Intensity of Ascaris lumbricoides infection was measured in terms of egg counts and worm burden in children 2–10 years of age. The expulsion of A. lumbricoides with a 3-day treatment of mebendazole occurred over 8 days, beginning on the second day of treatment. Ninety-seven percent of the worms were expelled between the second and seventh days. A rapid means of estimating eggs per gram (epg) by the Kato Katz technique correlated well with the method described by Martin & Beaver (1968). In spite of apparent density dependence in egg production, A. lumbricoides egg counts correlated well with worm burdens. It is concluded that, within the context of community surveys, epg is a reasonable means of identifying heavily infected individuals and that epg can be estimated rapidly by a slight modification to the standard Kato Katz technique.

Infective-stage larvae of trichostrongyle nematodes, either resistant or susceptible to thiabendazole (TBZ), were incubated in eserine, an acetylcholinesterase inhibitor. Paralysis occurred in larvae treated with eserine but significant differences were observed in the percentage of larva immobilized between TBZ-resistant and TBZ-susceptible strains of the nematodes. These differences are probably related to the presence of higher levels of acetylcholinesterase in the TBZ-resistant strains than in the susceptible strains. This could be used as a rapid and inexpensive method of detecting resistance to TBZ in trichostrongyles.

Four acidic glutathione (GSH) transferase forms were isolated from the cytosol of the adult cestode Hymenolepis diminuta by hydroxylapatite chromatography, glutathione-affinity chromatography and chromatofocusing, pH 7–5. The enzymes were dimers of subunit size approximately 24 kDa and accounted for at least 3% of the total soluble protein. The major GSH transferase had limited catalytic activity but may interact with a range of ligands and function as a binding/passive detoxification protein. An endogenous factor interfered with the binding of the crude cytosolic GSH transferase activity to glutathione-dependent affinity matrices but, following partial purification, the GSH transferase activity successfully interacted with the glutathione affinity matrix.

Killing of metacestodes by normal or post-infection macrophages and the regulation of this activity by cytokines were studied in vitro. The protoscolecidal activity of normal macrophages against Echinococcus granulosus was inhibited by a product of naive T-enriched lymphocytes co-cultured with protoscoleces (PSC). By contrast, supernates from co-cultures of Mesocestoides corti tetrathyridia (MCT) and T-enriched or B-enriched normal lymphocytes increased killing of MCT by normal macrophages. Larvicidal activity (against both PSC and MCT) was enhanced by high concentrations of macrophage-activating factors produced by Con A-stimulated rat lymphocytes (Con A-LK), but was reduced by low concentrations of these factors.

Taenia saginata cyst fluid proteins from 4, 8, 12 and 16-week-old cysticerci were analysed by a combination of direct I radio-isotope labelling, immunoprecipitation using a panel of sera from infected cattle infected with T. saginata and SDS–PAGE. Protein antigens of 12, 14, 16, 20 and 26 kDa were identified in all of the cyst fluids examined. These were immunogenic and were precipitated by serum taken from cattle from 8 weeks after infection onwards and were therefore considered to be of diagnostic potential. A 185 kDa protein antigen found only in the cyst fluid of 4-week-old cysticerci and a 43 kDa protein antigen first detected in cyst fluid from 8-week-old cysticerci were also identified but were considered to be of more limited diagnostic potential due to their restricted presence. An apparently non-immunogenic 67 kDa protein, found in all the cyst fluids examined, may have been host serum albumin.

Neonatal hamsters were exposed to varying doses of Necator americanus larvae and changes in the stability of the resulting worm burdens were monitored over a period of 25 weeks. No change in worm burdens was evident for the first 5 weeks of infection, irrespective of the infection intensity, but the more heavily infected groups subsequently lost worms in a density-dependent manner. Male and female hamsters lost comparable proportions of their established parasite burdens indicating that there was no host sex-linked difference in this respect. By week 15 infections had stabilized and the residual worm burdens, usually a maximum of 30 worms survived for a considerably longer period of time. Initially the percentage of male worms varied from 45% to 50% but as infection progressed male worms comprised a significantly increasing proportion of the total worm burden. By week 25 the percentage of male worms was usually in excess of 60%. The growth of infected animals was not severely affected by N. americanus, even when heavy worm burdens established initially, but a significant effect was detected particularly in week 5, prior to worm loss, when the adult worms would have been feeding on intestinal tissues and causing blood loss for a period of about 2 weeks. The most severe depression in the packed cell volume was also recorded in week 5, indicating that anaemia had been initiated in infected hamsters. Whilst, the regulation of parasite burdens in weeks 5–10 post-infection may have resulted from host immunity, the persistence of the residual worm burdens, the marked density-dependent anaemia and the subtle effect on host weight, all reflected well-documented aspects of chronic human necatoriasis.

Experiments showed that dead blowflies containing eggs of Taenia hydatigena can transmit infection if ingested by lambs during grazing. Rabbits became infected with T. pisiformis after grazing grass exposed to blowflies that had been in contact with dog faeces containing the eggs of this parasite. When captive blowflies were exposed first to dog faeces containing proglottids of T. hydatigena and then to cooked meat, 100% of pigs fed on this meat became infected. The experiments are intended to model the transmission dynamics that result in human larval tapeworm infections. The implications of the results to the epidemiology of human hydatid diseases caused by Echinococcus granulosus and E. multilocularis as well as of T. solium cysticercosis are discussed.

Baseline data from an immuno-epidemiological study of hookworm infection in a rural village in Madang Province, Papua New Guinea are reported. Necator americanus was found to be the commonest helminth infection, with a prevalence of near 100% and intensity of 40 worms per host in adults. Enterobius vermicularis, Ascaris lumbricoides and Trichuris trichiura were also present, at prevalences of 53, 10 and 3% respectively; Ancylostoma duodenale was absent. The frequency distribution of N. americanus was highly over-dispersed, and was well described by a negative binomial distribution with aggregation parameter, k, of 0·370. Intensity of infection was significantly related to host age, but did not differ between the sexes. Haemoglobin levels and haematocrit values were indicative of anaemia in the community, but were unrelated to hookworm infection. Levels of antibodies (IgG, IgA and 1gM combined) against adult Necator cuticular collagen and excretory-secretory (ES) products were determined.

We demonstrate, by truncating the expected negative binomial distribution, that the tracheal mite parasite, Acarapis woodi, causes mortality in the Europen honey bee, Apis mellifera, but, that this mortality can be documented only during periods of low mite densities (mites per bee). At high mite densities, this technique no longer reveals mite-induced mortality. We suggest that this paradox results from a reduction in the mortality threshold at high mite densities, concealing mortality from our truncation procedures. Longitudinal comparisons of hive and forager bee cohorts, nevertheless, suggests mortality at all levels of infestation. We propose that persistent parasitism overcomes a colony's ability to compensate for losses, leading to its sudden decline and death.

A Strain ofHaemonchus contortusshowing moderate levels of resistance to thiabendazole (TBZ) (egg hatch assay LC50 2.1 μM) was subjected, in alternating sequence, to 5 in vitro and 4 in vivo selections with TBZ. This resulted in a significant increase in resistance (egg hatch assay LC50 2.8 μM). The isolates obtained after each combined in vitro and in vivo selection were compared in terms of egg hatch assay, establishment, net egg output, per capita egg output and degree of pathology caused in infected hosts. The increase in resistance was accompanied by a significant increase in larval establishment sheep (22 %) and was associated with more severe pathology, higher egg count and worm recovery 3 months post- infection.

Strains of mice poorly (B10) or non-responsive (B10.BR) to a primary infection with Trichuris muris were protected against infection by vaccination with excretory/secretory (E/S) antigen in Complete Freund's Adjuvant (CFA). Protection in these mice was slow to be expressed compared to that in good responder strains. Vaccination boosted the IgG and IgG1 antibody responses to E/S antigen and altered the antigen recognition profiles, three high molecular weight antigens (80–85, 90–95, 105–110 kDa) being recognized by antibodies in sera from vaccinated but not control mice. B10. BR mice which had experienced a patent primary infection could not be protected against challenge infections by vaccination and this was correlated with depressed levels of IgG1, but not total IgG, to E'S antigen early post-challenge compared with vaccinated infected mice which had not seen an adult primary infection. There was also lack of recognition of the three high molecular weight antigens recognized by antibodies in sera from mice infected after vaccination. It is suggested that the rapid development of high levels of IgG1 antibodies, and the recognition of the three high molecular weight antigens, may reflect events that are important in protective immunity. Immunomodulation of host immunity by T. muris may therefore be achieved, at least in part, by the suppression of specific IgG1 levels, the production of an irrelevant IgG isotype and prevention of the recognition of critical antigens.

Comparisons were made of the infectivity and antigenicity of 4 Trichinella spiralis isolates (S, D, Y, W), of quite different geographical origins, and T. pseudospiralis (P) in rapid- and slow-responder inbred mice. Infectivity was measured by the Index of Reproductive Capacity (ICR) expressed as the ratio between the number of muscle larvae recovered on day 30 post-infection (p.i.) and the numbers of larvae given at infection. Antigen recognition was measured by the degree of proliferation of mesenteric lymph node cells (MLNC) to in vitro stimulation with crude muscle larvae antigen (CMLA) and by the total antibody responses to CMLA at day 25 p.i. as measured by ELISA. Regarding infectivity the isolates fell into two groups, high infectivity (S, D and Y) and low infectivity (W and P). Analysis of CMLA, detergent-stripped (CTAB) and I-labelled surface larval proteins was made by SDS—PAGE under reducing conditions. Differences in antigen profiles were seen in all antigen preparations, being most noticeable in CTAB and 125I-labelled proteins from W and P isolates. Antigen recognition by polyclonal infection-derived antisera and by monoclonal antibodies raised against the T. spiralis London strain (L) was studied in the W (Arctic) and S (Spanish) isolates. Polyclonal antisera recognized different antigens in the S and W isolates, as did the monoclonal antibody, although recognition was more restricted. Neither antibody recognized a 64 kDa band in the W isolate which was clearly visible in the others tested.

Recently the phenomenon of predisposition to helminth infection has been reported in a number of studies: those individuals which are heavily infected before treatment with an anthelmintic tend also to acquire heavy parasite burdens following a period of reinfection. This correlation between parasite burdens in initial and reinfections is generated by differences between hosts in their exposure to infective stages and in their susceptibility to infection. Inter-host differences in these factors also generate the aggregated or over-dispersed parasite distributions that are usually observed. This paper uses probability theory to predict the correlation between initial and reinfection parasite burdens assuming that those inter-host differences which generate over-dispersion remain constant for a given individual between initial and reinfection periods. The predicted correlation is considerably greater than is observed in most published data sets. Over-dispersion is thus generated by variability between hosts which has components that remain constant between initial and reinfection and also components which vary between infection periods. The model is modified to account for those two sources of variability, and the result applied to published data to determine the contributions made by short and long-term factors to the observed distributions.

Antineoplastic cyclophosphamide (CY) significantly reduced the survival and the weight of Hymenolepis microstoma in mice. Corticosteroid dexamethasone (DEX), on the other hand, did not influence the worm survival and the worms in DEX-treated mice became significantly heavier. Both immunosuppressants abolished H. microstoma-induced bile duct hypertrophy and submucous enteritis and lowered the number of mast cells (MC) in these regions. CY appeared to be more effective in depleting the bile duct MC whereas DEX seemed to affect more the duodenal MC population.