Haemonchus contortus worm populations isolated from naturally infected sheep at the Pastoral Research Laboratory, Armidale, N.S.W., were found to contain approximately 20% of worms resistant to a 50 mg/kg dose of thiabendazole. Following 3 generations of selection with 50 mg/kg thiabendazole the number of worms removed by the anthelmintic was too small to detect differences between treated and control groups. After more than 15 generations of selection, matings between males from the selected strain and non-resistant females produced resistant males and females in equal numbers. Thus, thiabendazole resistance does not appear to be sex-linked. A dose–response assay on the F2 adults indicated that worms from female resistant × male non-resistant crosses were more resistant than F2 adults of the reciprocal cross. An in vitro technique that identified thiabendazole-resistant eggs by their ability to hatch in a solution containing thiabendazole and 0·1% NaCl solution was also used to study the inheritance of resistance. F1 eggs had similar LC50's to the resistant parents. F2 and back-cross eggs from an original mating of thiabendazole-resistant females × non-resistant males had a higher LC50 than F2 and back-cross eggs from the reciprocal mating, indicating a degree of matroclinous inheritance of resistance. However, the resistant parents had tolerances to thiabendazole exceeding those of F2. F3 eggs had a resistance distribution that ranged from that of the resistant to the non-resistant parent. No significant deviation from linearity was observed in any of the dose–response lines. These results indicate that thiabendazole resistance in H. contortus worms is inherited as an autosomal and semi-dominant trait.

A technique for the transplantation of Trichinella spiralis worms directly into the host intestine is described. Infections established by the direct transfer of adult worms were essentially normal both in terms of their survival and reproduction and in their stimulation of, and susceptibility to, host immune responses. Worms transplanted from NIH mouse donors at intervals after infection had an equal ability to survive in the recipient, even when taken from the donor shortly before or during the process of worm expulsion, showing that expulsion does not require worms to be irreversibly damaged. It was noted, however, that after 7 days in the donor the ability of the worm to reproduce in the recipient was temporarily impaired.

The ovary of Aspiculuris tetraptera has a prominent terminal cap cell. This is considered to be part of the ovarian epithelium. Oogonia detach from the short rachis and increase in size from 6 to 60 μm; accumulating hyaline granules, shell granules and glycogen. The hyaline granules persist in the egg cytoplasm after shell formation has been completed and are considered to be lipoprotein yolk. The shell granules contribute to the non-chitin fraction of the chitinous layer. A classification of the cytoplasmic inclusions of the nematode oocyte is proposed. Upon fertilization a vitelline membrane is formed which constitutes the vitelline layer of the egg-shell. The chitinous layer is secreted in the perivitelline space, between the vitelline layer and the egg oolemma. Upon completion of chitinous layer synthesis, the egg cytoplasm contracts away from its inner surface. The material of the lipid layer is secreted at the surface of the egg cytoplasm and adheres to the inner surface of the chitinous layer. During secretion of the chitinous and lipid layers by the egg cytoplasm, the uterine cells secrete the unit membrane-like external uterine layer and the crystalline internal uterine layer. A complex system of interconnecting spaces develops in the internal uterine layer. This system is open to the exterior via breaks in the external uterine layer. There is no direct involvement of the uterine cells in the formation of this structure.

The egg of Aspiculuris tetraptera is an ellipsoid measuring 93 × 40 µm. The shell consists of 5 layers: the external uterine layer, internal uterine layer, vitelline layer, chitinous layer and the lipid layer. This nomenclature is based upon the formation and histochemistry of the shell layers. The internal uterine layer contains a system of interconnecting spaces, partly filled by uterine secretion, which open to the exterior of the egg via breaks in the external uterine layer. The surface of the egg is covered by a system of interconnecting grooves. Freeze-etching reveals that the internal uterine layer is open to the exterior via pores, which open into the grooves. Rod-shaped particles are also revealed in the external uterine layer. The operculum of the egg consists of a modification of the uterine and chitinous layers of the shell.

Propagation of Nosema eurytremae, a microsporidian pathogen of trematode larvae, was investigated by inoculation of spores into the haemocoele of insects and by growth in tissue cultures. Locusts and the larvae of three lepidopteran species were good hosts but cockroaches were not. Low replication was obtained in one lepidopteran species after per os infection. Antibiotics controlled bacterial growth in suspensions of microsporidian spores but fungi were unaffected by all antibiotics tested, except at concentrations detrimental to the microsporidia. All stages of the microsporidium developed in cell lines of Xenopus laevis and Aedes pseudoscutellaris when spores were induced to hatch in contact with cell monolayers: the Aedes culture was contaminated by yeasts. Repeated washing of the Xenopus cells with fresh medium, after the sporoplasms of N. eurytremae had penetrated the cells, removed yeast contaminants and sterile cultures were obtained. Replication during 4 passages over 53 days was only 100 to 200-fold compared with the original inoculum but spores harvested from the cultures were infective to a fresh culture and to Pieris brassicae by inoculation into the haemocoele.

CBA mice deprived of their T-cells by means of thymectomy and administration of rabbit anti-mouse thymocyte serum before a primary infection of Schistosoma mansoni, failed to resist re-infection to the same extent as immunologically intact controls. However, little difference was made to the degree of resistance to re-infection acquired by thymectomized S. mansoni-infected mice when the anti-thymocyte serum was administered after the primary infection and just before the challenge. Hydrocortisone acetate, when administered to primarily infected mice just before reinfection appeared to reduce the degree of acquired resistance, but the drug also had a schistosomicidal effect on the challenge-derived organisms. An attempt to specifically suppress the acquisition of resistance against S. mansoni by administering serum from homologously infected, resistant donors before and during the course of a primary infection failed, and partial depletion of complement activity with cobra venom factor that was administered just before challenge also failed to affect resistance. Serum obtained from mice with chronic S. mansoni infections and injected intradermally at the site of subsequent administration of a homologous percutaneous challenge infection failed to markedly inhibit maturation of the challenge in the recipient. Recipients of 3 ml of serum from heavily infected donors were also not significantly more resistant to challenge than untreated controls. However, isolated skin from heavily infected mice allowed fewer cercariae to penetrate and emerge transformed as schistosomula than did isolated skin from uninfected controls.

This paper describes further characteristics of the immunization of sheep against schistosomes using live, irradiated schistosomula. Sheep immunized with a non-virulent strain of Schistosoma mattheei were protected against a more virulent strain of the same species for over a year. As there was no evidence that the irradiated parasites were able to persist this long, it was concluded that the vaccine had induced a sterile resistance. Heterologous vaccination, using irradiated S. mattheei schistosomula to immunize against S. bovis or irradiated S. mansoni schistosomula to immunize against S. mattheei, failed to induce any protection.

Effects of thermal effluent on the incidence and abundance of gill and intestinal metazoan parasites of the black bullhead, Ictalurus melas, were investigated. A total of 472 bullheads from a thermal outfall area and an unaltered area of Lake Monona, Dane County, Wisconsin were examined. All parasites underwent a seasonal cycle in abundance with peak infections occurring in summer, except for the acanthocephalan, Pomphorhynchus bulbocolli, which underwent a seasonal cycle in abundance in the reference area but not in the outfall area. Thermal effluent had little effect on the incidence of the parasites. Differences in abundance between the outfall and reference areas were observed for all parasites but these differences were not always consistent nor statistically significant. P. bulbocolli was more abundant in the reference area than in the outfall area in summer (P ≤ 0·05). The monogenean, Cleidodiscus sp. was more abundant in the reference area than in the outfall area in August (P ≤ 0·05). The infections of the gill copepod, Achtheres ambloplitis, were higher in the reference area than in the outfall area in spring, June, August, and September (P ≤ 0·05). Availability of infective larvae and variability in host feeding patterns were suggested as the controlling factors of the patterns of abundance observed.

Stages seen in the life-cycle of Diplocystis tipulae sp.nov. parasitic in Tipula paludosa Mg., included a structure that was probably a trophozoite within the midgut epithelium of one host larva and gamonts that developed on the midgut wall in the haemocoele of the larvae. Syzygy occurred, usually in pairs, when the gamonts were about 200–300 μm in diameter. Initially, syzygous gamonts were bilobed but they quickly became spherical and were enclosed by a fine membrane to form a gametocyst 450–550 μm in diameter. Early stages of gametogony were seen in one pupa; sporogony occurred in pupae and adults. The mean size of the round–oval oocysts was 7·14 × 6·26 μm. Individuals of Tipula oleracea L. are also susceptible to infection with D. tipulae. This gregarine is considered to be a new species, independent of the gregarines of the gut lumen.

An examination of 2 strains of Eimeria acervulina var. mivati (since 1973 E. mivati has been regarded as a variant of E. acervulina) showed that previous confusion over the taxonomic status of E. mivati arose because the investigations were done using laboratory cultures of E. mivati which were contaminated with E. acervulina.

Electrophoretic analyses of enzymes, host specificity and cross-immunity tests have revealed that:

(1) The 1971 Houghton strain of E. acervulina var. mivati was a mixture of 2 parasites. (a) Passage of this strain in embryonating eggs resulted in a selection against that parasite previously characterized as E. acervulina. (b) The parasite which did reproduce in eggs did not immunize chickens against subsequent challenge with E. acervulina. This parasite is most likely E. mivati. (c) E. mivati recovered from eggs did, however, immunize chickens against challenge with a new field strain which was morphologically identical to E. mivati and characterized by the same electrophoretic forms of 2 enzymes.

(2) A strain of E. acervulina var. mivati from the USA was also a mixture of E. acervulina and E. mivati.

Oocysts of Eimeria maxima inoculated into guinea fowl do not develop. Infection occurs when intestinal mucosa or liver tissue from guinea fowl given E. maxima is transferred to susceptible chickens. By transferring material at different times after inoculation, it was shown that most of the stages are lost between 6 and 12 h and few, if any, survive to 48 h.

Sporozoites of E. tenella had low infectivity after 48 h contact in vitro with peritoneal macrophages from guinea fowls and turkeys. Sporozoites of E. grenieri from the guinea fowl appeared to be destroyed within macrophages taken from chickens.