Small nutrient molecules in fruit fuel efficient digestion and mutualism with plants in frugivorous bats.

Frugivorous bats often possess short intestines, and digest rapidly. These characters are thought to be weight-saving adaptations for flight. The hypothesis that they limit digestive efficiency was tested by assaying glucose and protein in fecal samples of a free-ranging bat, and in fruit of its main food plant. To assure the correct calculation of digestive efficiencies, seeds were used as a mass marker for nutrients in fruit and feces. Glucose represents 32.86%, and protein 0.65%, of the nutrient content of fruit. Digestive efficiencies for these nutrients respectively are 92.46% and 84.44%, clearly negating the hypothesis for glucose. Few studies have quantified protein in fruit. Instead, "crude protein", a dietary parameter solely based on nitrogen determinations, is used as a surrogate of protein content. This study shows that, for fruit consumed by bats, crude protein estimates typically are much greater than true protein values, implying that a large fraction of the crude protein reported in previous studies consists of free amino acids. The rapid digestion of frugivores has the potential to limit protein digestion, thus it may require free amino acids for efficient assimilation of nitrogen; therefore, the crude protein approach is inadequate for the fruit that they consume because it does not differentiate free amino acids from protein. Adding simple sugars and free amino acids, instead of protein, to fruit reduce metabolic costs for plants. Direct assimilation of these small nutrient molecules increases digestive and foraging efficiencies. Both factors contribute to the persistence of the mutualism between plants and frugivores, with community-wide repercussions.

The correct subgeneric name of Trypanosoma rangeli Tejera, 1920 (Euglenozoa: Trypanosomatidae), a human-infective endoparasite of neotropical mammals.

Trypanosoma rangeli Tejera, 1920 is peculiar in being transmitted to mammal hosts through the bite of triatomine bugs. For this reason, it has been placed in its own subgenus, Tejeraia Añez, 1982. This name is a junior homonym of Tejeraia Díaz-Ungría, 1963, used for the roundworm Tejeraia mediospiralis (Molin, 1860). The mandatory substitute name of Tejeraia Añez, 1982 is Aneza Özdikmen, 2009. T. (Aneza) rangeli Tejera, 1920 is often referred to as T. (Herpetosoma) rangeli Tejera, 1920. According to nomenclature rules, both name combinations are available. Which one to choose depends on evolutionary and taxonomic considerations. Phylogenetic knowledge indicates that T. (Aneza) rangeli should be used.

Trypanosoma brucei Plimmer & Bradford, 1899 is a synonym of T. evansi (Steel, 1885) according to current knowledge and by application of nomenclature rules.

Proper application of the principles of biological nomenclature is fundamental for scientific and technical communication about organisms. As other scientific disciplines, taxonomy inherently is open to change, thus species names cannot be final and immutable. Nevertheless, altering the names of organisms of high economical, medical, or veterinary importance can become a complex challenge between the scientific need to have correct classifications, and the practical ideal of having fixed classifications. Trypanosoma evansi (Steel, 1885), T. brucei Plimmer & Bradford, 1899 and T. equiperdum Doflein, 1901 are important parasites of mammals. According to current knowledge, the three names are synonyms of a single trypanosome species, the valid name of which should be T. evansi by the mandatory application of the Principle of Priority of zoological nomenclature. Subspecies known as T. brucei brucei Plimmer & Bradford, 1899, T. b. gambiense Dutton, 1902 and T. b. rhodesiense Stephens & Fantham, 1910 should be referred to respectively as T. evansi evansi (Steel, 1885), T. e. gambiense and T. e. rhodesiense. The polyphyletic groupings so far known as T. evansi and T. equiperdum should be referred respectively to as surra- and dourine-causing strains of T. e. evansi. Likewise, trypanosomes so far known as T. b. brucei should be referred to as nagana-causing strains of T. e. evansi. Though it modifies the scientific names of flagship human and animal parasites, the amended nomenclature proposed herein should be adopted because it reflects phylogenetic and biological advancements, fixes errors, and is simpler than the existing classificatory system.

The kinetic properties of hexokinases in African trypanosomes of the subgenus Trypanozoon match the blood glucose levels of mammal hosts.

We hypothesize that the hexokinases of trypanosomes of the subgenus Trypanozoon match the blood glucose levels of hosts. We studied the kinetic properties of purified hexokinase in T. equiperdum (specific activity=302U/mg), and compare with other members of Trypanozoon. With ATP (Km=104.7µM) as phosphate donor, hexokinase catalyzes the phosphorylation of glucose (Km=24.9µM) and mannose (Km=8.8µM). With respect to glucose, mannose and inorganic pyrophosphate respectively are a competitive, and a mixed inhibitor of hexokinase. With respect to ATP, both are mixed inhibitors of this enzyme. In T. equiperdum, hexokinase shows a high affinity for glucose. Pleomorphism-transformation of trypanosomes from a multiplicative to a non-multiplicative form-results in a self-limited growth stabilizing glucose consumption. It delays the death of the host, thus prolonging its exposure to tsetse flies. When glucose levels descend, top-down regulation allows trypanosomes to survive through the expression of alternative metabolic pathways. It accelerates the death of the host, but helps trypanosome density to increase enough to ensure transmission without tsetse flies. Pleomorphism, and a hexokinase with a high affinity for glucose, are two main adaptive traits of T. b. brucei. The latter trait, and a strong top-down regulation, are two main adaptive traits of T. equiperdum. For trypanosomes living in glucose-rich blood, a hexokinase with a high affinity for glucose would unnecessarily harm hosts. This may explain why the human parasites, T. b. gambiense and T. b. rhodesiense, possess hexokinases with a low affinity for glucose.

A new polytypic species of yellow-shouldered bats, genus Sturnira (Mammalia: Chiroptera: Phyllostomidae), from the Andean and coastal mountain systems of Venezuela and Colombia.

Sturnira is the most speciose genus of New World leaf-nosed bats (Phyllostomidae). We name Sturnira adrianae, new species. This taxon is born polytypic, divided into a larger subspecies (S. a. adrianae) widespread in the mountains of northern and western Venezuela, and northern Colombia, and a smaller subspecies (S. a. caripana) endemic to the mountains of northeastern Venezuela. The new species inhabits evergreen, deciduous, and cloud forests at mainly medium (1000-2000 m) elevations. It has long been confused with S. ludovici, but it is more closely related to S. oporaphilum. It can be distinguished from other species of Sturnira by genetic data, and based on discrete and continuously varying characters. Within the genus, the new species belongs to a clade that also includes S. oporaphilum, S. ludovici, S. hondurensis, and S. burtonlimi. The larger new subspecies is the largest member of this clade. The two new subspecies are the most sexually dimorphic members of this clade. The smaller new subspecies is restricted to small mountain systems undergoing severe deforestation processes, therefore can be assigned to the Vulnerable (VU) conservation category of the International Union for Conservation of Nature (IUCN).

Trypanosoma evansi is alike to Trypanosoma brucei brucei in the subcellular localisation of glycolytic enzymes.

Trypanosoma evansi, which causes surra, is descended from Trypanosoma brucei brucei, which causes nagana. Although both parasites are presumed to be metabolically similar, insufficient knowledge of T. evansi precludes a full comparison. Herein, we provide the first report on the subcellular localisation of the glycolytic enzymes in T. evansi, which is a alike to that of the bloodstream form (BSF) of T. b. brucei: (i) fructose-bisphosphate aldolase, glyceraldehyde-3-phosphate dehydrogenase (GAPDH), hexokinase, phosphofructokinase, glucose-6-phosphate isomerase, phosphoglycerate kinase, triosephosphate isomerase (glycolytic enzymes) and glycerol-3-phosphate dehydrogenase (a glycolysis-auxiliary enzyme) in glycosomes, (ii) enolase, phosphoglycerate mutase, pyruvate kinase (glycolytic enzymes) and a GAPDH isoenzyme in the cytosol, (iii) malate dehydrogenase in cytosol and (iv) glucose-6-phosphate dehydrogenase in both glycosomes and the cytosol. Specific enzymatic activities also suggest that T. evansi is alike to the BSF of T. b. brucei in glycolytic flux, which is much faster than the pentose phosphate pathway flux, and in the involvement of cytosolic GAPDH in the NAD+/NADH balance. These similarities were expected based on the close phylogenetic relationship of both parasites.

Trypanosoma evansi is alike to Trypanosoma brucei brucei in the subcellular localisation of glycolytic enzymes

Trypanosoma evansi, which causes surra, is descended from Trypanosoma brucei brucei, which causes nagana. Although both parasites are presumed to be metabolically similar, insufficient knowledge of T. evansi precludes a full comparison. Herein, we provide the first report on the subcellular localisation of the glycolytic enzymes in T. evansi, which is a alike to that of the bloodstream form (BSF) of T. b. brucei: (i) fructose-bisphosphate aldolase, glyceraldehyde-3-phosphate dehydrogenase (GAPDH), hexokinase, phosphofructokinase, glucose-6-phosphate isomerase, phosphoglycerate kinase, triosephosphate isomerase (glycolytic enzymes) and glycerol-3-phosphate dehydrogenase (a glycolysis-auxiliary enzyme) in glycosomes, (ii) enolase, phosphoglycerate mutase, pyruvate kinase (glycolytic enzymes) and a GAPDH isoenzyme in the cytosol, (iii) malate dehydrogenase in cytosol and (iv) glucose-6-phosphate dehydrogenase in both glycosomes and the cytosol. Specific enzymatic activities also suggest that T. evansi is alike to the BSF of T. b. brucei in glycolytic flux, which is much faster than the pentose phosphate pathway flux, and in the involvement of cytosolic GAPDH in the NAD+/NADH balance. These similarities were expected based on the close phylogenetic relationship of both parasites.

Importance of the horse and financial impact of equine trypanosomiasis on cattle raising in Venezuela.

In Venezuela, horses are indispensable for extensive cattle raising, and extensive cattle raising prevails in all regions. This determines the numerical relationship between horses and cattle (r = 0.93) to be relatively constant nationwide. At regional level, the average extension of cattle ranches varies greatly. However, in relation to the area covered by pastures, the numbers of horses (r = 0.95) and cattle (r = 0.93) are relatively uniform nationwide. Water buffalo occupy small fractions of the territory; therefore, their numbers are related to the area of pastures less strongly (r = 0.56). There is no information on the numerical relationship between the numbers of horses and water buffalo. In the Llanos region of the country, equine trypanosomiasis is responsible for a high mortality in horses, causing considerable financial losses to cattle ranches. So far, such losses have not been assessed. For this region, in 2008, it can be calculated that: (1) with no treatment, losses owing to horse mortality caused by this hemoparasitosis would have amounted to US$7,486,000; (2) the diagnosis and treatment of affected horses would have required an investment of US$805,000; and (3) in terms of horses saved, this investment would have resulted in benefit of US$6,232,000. Therefore, for every monetary unit invested, there would be a benefit 7.75 times greater, this ratio being applicable to any year and all regions of the country. It follows that the profitability of investing in the diagnosis and treatment of equine trypanosomiasis is guaranteed.