Helminth parasites in the intestinal tract of indigenous poultry in parts of Kenya.

A study was carried out on 456 indigenous poultry intestinal specimens from various towns in Kenya to determine the occurrence and distribution of helminth parasites in the intestinal tract of the birds. Of the specimens examined, 414 had parasites whereas the remaining 42 had none, which is an infection rate of 90.78%. The main species of helminths found in the intestines were Raillietina sp. (47.53%), Heterakis gallinarum (21.33%), Ascaridia galli (10.03%), Strongyloides avium (9.96%), Choanotaenia infundibulum (4.61%), Cotugnia digonopora (3.6%), Capillaria sp. (1.5%), Trichostrongylus tenius (1.04%) and Syngamus trachea (0.40%). Most helminths were present in both the mid- and hindguts. Syngamus trachea and C. digonopora were only found in the foregut and midgut, respectively. Although chickens from which the specimens were collected appeard healthy, the high prevalence of helminthiasis observed shows the poor level of helminth infection control practiced by the indigenous poultry keepers in the country, which might affect the health status of the birds and their growth rates. Poultry keepers should be encouraged to prevent, control and treat such cases.

Attempts to manipulate specific responses to induce resistance to Schistosoma mansoni in Kenyan baboons (Papio anubis).

Attempts were made to manipulate specific responses of baboons to protect them from infection with Schistosoma mansoni. In Experiment 1, eosinophilia was induced in naive baboons with Trichinella spiralis larvae given intravenously before intraperitoneal injection of globulin fractions from S. mansoni-infected baboon sera and subsequent percutaneous exposure to S. mansoni cercariae. In Experiment 2, baboons with 8- or 32-week-old primary S. mansoni infections received T. spiralis i.v. before an S. mansoni challenge. In experiments 3 to 5 respectively, naive baboons received intramuscularly before challenge: formalin-fixed S. mansoni schistosomula, with Bordetella pertussis as an adjuvant; a preparation of S. mansoni adult worm teguments; and a preparation of IgE-immune complexes obtained from S. mansoni-infected rat sera, with Freunds Complete Adjuvant. Minor, but statistically insignificant, protection was obtained in Experiments 2 (32-week infections) and 3, but was far less than that given by intact, irradiated living vaccines. There are signs on the horizon of non-living vaccines protecting rodents against S. mansoni infection and it would be prudent, as with drugs, to test these in primates before proceeding to man. The results of our experiments, though essentially negative, should help the design of any future vaccine trials in primates.

Attempts to induce resistance to Schistosoma mansoni and S. haematobium in Kenyan baboons (Papio anubis) using non-specific immunostimulants.

Non-specific immunostimulants were used in an attempt to protect baboons from infection by schistosomes. Subcutaneous vaccination with cord factor (4.50 mg) and muramyl dipeptide (4.56 mg) 6 days before percutaneous exposure to 3000 Schistosoma haematobium cercariae/baboon (c.p.b.) failed to protect naive baboons: baboons with a 7-month-old, 5000 c.p.b. S. haematobium primary infection had developed too strong a natural immunity to detect any protection attributable to vaccination. Subcutaneous vaccination with 0.4 ml of Bacillus Calmette-Guerin (BCG, 1-8 X 10(8) colony forming units/ml) 4 days before exposure to 1000 c.p.b. S. mansoni gave a significant (38%) reduction in worm load compared with controls. However, vaccination with 0.8 (intramuscular) and 0.2 (intradermal) ml of BCG 11 days before exposure to S. mansoni 800 c.p.b. did not protect naive baboons, nor did it significantly reduce challenge worm recovery from baboons with a 13-week-old, 500 c.p.b. S. mansoni primary infection. Obvious pathology was seen at the site of vaccination in the first but not the second BCG experiment. These results partly support the findings in mice that non-specific macrophage and monocyte activators give partial protection against schistosome infections but they also illustrate that rodents and primates do not necessarily react identically. Hence, findings from rodent models should be extrapolated to man with some caution.

Observations on the ability of repeated, light exposures to Schistosoma mansoni cercariae to induce resistance to reinfection in Kenyan baboons (Papio anubis).

Using groups of 4 baboons (Papio anubis), 21.0% of a trickle exposure of 480 Schistosoma mansoni cercariae/baboon (10/week for 48 weeks) were recovered as adult worms (Group A) compared with 72.6% from a single massive exposure of 2500 cercariae/baboon (Group C). Group B, exposed first to the trickle and then to the massive exposure simultaneously with Groups A and C, yielded a worm recovery of 54% which was slightly but significantly less than Group C. The trickle infection apparently induced a substantial resistance to light re-exposure but only a partial, although significant, resistance to a massive re-exposure. In Group B, however, there was a marked reduction in the degree of gross pathology, despite high tissue egg production by the mature challenge worms. The parasitological results, in terms of resistance to reinfection by and development of pathology to a trickle infection, are not materially different from those obtained in studies using conventional heavy primary and challenge exposures with S. mansoni. The significance of these findings is discussed in relation to the epidemiology of human schistosomiasis mansoni in which heavy exposures are believed to be the exception rather than the rule.

Experimental Schistosoma mansoni infection in vervet monkeys (Cercopithecus aethiops) in Kenya: I. Susceptibility to a primary infection.

Groups of five 3-kg Kenyan monkeys, Cercopithecus aethiops, were exposed individually to 150,600 or 1500 Schistosoma mansoni cercariae per monkey. Three monkeys died soon after the infections became patent and the survivors were autopsied 4 months after exposure. Mortality and most haematological, parasitological and pathological sequelae of infection were dose-related, but not the white cell response or changes in the levels of serum proteins or fibrinogen. No gross liver fibrosis was seen. Comparison of this study with earlier ones on related cercopithecine monkeys suggests that the vervet closely resembles the baboon in its response to S. mansoni infections. Difficulties in managing and maintaining vervets can be overcome by using colony-bred or properly adapted feral animals. Thus, the vervet provides a cheaper, more readily available primate model for experimental S. mansoni studies. A prolonged infection, sufficiently heavy to permit reliable parasitological monitoring without undue mortality, should be provided by 150 S. mansoni cercariae per kg body-weight, using the Kenyan strains of vervet and parasite.

Observations on possible immunity to reinfection among Kenyan schoolchildren after treatment for Schistosoma mansoni.

In February 1977, 306 out of 409 six- to 16-year-old Kenyan schoolchildren were found to be infected with Schistosoma mansoni. Prevalence and intensity were directly related to age and indirectly to the distance between the child's home and the transmission site, but were not related to the child's sex. Most children were treated with hycanthone in July 1977. Pretreatment blood samples were taken from 100 study children for eosinophil counts and measurements of cytotoxic anti-schistosomular antibody levels. Blood and faecal samples were re-examined five times between November 1977 and July 1979. Whole school resurveys in July 1978 and 1979 confirmed the continuation of transmission after chemotherapy. 'Reinfection' rates in the study children, incorporating both failed treatment and true reinfections, were significantly reduced in children, with both detectable antibody and eosinophil counts above 400/mm3, compared with children with neither. Children with either detectable antibodies or high eosinophil counts (mainly the latter) had intermediate reinfection rates. Neither sex, age nor pretreatment intensities influenced reinfection rates, but location of dwelling did: children from distant homes had lower rates. However, the effects of residence and 'protection' were not directly linked. The implication of these results, namely that infection can confer immune protection to reinfection after treatment, is being explored in further studies.

Marburg, Ebola and Rift Valley Fever virus antibodies in East African primates.

Sera from 464 primates held at four institutes in Kenya were tested by indirect immunofluorescence for the presence of antibodies against Marburg, Ebola, Congo haemorrhagic fever, Rift Valley fever and Lassa viruses. Four of 136 vervet monkeys were positive for Marburg virus antibodies and three of 184 baboons had antibodies against Ebola virus. One baboon was positive for Marburg virus antibodies. Two vervet monkeys, three baboons and one grivet monkey (of 56 tested) had antibodies against Rift Valley fever virus. No Congo or Lassa virus antibodies were detected. A sample of 88 sera of more arboreal primates (Sykes, blue and colobus monkeys) were negative against all five antigens, as were sera from 58 staff members of the institutes who worked with or near the animals.

Heat-labile and heat-stable anti-schistosomular antibodies in Kenyan schoolchildren infected with Schistosoma mansoni.

Two in vitro cytotoxicity assays using 51Cr-labelled Schistosoma mansoni schistosomula were performed on serum samples collected from 91 schoolchildren infected with S. mansoni from Machakos District, Kenya. One assay, which is believed to detect IgE/antigen complexes, uses unheated serum and human monocytes; the other, believed to detect IgG antibodies, uses heat-inactivated serum and unpurified peripheral blood leucocytes. Analysis of the data was complicated because the children were drawn from two separate studies and the data was extremely variable, probably because of the manner in which infections are acquired under natural conditions. There was a strong, positive regression of intensity of infection on age of the children, and evidence that IgG, but not IgE, activity was related to intensity of infection. There was no clear-cut relationship of IgE and IgG activities with the age of the children, and little evidence of any correlation between IgE and IgG activities within individual children. The implications of this latter dissociation and the possibility of either mechanism acting as the effector mechanism for concomitant immunity in man are discussed in the light of these results.

Functional studies on purified eosinophils and neutrophils from patients with Schistosoma mansoni infections.

Unpurified peripheral blood leucocytes or purified eosinophils and neutrophils from patients with schistosomiasis and from normal individuals were compared for their ability to interact with antibody coated schistosomula of Schistosoma mansoni. There was no difference in the ability of buffy coat cells or neutrophils from patients and from normal individuals to mediate antibody-dependent 51Cr release from labelled schistosomula. However, eosinophils from patients were significantly better than those from normal individuals in causing antibody-dependent 51Cr release. This enhanced activity of eosinophils from patients with schistosomiasis was found to correlate with the intensity of their infection as judged by faecal egg counts. Eosinophils from patients also contained a higher proportion of cells with detectable Fc receptors than those from normal individuals. It is suggested that the difference in the behaviour of eosinophils from patients and from normals may reflect an 'activated' state of these cells in the infected individuals.

Schistosoma mansoni in the Kenyan baboon (Papio anubis): the development and predictability of resistance to homologous challenge.

Groups of baboons were exposed to primary infections of either 500 or 2,000 Schistosoma mansoni cercariae per baboon (c.p.b.). Five from each infection level and five uninfected baboons were challenged with 2,500 c.p.b. at one of four intervals of time after primary infection and killed ten weeks later, together with unchallenged appropriate primary infection controls. Primary faecal egg excretion was related to the cercarial dose, showing some systematic fluctuations during the 78 weeks of the experiment. Challenge infections increased faecal egg excretion in certain cases only. Faecal and tissue egg production were usually suppressed in the challenge worms. In contrast to less heavily infected, challenge-control baboons bearing primary infections, the challenged baboons had minimal gross pathology and there were no deaths due to acute schistosomiasis from the challenge infection. Over-all resistance to reinfection was low and unrelated to the age or intensity of the primary infections. However, seven baboons yielded less than 50% of the expected challenge worms. An in vitro assay, measuring anti-schistosomula antibody and peripheral leucocyte cytotoxic activity, successfully identified the in vivo immune status at thetime of challenge of 14/18 baboons tested. The in vivo significance of the immunological mechanism upon which the test is based is discussed in relation to possible future baboon and human studies.

Eosinophilia in Kenyan baboons (Papio anubis) induced by Trichinella spiralis and Schistosoma mansoni.

High primary doses of Trichinella spiralis administered orally to Kenyan baboons (Papio anubis) induced a marked but unpredictable eosinophilia which started 2--3 weeks after infection and persisted as erratic waves for at least 6 months. Low primary oral doses induced no eosinophilia but a later, high challenge gave an accelerated eosinophilic response, although the peak was lower than in high primary infection. Intravenous injection of infective T. spiralis larvae resulted in a predictable, rapid eosinophilic response which persisted for several weeks. Intravenous injection of a particulate material, Sepharose, gave no oesinophilic response. Percutaneous Schistosoma mansoni infection of baboons resulted in a two-stage eosinophilic response: an initial rise occurred about 2/3 of the way through the pre-patent period and was followed by a second rise at the onset of patency. After peaking, the eosinophilia waned erratically over the next 3 or 4 weeks. A strong antibody response, measured by countercurrent immunoelectrophoresis, was given in oral infections with T. spiralis, but intravenous injections elicited little or no antibody formation. Parasitological evidence indicated no cross-resistance to S. mansoni in baboons injected with T. spiralis 9 days previously. Thus, the intravenous injection of infective T. spiralis larvae appears to be a suitable method of inducing experimentally a non-specific eosinophilia to investigate possible immune mechanisms to S. mansoni in the baboon.