R. Barclay McGHEE

Anemia in Ducklings treated with Malarious Plasma.

Abstract Plasma from ducklings infected with Plasmodium lophurae was filtered to insure the removal of parasites and donor red blood cells; this was administered intravenously in a series of three inocula per recipient duckling. Birds receiving the plasma underwent an anemia and a radical loss of polychromatophil erythroblasts. These manifestations were similar to those observed in ducklings with low-grade infections. In one of three groups of experimental ducklings which received no further treatment, the total red blood cell count reached a mean of less than 1.00 million per cubic millimeter. The birds became moribund and died or were killed. In the other two groups, there was a replacement of red blood cells by the influx of basophil erythroblasts. This alleviated the anemia and recovery followed. From a review of the literature and examination of our own work, we believe that we are observing the effects of one or more soluble antigens in the malarious plasma and of corresponding antierythrocytic antibodies.

Redescription of Coccidiascus legeri chatton, 1913 (Nematosporaceae: Hemiascomycetidae), an intracellular parasitic yeastlike fungus from the intestinal epithelium of Drosophila melanogaster

Abstract Utilizing light and electron microscopy, development of Coccidiascus legeri is described. The fungus develops within vacuoles in the intestinal epithelium of Drosophila melanogaster . The initial stages are round to ovoid vegetative cells which reproduce by budding in a typical yeastlike manner. Later, elongate cells form asci which, when mature, contain two ascospores while still within host tissues. During ascosporogenesis lomasomelike vesicles fuse with the cytomembrane, releasing their contents and producing a dense bilayered ascus wall. Mature asci measure 15 μm in length (range 13–18 μm) and contain ascospores without cytoplasmic appendages. Attempts to cultivate the fungus on artificial media were unsuccessful. Conjugation was not observed. The taxonomic position of C. legeri with relation to other members of the Nematosporaceae (Hemiascomycetidae) is at present undetermined.

Plasmodium gallinaceum: Variation in susceptibility of dove erythrocyte

Abstract Indices of susceptibility for the erythrocytes of three doves (Streptopelia risoria) were calculated on the basis of parasite invasion when injected into chicken embryos infected with Plasmodium gallinaceum. The red blood cells of two of the animals were quite comparable while those of Dove 3 were nearly twice as susceptible. In a 13-month period there was a trend toward increased susceptibility in all doves, with each animal retaining its susceptibility relative to the other. Thus, individual and temporal fluctuations of susceptibility exist as regards erythrocytes of ring doves, S. risoria.

Plasmodium gallinaceum: Hereditary transmission of erythrocyte susceptibility☆

Abstract Calculations of indices of susceptibility based on incidence of parasite invasion of exotic erythrocytes in chicken embryos infected with Plasmodium gallinaceum were carried out. Erythrocytes of the pigeon ( Columba livia ) were essentially refractory to infection; those of the ring dove (R.D.) were quite susceptible. The erythrocytes of an F 1 hybrid between these two parents were somewhat more susceptible than those of the pigeon but much less susceptible than those of the dove parent. Transmission of partial susceptibility to malaria follows that observed for the total inheritance of pigeon but only partial inheritance of dove antigen into F 1 .

A filterable, proliferating factor simulating autoimmunity in malarious and nonmalarious ducklings.

Abstract Ducklings receiving 9.0 ml or 0.2 ml of filtered malarious plasma underwent comparable anemic responses. Recipients of the larger injection demonstrated a reduction in the level of polychromatophil erythroblasts whereas the recipients of the smaller injection did not. Two tenths milliliter of whole blood or filtered plasma from these ducklings also produced and continued to produce anemia during 24 successive passages in ducklings without any apparent reduction of its efficacy. The anemia-producing agent resides on or in erythrocytes and occurs in the plasma. Transfer of the agent in conjunction with a Plasmodium lophurae infection maintained by transfer of infected blood every four days was demonstrated. Preliminary attempts to characterize the agent beyond being filterable and proliferating met with no success. From consideration of our results we believe that we are observing the effect of a virus that can be transferred either with or without the malaria parasite and is responsible for at least part of the anemia observed in infections of P. lophurae in ducklings.

Plasmodium gallinaceum: changing virulence patterns of malaria parasites during adaptation from neonate chick to chicken embryos.

Abstract Infections of avian embryos with Plasmodium gallinaceum from a malaria strain adapted to continuous passage in chicks were characterized by reduced virulence. Five passages through embryos were required to produce infections comparable to those observed in established infections. If blood from a chicken infected by sporozoites was injected into 10-day chicken embryos there were a marked loss of virulence, heightened pathogenicity, and morphological aberrations. Increasing the dosage from a million to 20 × 10 6 parasites resulted in parasitemias more nearly resembling those in fully adapted passages in chicken embryos. Blood passages from chicken to chicken somehow changed the parasite to the point that after four passages acute virulent infections could be obtained in the embryo. It is postulated that the chicken embryo by virtue of its difference from neonates as regards plasma elements and physiochemical composition of its erythrocytes, especially in the hemoglobin, constitutes essentially a foreign host to which a few parasites are preadapted. During blood passages selection toward virulence ensues.

Plasmodium gallinaceum: Response of malarious chicken embryos to injection of serum from hyperimmunized chickens

Abstract The injection of serum from chickens hyperimmune to the avian malaria parasite, Plasmodium gallinaceum , or of nonimmune serum into the chorioallantoic cavity of chicken embryos infected with the same parasite resulted in changes in the blood picture of such embryos. In those embryos receiving serum from hyperimmunized birds: The level and rate of parasite increase were depressed; the maturation of the erythroid elements was reduced; the hematocrit values increased only by 27% as compared with 69% in untreated embryos. While hematocrit levels and rates of erythrocytic maturation were depressed in those embryos injected with nonimmune serum, there was no suppression of parasitemia. The results suggest a definite role of immunity in the anemia accompanying malaria.

Absence of anemia in the immunoincompetent malarious chicken embryo

Abstract Contrasted with severe anemia followed by compensation by erythroid hyperplasia in neonate chicks infected with Plasmodium gallinaceum , embryonic chickens displayed neither anemia nor significant deviation from normalcy in the blood picture. In view of the fact that no volume changes in erythrocytes were observable it appeared that in these immunoincompetent animals there was destruction of neither uninfected nor infected erythrocytes. A corollary would imply the egress of merozoites from host cells without erythrocyte destruction.

Plasmodium gallinaceum: Avian immunologic tolerance to serum antigens

Abstract Neonatal chicks were injected with malarious or normal serum and later challenged with malarious serum. Eleven days after challenge serum was taken from both groups and titered by the indirect fluorescent antibody test. Those chicks initially injected with malarious serum were completely tolerant to challenge. Those given normal serum responded to challenge. Rechallenge of both groups with malarious serum resulted in similar findings to those above indicating the induction of immunologic tolerance in those initially given malarious serum for a period of at least 30 days.