Toxoplasmosis in Chickens

Abstract

Pools of tissues from the ovaries and oviducts of apparently healthy hens, obtained at a poultry processing plant, were examined for Toxoplasma gondii cysts by the digestion-inoculation technique. Each pool contained organs from ten birds. Twelve pools of a total of 62 were found positive. A subsequent survey of 108 individual hens revealed four with chronic toxoplasma infection; none of 108 shelled eggs taken from these birds was positive for toxoplasma. Three hundred and twenty-seven eggs laid by 16 chickens during the chronic stage of infection produced experimentally with chicken strains of T. gondii were also tested and one positive egg was found. Parasitemia was demonstrated in all experimental birds during the acute stage of infection. All birds had toxoplasma cysts in one or more of the following organs or tissues, when killed 3 to 10 months postinoculation: brain, muscle, ovary, oviduct, kidney, gizzard, and intestine. A recent review by Siim, Biering-S0rensen, and M0ller (1963) on toxoplasmosis in domestic animals summarizes most of the reports on this infection in chickens. To our knowledge, the only additional citations needed to complete their list is a report of a spontaneous case in Argentina (Mayer, 1961), one by Kulasiri (1965) on experimental infection of chickens with an avirulent strain of toxoplasma, and another report of experimental infection by Kinjo (1961) that we have not seen. (One paper cited by Siim et al., by Pande, Shukla, and Sekariah, 1961, on toxoplasma from the eggs of domestic fowl, was subsequently questioned, Science 134: 945, 29 September 1961.) In earlier work done in two laboratories of this Institute and reported by Jones et al. (1959), it was found that the chicken is relatively tolerant to toxoplasmosis. Only very large inocula produced disease in mature birds, or even in young chickens. This was true despite hematogenous spread of the organisms early in the course of infection. Furthermore, when tissues of experimentally infected chickens were examined for residual parasites 4 weeks or longer after inoculation, the brain, liver, lung, or muscles were only occasionally found positive. However, these experimental results were in contrast to the observations of others on disease due to toxoplasmosis in naturally infected chickens (Hepding, 1939; Ericksen and Harboe, 1953; Fankhauser, 1951; Nobrega et al., Received for publication 14 May 1966. * Present address: Division of Biologics Standards, NIH, Bethesda, Maryland 20014. 1955). Also, while Ericksen and Harboe had not been able experimentally to reproduce the disease they had observed in epidemic form, Geissler (1955) did produce the clinical picture in experimentally infected chickens. The question of the importance of birds in the epidemiology of toxoplasmosis also requires more study. Gibson and Eyles (1957) found infected chickens among other infected animals in an area adjacent to the home of a case of human toxoplasmosis. Kimball and her associates (1959), in a survey of human beings in Minnesota, reported a correlation of dye test positivity and contact with chickens and other birds, although not with the ingestion of raw eggs. Sparapani (1950) found toxoplasma cysts in developing eggs from the ovaries of hens dead of toxoplasmosis. Biering-S0rensen (1956) also found toxoplasma cysts in the ovaries of chickens with disease due to toxoplasma. Geissler demonstrated, by inoculation into mice, toxoplasma in five eggs from experimentally infected hens and also found complement fixing antibodies in the sera of eight chicks hatched from the eggs of such hens. [He claims much more usefulness for the complement fixation test than do Harboe and his co-workers (Ericksen and Harboe, 1953; Harboe and Ericksen, 1954)]. The reports just cited all have dealt with chickens showing overt disease. It seemed worthwhile to us to reexamine the apparently healthy chicken as a natural host of toxoplasma, and to attempt to appraise the possible importance of eggs as a source of infection for other animals.