Biomedical subjects
Publications and source records attributed to B Mulder.
Monoclonal antibodies (mAbs) and human sera from gametocyte carriers were applied in the bio-assay to test for their transmission-blocking capacity. Competition ELISA's have been developed for the detection of natural transmission blocking antibodies. Approximately 55% of the sera blocking in the bio-assay gave positive results in these competition ELISA's.
Factors which could influence the success of experimental infections of Anopheles gambiae with Plasmodium falciparum were investigated in Cameroon. 139 experimental infections with different gametocyte carriers were performed. 86 (62%) gave rise to mosquito infection after dissection of at least 20 mosquitoes. Among succeeding infections, the mean percentage of infected mosquitoes was 18.6% and mean oocyst load per positive midgut was 2.56. Only gametocyte density was identified as a factor which determined the success and the level of mosquito infection. No significant influence was found for sex and age of the gametocyte carrier, body-temperature, presence of asexual erythrocyte stages, rhesus factor, blood group and use of antimalarial drugs (chloroquine and amodiaquine).
Experimental infections of Anopheles gambiae were carried out with Plasmodium falciparum gametocytes from 65 naturally infected patients in Cameroon. A comparison was made between infections with blood containing autologous plasma and blood in which the plasma was replaced by plasma from donors without previous malaria exposure. A lower mosquito-infection rate was observed in 50 out of 65 autologous plasma samples. The transmission was completely blocked in 8 infections, whilst belonging exposures to heterologous plasma led to infected mosquitoes. Evidence is shown that blood plasma factors of gametocyte carriers from a population living in a malaria-endemic area are able to reduce transmission capacity.
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Growth of yersiniae is restricted at 37 degrees C in the absence of calcium ions. This phenomenon correlates with the massive release of a set of proteins called Yops. Growth restriction and Yops production are governed by a 70 kb plasmid called pYV. yop genes are distributed throughout pYV and constitute a thermoactivated regulon controlled by the gene virF. The transcription activator VirF is a member of a new family of regulators including those of the arabinose and rhamnose operons as well as a regulator of enteric colonization pili. The role of calcium ions on the release of Yops remains largely unknown.
This paper describes the mutagenesis of the pYV plasmid from Yersinia enterocolitica W22703 (serotype O:9) with Tn2507, a new element generating operon fusions. Analysis of the mutants allowed the identification of an additional Yop protein called Yop20 and the mapping of yop20, yop44, yop48, and lcrV, the gene encoding the V antigen. The last gene appeared to be part of an operon that also may contain yop37 and yop44. At 37 degrees C, mutants affected in this operon grew poorly, irrespective of the presence of Ca2+, or they even died in the presence of Ca2+. This operon is thus involved in the regulation by Ca2+, and we called it car, for Ca2+ regulation. It is presumably the Y. enterocolitica counterpart of the lcrGVH operon of Yersinia pestis. Transcription of yop20 and of the car operon was strongly regulated by temperature and only slightly by calcium. Hence, these genes behaved like the other genes of the yop regulon. Mutants affected in yop20 or in yop48 were markedly less virulent for the desferrioxamine-treated mouse than was the parental strain. Yop20 and Yop48 thus probably are Yersinia virulence factors.
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The effect of 7 consecutive days dosing with anti-inflammatory drugs on rat gastric mucosal PGE2 and 6-keto-PGF1 alpha concentrations were studied. Normal adult rats were given daily, single oral doses of etodolac (3 or 8 mg/kg/day), naproxen (3 mg/kg/day), or aspirin (300 mg/kg/day). Two hours after administration of the last dose, the animals were killed and the gastric mucosal PGE2 and 6-keto-PGF1 alpha were extracted and measured by radioimmunoassay. At equieffective anti-inflammatory doses in the rat, etodolac (3 mg/kg/day) did not significantly lower the concentrations of either PGE2 or 6-keto-PGF1 alpha, whereas both 3 mg/kg/day of naproxen and 300 mg/kg/day of aspirin significantly lowered the concentrations of both prostaglandins. The effects of naproxen and aspirin on the 6-keto-PGF1 alpha concentrations were also significantly different from that of etodolac at 3 mg/kg/day. At a higher dose of 8 mg/kg/day, etodolac did significantly lower the concentrations of PGE2 (by 33%) but not of 6-keto-PGF1 alpha. Our present data thus supports the hypothesis that the relatively weak inhibiting effect of etodolac on the gastric mucosal prostaglandin concentrations may contribute to its excellent GI profile observed in man.
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Experimental infections of anopheline mosquitoes were carried out with Plasmodium falciparum gametocytes from 65 naturally infected patients in Cameroon. A comparison was made between infections with blood containing autologous plasma and blood in which the plasma was replaced with plasma from a donor without previous malaria exposure. A lower infection rate was observed in 50 of 65 autologous plasma samples. Transmission was significantly blocked in 3 infections. This indicates that, in a population living in an area endemic for malaria, blood plasma factor(s) can reduce the transmission capacity of gametocyte carriers to mosquitoes.
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Insectary-reared Anopheles gambiae were experimentally fed with the blood of 90 naturally infected human volunteers carrying gametocytes of Plasmodium falciparum. At least one mosquito was successfully infected in 74% of experiments. The probability that a gametocyte carrier was infective, the probability that a mosquito became infected, and the number of oocysts harboured were related to gametocyte density. The mean proportion of male gametocytes was 0.217 (i.e., 3.6 females for every male). Sex ratios differed significantly between gametocyte carriers. Variation in sex ratio was not related to the probability that a gametocyte carrier was infective. Among infective people whose sex ratio estimates were based on a reasonable number of gametocytes, sex ratio significantly predicted the proportion of infected mosquitoes and mean oocyst load, with infectivity rising as the proportion of the male gametocytes increased towards 50%. There was no indication that infectivity reached a peak at some intermediate sex ratio, as would be expected if random mating of gametes was the primary determinant of fertilization success. These results raise 2 interesting questions: why should higher sex ratios be more infective, and why is the observed population sex ratio lower than that which produces the greatest infectivity?
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