Theo Schetters

Canine babesiosis in Europe : how many diseases?

Babesiosis, recognized since ancient times as an important disease of livestock and more recently as an emerging disease in dogs worldwide, is caused by intraerythrocytic protozoa of the genus Babesia and is transmitted by ticks. The pathophysiology of canine babesiosis has been extensively studied but many questions remain unanswered, especially regarding the diversity of disease manifestations in different European countries. Continued investigation of the similarities and differences in host-parasite interplay in canine babesiosis in different European countries should lead to a better understanding of the disease process, potentially leading to better prediction of disease outcome and the development of new treatment modalities. From the European point of view it is important to conduct these studies on Babesia canis.

ANTIDotE: anti-tick vaccines to prevent tick-borne diseases in Europe

Ixodes ricinus transmits bacterial, protozoal and viral pathogens, causing disease and forming an increasing health concern in Europe. ANTIDotE is an European Commission funded consortium of seven institutes, which aims to identify and characterize tick proteins involved in feeding and pathogen transmission. The knowledge gained will be used to develop and evaluate anti-tick vaccines that may prevent multiple human tick-borne diseases. Strategies encompassing anti-tick vaccines to prevent transmission of pathogens to humans, animals or wildlife will be developed with relevant stakeholders with the ultimate aim of reducing the incidence of tick-borne diseases in humans.

Cattle tick vaccine researchers join forces in CATVAC

A meeting sponsored by the Bill & Melinda Gates Foundation was held at the Avanti Hotel, Mohammedia, Morocco, July 14–15, 2015. The meeting resulted in the formation of the Cattle Tick Vaccine Consortium (CATVAC).

Living apart or together

Symbiosis is defined as two organisms living together. This definition assumes that the organisms are separate entities. However, it becomes more and more clear that the level of integration can go much further and evidence is accumulating that this integration is an ongoing process. Apicomplexans including Plasmodium and Toxoplasma appear to have acquired plastid genes that are of bacterial origin. When tracing back the origin of these genes, it is assumed that the ancestor of these apicomplexans engulfed a plastid-containing alga. Prior to that event, the ancestor of all algae had engulfed a cyanobacterium, which formed the plastid organelle. This integration was taken one step further when many of the plastid genes transferred to the nuclear genome in apicomplexans. It has now been found that these genes subsequently accquired new introns [Schaap, D. et al. (2001) Mol. Biochem. Parasitol. 115, 119–121]. Furthermore, the results showed that, in Toxoplasma, intron invasion must have occurred relatively recently – after the separation of Plasmodium and Toxoplasma from their common ancestor. The significance of this finding is that through intron invasion new or altered genes can evolve and this could be crucial for adaptation of these parasites to ever-changing environments. TS

Why are the French different from the British

Parasites affect the physiological and immunological systems of their host to increase the chance of successful transmission. It has been reported that Toxoplasma gondii, which also infects the brain, can change the behaviour of the host. When rats are infected with T. gondii, the propensity to explore novel stimuli in their environment was increased, whereas there was no effect on social status in the group or mating success. This selective change in behaviour would increase the chance of rats to be captured by cats and consequently increase the transmission of the parasite. Manuel Berdoy from the University of Oxford, UK, states that such effects of T. gondii on the brain could explain the reports of altered personality and IQ levels in some humans following parasite infection. Interestingly, ∼22% of the UK population carries the organism, whereas in France the level is 87% (source: http://www.webmesh.co.uk). TS

Towards a Psoroptes ovis vaccine

Sheep scab is an exudative dermatitis of the skin caused by the mite Psoroptes ovis. Mainly owing to safety reasons and the development of resistance to antiparasitics, new ways to control sheep scab are being sought. It has now been reported that sheep develop immunity after infection with the parasite [reviewed in Smith, W.D. et al. (2001) Res. Vet. Sci. 70, 87–91]. It was found that not only the affected surface area after infection was reduced in previously infected sheep, but compared with challenge controls, fewer mites were detected on the sheep also. This type of immunity was associated with a rapid increase in circulating IgE antibody concentration after challenge infection. Furthermore, a series of experiments by other research groups suggested that soluble extracts of mites could induce a certain degree of protection, whereas membrane-extracted extracts fail to do so. In the light of developing a vaccine against sheep scab, these findings are encouraging, and further research will aim to identify the molecules and genes encoding them. TS

Research or re-search?

In the past decade, the Internet has proven to be a valuable tool to obtain information. Many scientists keep up with the literature through services such as BioMedNet, which provides access to a number of scientific journals. However, some scientific journals are still only available as printed copies and this creates a threshold to access such journals and interest in these journals is decreasing. Furthermore, unless the institutional library has a subscription to an electronic version of the journal, services are limited to listings of titles and abstracts. This holds the risk that most of the interpretation of data (although peer-reviewed) is left to the authors because it is often too much effort to obtain a copy of the original article. Much of the original work on parasitology was carried out around the turn of the 20th century using natural parasite–host combinations, something that, because of the change in ethical attitude towards in vivo experimentation, would not be possible today. Exemplary is the treatment of neurosyphillis patients with malaria parasites in the period before the Second World War. Because the electronic databases do not go further back than 1966, the risk of missing the basic literature is increasing. Unless this information becomes available as readily as more recent literature, we will enter an era of re-search rather than developing research. TS

Parasites on the move

Global changes as diverse as changes in climate, mobility of people and animals, deforestation and forestation affect the ecology of a variety of organisms, including parasites. The re-emergence of recognized diseases, such as malaria and trypanosomiasis in countries where these diseases have been effectively controlled, is exemplary. In 1977, two years after the WHO declared Europe free of malaria, 83% of the world population was living in malaria-free areas or in areas where control programs were in progress. Today, however, this figure has decreased to 60%. The resurgence of malaria could not be attributed solely to the development of resistance of both the parasite and the mosquito vector to drugs and chemotherapeutics, respectively. In a recent article, Ronald Fayer points out that several other parasitic diseases are increasing globally [Fayer, R.J. (2000) J. Parasitol. 86, 1174–1181]. Dazzling figures on the number of cryptosporidiosis cases (from two human cases reported in the USA in 1976, to an estimated 300 000 cases reported annually today), and trichinosis (a 17-fold increase since 1983 in Romania to over 16 000 cases in the 1990s) support the notion that parasites are on the move. In an era when budgets on teaching and research in parasitology have been drastically reduced, it appears that with this increase in the occurrence of parasitic diseases, the parasitologists have the next move. TS

Setting the stage for Leishmania

When a host is infected with a parasite, a symbiosis ensues that functions as a new complex organism; the infected host. The co-existence of these organisms requires integration of both physiological complexes. It has been shown that the immune system plays an important role in the fate of Leishmania in the host. White blood cells produce a cytokine context that either allows survival of the parasite or its elimination. This is dependent on the type of T-cell response activated upon infection. A T-helper 1 (Th1) response (characterized by the production of IFN-γ and IL-12) that leads to parasite killing owing to the activation of infected macrophages by IFN-γ. By contrast, a Th2 response (characterized by the production of IL- 4) allows survival of the parasite, probably because of downregulation of IFN-γ production by IL-10. Results from a mouse model indicated that salivary gland lysates of Plebotomus papatasi, the mosquito vector that transmits Leishmania major, provokes a Th2 response, which allows parasite survival (M.L. Mbow. et al., J. Immunol. 161, 5571–5577, 1998). Recently, it was shown that prior exposure of mice to bites of uninfected sandflies induced strong Th1 responsiveness with IFN-γ production, and associated resistance to Leishmania infection. These results suggest an alternative means of immunization against Leishmania infection (S. Kamhawi et al., Science 290, 1351–1354, 2000) and might have implications to the epidemiology of the disease. TS

Life beyond death

The strategy of inducing apoptosis in cells that are infected with intracellular parasites might not be as effective at reducing infection as was once thought [Lopes, M.F. et al. (2000) Immunol. Today 21, 489–494]. Apoptotic cells do not lyse, and are subsequently cleared by macrophages through a specific receptor (apoptotic cell receptor αv β3, vitronectin receptor). In vitro cultivation of Trypanosoma cruzi in macrophages demonstrated that apoptosis occurred in co-cultured splenic T cells. Furthermore, apoptosis led to a marked increase in parasite replication within the macrophages. Importantly, apoptotic rather than necrotic cells increased parasite proliferation. Although it was not clear whether the apoptotic cells arose after infection with the parasite in this case (e.g. cells can also be triggered to become apoptotic through the Fas receptor), intracellular parasite death resulting from induction of apoptosis could actually promote further parasite proliferation in macrophages that take up the apoptotic cells. TS