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Biomedical subjects

I A Clark

Publications and source records attributed to I A Clark.

At least 109 records · Page 6Linked to original sources
PubMed1979

Protection of mice against Babesia microti with cord factor, COAM, zymosan, glucan, Salmonella and Listeria.

Cord factor (trehalose 6-6' dimycolate). COAM (chlorite-oxidized oxyamylose), zymosan, glucan, Salmonella enteritidis 11RX and Listeria monocytogenes were found to protect mice against subsequent infection with Babesia microti, an intra-erythrocytic protozoan parasite. This protection was not observed after injection of Staphylococcus epidermidis, a viridans group Streptococcus, thioglycollate, or colloidal carbon. All the agents which protect against B. microti have also been reported to induce non-specific protection against experimental tumours. The parasites appear to die inside circulating red cells. This implies that these can exert non-specific protection against this parasite through the mediation of a soluble factor.

Amylose↗
PubMed1979

Resistance to Babesia spp. and Plasmodium sp. in mice pretreated with an extract of Coxiella burnetii.

Mice injected intravenously with a commercially available extract of Coxiella burnetii prepared for use as the antigen in the complement fixation diagnostic test for Q fever were subsequently resistant to infection with Babesia microti, Babesia rodhaini, and Plasmodium vinckei petteri. The parasites appeared to die inside circulating erythrocytes. Protection was unaffected by exposing the pretreated mice to 900 rads on the day before they were infected. To explain these findings, it is postulated that pretreatment with Coxiella extract protects by potentiating the interferon-inducing capacity of the challenge dose of protozoa, which perhaps leads to enhanced of natural killer cells. Tumor necrosis factor also warrants investigation.

Animals↗
PubMed1978

Does endotoxin cause both the disease and parasite death in acute malaria and babesiosis?

When mice are infected with either of several species of Plasmodium or Babesia the amount of Escherichia coli lipopolysaccharide (L.P.S.) required to kill them is decreased several hundred fold. The higher their parasitaemia the greater their susceptibility. There is indirect evidence that more L.P.S. than usual is present during infection with these parasites. In a very susceptible host this may be sufficient to produce endotoxin shock. Non-antibody mediators able to kill rapidly dividing cells, which are released during endotoxin shock, may then control the parasitaemia of acute primary attacks. This may explain why agents such as B.C.G., which produce responsiveness to abnormally low concentrations of L.P.S., protect against infection with certain of these parasities. It may also explain why host species naturally resistance to L.P.S. become ill only at high parasite concentrations, and why others with a naturally high susceptibility to L.P.S. become ill when infected with relatively few parasites. In the individual host convalescence from certain bacterial infections or concomitant infection with L.P.S.-producing organisms may vary the parasitaemia required to produce illness.

Animals↗
PubMed1978

Protection of mice against haemoprotozoan Babesia microti with Brucella abortus strain 19.

When Brucella abortus strain 19 is given intraperitoneally to mice it protects them against subsequent infection with large doses of Babesia microti. The protection obtained was more effective when B. abortus was given intraperitoneally than when it was injected subcutaneously. This non-specific protection seems to be best explained by the stimulation of macrophages so as to release a mediator which limits the intracellular replication of the parasites.

Animals↗
PubMed1977

Protection of mice against Babesia spp. and Plasmodium spp. with killed Corynebacterium parvum.

Mice which had been pre-treated with killed Corynebacterium parvum given intravenously or intraperitoneally, but not subcutaneously, were completely resistant to infection with Babesia microti or B. rodhaini, and were protected from death caused by Plasmodium vinckei or P. chabaudi infection. There is evidence that the parasites died within circulating erythrocytes. This occurred much too soon for a specific antibody response to be evoked, and no antibody could be detected by the indirect fluorescent-antibody technique. Thus it is suggested that a non-specific soluble mediator may play an important role in the protection observed.

Animals↗
PubMed1977

Intra-erythrocytic death of the parasite in mice recovering from infection with Babesia microti.

As mice recover from infection with Babesia microti, abnormal forms of the parasite are present in some red cells. These forms are non-infective, indistinguishable by light microscopy from those present after treatment with amicarbalide, a babesicidal drug, and persist in splenectomized mice. Electron microscopy confirmed that these abnormal forms are degenerating intra-erythrocytic parasites. In the absence of evidence for death of B. microti elsewhere in the body, it appears that infections of mice with this parasite are normally terminated by their death within circulating red cells. This has important implications for the mechanism of immunity to both this parasite and those Plasmodium spp. with which it cross-protects in this host.

Animals↗
PubMed1977

Suppression of babesiosis in BCG-infected mice and its correlation with tumor inhibition.

Infection of mice with Bacillus Calmette-Guérin (BCG) provided good protection against Babesia species. The intensity and duration of this protection was similar to that established after natural recovery from babesiosis. It developed too soon after the first exposure to the parasite, and was too radioresistant, to be attributable to specific antibody production. In addition, the parasites degenerated within circulating erythrocytes. This phenomenon is inconsistent with phagocytosis or lysis of parasites or parasitized cells, or prevention of entry of parasites into erythrocytes, causing the observed protection. Hence the phenomenon is best explained by the release of a nonspecific mediator that can limit multiplication of parasites within erythrocytes. These results not only throw light on mechanisms of immunity against hemoprotozoa. There are many points of similarity between the nonspecific protection BCG and Corynebactium parvum provide against Babesia species and inhibition of tumor growth by these agents. Therefore, babesiosis in mice may be a convenient experimental model for assessing stimulation of the mononuclear phagocyte system, which appears to be the basis of nonspecific immunity against bacteria, parasites, and tumors.

Animals↗
PubMed1976

The experimental production of haemolytic disease of the newborn in calves.

Haemolytic disease in varying degrees of severity was produced experimentally in 15 newborn calves. Blood group antibodies, incompatible with some of the blood group factors of the calves, were produced in the dams of these calves by inoculation with non-parasitised red blood cells from the sire in most cases. These antibodies were absorbed by the calves from the colostrum. The resultant sensitisation of the calves' red cells produced acute intravascular haemolysis causing haemoglobinuria and anaemia. The principal factor governing the severity of the condition appeared to be the amount of sensitising antibody absorbed by the calf. The finding of leucopenia, thrombocytopenia, hypofibrinogenaemia, a reduction in plasma coagulation factors and the detection of fibrinogen degradation products indicated that disseminated intravascular coagulation occurs in this condition and is the cause of death in the acute cases where a haemorrhagic diathesis, fibrin deposition and oedema of the lungs are the main clinical and post mortem observations.

Animals↗
PubMed1975

Immunity to intra-erythrocytic protoza.

Intra-erythrocytic inclusion bodies were seen in Giemsa-stained smears of peripheral blood from mice infected with Babesia microti. These bodies, which were probably the pyknotic remnants of dead protozoa, increased as parasitaemia fell and the animal recovered. It is suggested that a soluble mediator liberated by cells of the host during infection penetrates the red blood-cell and leads to degeneration of the parasite.

Animals↗