Scabies is an infectious disease that is endemic in poorly resourced communities, and also common in industrialized countries. Although the disease, which is caused by infestation of Sarcoptes scabiei, is generally mild, the need for a vaccine against S. scabiei is proposed. The immunological mechanisms that control S. scabiei infection are discussed and the current status of scabies vaccine development reviewed. Future directions for scabies vaccine development are also addressed.

Members of the family Trichomonadidae, mainly Trichomonas gallinae and Tetratrichomonas gallinarum, represent important parasites in birds with worldwide presence, since being reported in the 19th century. Especially Columbiformes, Falconiformes and Strigiformes can be severely affected by trichomonads, whereas the majority of infections in Galliformes and Anatiformes are subclinical although severe infections are occasionally reported. With the recent appearance of deadly infections in wild Passeriformes the protozoan parasite T. gallinae obtained greater attention which will be addressed in this review. Although light microscopy remains the method of choice to confirm the presence of trichomonads molecular studies were introduced in recent years, in order to characterize the parasites and to establish relationships between isolates. Isolation of trichomonads is a prerequisite for detailed in vitro and in vivo studies and different media are reported to obtain suitable material. The limited information about virulence factors will be reviewed in context with the pathogenicity of trichomonads which varies greatly, indicating certain strain heterogeneity of the parasites. Options for treatment characterized by the leading role of imidazoles whose activity is sometimes hampered by resistant parasites remains a challenge for the future. Introducing more standardized genetic studies and investigations concentrating on the host-pathogen interaction should be helpful to elucidate virulence factors which might lead to new concepts of treatment.

Considering the epidemic situation of gambiense human African trypanosomiasis (HAT) at the end of the twentieth century, the World Health Organization (WHO) and partners strengthened disease control and surveillance. Over the last 15 years, the activities implemented through the National Control Programmes have brought gambiense HAT under control and now its elimination is deemed as an achievable goal. In 2012, WHO targeted gambiense HAT for elimination as a public health problem by 2020. The final goal will be the sustainable disease elimination by 2030, defined as the interruption of the transmission of gambiense HAT. The elimination is considered feasible, because of the epidemiological vulnerability of the disease, the current state of control, the availability of strategies and tools and international commitment and political will. Integration of activities in the health system is needed to ensure the sustainability of the elimination. The development of user-friendly diagnostic and treatment tools will facilitate the integration process. Adequate funding is needed to implement activities, but also to support research that will make the elimination sustainable. A long-term commitment by donors is needed and ownership of the process by endemic countries is critical.

This study aimed to develop and test the in vitro and in vivo effectiveness of diminazene aceturate encapsulated into liposomes (L-DMZ) on Trypanosoma evansi. To validate the in vitro tests with L-DMZ, the efficacy of a commercial formulation of diminazene aceturate (C-DMZ) was also assessed. The tests were carried out in culture medium for T. evansi, at concentrations of 0·25, 0·5, 1, 2 and 3 μg mL−1 of L-DMZ and C-DMZ. A dose-dependent effect was observed for both formulations (L-DMZ and C-DMZ), with the highest dose-dependent mortality of trypomastigotes being observed at 1 and 3 h after the onset of tests with L-DMZ. The results of in vivo tests showed the same effects in the animals treated with L-DMZ and C-DMZ in single doses of 3·5 mg kg−1 and for 5 consecutive days (3·5 mg kg−1 day−1). It was possible to conclude that T. evansi showed greater in vitro susceptibility to L-DMZ when compared with C-DMZ. In vivo tests suggest that treatment with the L-DMZ and C-DMZ showed similar efficacy in vivo. The potential of the formulation developed in this study was clearly demonstrated, as it increased the efficacy of the treatment against trypanosomosis, but more studies are needed to increase the effectiveness in vivo.

We studied a total of eight developmental stages of capped brood and newly emerged workers of Apis mellifera carnica colonies naturally parasitized with Varroa destructor. During winter and early spring four colonies were fed syrup containing 1·8 mg vitamin C kg−1 (ascorbic acid group; group AA) while four colonies were fed syrup without the vitamin C (control group C). Selected elements of the antioxidative system were analysed including total antioxidant status (TAS), glutathione content and antioxidative enzyme activities (superoxide dismutase, catalase, peroxidase and glutathione S-transferase). Body weight, protein content and indices of infestation were also determined. The prevalence (8·11%) and intensity (1·15 parasite per bee) of the infestation were lower in group AA compared with group C (11·3% and 1·21, respectively). Changes in the indicators of antioxidative stress were evidence for the strengthening of the antioxidative system in the brood by administration of vitamin C. In freshly emerged worker bees of group AA, despite the infestation, protein content, TAS, and the activity of all antioxidative enzymes had significantly higher values in relation to group C.

Two single nucleotide polymorphisms (SNP TXNIP and SNP ARNT), both on chromosome 4, have been reported to be associated with roundworm (Ascaris suum) burden in pigs. In the present study, we selected pigs with two SNP TXNIP genotypes (AA; n = 24 and AB; n = 24), trickle-infected them with A. suum from 8 weeks of age until necropsy 8 weeks later, and tested the hypothesis that pigs with the AA genotype would have higher levels of resistance than pigs of AB genotype. We used different indicators of resistance (worm burden, fecal egg counts (FEC), number of liver white spots and A. suum-specific serum IgG antibody levels). Pigs of the AA genotype had lower mean macroscopic worm burden (2·4 vs 19·3; P = 0·06), lower mean total worm burden (26·5 vs 70·1; P = 0·09) and excreted fewer A. suum eggs at week 8 PI (mean number of eggs/g feces: 238 vs 1259; P = 0·14) than pigs of the AB genotype, as expected based on prior associations. The pigs were also genotyped at another locus (SNP ARNT) which showed a similar trend. This study provides suggestive evidence that resistant pigs may be selected using a genetic marker, TXNIP, and provides further support to the quantitative trait locus on chromosome 4.

Protozoan parasites of genus Leishmania are the causative agents of leishmaniasis. Leishmania promastigotes primarily infect macrophages in the host, where they transform into amastigotes and multiply. Lipophosphoglycan (LPG), the most abundant surface molecule of the parasite, is a virulence determinant that regulates the host immune response. Promastigotes are able to modulate this effect through LPG, creating a favourable environment for parasite survival, although the mechanisms underlying this modulation remain unknown. We analysed the participation of TLR2 and TLR4 in the production of cytokines and explored the possible phosphorylation of ERK and/or p38 MAP kinase signalling cascades in human macrophages stimulated with Leishmania mexicana LPG. The results show that LPG induced the production of TNF-α, IL-1β, IL-12p40, IL-12p70 and IL-10 and led to phosphorylation of ERK and p38 MAP kinase. Specific inhibitors of ERK or p38 MAP kinases and mAbs against TLR2 and TLR4 reduced cytokine production and phosphorylation of both kinases. Our results suggest that L. mexicana LPG binds TLR2 and TLR4 receptors in human macrophages, leading to ERK and MAP kinase phosphorylation and production of pro-inflammatory cytokines.

Protein deficiency impairs local and systemic immune responses to Heligmosomoides bakeri infection but little is known about their individual and interactive impacts on tissue architecture of maternal lymphoid (thymus, spleen) and visceral (small intestine, kidney, liver, pancreas) organs during the demanding period of lactation. Using a 2×2 factorial design, pregnant CD1 mice were fed a 24% protein sufficient (PS) or a 6% protein deficient (PD) isoenergetic diet beginning on day 14 of pregnancy and were infected with 100 H. bakeri larvae four times or exposed to four sham infections. On day 20 of lactation, maternal organs were examined histologically and serum analytes were assayed as indicators of organ function. The absence of villus atrophy in response to infection was associated with increased crypt depth and infiltration of mast cells and eosinophils but only in lactating dams fed adequate protein. Infection-induced lobular liver inflammation was reduced in PD dams, however, abnormalities in the kidney caused by protein deficiency were absent in infected dams. Bilirubin and creatinine were highest in PD infected mice. Infection-induced splenomegaly was not due to an increase in the lymphoid compartment of the spleen. During lactation, infection and protein deficiency have interactive effects on extra-intestinal pathologies.

Chagas disease, which is caused by the parasite Trypanosoma cruzi, affects approximately 7–8 million people in Latin America. The drugs available to treat this disease are ineffective against chronic phase disease and are associated with toxic side effects. Therefore, the development of new compounds that can kill T. cruzi at low concentrations is critically important. Herein, we report the effects of a novel 3-arylideneindolin-2-one that inhibits sirtuins, which are highly conserved proteins that are involved in a variety of physiological processes. The compound KH-TFMDI was tested against the epimastigote, trypomastigote and amastigote forms of T. cruzi, and its effects were evaluated using flow cytometry, light and electron microscopy. KH-TFMDI inhibited the replication of T. cruzi intracellular amastigotes with an IC50 of 0·5±0·2 μm, which is significantly lower than the IC50 of benznidazole. The compound also lysed the highly infectious bloodstream trypomastigotes (BST) with LC50 values of 0·8±0·3 μm at 4 °C and 2·5±1·1 μm at 37 °C. KH-TFMDI inhibited cytokinesis and induced several morphological changes in the parasite, leading to its death by apoptosis and autophagy. This study highlights sirtuins as a potential new target for Chagas disease therapy.

The effect of gastrointestinal helminths on Pb accumulation in the host body is ambiguous. A laboratory experiment with Rattus norvegicus/Hymenolepis diminuta model was conducted to determine Pb toxicokinetics in a terrestrial host-parasite system. The ET-AAS or ICP–OES techniques were used to determine Pb concentrations (CPb) in both tapeworms and host tissues (kidney, liver, bone, testes, muscle and intestinal wall). Concerning the entire host-parasite system, the highest CPb were detected in H. diminuta. Rat kidneys and bone were the only two tissues whose mean Pb levels were lower in parasitized animals than they were in non-infected subjects after both levels of exposure. At low Pb exposure, parasitization slightly changed the Pb toxicokinetics in the host body. However, with respect to tissue at the same exposure level, no significant differences were detected between the parasitized and non-parasitized animals and no significant correlations were found between CPb in tapeworms and those of host tissues. The results of this study indicate that H. diminuta does not protect rat from elevated Pb exposure even if tapeworm accumulates a higher portion of ingested Pb dose compared with that of the most Pb-loaded host soft tissue. The portion of Pb dose accumulated in H. diminuta correlates positively with parasite biomass.

Transmission of Trypanosoma cruzi, the causal agent of Chagas disease, has expanded from rural endemic to urban areas due to migration. This so-called urban Chagas is an emerging health problem in American, European, Australian and Japanese cities. We present a mathematical model to analyse the dynamics of urban Chagas to better understand its epidemiology. The model considers the three clinical stages of the disease and the main routes of inter-human transmission. To overcome the complexities of the infection dynamics, the next-generation matrix method was developed. We deduced expressions which allowed estimating the number of new infections generated by an infected individual through each transmission route at each disease stage, the basic reproduction number and the number of individuals at each disease stage at the outbreak of the infection. The analysis was applied to Buenos Aires city (Argentina). We estimated that 94% of the new infections are generated by individuals in the chronic indeterminate stage. When migration was not considered, the infection disappeared slowly and R 0 = 0·079, whereas when migration was considered, the number of individuals in each stage of the infection tended to stabilize. The expressions can be used to estimate different numbers of infected individuals in any place where only inter-human transmission is possible.

Chagas heart disease is a major public concern since 30% of infected patients develop cardiac alterations. The relationship between Trypanosoma cruzi discrete typing units (DTUs) and the biological properties exhibited by the parasite population has yet to be elucidated. In this study, we analysed the expression of α-smooth muscle actin (α-SMA) and galectin-3 (Gal-3) associated with cardiac extracellular matrix (ECM) remodelling a murine chronic cardiomyopathy induced by Tc I genotypes. We found the induction of myocarditis was associated with the upregulation of Col I, α-SMA, Gal-3, IFN-γ and IL-13, as analysed by q-PCR. In myocardial areas of fibrosis, the intensity of myocarditis and significant ECM remodelling correlated with the presence of Col I-, Gal-3- and α-SMA-positive cells. These results are promising for the further efforts to evaluate the relevance of Gal-3 in Chagas heart disease, since this galectin was proposed as a prognosis marker in heart failure patients.

Infections with the malaria parasite Plasmodium vivax are noteworthy for potentially very long incubation periods (6–9 months), which present a major barrier to disease elimination. Increased sporozoite challenge has been reported to be associated with both shorter incubation and pre-patent periods in a range of human challenge studies. However, this evidence base has scant empirical foundation, as these historical analyses were limited by available analytic methods, and provides no quantitative estimates of effect size. Following a comprehensive literature search, we re-analysed all identified studies using survival and/or logistic models plus contingency tables. We have found very weak evidence for dose-dependence at entomologically plausible inocula levels. These results strongly suggest that sporozoite dosage is not an important driver of long-latency. Evidence presented suggests that parasite strain and vector species have quantitatively greater impacts, and the potential existence of a dose threshold for human dose-response to sporozoites. Greater consideration of the complex interplay between these aspects of vectors and parasites are important for human challenge experiments, vaccine trials, and epidemiology towards global malaria elimination.