Two key biological features distinguish Trypanosoma evansi from the T. brucei group: independence from the tsetse fly as obligatory vector, and independence from the need for functional mitochondrial DNA (kinetoplast or kDNA). In an effort to better understand the molecular causes and consequences of these differences, we sequenced the genome of an akinetoplastic T. evansi strain from China and compared it to the T. b. brucei reference strain. The annotated T. evansi genome shows extensive similarity to the reference, with 94.9% of the predicted T. b. brucei coding sequences (CDS) having an ortholog in T. evansi, and 94.6% of the non-repetitive orthologs having a nucleotide identity of 95% or greater. Interestingly, several procyclin-associated genes (PAGs) were disrupted or not found in this T. evansi strain, suggesting a selective loss of function in the absence of the insect life-cycle stage. Surprisingly, orthologous sequences were found in T. evansi for all 978 nuclear CDS predicted to represent the mitochondrial proteome in T. brucei, although a small number of these may have lost functionality. Consistent with previous results, the F₁F_O-ATP synthase γ subunit was found to have an A281 deletion, which is involved in generation of a mitochondrial membrane potential in the absence of kDNA. Candidates for CDS that are absent from the reference genome were identified in supplementary de novo assemblies of T. evansi reads. Phylogenetic analyses show that the sequenced strain belongs to a dominant group of clonal T. evansi strains with worldwide distribution that also includes isolates classified as T. equiperdum. At least three other types of T. evansi or T. equiperdum have emerged independently. Overall, the elucidation of the T. evansi genome sequence reveals extensive similarity of T. brucei and supports the contention that T. evansi should be classified as a subspecies of T. brucei. The single-cell parasite Trypanosoma evansi is the disease-causing trypanosome with the widest geographical distribution. The disease, called surra, has significant economic impact primarily due to infections of cattle, horses, and camels. Morphologically the parasite is indistinguishable from bloodstream stage T. brucei, a parasite causing sleeping sickness in humans and the disease nagana in animals. T. brucei, however, is strictly bound to sub-Saharan Africa where its obligate vector, the tsetse fly, resides. The lack of a complete mitochondrial genome in T. evansi further distinguishes this parasite from T. brucei. Important questions regarding the biology of T. evansi include how it escaped from Africa, whether this has happened more than once, and how exactly it is related to T. brucei. To help answer these questions we have sequenced the T. evansi nuclear genome. Our phylogenetic analysis demonstrates that T. evansi, and the closely related horse parasite T. equiperdum, evolved more than once from T. brucei. We also demonstrate extensive similarity to T. brucei, including the maintenance of numerous genes that T. evansi no longer requires. Therefore, despite the significant functional and pathological differences between T. evansi and T. brucei, our analysis supports the notion that T. evansi is not an independent species.

SUMMARY: Visceral leishmaniasis (VL) caused by Leishmania spp. is an important vector-borne and largely zoonotic disease. In China, three epidemiological types of VL have been described: anthroponotic VL (AVL), mountain-type zoonotic VL (MT-ZVL), and desert-type ZVL (DT-ZVL). These are transmitted by four different sand fly species: Phlebotomus chinensis , P. longiductus , P. wui , and P. alexandri. In 1951, a detailed survey of VL showed that it was rampant in the vast rural areas west, northwest, and north of the Yangtze River. Control programs were designed and implemented stringently by the government at all administrative levels, resulting in elimination of the disease from most areas of endemicity, except the western and northwestern regions. The control programs consisted of (i) diagnosis and chemotherapy of patients, (ii) identification, isolation, and disposal of infected dogs, and (iii) residual insecticide indoor spraying for vector control. The success of the control programs is attributable to massive and effective mobilization of the general public and health workers to the cause. Nationally, the annual incidence is now very low, i.e., only 0.03/100,000 according to the available 2011 official record. The overwhelming majority of cases are reported from sites of endemicity in the western and northwestern regions. Here, we describe in some depth and breadth the current status of epidemiology, diagnosis, treatment, and prevention of the disease, with particular reference to the control programs. Pertinent information has been assembled from scattered literature of the past decades in different languages that are not readily accessible to the scientific community. The information provided constitutes an integral part of our knowledge on leishmaniasis in the global context and will be of special value to those interested in control programs.

Toxoplasma gondii infects humans and warm blooded animals causing devastating disease worldwide. It has long been a mystery as to why the peritoneal macrophages of rats are naturally resistant to T. gondii infection while those of mice are not. Here, we report that high expression levels and activity of inducible nitric oxide synthase (iNOS) and low levels of arginase-1 (Arg 1) activity in the peritoneal macrophages of rats are responsible for their resistance against T. gondii infection, due to high nitric oxide and low polyamines within these cells. The opposite situation was observed in the peritoneal macrophages of mice. This discovery of the opposing functions of iNOS and Arg 1 in rodent peritoneal macrophages may lead to a better understanding of the resistance mechanisms of mammals, particularly humans and livestock, against T. gondii and other intracellular pathogens.

Toxoplasma gondii (T. gondii) is a very successful parasite that can infect virtually all warm blooded animals with a worldwide distribution. It causes a large range of clinical manifestations in both humans and domesticated animals. In addition, marked biological differences exist among T. gondii strains in the pathogenicity and geographical distribution. Molecular epidemiology studies primarily based on restriction fragment length polymorphism (RFLP) method revealed that three main types are predominant in North America and Europe, whereas other diverse genotypes are found in other parts of the world. Microsatellite (MS) as a type of genetic marker has been widely used in many organisms. Limited MS genotyping, however, to fingerprint T. gondii isolates has been reported and little is known about the MS data of the strains predominantly prevalent in China.