The effect of vaccinating S. mansoni–infected BALB/c mice either before or after treatment

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. African Journal of Health Sciences Vol. 13 (1-2) 2008: pp. 55-6

Studies on the interaction of Schistosoma mansoni and Leishmania major in experimentally infected Balb/c mice

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.a 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. majorresponse. African Journal of Health Sciences Vol. 14 (1-2) 2007: pp. 80-8

Influence of age of mice on the susceptibility to murine schistosomiasis infection

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 (

Do schistosome vaccine trials in mice have an intrinsic flaw that generates spurious protection data?

The laboratory mouse has been widely used to test the efficacy of schistosome vaccines and a long list of candidates has emerged from this work, many of them abundant internal proteins. These antigens do not have an additive effect when co-administered, or delivered as SWAP homogenate, a quarter of which comprises multiple candidates; the observed protection has an apparent ceiling of 40–50 %. We contend that the low level of maturation of penetrating cercariae (~32 % for Schistosoma mansoni) is a major limitation of the model since 68/100 parasites fail to mature in naïve mice due to natural causes. The pulmonary capillary bed is the obstacle encountered by schistosomula en route to the portal system. The fragility of pulmonary capillaries and their susceptibility to a cytokine-induced vascular leak syndrome have been documented. During lung transit schistosomula burst into the alveolar spaces, and possess only a limited capacity to re-enter tissues. The acquired immunity elicited by the radiation attenuated (RA) cercarial vaccine relies on a pulmonary inflammatory response, involving cytokines such as IFNγ and TNFα, to deflect additional parasites into the alveoli. A principal difference between antigen vaccine protocols and the RA vaccine is the short interval between the last antigen boost and cercarial challenge of mice (often two weeks). Thus, after antigen vaccination, challenge parasites will reach the lungs when both activated T cells and cytokine levels are maximal in the circulation. We propose that “protection” in this situation is the result of physiological effects on the pulmonary blood vessels, increasing the proportion of parasites that enter the alveoli. This hypothesis will explain why internal antigens, which are unlikely to interact with the immune response in a living schistosomulum, plus a variety of heterologous proteins, can reduce the level of maturation in a non-antigen-specific way. These proteins are “successful” precisely because they have not been selected for immunological silence. The same arguments apply to vaccine experiments with S. japonicum in the mouse model; this schistosome species seems a more robust parasite, even harder to eliminate by acquired immune responses. We propose a number of ways in which our conclusions may be tested

Prevalence and Intensity of Gastrointestinal Parasites in Wild -trapped Pabio anubis and Cercopithecus aethiops in Kenya

Gastrointestinal parasite infections by multiple parasite species involving helminths and protozoans occur in non-human primates. The objective of the study was to screen for gastrointestinal parasite infections from sixty five wild-trapped Pabio anubis (olive baboons) and sixty four Cercopithecus aaethiops (African green monkeys) from various locations in Kenya and at the Institute of Primate Research (IPR), Nairobi, in March 2008 to June 2009 to obtain preliminary data as baseline for proposed further study on coccidian parasites. Four faecal samples per individual animal were collected on Mondays and Thursdays for two consecutive weeks and processed for parasitological examination for gastrointestinal parasites. The animals were asymptomatic at the time of faecal sampling. Twelve taxa of intestinal parasites, 5 helminth and 7 protozoan parasites were identified. The helminth genera observed were Oesophagostomum, Trichuris, Strongyloides, Trichostrongylus and Enterobius with species prevalence of 33.6%, 30.4%, 26.2%, 8.8%, 0.8%, 0.4%, and 10.0%, 47.6%, 16.0%, 3.2%, 0.4% for olive baboons and African green monkeys, respectively. The intensity of infections ranged from 0-2350 eggs per gram (epg). Most individuals (56.2%) had mild infections of 1-300 epg and only 8% had egg counts greater or equal to 400. The protozoan parasites identified in this study were Entamoeba coli, Entamoeba histolytica, Cyclospora spp, Cryptosporidia spp, Isospora spp, Iodamoeba butschilii and Paramecium spp with prevalence of 77.3%, 23.1%, 3.8%, 2.7%, 2.2%, 1.2%, 0%, and 76.8%, 23.6%, 63.6%, 6.2%, 0.4%, 0%, 0.4% for olive baboons and African green monkeys, respectively. Majority (63.1%) of the animals had 2-3 parasite infections. Though the infections were asymptomatic in these non-human primates, they harbour important parasites that pose potential danger to public health, livestock and wildlife animals

Enzootic simian piroplasm (Entopolypoides macaci ) in wild-caught Kenyan non-human primates

BACKGROUNDThree 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.METHODSObservation 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.RESULTSGender 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 &gt; 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.CONCLUSIONThis 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.</p