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Biomedical subjects

L H Miller

Publications and source records attributed to L H Miller.

At least 19 recordsLinked to original sources
PubMed1979

Severe malaria and glucose-6-phosphate-dehydrogenase deficiency: a reappraisal of the malaria/G-6-P.D. hypothesis.

Nigerian children with convulsions and Plasmodium falciparium parasitaemia above 100,000/microliter did not show a decreased frequency of glucose-6-phosphate-dehydrogenase (G.-6-P.D.) deficiency. A re-evaluation of earlier studies has led to the conclusion that clinical evidence of protection against falciparum malaria in G.-6-P.D.-deficient individuals is lacking. Evidence for the possible role of malaria in selecting for G.-6-P.D.-deficient genes consists solely of the geographical association of high frequencies of G.-6-P.D. deficiency with endemic malaria.

Child↗
PubMed1979

Interaction between cytochalasin B-treated malarial parasites and erythrocytes. Attachment and junction formation.

We have previously demonstrated that invasion of erythrocytes (RBCs) by malaria merozoites follows a sequence: recognition and attachment in an apical orientation associated with widespread deformation of the RBC, junction formation, movement of the junction around the merozoite that brings the merozoite into the invaginated RBC membrane, and sealing of the membrane. In the present paper, we describe a method for blocking invasion at an early stage in the sequence. Cytochalasin-treated merozoites attach specifically to host RBCs, most frequently by the apical region that contains specialized organelles (rhoptries) associated with invasion. The parasite then forms a junction between the apical region and the RBC. Cytochalasin blocks movement of this junction, a later step in invasion. Cytochalasin-treated (Plasmodium knowlesi) merozoites attach to Duffy-negative human RBCs, although these RBCs are resistant to invasion by the parasite. The attachment with these RBCs, however, differs from susceptible RBCs in that there is no junction formation. Therefore the Duffy associated antigen appears to be involved in junction formation, not initial attachment.

Animals↗
PubMed1979

Frequency of blood group antigens in Nigerian children with falciparum malaria.

The frequencies of the following blood group antigens: A, B, O, M, N, S, s, U, Fya, FyB, Lea, Jsa and K have been determined in Nigerian children with severe falciparum malaria. The frequency distribution of M, N, S, s, U, Fya and Fyb were not significantly different in children with life-threatening falciparum malaria and controls. The frequencies of A, B, O, Lea, Jsa and K found in the children with severe malaria were similar to those previously reported for healthy adults in this population. The Duffy blood group antigens Fya and Fyb were virtually absent from both infected and control children. This finding is in variance with a Fya frequency of 23% reported by Worlledge et al. (1974) for healthy adults in this population.

ABO Blood-Group System↗
PubMed1979

Evidence for environmental modulation of gametocytogenesis in Plasmodium falciparum in continuous culture.

With the introduction of continuous culture of Plasmodium falciparum it has become possible to study the factors involved in gametocyte production in vitro and thus eliminate the uncontrollable in vivo variables of the host. The authors have developed a method for measuring quantitatively the rate of production of gametocytes at any time in such cultures. The method is based on an estimation of the percentage of ring forms that develop into stage II gametocytes.Using this approach, it was found that dilution of cultures with fresh red blood cells so as to lower the parasitaemia led to rapid fall in the rate of conversion to gametocytes. The conversion rates subsequently rose again to levels typically in the order of 10% after several days of growth in the new culture. In the parental cultures from which the dilutions were made, conversion rates remained high at all times. This pattern was consistently observed in three different isolates of P. falciparum from Africa and the results indicate that the reduction of parasitaemia by addition of fresh cells was responsible for reducing production of gametocytes and that conditions associated with a period of growth in culture induced renewed gametocytogenesis. The authors conclude, therefore, that environmental conditions directly modulate the rate of gametocyte production by P. falciparum in culture.After 1(1/2) years in culture, parasites have retained their ability to produce gametocytes and the gametocytes to undergo exflagellation.

Animals↗
PubMed1978

Low erythrocyte pyridoxal-kinase activity in Blacks: Its possible relation to falciparum malaria.

The red-cell glucose-6-phosphate dehydrogenase (G.-6-P.D.) activity and red-cell pyridoxal-kinase (P.L.K.) activity of 27 Nigerian children with severe Plasmodium falciparum parasitaemia were compared with those of 26 healthy Nigerian children and 6 White adults. The mean P.L.K. activity of the malaria patients was similar to that of the Whites but significantly higher than that of the Nigerian controls. Correction for reduced mean red-cell age in patients was made by comparing the P.L.K.: G.-6-P.D. ratio for those subjects with stable G.-6-P.D. phenotypes. The mean P.L.K.:G.-6-P.D. ratio was the same for malaria patients and adult White but significantly higher than that for the Nigerian controls. These results suggest that the relatively high frequency of low red-cell P.L.K. activity among Blacks may have been selected for by falciparum malaria.

Adult↗
PubMed1978

Erythrocyte entry by malarial parasites. A moving junction between erythrocyte and parasite.

Invasion of erythrocytes by merozoites of the monkey malaria, Plasmodium knowlesi, was investigated by electron microscopy. The apical end of the merozoite makes initial contact with the erythrocyte, creating a small depression in the erythrocyte membrane. The area of the erythrocyte membrane to which the merozoite is attached becomes thickened and forms a junction with the plasma membrane of the merozoite. As the merozoite enters the invagination in the erythrocyte surface, the junction, which is in the form of a circumferential zone of attachment between the erythrocyte and merozoite, moves along the confronted membranes to maintain its position at the orifice of the invagination. When entry is completed, the orifice closes behind the parasite in the fashion of an iris diaphragm, and the junction becomes a part of the parasitophorous vacuole. The movement of the junction during invasion is an important component of the mechanism by which the merozoite enters the erythrocyte. The extracellular merozoite is covered with a prominent surface coat. During invasion, this coat appears to be absent from the portion of the merozoite within the erythrocyte invagination, but the density of the surface coat outside the invagination (beyond the junction) is unaltered.

Animals↗
PubMed1978

The Duffy blood group phenotype in American blacks infected with Plasmodium vivax in Vietnam.

We determined blood group phenotypes of 13 blacks who were infected with Plasmodium vivax in Vietnam. All were Duffy blood group positive as compared to 40--50% Duffy positive in surveys of black blood donors in the United States. The probability that 13 of 13 were Duffy positive by chance alone was P less than 0.001. All other blood groups occurred at the expected frequency. This study is further support for the hypothesis that the Duffy negative genotype (FyFy) is the basis for resistance of blacks to P. vivax.

Black or African American↗
PubMed1978

The Duffy blood group and resistance to Plasmodium vivax in Honduras.

To test the hypothesis that the Duffy blood group negative genotype is a factor in resistance to Plasmodium vivax, we determined the Duffy blood group, the malaria antibodies, and the slide-demonstrated infection rates with P. vivax and P. falciparum of 420 persons living in Nueva Armenia, Honduras. In all, 247 persons were Duffy negative. Demonstrated infections with P. falciparum were almost equally distributed between Duffy-positive (5,8%) and Duffy-negative (4.9%) persons. Similarly, Duffy-positive (25.6%) and Duffy-negative (28.2%) persons had equal proportions of indirect fluorescent antibody test titers suggestive of past or present P. falciparum infection. In contrast, all 14 P. vivax infections were found in Duffy-negative persons. There was no evidence suggesting that Duffy-positive and Duffy-negative persons had different exposures to malaria. The Duffy negative genotype FyFy appears to be a factor in resistance to P. vivax.

Antibodies↗
PubMed1978

Selection of increased quinine resistance in Plasmodium falciparum in Aotus monkeys.

Although partial resistance (RI) of Plasmodium falciparum to quinine is common in some areas of the world, failure to obtain an initial response (RII or RIII) is unusual. Furthermore, emergence of quinine resistance during therapy of malaria infections in humans and animals is uncommon. In the current study, exposure of the Panama II strain of P. falciparum in Aotus monkeys to subcurative quinine therapy during six serial passages over 6 months resulted in a shift in the quinine responsiveness of the strain from mild insensitivity to quinine to uniform resistance of a marked degree. Treatment with quinine for 14 days of infections in 12 monkeys with the original isolate resulted in cure in 8 monkeys and RI resistance in 4. Infections with the resistant isolate (selected under quinine pressure) were uniformly resistant to cure by 14 days of quinine; resistance to quinine was RIII in 4 of 12 monkeys and was RII in 5. These results suggest that extensive usage of quinine or related drugs (e.g., mefloquine) in the field may result in decreasing sensitivity of falciparum malaria to quinine.

Animals↗
PubMed1978

Failure of chloroquine in human babesiosis (Babesia microti): case report and chemotherapeutic trials in hamsters.

The failure of a 3-week course of chloroquine to eliminate an infection of Babesia microti acquired on Martha's Vineyard led to tests of selected drugs in hamsters infected with the strain from this patient. The results showed response to several antitrypanosomal drugs (pentamidine and 4,4'-diazoaminobenzamidine) but not to antimalarial drugs (chloroquine, sulfadiazine, and pyrimethamine).

Animals↗
PubMed1977

Evidence for differences in erythrocyte surface receptors for the malarial parasites, Plasmodium falciparum and Plasmodium knowlesi.

Human erythrocytes lacking various blood group determinants were susceptible to invasion by Plasmodium falciparum including Duffy-negative erythrocytes that are refractory to invasion by Plasmodium knowlesi. Erythrocytes treated with trypsin or neuraminidase had reduced susceptibility of P. falciparum and normal susceptibility to P. knowlesi. Chymotrypsin treatment (0.1 mg/ml) blocked invasion only by P. knowlesi. The differential effect of enzymatic cleavage of determinats from the erythrocyte surface on invasion by these parasites suggests that P. falciparum and P. knowlesi interact with different determinants on the erythrocyte surface.

Chymotrypsin↗