An avian model for the study of acute hemolytic anemia in the domestic fowl (Gallus domesticus).

Acute hemolytic anemia was experimentally induced in chickens with the oxidant chemical phenylhydrazine. From results of the graded doses trial, subcutaneously injected 6 mg/100 g body weight single dose was designated as standardised. The anemic response, characterized by marked reductions in hemoglobin, packed cell volume and total erythrocyte count, was perceptible on day 1 post-injection. Peak anemia was observed on day 3. Compensatory erythropoiesis was discernible on day 5. The hematological profile indicated near complete recovery on day 11 post-injection. This avian model is proposed for study of the basic mechanisms of hemolytic anemia in chickens.

Sequential morphological changes in chicken erythrocytes after in vivo and in vitro exposure to phenylhydrazine-hydrochloride.

In acute haemolytic anaemia of chickens, induced with the oxidant chemical phenylhydrazine-hydrochloride, maximum degenerative changes in the in vivo exposed erythrocytes occurred on day 3 after injection. Microspherocytic transformation, dumb-bell shaped red blood cells and foamy squashed nuclei predominated. Heinz body formation was the cytoplasmic hallmark of the haemolytic anaemia. Marked reticulocytosis on day 5 indicated spontaneous regeneration. In vitro exposure to the chemical agent evoked similar morphological aberrations/Heinz bodies, microspherocytic transformation and nuclear degeneration. These were induced much earlier, presumably because of the absence of a protective internal milieu. Nevertheless, a basic similarity in morphology was evident. The in vitro test system might be suitable for screening oxidant chemicals and drugs.

Erythrophagocytosis in phenylhydrazine induced acute anaemia in chickens.

Acute anaemia was experimentally induced in chickens with a single subcutaneous injection of phenylhydrazine-hydrochloride. The birds were necropsied at fixed intervals. Liver, spleen and red bone marrow (from middle of tibia) were promptly dissected out. Impression smears were stained and examined under dry high power. Erythrophagocytosis was massive in the liver, moderate in the spleen and less conspicuous in bone marrow. Extensive erythrophagocytosis by the mononuclear cells might be associated with extravascular haemolysis. This appeared to be a major factor in the induction of anaemia.

Sequential changes in tissue D-fructose-1,6-diphosphate aldolase activity in chickens experimentally infected with Borrelia anserina.

Following experimental Borrelia anserina infection of chickens, aldolase activity increased in the proventriculus, heart and bone marrow but declined in the kidney and cervical spinal cord.

Fractionation of cock spermatozoa.

An account is given of the methodology for fractionation of cock spermatozoa into head and tail fractions by ultrasonication, followed by sucrose density gradient centrifugation. Quantitative estimates of DNA attested to 89.4% purity of the head fraction and low contamination of tails with heads. Recovery of protein and malic dehydrogenase (MDH) activity, following sperm fractionation, averaged 94.3% and 95.7%, respectively. Contamination of the head fraction with tails, as assessed by MDH assay, was only 4.65%, and the purity of the tail fraction was 91%. Intensive succinic dehydrogenase (SDH) activity was histochemically localised in the separated tail fraction and in the tail portion of intact spermatozoa. However, SDH activity was discernible neither in the head fraction nor in the head of intact spermatozoa.

Effect of orally administered furazolidone on volume and sperm concentration of dwarf and non-dwarf cock semen.

2 groups of 20 cocks each were selected at random from non-dwarf White Leghorn (28 weeks post-hatch) and dwarf Krishna-J (38 weeks post-hatch) genotypes. The treated groups comprised 10 White Leghorn and 10 Krishna-J cocks. The remaining birds served as controls. 8 weeks prior to furazolidone treatment, semen was collected from both control groups at regular 4-day intervals, for 4 weeks. Cocks of the treated groups of both genotypes were administered furazolidone (0.14 g/bird/day) for 7 consecutive days. Semen was collected from all cocks at regular 4-day intervals for 4 weeks. Semen from the cocks of the same group was pooled. The pooled ejaculate volume and sperm density did not differ significantly in the 2 genotypes. The semen output as well as sperm density increased along with progressive attainment of sexual maturity. Furazolidone treatment caused significant reduction in semen volume as well as sperm concentration in either genotype.