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Trichomonas gallinae is a common flagellate protozoan found in the upper digestive tracts of birds, especially columbiformes (doves and pigeons). It is the causative agent of “canker” in pigeons and “frounce” in raptors. T. gallinae is present in nearly 80-90% of pigeons, but most show no signs of disease.1,2 It is also the most universal and most easily recognized form of internal parasitism in raptors. Trichomonas infections occur in all species of mammals and birds, with the peculiar exception of rabbits. They have also been isolated in many species of reptiles, amphibians, fish and invertebrates. Structure and Physiology The name trichomonas was first given to a genus that was believed to possess three anterior flagella. However, several species have more than three flagella, but the name remains . Most trichomonads are 5 x 19 um and have a clearly visible axostyle which projects beyond the posterior end. The life cycle of trichomonads is simple; they reproduce by binary fission and no sexual or cystic stages are known. Trichomonads are generally anaerobic. They can, however, grow under low oxygen tensions. Mitochondria, cytochromes and functional TCA cycle are absent. In the cytoplasm, energy is derived from glucose which is broken down into pyruvate or succinate. Trichomonads have morphologically distinct organelles called hydrogenosomes which contain the enzymes responsible for pyruvate metabolism. These organelles produce H2 and therefore Flagyl (metronidazole), which blocks H2 production, is an affective treatment.5 Pathogenesis Most trichomonads are nonpathogenic commensals, but a few are pathogenic. T. gallinae varies greatly in its virulence, with virulent strains linked to epizootics.1 Interestingly, infection and mortality rates are not closely linked. The disease varies from a mild condition to a rapidly fatal one with death in 4-18 days post infection.6 Transformation of T. gallinae into pathogenic forms was described by Narcisi, et al. They exposed an avirulent strain, no longer infective to nonimmune pigeons, to a virulent strain. The avirulent strain was injected into mice where it showed increased pathogenicity.7 Apparently lentogenic infection may cause no lesions whereas velogenic strains may cause rapid mortality.5 Immunity conferred on the host as a result of infection is apparently temporary, but one report states infection with a nonvirulent strain can result in subsequent resistance to lethal strains.1 Therefore, flocks lacking previous exposure to the organism are at particular risk of infection. T. gallinae is transmitted directly from adults to squabs in pigeon milk and drinking water. Raptors acquire the protozoan by eating infected pigeons, however, feces, saliva, and crop secretions also serve as vehicles of dissemination.8 Pathogenic changes associated with trichomonas infection range from mild inflammation of the oral mucosa to large caseous lesions that block the lumen of the esophagus. The early lesions in the mouth are small, yellowish, circumscribed plaques on the mucosa. More velogenic strains can cause caseated abscessation of the oropharynx. Eventually these space occupying lesions obstruct the esophagus and trachea resulting in emaciation and asphyxiation. Although lesions are usually seen in the mouth and oropharynx in raptors, it can also affect other mucus membranes. Jessup reports one owl having eye lesions from infection spreading into the nasolacrimal duct.2 Bony involvement can occur after soft tissue destruction. The organism does not survive posterior to the proventriculus, except in pigeons. Unlike other birds infected with T. gallinae, pigeons are susceptible to secondary organ invasion by virulent strains of the parasite. The visceral form of the disease involves the liver and gastrointestinal tract, causing organ dysfunction. Diagnosis and Treatment Diagnosis can be accomplished by clinical signs and direct exam or culture. Clinical signs of trichomoniasis include pronounced swallowing motions, excessive salivation and caseous-diphtheritic membranes of the mouth, crop and pharynx.3 Differential diagnoses should include capillariasis, hypovitaminosis A. Positive identification of the organism can be made by microscopic examination of material scraped from the oral cavity of infected birds. Inoculation of the material into growth medium can also be done, as both methods provide satisfactory results. A new culture system called InPouch has practical advantages over the usual in vitro system.9 If a bird is dyspneic or cannot swallow food, oral plaques can be removed with thumb foreceps. Most treatment regimens use imidazole-class antiprotozoals with good success (dimetridazole, metronidazole) at 20-25 mg/lb for 1-2 days.2,8 Conclusion Trichomonas gallinae is a flagellate parasite of many animals, but is most prevalent in columbiformes and raptors. The parasite initially infects the upper digestive tract, causing ulcers and plaques. More virulent strains lead to caseous masses that can occlude the oropharynx causing emaciation, asphyxiation and death. In pigeons, the protozoan can gain access to the circulatory system via oral lesions and infect visceral organs. T. gallinae can be diagnosed by direct exam or various culture methods. It can be successfully treated using imidazole drugs. |
