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K Vickerman

Publications and source records attributed to K Vickerman.

13 recordsLinked to original sources

Multinuclear forms in a dyskinetoplastic strain of Trypanosoma evansi in mice.

The production of short stumpy and multinuclear trypanosomes in a Chinese strain of dyskinetoplastic Trypanosoma evansi maintained in rabbits and mice is described. Production of multinuclear trypanosomes was increased following passage through a reptile (gecko), in which the trypanosomes did not multiply, and transfer back to mice. The multinuclear trypanosomes showed more nuclei than flagella indicating that disruption of the normal cell cycle had taken place and not simply inhibition of cleavage. A Chinese kinetoplastic T. evansi treated similarly rarely produced stumpy or multinuclear forms.

Animals

The glycosomes of trypanosomes: number and distribution as revealed by electron spectroscopic imaging and 3-D reconstruction.

Computer-aided 3-D reconstruction of trypanosomes from 0.35-micron-thick sections imaged on the Zeiss 902 electron microscope are being used to study the dynamics of cell organization. Segregation of glycolytic enzymes into glycosomes raises questions concerning the distribution and biogenesis of these organelles. Direct counts of glycosomes from Trypanosoma evansi indicate 30-40 per cell and for the closely related T. brucei, 65 per cell. These figures contrast with the estimates of others who have used model-based morphometric methods to obtain a value of 230 per cell.

Animals

A comparison of multiplication rates in primary and challenge infections of Trypanosoma brucei bloodstream forms.

The hypothesis that division of Trypanosoma brucei slender bloodstream forms is dependent upon the availability of a host-derived growth factor has been tested by superimposing challenge doses of slender-form trypanosomes onto preexisting infections at a time during the primary infection when stumpy forms predominated. The challenge populations grew in the doubly-infected mice indicating that depletion of a putative growth factor by the expanding population of the primary infection had not prevented division of the trypanosomes although slight reductions in multiplication rates were observed. This effect was independent of the variable antigen type (VAT) of the trypanosomes and of their stock of origin.

Animals

Trypanosome sociology and antigenic variation.

Survival of the trypanosome (Trypanosoma brucei) population in the mammalian body depends upon paced stimulation of the host's humoral immune response by different antigenic variants and serial sacrifice of the dominant variant (homotype) so that minority variants (heterotypes) can continue the infection and each become a homotype in its turn. New variants are generated by a spontaneous switch in gene expression so that the trypanosome puts on a surface coat of a glycoprotein differing in antigenic specificity from its predecessor. Homotypes appear in a characteristic order for a given trypanosome clone but what determines this order and the pacing of homotype generation so that the trypanosome does not quickly exhaust its repertoire of variable antigens, is not clear. The tendency of some genes to be expressed more frequently than others may reflect the location within the genome and mode of expression of the genes concerned and may influence homotype succession. Differences in the doubling time of different variants or in the rate at which trypanosomes belonging to a particular variant differentiate into non-dividing (vector infective) stumpy forms have also been invoked to explain how a heterotype's growth characteristics may determine when it becomes a homotype. Recent estimations of the frequency of variable antigen switching in trypanosome populations after transmission through the tsetse fly vector, however, suggest a much higher figure (0.97-2.2 x 10(-3) switches per cell per generation) than that obtained for syringe-passed infections (10(-5)-10(-7) switches per cell per generation) and it seems probable that most of the variable antigen genes are expressed as minority variable antigen types very early in the infection. Instability of expression is a feature of trypanosome clones derived from infective tsetse salivary gland (metacyclic) trypanosomes and it is suggested that high switching rates in tsetse-transmitted infections may delay the growth of certain variants to homotype status until later in the infection.

Animals

Kinetoplast DNA of Bodo caudatus: a noncatenated structure.

The kinetoplast DNA (kDNA) of trypanosomes and other parasitic members of the order Kinetoplastida is organized as a complex network containing thousands of catenated circular DNA molecules. We found that the kDNA of a free-living kinetoplastida, Bodo caudatus, exists as a noncatenated structure. The kDNA of B. caudatus represents about 40% of the total cellular DNA, and the major components of this DNA are large circles of 10 and 12 kilobases (kb). Our results indicate that these circles are analogous to trypanosome kDNA minicircles despite their large size and noncatenated form. The kDNA of B. caudatus also contains a minor component of 19 kb which is transcribed. The 19-kb molecules are probably analogous to the maxicircles of trypanosomes. The properties of the B. caudatus kDNA suggest that the catenated network structure of trypanosome kDNA is not required for maxicircle segregation during kinetoplast division or for the expression of the maxicircle genome.

Animals

Detection of multiple variable antigen types in metacyclic populations of Trypanosoma brucei.

The identification of antigen types in tsetse salivary gland metacyclic populations of Trypanosoma brucei requires the production of monospecific antisera to the corresponding bloodstream variable antigen types. Monospecific antisera against clones from cyclically transmitted populations are difficult to prepare, however, owing to the antigenic lability of such clones. This problem has been overcome by isolating an antigenically stable clone from a syringe-infected rabbit at a time when its serum showed incipient activity towards metacyclic trypanosomes. Monospecific antisera raised against this clone reacted with up to 20% metacyclics in trypanolysis and immunofluorescence tests, confirming that a clone-derived metacyclic population of T. brucei is heterogeneous with respect to variable antigen type.

Animals

Antigenic variation in trypanosomes.

In its mammalian host, Trypanosoma brucei is able to change the antigenic character of its glycoprotein surface coat and so evade the host's immune response. This phenotypic change seems to occur spontaneously in 1 in 10,000 individuals but is not due to genetic mutation: host antibody is not necessary for its induction but plays a selective part in bringing about the gross changes in parasite numbers and antigenic character observed in the bloodstream by destroying the main component of what is actually a heterogeneous population. The infecting trypanosome population injected into the mammalian host by the tsetse fly vector may also be heterogeneous. Such heterogeneity complicates plans to vaccinate cattle and people against the African trypanosomes based on the premise that the metacyclic trypanosomes of a clone bear the same surface antigen.

Animals

Fusion of host cell secondary lysosomes with the parasitophorous vacuoles of Leishmania mexicana-infected macrophages.

Secondary lysosomes of cultured mouse peritoneal macrophages were labeled with the electron-dense colloid saccharated iron oxide; the identity of the labeled structures was checked by the Gomori reaction for acid phosphatase. Amastigotes of Leishmania mexicana mexicana derived from mouse lesions were used to infect these macrophages in vitro. In electron micrographs of thin sections of infected macrophages the labeled secondary lysosomes were seen fused with the parasitophorous vacuoles without preventing subsequent multiplication of the parasites. A similar fusion probably occurs in vivo, and may provide a pathway through which not only nutrients but also drugs and host antibodies could reach the intracellular parasite.

Acid Phosphatase