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Scores of millions of people around the world are infected by Schistosoma mansoni causing considerable morbidity, mortality and loss of productivity. Safe chemotherapeutic agents have been used though there are challenges of re-infection due to resistance. Both epidemiological and experimental data suggest that acquired cell mediated immunity play significant roles in regulating the intensity of S. mansoni infection as well as its patho-physiologic sequelae. Improved control of this trematode parasite may be obtained with immunization to enhance the resistance of individuals to risk of infection. This study investigated the cellular responses of mice immunized with soluble proteins from foot and digestive gland of the vector snail and challenged with S. mansoni. The proteins were used to immunize the experimental groups then challenged with the S. mansoni. The experimental groups were FT (immunized with foot protein) and DG (immunized with digestive gland). The parameters, which were analyzed to demonstrate protection, included; the worm counts and cellular (IFN-γ, IL-5 cytokines) responses. It was observed that, the experimental groups showed significant protection in terms of worm reduction and immune responses. The group vaccinated with foot protein showed higher protection (87.5%) as compared to the group vaccinated with the digestive gland (50%) in terms of worm reduction. Cytokines (IFN-γ and IL-5) production was present in different levels during the assay time points which showed an aspect of protection. The Foot protein of the vector showed more immunizing power than the digestive gland. Research towards utilizing the two proteins as feasible vaccine candidates is encouraged.

Purity N Nguhiu1, Claire N Wamae2,3, Japheth K Magambo4, Paul G Mbuthia5, Daniel C Chai6, Dorcas S Yole61Department of Veterinary Services, Kabete, Ministry of Livestock Development, Nairobi, 2Directorate of Research and Development, Kenya Methodist University, Meru, 3Kenya Medical Research Institute, Nairobi, 4Meru University College of Science and Technology, Meru, 5Department of Veterinary Pathology, Microbiology and Parasitology, University of Nairobi, 6Department of Tropical Infectious Diseases, Institute of Primate Research, Karen, Nairobi, KenyaAbstract: In 2009, experimental Cyclospora infections were established in two juvenile female and two adult male Cercopithecus aethiops (African green monkeys) at Nairobi's Institute of Primate Research (IPR). The study animals were humanely sacrificed, and gross and histopathological evaluation was done at seven weeks post-infection. On gross examination, the juveniles had no abnormalities except for a slight enlargement of the mesenteric lymph nodes, while the adults displayed more pathology of enlarged lymph nodes, hemorrhagic gastrointestinal tracts, widespread necrotic foci of the liver, and enlarged spleens. Significant histopathological findings were observed in both the juveniles and adults, which ranged from mild inflammatory reactions in the stomach and intestines to intense cellular infiltrations with mitotic activity and lymphocytic infiltrations around the periportal area of the livers. The lymph nodes had extensive hyperplasia with many mitotic cells.Keywords: Cyclospora spp., cyclosporiasis, nonhuman primates, pathological findings, histopathological findings, African green monkeys

BACKGROUND Three species of non-human primates comprising African green monkeys (AGMs), (Cercopithecus aethiops, n = 89), Syke's monkeys (Cercopithecus mitis, n = 60) and olive baboons (Papio cynocephalus anubis, n = 30), were screened for Entopolypoides macaci. METHODS Observation of blood smears prepared from these animals revealed E. macaci infection rate of 42.7% in AGMs, 35% in Syke's monkeys and 33.3% in baboons. RESULTS Gender infection rate was 38.2% in females and 29% in males. Statistically, there was no significant difference in infection rates between the monkey species and sexes (P > 0.05). Subsequent indirect immuno fluorescent antibody test supported the morphological appearance of E. macaci observed by microscopy. Sera from infected animals reacted positively (1:625) with E. macaci antigen, but not to Babesia bigemina or B. bovis antigen at 1:125 titer. CONCLUSION This study has revealed high prevalence of E. macaci infection in all three widely distributed Kenyan non-human primates. With the continued use of these animals as models for human parasitic diseases, the presence of this highly enzootic parasite should be noted.

Schistosoma haematobium is widely distributed in Africa. In Kenya, endemic areas include the upper and the lower regions of the Coast Province, Lake Victoria and the Kano plains. Low infection rates over prolonged periods of time characterize schistosome infections of people living in endemic areas. However, the common laboratory practice is to expose the definitive host to a single high dose. In order to utilize the laboratory results appropriately, it is important to know whether or not a large single infection has similar results to multiple small doses. In this study, immune responses, worm burden, gross and histopathological patterns of multiple infection of S. haematobiumium in the Golden hamster ( Mesocricetus auratus ) were compared with those of single exposure. Multiple infections with low doses of the parasite did not seem to be protective, as suggested by; more worms, worse gross and histopathology in multiple low dose group compared to single high dose group. Most probably there is an antigenic threshold, which needs to be attained before protective mechanisms come into play. Although necessary for protection, there was no direct correlation between IgG levels and degree of protection.

Schistosoma mansoni and Leishmania major are important tropical human parasites. It is crucial to know the effect of the two infecting man concurrently. Two groups of BALB/c mice were infected with each of the parasites separately; another group was co-infected with both parasites and there was a naïve control. Draining lymph node and spleen cells from mice infected with either of the parasites showed high proliferative responses to their specific parasite antigen. However, crossreactivity occurred between S. mansoni and L. major. Spleen and Lymph node cells from co-infected group demonstrated high and sustained proliferative responses to schistosome soluble worm antigen preparation and killed Leishmania major antigen, respectively. There was high and sustained IgG levels for both the single and coinfected groups. At 10 weeks post-infection, co-infected mice had significantly larger nodules than mice with L. major infection alone. However, co-infected animals had less severe liver pathology and less enlarged mesenteric lymph nodes than those infected with S. mansoni only. This work shows that co-infection results in two different outcomes: protection against S. mansoni and exacerbated pathogy in L. major. We suggest that cellular responses possibly protect against S. mansoni, while high IgG levels lead to exacerbated L. major response.

In Schistosoma mansoni endemic areas, there are people with ongoing S. mansoni infection, others have been infected and treated while others have never been infected. What would happen if these different groups of people were vaccinated against S. mansoni? BALB/c mice were divided into five groups: Infected-Treated-Vaccinated; Infected-Vaccinated-Treated; Vaccinated-Treated Control; Challenge Control and Untreated challenge Control. Vaccination (500 20krad irradiated S. mansoni cercariae), Treatment (praziquantel), Infection and Challenge (150 S. mansoni cercariae) were carried out at specified times. Proliferation assay, Enzyme linked immunosorbent assay, gross pathology, histopathology and perfusion were performed. High protection levels were obtained in mice treated after vaccination: Vaccinated-Treated control, 96.5%; Infected-Vaccinated-Treated, 68.9%; and Infected-Treated-Vaccinated, 41%. A good correlation was obtained between proliferative responses and protective levels, implying cellular involvement in protection. Although all protected animals had high IgG levels, there was no strong correlation between the two. Specificity rather than amounts of IgG, seem more important in protection. Praziquantel seemed to boost protective immunity when administered after vaccination. Granuloma development and modulation in the two test groups was similar. It seems better to vaccinate infected patients before treatment, the ideal situation being vaccinating people who have not encountered S. mansoni .

Intensity of human schistosomiasis infection increases with age, a peak being attained at early puberty. Hormones could be involved in the age-related changes in susceptibility to schistosomiasis. Male BALB/c mice were infected with Schistosoma mansoni either before or after puberty and worm numbers, cellular immune responses, hormonal levels and pathology analysed. Pre-puberty infected mice had a significantly higher number of adult worms (p<0.05), more severe granulomas, higher mortality rate and higher proliferative responses as compared to postpuberty infected mice. Levels of the hormones were lower in the pre-puberty infected mice as compared to the post-puberty group early in the infection. Plasma levels of testosterone and luteinizing hormones decreased significantly (p<0.05) in infected mice when compared to controls. Susceptibility to S. mansoni in male BALB/c mice seems to be influenced by levels of testosterone and leutenizing hormone at infection. Albeit, an infection with S. mansoni seems to lower the hormonal levels.