The distribution and location of the symbiont Lagenophrys aselli on the freshwater isopod Asellus aquaticus

1. The distribution and location of the ciliated protozoan Lagenophrys aselli on the freshwater isopod Asellus aquaticus were studied in relation to water flow over the third pleopod surface. 2. At low densities L. aselli had a significant preference for the anterior centre of the pleopod; however, at the highest densities this preference was no longer significant. The distribution ranged from closer than random at low densities to further than random at the highest densities, and may have been a product of feeding and reproduction of L. aselli as well as the short intermoult period of the host. 3. An individual L. aselli has an effective area of both the lorica and the ciliated feeding disc. The ciliated feeding disc, when extended, may contribute to the presence of a small anterior–posterior gap being left between individuals.     

Distribution of the ticks <Emphasis Type="Italic">Ixodes persulcatus</Emphasis> and <Emphasis Type="Italic">Ixodes pavlovskyi</Emphasis> on the boundary of the forest and forest-steppe zones in the Ob region

Surveys of ixodoid ticks were performed in Novosibirsk Province (Novosibirsk and Toguchin Districts) and in the vicinity of Akademgorodok (Novosibirsk) in 2009–2010. The abundance and distribution of ticks were assessed in 8 types of habitats. Ixodes persulcatus (Schulze, 1930) was collected by flagging in Novosibirsk and Toguchin Districts, with the highest densities of 19 ind./km being observed in habitats with small-leaved trees. Three species of ticks: Ixodes persulcatus, I. pavlovskyi (subspecies I. pavlovskyi occidentalis Filip. et Pan., 1998), and Dermacentor reticulatus (Fabricius, 1794) were recorded in a recreational forest of Akademgorodok. A high abundance (22 ind./km) of I. pavlovskyi was observed in pine forests subjected to considerable recreational load. The abundance of I. persulcatus was the highest in aspen-birch and birch-aspen forests. D. reticulatus was captured in pine forests and fallow lands, its abundance varying from 0.2 to 2 ind./km.     

African trypanosomes and brain infection – the unsolved question

African trypanosomes induce sleeping sickness. The parasites are transmitted during the blood meal of a tsetse fly and appear primarily in blood and lymph vessels, before they enter the central nervous system. During the latter stage, trypanosomes induce a deregulation of sleep–wake cycles and some additional neurological disorders. Historically, it was assumed that trypanosomes cross the blood–brain barrier and settle somewhere between the brain cells. The brain, however, is a strictly controlled and immune‐privileged area that is completely surrounded by a dense barrier that covers the blood vessels: this is the blood–brain barrier. It is known that some immune cells are able to cross this barrier, but this requires a sophisticated mechanism and highly specific cell–cell interactions that have not been observed for trypanosomes within the mammalian host. Interestingly, trypanosomes injected directly into the brain parenchyma did not induce an infection. Likewise, after an intraperitoneal infection of rats, Trypanosoma brucei brucei was not observed within the brain, but appeared readily within the cerebrospinal fluid (CSF) and the meninges. Therefore, the parasite did not cross the blood–brain barrier, but the blood–CSF barrier, which is formed by the choroid plexus, i.e. the part of the ventricles where CSF is produced from blood. While there is no question that trypanosomes are able to invade the brain to induce a deadly encephalopathy, controversy exists about the pathway involved. This review lists experimental results that support crossing of the blood–brain barrier and of the blood–CSF barrier and discuss the implications that either pathway would have on infection progress and on the survival strategy of the parasite. For reasons discussed below, we prefer the latter pathway and suggest the existence of an additional distinct meningeal stage, from which trypanosomes could invade the brain via the Virchow–Robin space thereby bypassing the blood–brain barrier. We also consider healthy carriers, i.e. people living symptomless with the disease for up to several decades, and discuss implications the proposed meningeal stage would have for new anti‐trypanosomal drug development. Considering the re‐infection of blood, a process called relapse, we discuss the likely involvement of the newly described glymphatic connection between the meningeal space and the lymphatic system, that seems also be important for other infectious diseases.