upper digestive tract trichomoniasis
OverviewTop of page
Trichomonas gallinae (Rivolta, 1878) is a flagellate protozoan that infects a variety of birds, especially columbids (doves and pigeons) worldwide (BonDurant and Honigberg, 1994). This trichomonad species occurs in the upper digestive tract, and some virulent isolates can spread to other parts of the body. T. gallinae is the organism originally described by Rivolta (1878) as Cercomonas gallinae from the mouth and crop of a pigeon. The taxonomic position of the genus Trichomonas was reported by Levine et al. (1980):
Phylum: Sarcomastigophora Honigberg and Balamuth, 1963
Subphylum: Mastigophora Diesing, 1866
Class: Zoomastigophorea Calkins, 1909
Order: Trichomonadida Kirby, 1947 emend. Honigberg, in Camp, Mattern and Honigberg, 1974
Family: Trichomonadidae Honigberg, 1963
Subfamily: Trichomonadinae Honigberg, 1963
T. gallinae, a very common parasite of pigeons, causes serious losses in these birds, and also in turkeys. In columbids, T. gallinae is typically transferred in pigeon ‘milk’ from the crop of an infected parent bird to the offspring within a short time after the latter have hatched from the eggs. All the offspring become infected. Once acquired, the infection can be very long-lasting, some infections persisting for up to 2 years (BonDurant and Honigberg, 1994).
Experimental infections have been used in pathogenic studies, especially subcutaneous mouse assay (Honigberg, 1961; Frost and Honigberg, 1962). A number of birds have been infected experimentally. They include the bobwhite quail (Colinus virginianus), canary (Serinus canaria), English sparrow (Passer domesticus), barn swallow (Hirundo rustica), goldfinch and song sparrow (Melospiza melodia), Tovi parakeet (Brotogeris jugularis) and cardinal (Cardinalis cardinalis) (Levine, 1973). Parenteral infections have also been produced experimentally in rats and kittens (Levine, 1973). T. gallinae caused abscesses following subcutaneous injection in mice (Frost and Honigberg, 1962).
T. gallinae is an exceptionally hardy parasite, and can survive sub-optimal environmental conditions without a cyst form (indeed, no such form is known in the genus). Survival in tap water for short periods ensures that drinking water can be a source of infection for domestic fowl. An individual bird may lose the parasite, but since pigeons live in groups, the close contact among them ensures reinfection. The behaviour of pigeons is conducive to spread of the parasite. The behaviours important in transmitting infection are billing during courtship and feeding (involving ‘pigeon milk’) of the young by infected parent birds. However, adults can also be reinfected from water sources frequented by infected pigeons. An infection may also be established in a raptor that has fed on an infected prey bird (BonDurant and Honigberg, 1994).
The spread of T. gallinae to domestic fowls such as turkeys and chickens, is dependent primarily on obtaining the parasite from drinking water from sources visited by feral pigeons. It seems that, in view of the feeding habits of domestic fowls, in these birds epizootics of T. gallinae are dependent on the presence of pigeons as the reservoir hosts. In chickens and turkeys, the organism may be transmitted in drinking water, but not from one generation to the next as in the Columbiformes.
Since T. gallinae is not found in the intestinal tract beyond the muscular stomach, the parasite cannot be transmitted in faecal droppings. The routes of escape can only be the nares, eyes and mouth, the last being the most important portal of exit. In all birds other than columbids, water is the main medium of infection (BonDurant and Honigberg, 1994).
In the pigeon, trichomonosis is mainly a disease of young birds; 80-90% of the adults are infected but show no signs of disease (Levine, 1973).
DistributionTop of page
Trichomonas gallinae infects a variety of birds all over the world. The domestic pigeon, Columba livia, is the primary host of this flagellate. Other columbiform hosts have been found to harbour the parasite, as have domestic fowls (especially turkeys), Java sparrows, various raptors, and sea gulls. Experimental infections have been established in many kinds of passerine birds.
Distribution TableTop of page
The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.
|Continent/Country/Region||Distribution||Last Reported||Origin||First Reported||Invasive||Reference||Notes|
|Bahrain||Present||Samour et al., 1995|
|China||Present||Zhang et al., 1982|
|India||Present||Bhattacharya et al., 1997|
|Iran||Present||Bozorgmehri-Fard and Moeinvaziri, 1985|
|Saudi Arabia||Present||Silvanose et al., 1998; Samour and Naldo, 2003|
|Turkey||Present||Aydin et al., 2000|
|United Arab Emirates||Present||Silvanose et al., 1998|
|Egypt||Present||Abd-El-Motelib and Galal, 1994|
|South Africa||Present||Huchzermeyer, 1978; Pepler and Oettlé, 1992|
|Canada||Present||Present based on regional distribution.|
|-British Columbia||Present||Rosenfield et al., 2002|
|Mexico||Present||Moedano and Moreno, 1976|
|USA||Present||Present based on regional distribution.|
|-Arizona||Present||Boal et al., 1998; Rosenfield et al., 2002|
|-California||Present||Rupiper and Harmon, 1988; Willoughby et al., 1995|
|-Connecticut||Present||Sasseville et al., 1988|
|-Florida||Present||Conti and Forrester, 1981|
|-Hawaii||Present||Kocan and Banko, 1974|
|-New York||Present||Tangredi, 1978; Stone and Nye, 1981|
|-North Dakota||Present||Rosenfield et al., 2002|
|-Texas||Present||Glass et al., 2001|
|-Utah||Present||Ostrand et al., 1995|
|-Wisconsin||Present||Rosenfield et al., 2002|
Central America and Caribbean
|Trinidad and Tobago||Present||Kaminjolo et al., 1988|
|Brazil||Present||Present based on regional distribution.|
|-Rio Grande do Sul||Present||Tasca and Carli, 1999a; De et al., 1979|
|-Sao Paulo||Present||Pereira and Almeida, 1943|
|Chile||Present||Toro et al., 1999|
|Croatia||Present||Greguric et al., 1986|
|Greece||Present||Githkopoulos and Liakos, 1987|
|Italy||Present||Catelli et al., 1999|
|Macedonia||Present||Kulisic et al., 1996|
|Poland||Present||Native||Wieliczko et al., 2003|
|Portugal||Present||Ponce et al., 2002|
|Russian Federation||Present||Greguric et al., 1986|
|Slovenia||Present||Dobeic, 2003; Dovc et al., 2004|
|Spain||Present||Martínez-Moreno et al., 1989; Ponce et al., 2002|
|UK||Present||Cooper and Petty, 1988; Cousquer, 2003|
|Yugoslavia (former)||Present||Kulisic et al., 1996|
|Australia||Present||McKeon et al., 1997|
PathologyTop of page
Lesions of T. gallinae trichomonosis appear as firm, yellow, caseous areas. In the brains and liver they may replace considerable amounts of the organ involved. In the upper digestive tract they may appear as huge, firmly attached masses (mouth) or as disc-shaped lesions -‘yellow buttons’- with central, spur-like projections (oesophagus and crop). Massive lumps may occur in the tissues of the neck, or encircling caseous regions may involve the mucosa of the oesophagus, crop, or proventriculus (Samour et al., 1995).
Certain isolates of the parasite appear to have a predilection for some tissues. The Jones’ Barn isolate almost invariably attacks the liver of infected pigeons, only moderately involving the regions of the head and neck. The Mirza isolate, on the other hand, causes extensive damage to the tissues of the head and the mucosa of the upper digestive tract, only rarely entering the abdominal cavity (Perez-Mesa et al., 1961; BonDurant and Honigberg, 1994).
The lining of the mouth, pharynx, oesophagus crop, and glandular stomach have commonly been involved. The head sinuses, orbital regions, and brain are sometimes infected. Caseous masses in the neck tissues are common. The most frequently involved visceral organ is the liver. The liver surface may become almost entirely covered with caseous lesions which, by contact extension, may involved the intestinal and gizzard surfaces, sub-sternal membranes, air sacs, lungs and pericardium. The myocardium may become caseous, apparently as an extension of processes in the pericardium. The pancreas is also sometimes infected. In young squabs the navel region is sometimes so thoroughly involved that the skin and adjacent tissues, as well as the local organs, are cemented in one huge caseous mass. The caseous lesions of the upper digestive tract may become so extensive that they completely occlude the lumen, making passage of food an impossibility. Large quantities of fluid frequently accumulate in the crop.
The more rarely involved sites include spleen, kidney, trachea and upper respiratory tract, bone marrow, and the middle ear. It has been noted by several observers that lesions of the upper digestive tract frequently end abruptly at the glandular stomach (Samour et al., 1995).
The histopathology of infection with T. gallinae has not been extensively treated, although some observations have been made (Stabler, 1954).
Factors affecting pathogenicity
In vitro cultivation of T. gallinae affects inherent pathogenicity levels in infections of mice (Honigberg, 1961) and pigeons (Stabler et al., 1964). In mice there is a progressive decrease in the mean volume of subcutaneous abscesses with cultivation time (Honigberg, 1961). In avian hosts, after between 17 and 21 weeks of cultivation, virulence for pigeons was lost by the JB isolate, although it could be restored after at least up to 28 weeks of cultivation, by serial passages in non-immune pigeon squabs (Stabler et al., 1964).
It was also demonstrated by Stabler et al. (1964) that the presence of antibiotics, such as penicillin and streptomycin, in the culture medium results in more rapid attenuation of virulence. When isolated in the presence of these antibiotics, the JB isolated became avirulent within 7.5 to 9 weeks of in vitro culture.
DiagnosisTop of page
Upper digestive tract trichomonosis (oral cavity, choanae, tongue, pharynx, crop, upper oesophagus and infraorbital sinuses) is readily diagnosed by observation of the lesions together with finding of the protozoa (Levine, 1973; Samour et al., 1995).
The throats of pigeons are swabbed and the swabbings used to inoculate trypticase-yeast extract-maltose (TYM) medium for incubation. Samples are cultured axenically in vitro,without antibiotics, in a TYM medium without agar; pH 7.2, supplemented with 10% (v/v) heat inactivated horse serum, at a temperature of 37°C (±0.5). Some cultures can be established without the use of antibiotics, others are isolated with 5000 units of penicillin and 1000 µg of dihydrostreptomycin per ml of the original culture. Dying of parasites is strongly recommended to observe morphological features. Parasites from a 24-h culture in TYM medium are stained by the Giemsa method (Carli et al., 1979; Tasca and Carli, 1999).
List of Symptoms/SignsTop of page
|Digestive Signs / Anorexia, loss or decreased appetite, not nursing, off feed||Sign|
|Digestive Signs / Congestion oral mucous membranes, erythema, redness oral mucosa||Poultry:Day-old chick,Poultry:Young poultry,Poultry:Mature female,Poultry:Cockerel,Poultry:Mature male||Sign|
|Digestive Signs / Dysphagia, difficulty swallowing||Sign|
|Digestive Signs / Erythema, redness of pharynx||Poultry:Day-old chick,Poultry:Young poultry,Poultry:Mature female,Poultry:Cockerel,Poultry:Mature male||Sign|
|Digestive Signs / Esophageal obstruction||Poultry:Day-old chick,Poultry:Young poultry,Poultry:Mature female,Poultry:Cockerel,Poultry:Mature male||Sign|
|Digestive Signs / Excessive salivation, frothing at the mouth, ptyalism||Sign|
|Digestive Signs / Inability to open (trismus) and / or close jaw, mouth||Sign|
|Digestive Signs / Oral mucosal ulcers, vesicles, plaques, pustules, erosions, tears||Sign|
|Digestive Signs / Pharyngeal ulcers, vesicles, erosion, papules, sores pharynx||Sign|
|Digestive Signs / Tongue protrusion||Sign|
|Digestive Signs / Tongue ulcers, vesicles, erosions, sores, blisters, cuts, tears||Sign|
|General Signs / Ataxia, incoordination, staggering, falling||Sign|
|General Signs / Dysmetria, hypermetria, hypometria||Sign|
|General Signs / Increased mortality in flocks of birds||Sign|
|General Signs / Lack of growth or weight gain, retarded, stunted growth||Sign|
|General Signs / Laryngeal, tracheal, pharyngeal swelling, mass larynx, trachea, pharynx||Sign|
|General Signs / Neck swelling, mass cervical region||Diagnosis|
|General Signs / Oral cavity, tongue swelling, mass in mouth||Sign|
|General Signs / Orbital, periorbital, periocular, conjunctival swelling, eyeball mass||Sign|
|General Signs / Sudden death, found dead||Sign|
|General Signs / Underweight, poor condition, thin, emaciated, unthriftiness, ill thrift||Sign|
|General Signs / Weight loss||Sign|
|Nervous Signs / Dullness, depression, lethargy, depressed, lethargic, listless||Sign|
|Ophthalmology Signs / Blindness||Sign|
|Ophthalmology Signs / Lacrimation, tearing, serous ocular discharge, watery eyes||Sign|
|Ophthalmology Signs / Purulent discharge from eye||Sign|
|Pain / Discomfort Signs / Mouth, oral mucosal or tongue pain||Sign|
|Respiratory Signs / Abnormal breathing sounds of the upper airway, airflow obstruction, stertor, snoring||Sign|
|Respiratory Signs / Dyspnea, difficult, open mouth breathing, grunt, gasping||Sign|
|Respiratory Signs / Epistaxis, nosebleed, nasal haemorrhage, bleeding||Diagnosis|
|Respiratory Signs / Mucoid nasal discharge, serous, watery||Sign|
|Respiratory Signs / Nasal mucosal ulcers, vesicles, erosions, cuts, tears, papules, pustules||Diagnosis|
|Respiratory Signs / Purulent nasal discharge||Sign|
Disease CourseTop of page
Trichomonas gallinae causes a variety of pathological manifestations depending on the isolate of the parasite and species of bird infected (Jessup, 1980; Baker, 1986; Cooper and Petty, 1988; Henderson et al., 1988). The normal sites of this parasite are the mouth, pharynx, oesophagus and crop, with most of the isolates never leaving the upper digestive tract. The virulent isolates may cause lesions in the upper digestive tract of birds; some of these isolates spread to other parts of the body. The parasite initially infects the upper digestive tract, causing the formation of ulcers in the mouth, sinuses, orbital region, pharynx, oesophagus, crop and even the proventriculus (Levine, 1973), which allow the pathogen to enter the circulatory system. The trichomonads later gain access to the liver, and cause the formation of caseous lesions. Non-immune pigeons may die of liver dysfunction within 14 to 17 days after inoculation. Other virulent isolates include those that invade the head and neck sinuses and from there enter the eye regions and brain. Other virulent T. gallinae establish in the organs of the thoracic and abdominal cavities, such as, lungs, heart, liver, and pancreas. Transmission of T. gallinae is horizontal (BonDurant and Honigberg, 1994).
EpidemiologyTop of page
Trichomonas gallinae infects pigeons and a variety of birds, including turkeys, and has caused important economic losses in this species as well as in chickens and pet birds (BonDurant and Honigberg, 1994). In pigeons and mourning doves, trichomonosis is transmitted from adults to the squabs in the pigeon milk, which is produced in the crop. The squabs are infected within minutes after hatching. Hawks and other wild raptors become infected by eating infected birds. Turkeys and chickens are infected through contaminated drinking water. Feral pigeons and other columbid birds are usually the original source of infection (Levine, 1973).
Impact: EconomicTop of page
Trichomonas gallinae is very common in domestic pigeons, in which it often causes serious losses. Present data regarding economic losses are not available. In 1954 the US Department of Agriculture estimated that the parasite causes an annual loss of US $47,000 in turkeys; in 1965, it was estimated that the flagellate caused an annual loss of US $23,000 in chickens and US $1,186,000 in turkeys. T. gallinae is common in mourning doves, and may cause serious losses in these birds (Levine, 1973).
Disease TreatmentTop of page
Treatment is only feasible in captive birds because the drugs used for treatment must be administered orally, either by force feeding or by treating the food and/or water. Antiprotozoal medications that have been used are dimetridazole, metronidazole, copper sulfate, quaternary ammonia, carnidazole, 2-amino-5-nitrothiazole and aminonitrothiazole. Some of these medications are under review and some can be specifically used only on non-food birds (metronidazole) (Frank, 2004). Ronidazole presents excellent activity against T. gallinae with high safety margin (Samour and Naldo, 2003). Dimetridazole was formulated for drinking water medication and as a prolonged-release tablet. To suppress T. gallinae infection, successfully, medicated drinking water containing dimetridazole (400 mg/L) has to be administered for at least 3 days (Inghelbrecht et al., 1996).
Treatment of wild birds is difficult because of the availability of natural food and water sources.
Resistance of T. gallinae isolates to the nitroimidazole drugs ronidazole, carnidazole and metronidazole has been reported (Franssen and Lumeij, 1992; Munoz et al., 1998). Although ronidazole showed a greater potency than the other nitroimidazole derivatives, 8-22 times more drug was necessary for efficacy compared with the others (Munoz et al., 1998).
Prevention and ControlTop of page
Effective treatment of a population of susceptible birds involves removal of the source of infective organisms and treatment of treatable infected individuals. Source removal often requires the destruction of chronically infected birds and protection of water sources from wild birds. Drugs have been employed, either in drinking water or topically in the mouth and throats of the birds. Older remedies included anise and aniline oil, tartar emetic, acriflavin, iodine with or without glycerine, carbolic acid with glycerine, ‘sulfoliquid’, sulfathizole and sulfanilamide, nitrate stick, powdered alum, and writers ink (Stabler, 1954; BonDurant and Honigberg, 1994).
In addition, the following preventive measures are advised: practice a high standard of sanitation at all times; do not add birds to an established flock without quarantine for 30 days; and provide a source of clean, fresh water and eliminate all sources of stagnant water (Butcher, 2003). In captive birds, cull or treat carrier birds, cull adults whose offspring become infected, regularly disinfect food and water sources with 10% bleach solution, screen out (exclude) wild birds to protect from contamination by wild pigeons and other birds, segregate young birds from adults, and segregate susceptible birds from recovered or carrier birds. To minimize infections in wild birds, minimize dove and pigeon concentrations at feeders (or do not feed) and at water receptacles. Severely affected captive or wild birds should be killed.
ReferencesTop of page
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