Search PubMed⌕ Search

Biomedical subjects

I G Wright

Publications and source records attributed to I G Wright.

At least 109 records · Page 6Linked to original sources
PubMed1977

Acute Babesia bigemina infection: changes in coagulation and kallikrein parameters.

Plasma from splenectomized calves infected with B. bigemina were assayed for disturbances in the coagulation system. Changes were observed in the WBCT, PTT, PT, TT and RT as well as in fibrinogen, calcium and thrombocyte levels. These changes were most marked during days 6--7 when parasite numbers were greatest. Massive intramuscular haemolysis coincided with these changes. The plasma kallikrein level fell progressively from days 6--11 and the level of activated kallikrein rose slightly. Parasite doubling time was calculated at 8.13 h. The similarities and differences between this disease and B. argentina infections of cattle are discussed.

Animals↗
PubMed1977

Kinin, kininogen and kininase levels during acute Babesia bovis (= B. argentina) infection of cattle.

1. Kinin levels began rising on day 3 after infection of cattle with Babesia bovis (= B. argentina) and attained a maximum value of 98% above preinfection levels by day 7. 2. Kininogen levels began falling on day 3 and reached minimum levels of 83% below preinfection levels on day 8. 3. Changes in both kinin and kininogen levels on day 3 coincided with the detection of low levels of parasites, and with a fall in packed cell volume. 4. Plasma kininase levels rose significantly 6 to 9 days after infection. Preparations of lysed and sonicated uninfected and infected red cells contained kininase activity, the respective red cell preparations being 23.9 and 11.4 times more active per mg protein than uninfected red cell preparations. The effect of pH, and the inhibitors disodium edetate, 1,10 phenanthroline and aprotinin on normal and infected plasma and on the various red cell preparations suggested that the rise in plasma kininase levels during infection was probably at least partly due to parasite products. 5. These results are discussed in relation to previous data showing that both kallikrein activation and the onset of hypotension also occur on or about day 3.

Animals↗
PubMed1977

The identification of Babesia equi in Australia.

A Babesia parasite, isolated from the blood of a horse at Bowral, New South Wales, was identified on the basis of its morphological features, host specificity and serological reactions, as Babesia equi (Laveran 1901). The case was originally reported by Churchill and Best (1976, Aust. vet. J. 52: 487) and is the first record of equine babesiosis in Australia. In preliminary studies, the organism produced only a mild disease in an intact horse, but caused the typical clinical syndrome of acute babesiosis in a splenectomised horse, which died 19 days after the intravenous inoculation of the parasites.

Animals↗
PubMed1976

Hypotension in rabbits infected with Trypanosoma brucei.

1 Blood pressures and heart rates of 12 anaesthetized rabbits chronically infected with T.brucei were measured (average infection time 39 days (range 25-67). The systolic BP was 31.4 +/- 5.7 mmHg, the diastolic BP 25.0 +/- 7.2 mmHg, and the heart rate 120.5 +/- 24.2 beats/minute. Two rabbits were already hypotensive 10 days after infection. In 12 anaesthetized control rabbits, the systolic BP was 66.2 +/- 7.3 mmHg (mean +/- s.e.), the diastolic BP 60.2 +/- 7.3 mmHg, and the heart rate 116.3 +/- 15.9 beats/minute. 2 The intravenous injection of 3 X 10(8) disintegrated trypanosomes into infected rabbits lowered the blood pressure by 41.4 +/- 22.0%. Pretreatment of two rabbits with aprotinin prior to administration of parasites prevented the fall in blood pressure. 3 Injection of 3 X 10(8) live trypanosomes complexed with hyperimmune sera produced a fall of 68.3 +/- 38.4% in the systolic BP of normal rabbits. Disintegrated or live trypanosomes, or hyperimmune sera alone had no effect. Pretreatment of animals with aprotinin prior to administration of the immune complex abolished the fall in BP. 4 The results suggest that the profound hypotension in chronic trypanosomiasis is caused by complex formation of trypanosomes with antibody. Since it can be prevented by pretreatment with aprotinin, it is likely that activation of plasma kallikrein with a subsequent release of plasma kinins contributes to this effect.

Animals↗
PubMed1975

Effect of trasylol on packed cell volume and plasma kallikrein activation in acute Babesia argentina infection of splenectomised calves.

Three groups of four splenectomised calves, three months old, were infected with Babesia argentina parasites. One group was inoculated intravenously with 2000 kallikrein inhibitor units (kiu)/kg body weight of the broad-spectrum proteinase inhibitor, Trasylol, three times a day for 5 days commencing on the 3rd day after infection (early treatment). The same dose of Trasylol was given to a second group for 3 days commencing 8 days after infection (late treatment). The third group was untreated. Parasite multiplication rates were similar in the three groups. In the early treated group levels of activated kallikrein in plasma were significantly lower than those in the other two groups. The early treatment group also showed significantly higher levels of plasma kallikrein inhibitor. No significant differences in total plasma kallikrein levels were seen among the three groups. Packed cell volumes in the treated groups remained significantly higher than those in the controls. The implications of these findings are discussed.

Analysis of Variance↗