Encystment of Colpoda cucullus is induced by an increase in external Ca2+ concentration. When the Colpoda vegetative cells were induced to encyst by being suspended in Ca2+-containing medium, the cells that had swum linearly began to turn round which may have modified their ciliary movement, and then stopped prior to the formation of a cyst wall. Such a behavioral modification may be responsible for an elevation of intracellular Ca2+ concentration. Slowly and spontaneously induced encystment in Ca2+-free medium was suppressed by the addition of EGTA, suggesting that Ca2+ contaminating the medium may be partially responsible for the induction of such spontaneous encystment. A cAMP enzyme immunoassay (EIA) revealed that the cAMP level was raised when the vegetative cells were transferred into Ca2+-containing medium for encystment induction. This result suggests that Ca2+ may activate a signaling pathway leading to encystment events including elevation of the cAMP concentration.
A study was undertaken to detect Trypanosoma evansi infection by polymerase chain reaction (PCR) among clinically ill cattle, buffaloes and horses which were suspected for 'surra', but found negative by parasitological and immunological tests. Detection of trypanosomal DNA based on PCR have been found more useful tool for diagnosis of the infection in clinically ill animals which were declared as negative by examination of Giemsa stained blood smears, mouse inoculation test and antibody detection enzyme linked immunosorbent assay (ELISA) test.
A cross-sectional study was conducted in 2003 on sleeping sickness (SS) patients in the Ibba hospital in Maridi County, western Equatorial province of southern Sudan. The occurrences of co-infection with blood-borne infections and hematological profiles were investigated in SS patients. Fifty SS patients (23 males and 27 females) were included in the study. Most (49) of the patients were in second stage disease, but trypanosomes could be demonstrated in the cerebrospinal fluid (CSF) of only eight of them. Majority of the patients had co-infection with loiasis (36%), malaria (30%) or both loiasis and malaria (10%), and only 24% were free from other infections. Other parasitic infections observed from symptomatic patients were onchocerciasis (2), giardiasis (2), trichomoniasis (2), helminthosis (2) and amoebiasis (2). Co-infection was more common in female (85%) than in male patients (65%), which may be attributed to occupational activities by females. The patients had various disease symptoms including headache (96%), arthralgia/myalgia (88%), pruritus (82%), fever (52%), insomnia (26%) and mental disturbance (20%）. The nutritional status of most of them (84%) was below normal Body Mass Index (20-13), and anemia was common (79%). Despite most patients having either normal (66%) or low (12%) white blood cell (WBC) counts, further analysis in 23 of them revealed that majority had lymphocytosis (83%), eosinophilia (96%) and neutropenia (61%), some of which are indicative of a depressed or exhausted immune system. Loa loa parasites obstructed microscopic observation of trypanosomes at the buffy coat interphase of a microhematocrit tube. This study has shown that co-infections of malaria and loiasis are common in SS patients in this region. Apart from the SS and malaria control it would be important to also introduce control programs against nematode infections and particularly loiasis in this region. Combined control of the three diseases would decrease morbidity and co-morbidity due to multiple parasitic diseases.
CD4+CD25+ regulatory T cells (Treg cells) work as an immunoregulatory suppressor for the effector function of cell-mediated immunity. In the present study, we depleted a population of Treg cells by hyper-treatment with an anti-mouse CD25 monoclonal antibody and evaluated the infectious development of two murine Babesia parasites,B. microti (non-lethal) and B. rodhaini (lethal), in mice. The Treg cell-depleted mice were more resistant to the infection of B. microti than the control mice, as indicated by the lower development of parasitemia and faster recovery of anemia in the mice. On the other hand, in B. rodhaini infection, the depleted mice showed a severer clinical response than the control mice, as indicated by the parasitemia development and lethal rate dynamics. These findings indicated different effects of Treg cell-depletion in Babesia infections, suggesting that cell-mediated immunity, which can be suppressed by Treg cells, might be responsible for the control of B. microti infection but not for the B. rodhaini infection in mice.