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J L Soni

Publications and source records attributed to J L Soni.

At least 19 recordsLinked to original sources
PubMed1991

Hemato-clinical changes in phenylhydrazine-induced acute hemolytic anaemia in calves.

Acute anaemia was induced in calves aged 1 week, using the oxidant chemical phenylhydrazine-hydrochloride (PHH). The hematoclinical responses to graded doses were evaluated. Mild anaemia was observed with the 60 mg/kg body weight (B.W.) dose. The 100 mg/kg B.W. dose was too toxic. The sublethal 80 mg/kg B.W. dose produced the desired type of hemolytic anaemia, the peak of which being observed on d 4 post-injection (p.i.). Hemolytic anaemia was evidenced by hemoglobinaemia and hemoglobinuria. The acute toxicity symptoms lasted for about 30 min. Thereafter, the animals appeared to overcome the stress. In general, increases in pulse and respiration coincided with progress of the hemolytic syndrome. Peak response occurred 48 to 60 h p.i.

Acute Disease↗
PubMed1991

Pathomorphological changes in calf erythrocytes during phenylhydrazine-induced acute hemolytic anaemia.

In acute hemolytic anaemia of calves induced with phenylhydrazine-hydrochloride, accentuated degenerative changes in circulating erythrocytes occurred on the 5th d post-injection. Marked anisocytosis and poikilocytosis were observed. Crenated cells, acanthocytes (star-shaped cells), dacrocytes (tear drop cells), bite cells, and schistocytes predominated. Heinz bodies were the cytoplasmic hallmark of hemolytic anaemia. The regenerative nature of anaemia was evidenced by early appearance of reticulocytes in peripheral blood.

Acute Disease↗
PubMed1990

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.

Acute Disease↗
PubMed1990

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.

Anemia, Hemolytic↗
PubMed1989

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.

Acute Disease↗
PubMed1975

Pathogenesis of acute avian malaria. IV. Immunologic factors in nephritis of acute Plasmodium gallinaceum infections of chickens.

Study of urinary waste of chickens with acute Plasmodium gallinaceum malaria indicated that serum proteins of the globulin and albumin classes were passed. Protein extravasation did not begin until globulin-associated serum antigen and its antibody were detected in the blood. Both serum antigen and antibody were found in the wastes for as long as the antigen was present in the blood. Extracts of kidney tissues contained serum proteins that were not present in extracts from normal kidneys, and serum antigen and its antibody were both present. Frozen kidney sections reacted strongly with fluorescein-conjugated antibody to serum antigen, showing diffuse granular immunofluorescence characteristic of immune complex nephritis. Sections from chickens with nephritis induced by injections of malarious plasma also showed deposits of extravasated antigen. The experiments suggested that complexes of serum antigen and antibody served as a permeability factor, or activated other permeability factors and may have caused the glomerulonephritis associated with acute avian malaria. The passing of serum proteins in the urinary wastes after chickens had recovered from acute malaria suggested that persisting damage may have resulted.

Acute Disease↗
PubMed1975

Pathogenesis of acute avian malaria. III. Antigen and antibody complexes as a mediator of anemia in acute Plasmodium gallinaceum infections of chickens.

In a study of antigens and antibodies found in malarious chicken blood, antigen activity was found in plasma, and in hypertonic saline eluates of blood cells. A soluble antigen was extracted from parasites liberated from erythrocytes. Two classes of antigen were differentiated, one a globulin associated "serum antigen" which was found to show identity with a serum antigen from blood of rats with acute Babesia rodhaini infection, and another that was associated with the Plasmodium gallinaceum parasite. The plasma also contained antibody to both classes of antigen. Study of blood cells from normal chickens made anemic by injections of autohemagglutinin-free malarious plasma indicated that both serum antigen and its antibody were present in eluates of the washed blood cells. Direct immunofluorescent tests of these cells with conjugated antibody to serum antigen, and with conjugated antibody to P. gallinaceum parasite antigen showed that they reacted with the antibody to serum antigen but gave no reaction with antibody to parasite antigen. From this information it is suggested that soluble complexes of serum antigen and its antibody combined with the erythrocytes, and that these complexes acted as opsonin to cause the cells to be sequestered and destroyed in the spleen, or may have fixed complement to cause intravascular hemolysis. The serologic identity of serum antigen from malarious chickens and from rats with babesiosis, and its distinction from parasite antigen, led to the speculation that it might be an autoantigenic macroglobulin.

Anemia, Hemolytic, Autoimmune↗
PubMed1975

Pathogenesis of acute avian malaria. II. Anemia mediated by a cold-active autohemagglutinin from the blood of chickens with acute Plasmodium gallinaceum infection.

A cold-active hemagglutinin for trypsinized human type "O" erythrocytes (CAH) from blood of chickens with acute Plasmodium gallinaceum malaria was found to be associated with 19 S and 7 S globulin fractions of malarious chicken blood, but cleavage with 2-mercaptoethanol indicated that it was primarily of the IgM class of antibody. In serologic tests CAH reacted with trypsinized erythrocytes, and anti-chicken globulin. It did not react with other of the antigens or antibodies detected in the blood of malarious chickens. When the absorbed and eluted CAH was injected into normal chickens it produced an anaphylactic-like shock and caused a 25% reduction in red blood cell counts within 48 hours. Plasma samples collected during this interval showed signs of hemolysis. Reactions of blood cells from the recipient birds with fluorescein conjugated anti-chicken globulin indicated that CAH reacted with erythrocytes. The absence of fluorescent activity 3 days after injection suggested that these erythrocytes had been removed from the circulation. When normal chickens were injected with trypsinized autologous blood cells, CAH was detected within 3 days. The agglutination test again was active at temperatures below 22 degrees C and was negative when tested at 37 degrees C. In these birds the appearance of CAH was accompanied by reductions in red blood cell counts and by hemolysis. The results of these experiments suggest that CAH was not stimulated by plasmodial parasite antigen, but rather by autoantigens, which appear to be common to heterologous animal species, and which were in some manner expressed by the presence of the intracellular parasites, or by trypsin treatment. The experiments further suggest that this autohemagglutinin was partially causal of malarial anemia. The presence of other anemia factor(s) was indicated by anemia following injection of plasma that had been absorbed free of CAH.

Agglutinins↗