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These types of developmental events appear to occur in many members of the family Trypanosomatidae.

For example, Trypanosoma cruzi undergoes morphological transitions in the amastigote to trypanomastigote stage in the mammalian host and develops to the infective metacyclic stage in the hindgut of the vector. A similar change would appear to take place in the vector stages of Leishmania species in the transition of rapidly dividing gut stages to a non-dividing, infective metacyclic stage.

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The metacyclic stage ultimately dies if it is not inoculated into a mammalian host. It has been suggested that in the African trypanosomes there are two possible reasons for the evolution of the LS to SS transition. The first is that the LS to SS is necessary for the transition of the trypanosomes from life in their glucose-rich, highly-oxygenated blood environment into the glucose-poor, poorly-oxygenated environment of the tsetse gut.

In most texts or research papers on this topic, it is suggested that it is the SS stage that is vector transmissible and there is good evidence to support this statement. The SS stage appears to be pre-adapted for life in the vector. There are changes in enzyme and mitochondrial functions suggesting preparation for survival in an environment that is low in glucose and oxygen [ 8 ].


The trypanosome populations enriched for the SS stage have been shown to be tsetse infective. However, there are also suggestions in the literature that the LS stage can be tsetse infective [discussed in [ 13 ]].

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In addition, monomorphic strains can be induced to grow as procyclics in in vitro culture [ 14 ]. Equally important is the question as to whether the SS population is homogenous with respect to tsetse infectivity. We hypothesize that aging SS forms eventually reach a stage in which they are no longer fly infective but in fact are programmed to die. It is, therefore, suggested that the SS population is heterogeneous: The second reason that has been suggested for the evolution of the LS to SS transition is to control the trypanosome parasitemia in the mammalian host and thereby prolong host survival.

This would increase the time available for the successful transmission of the trypanosomes to the vector. There is considerable experimental evidence to support this hypothesis. It has been repeatedly demonstrated that monomorphic strains of the African trypanosomes are highly virulent [ 15 ]. For example one clone that we have used, the monomorphic, T. If one injected into the moribund mouse one ml of a concentrated glucose solution, the mouse would survive significantly longer and the parasitemia would more that double during that time period Seed and Sechelski, unpublished.

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Others have reported similar results using mice and rats [ 16 , 17 ]. We suggest that our mice died of hypoglycemia, oxygen depletion, and acidosis as originally proposed by Von Brand [ 18 ]. This is an enormous energy drain on the host. Susceptible C3H mice infected with monomorphic and pleomorphic trypanosomes. C3H mice infected with either the monomorphic TXTat-1 clone of Trypanosoma brucei gambiense or the pleomorphic Loutat-1 clone of Trypanosoma brucei rhodesiense.

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Panel A shows the number of trypanosomes per ml of blood. Panel B shows the percentage of the pleomorphic trypanosomes that are in the LS stage. Louis Missouri, Personal Communication, that would be consumed by the circulating trypanosomes. The ability of the trypanosome population to switch from the LS to the SS stage lowers the parasitemia in the complete absence of any detectable host immune response Figure 1A,1B ; [ 19 ]; and others. If one calculates the carbohydrate utilization by the trypanosomes during the early peak in parasitemia of a pleomorphic population in the C3H mouse, the mouse should be able to maintain its energy balance.

It is only during the later phase with the rise in parasitemia that the consumption of host carbohydrate by the trypanosomes dramatically increases. This is observed in small rodent models, in which blood glucose levels are maintained until the very terminal stages of the infection [ 20 ].

Furthermore mice infected with a pleomorphic strains show no obvious weight loss during the infection. If the SS stage has a metabolic rate for glucose similar to the LS stage the energy drain on the host would be considerably greater. Although mice infected with a pleomorphic clone are able to survive significantly longer than animals infected with a monomorphic clone approximately 20 days versus 5 days , the mice do not survive as long as animals that have a relapsing type infection. Immunocompetent, resistant B10BR mice have a relapsing type infection and survive an average of 38 days.

In B10BR mice it can be observed that the percentage of host carbohydrate utilized by the trypanosomes mimics the relapsing nature of the parasitemia Figures 2A,2C. There are short peaks of large energy loss followed by longer periods of minimal carbohydrate utilization.

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This of course assumes that the host's eating habits are normal. This lowering of parasitemia would presumably allow for longer host survival. B10BR mice infected with the pleomorphic Loutat-1 clone of Trypanosoma brucei rhodesiense. Panel B shown the percentage of these trypanosomes that are in the LS stage; at hours, nearly all of the remaining parasites are the SS form. In the above discussion, we are not trying to suggest that host carbohydrate depletion is responsible for triggering the LS to SS transition, nor do we believe that in large naturally infected mammals that energy losses are solely responsible for the pathology observed.

What we are hypothesizing is that if trypanosome growth is not controlled in large animals and the parasitemia approached that found in a mouse infected with a monomorphic clone, the host would be severely energy depleted. It is suggested that one of the critical factors in the control of parasitemia is the LS to SS transition. The earlier during an infection that the LS to SS transition takes place, resulting in lower parasitemia, the less energy is lost by the host as a result of the trypanosomes' high energy demand.

Although in large mammals carbohydrate catabolized by the trypanosomes is not believed to be solely responsible for the pathology, it is conceivable that, particularly in the central nervous system, local concentrations of trypanosomes could alter or damage cells by simply out-competing host cells for essential nutrients. The calculations of glucose use by the trypanosomes in relation to the mouse intake illustrate the large energy demand that uncontrolled parasite growth places on the host.

We should note that in addition to glucose the trypanosomes are also know to dramatically reduce the aromatic amino acid levels in animals with high parasitemia. It is, therefore, also conceivable that trypanosomes localized in the CNS could out compete host cells i. Several other points should be noted at this time. The first is that there is evidence to suggest that the LS form is more sensitive that the SS stage to antibody plus complement mediated lysis [ 1 , 21 ].

This would insure that the SS stages are available for transmission for a greater time period in the blood of their host. The second point is that experimental evidence has been presented demonstrating that it is the SS form that is primarily responsible for inducing the protective anti-variant specific antibody response in chronically infected mice [ 22 ].

Therefore, it would appear that the LS to SS transition is responsible for the initial non-immunological control of the peak in parasitemia, that SS forms persist in the presence of antibody for a greater period of time, and finally that it is the SS stage that is predominantly responsible for the antibody induced relapse. Earlier, it was asked if LS stage trypanosomes could infect tsetse as well as whether all SS forms were fly-infective. It was suggested that the SS population is not homogeneous but rather consists of young fly infective SS forms and old dying SS forms.

There is little question that the SS forms in the absence of being taken up by the vector will die. It would appear that they are programmed to die during an apoptosis-like phenomenon. It seems reasonable to assume that SS forms once in their final death phase are no longer fly infective. It has been shown that the transition from LS to SS is not reversible and one can suggest that the transition from SS fly infective to SS dying is also not reversible.

Only the rapidly dividing LS form and the old SS form are predicted not to infect tsetse. Small in amount or extent; meager: As applied to the human body, slender implies a generally attractive and pleasing thinness: Switch to new thesaurus. Having little flesh or fat on the body: Small in degree, especially of probability: His chances of winning are extremely slender. References in classic literature? Arachnodactyly has been linked to mutations in both fibrillin-1 and fibrillin-2 genes.

It remains unconfirmed whether composer Sergei Rachmaninoff 's abnormally large reach on a piano was a result of arachnodactyly due to Marfan syndrome , as the pianist exhibited no other signs of the disease. From Wikipedia, the free encyclopedia. Journal of Medical Genetics. Retrieved 25 September Recognition and management for physiotherapists". Cleidocranial dysostosis Sprengel's deformity Wallis—Zieff—Goldblatt syndrome.

Madelung's deformity Clinodactyly Oligodactyly Polydactyly. Genu valgum Genu varum Genu recurvatum Discoid meniscus Congenital patellar dislocation Congenital knee dislocation. Acheiropodia Ectromelia Phocomelia Amelia Hemimelia.