Trypanosomes of birds

Trypanosomes have been reported under a large number of names from many species of birds. They all look very much alike and probably belong to relatively few species. However, extensive cross transmission studies are needed to establish their relationships, and, until these are carried out, it is probably best to refer to them by the names under which they were first described.

Trypanosoma avium Danilewsky, 1885 was first described from owls (scientific name not given) and roller-birds (Coracias garrulus) in Europe, and has since been reported from a wide variety of birds, including crows (Baker, 19 56) and Canada geese (Diamond and Herman, 1954). Baker (1956 a, b) transmitted it from the rook (Corvus frugilegus) and jackdaw (C. monedula) to canaries, but failed to transmit it to a single 3-day-old chick.

T. calmettei Mathis and Leger, 1909 was described from the chicken in southeast Asia; it is about 36 u long. T. gallinarum Bruce ei al., 1911 was described from the chicken in central Africa; it is about 60 u long. T. hannai was described from the pigeon, and T. numidae from the guinea fowl.

Avian trypanosomes are very polymorphic, sometimes attaining great size. They may be 26 to 60 u long or even longer. The kinetoplast is generally a long distance from the posterior end. There is a free flagellum, and the body is often striated.

Blood-sucking arthropods such as mosquitoes and hippoboscids are believed to be the vectors of avian trypanosomes, but the only complete life cycle was worked out by Baker (1956,a, b) for T. avium from rooks and jackdaws. He found that in England the hippoboscid fly, Ornithomyia avicularia, acts as the vector. Upon ingestion with a blood meal, the trypanosomes change into the crithidial form in the midgut, multiply by binary fission in this form, and pass to the hindgut. They multiply further and then turn into a piriform stage which develops in turn into a small, metacyclic trypanosome form. Birds become infected when they eat infected insects. The metacyclic trypanosomes penetrate the membranes of the mouth, esophagus and/or crop and probably invade the lymphatic system, developing into large forms which first appear in the blood 18 to 24 hours after infection.

According to Baker, there is no multiplication in the avian host, the trypanosomes simply becoming larger. This would account for their sparse numbers in the blood. They persist in the rook and jackdaw over-winter, being more or less restricted to the bone marrow, and reappear in the peripheral blood in the spring. Diamond and Herman (1954), too, found that T. avium could be isolated from the bone marrow of Canada geese much more readily than from the blood.

Nothing is known of the pathogenicity of the avian trypanosomes. They are presumably non-pathogenic.

Avian trypanosomes can be readily cultivated on several media, including NNN medium and the SNB-9 (saline-neopeptone-blood) medium described by Diamond and Herman (1954).