Observations on 5 different isolates of Eimeria stiedai from pure infections in laboratory-reared rabbits have confirmed the presence of an oocyst residuum. This structure was seen in 89–100% of the oocysts in cultures prepared both from the liver and from the faeces at different times during the patent period. The residuum consisted of 1–7 or more granules situated centrally in the oocyst and partially concealed by 4 sporocysts. The differential diagnosis of E. stiedai and E. coecicola is discussed.

RNA with messenger activity has been extracted from both blood and culture (insect mid–gut) forms of Trypanosoma brucei and translated in a reticulocyte cell–free system. The products of this cell–free system have been compared, and many common polypeptides demonstrated. A major polypeptide of 58000–65000 molecular weight was made when both blood and culture from RNA was added to the cell–free system.

Antiserum raised against purified variant antigen from a cloned variant (MIAG 099) was used to detect specific products of this system. A major polypeptide of approximately 58000–65000 molecular weight was precipitated when the homologous trypanosome (MIAG 099) blood form RNA was used in the cell–free system. No such polypeptide was precipitated when RNA from a heterologous strain culture or blood form was used in the system. Competition experiments, in which excess purified variant antigen was added after incubation but before addition of specific antiserum, confirmed that the polypeptide of 58000–65000 molecular weight is the variant antigen.

Poly(A)–containing RNA from trypanosomes was shown to contain the mRNA for the variant antigen.

Although superseded by more recent and biologically realistic studies, Crofton's (1971b) model of host–parasite associations remains of interest as the simplest model which captures the essentials. Even if its simplifying assumptions are all accepted, Crofton's model has two defects: the first is that its general conclusions are drawn from numerical simulations for a very restricted range of parameter values; the second is that the probability for a parasite transmission stage to succeed in establishing itself in a host is not constrained to be less than unity, as biologically it must be. The present paper remedies these two defects, by giving analytical results valid for all values of the parameters, and by demanding that the parasite transmission factor indeed saturates to unity. Some of Crofton's conclusions remain intact, others are significantly altered.

(1) Crofton (1971b) has presented a mathematical model which aims to exhibit some of the essential dynamical properties of host–parasite associations. The extreme biological simplicity of this model (e.g. hosts and parasites have the same generation time) makes it applicable to few real systems, and later models (Anderson & May, 1977; May & Anderson, 1977) have added many more general biological features in an effort to makecontact with empirical data. Nevertheless, Crofton's model retains pedagogical value as the basic model.

(2) Even within its own framework ofsimple assumptions, Crofton's model has two defects. The first is thatthe general conclusions about its dynamical behaviour are drawn from numerical stimulations for a re stricted, and not necessarily representative, range of parametervalues. The second is that the factor describingthe input of parasite transmission stages into the next generation of hostsdoes not saturate to unity, as its biological definition implies it must. Thepresent paper gives an analytical account of the dynamical behaviour of Crofton's model, valid for all values of the relevant biological parameters, and with a parasite trans mission factor that does saturate to unity. The ensuing conclusions are in several respects significantly differentfrom Crofton's

(3) The intrinsic growth rates of the host and parasite populations are defined as λ and A; the negative binomial parameter k measures the overdispersion of parasites among hosts (small k corresponds to high overdispersion); and L characterizes thelethal level of parasites per host.Then unless λ1+1/k λ A exp (– 1[L) no equilibrium state is possible, andthe host population undergoes Malthusiangrowth that the parasites cannot check. This inequality tends to be satisfied if k is not too small, λ not too large, and A significantly larger than λ: see Figs 1, 2, and 4.This aspect of the model derives from the saturation of the parasite transmission factor, and is omitted fro Crofton's discussion.

(4) When an equilibrium does exist, the following observations can be made. The equilibrium host population H* is given by eq. (15): it de creases with increasing A; increases with increasing λ; is roughly inde pendent of L; and increases with increasing parasite overdispersion for small k (k < In λ);, while being roughly independent of k for larger k. Theequilibrium number of parasites per host m* is given by eq. (9): it is independent of A; increases roughly linearly with L; increases with increasing overdispersion or λ for small k (k < in λ); and increases slowly with λ, and is roughly independent of k, for larger k. The totalpopulation of parasites at equilibrium is given by P* = H*m*.

(5) The stability of the equilibrium, i.e. its ability to recover from disturbance, depends mainly on λ and on k, as illustrated in Fig. 4. Except for values of λ and k perilously close to the boundary where no equili brium is possible, the disturbed host and parasite populations will return to their equilibrium values by undergoing damped oscillations. The damping will tend to be weak if k is large, or if λ is small.

(6) These conclusions accord with those derived from more detailed and realistic host–parasite models.

(7) The general process, whereby thehost–parasite association can be stabilized by overdispersion of parasites, is dynamically similar to that whereby prey–predator or host–parasitoid associationscan be stabilized by differential aggregation of predators or by explicit refuges for the prey.

Relapse of infection after drug treatment of trypanosome infections under conditions precluding re-infection has usually been ascribed to drug resistance on the part of the parasite or to under-dosage of the drug. With Trypanosoma brucei infection in mice we have obtained evidence of another type of relapse. In infections resulting from the inoculation of 1 × 105 trypanosomes, derived from a stabilate T. brucei TREU 667, treatment with diminazene aceturate (Berenil) at 40 mg/kg at either 3 or 7 days after infection elicited a permanent cure. If, however, treatment was delayed later than 14 days after infection, then all the mice relapsed. These relapses generally occurred between 20 and 50 days after treatment, but some mice remained aparasitaemic for up to 60 days. The relapsed infections were apparently not due to the survival of ‘drug-resistant’ trypanosomes, as infections derived from a stabilate isolated from a relapsed Berenil-treated mouse were also permanently cured with Berenil if treated 3 days after infection; however, if treatment was delayed until 21 days post-infection, all the mice relapsed. The cause of relapse was not related to the number of parasites inoculated, as infection resulting from initial inocula of 1 × 105 to 1 × 108 trypanosomes were all cured if treated at 3 days after infection, and all eventually relapsed if treatment was delayed until day 21. This type of relapse phenomenon was not confined to T. brucei TREU 667 but also occurred with 5 other stabi-lates of T. brucei after Berenil treatment. Treatment of T. brucei TREU 667 infections with Ethidium and Prothidium at dose levels of 7.5 and 10 mg/kg respectively was also followed by relapse if treatment was delayed for 3 weeks after infection. The possible causes of relapse under these conditions, and its implications in the study of the natural disease, are discussed.

In Hymenolepis diminuta the in vitro rate of absorption of glucose/unit dry weight of worm falls with increasing worm age, with increasing worm weight and as the number of worms in an infection is increased. In a 6 mM solution of glucose, a 5 mg (dry weight) worm from a 7 or 8 worm infection absorbed 80 µmoles/g dry weight/5 min whereas a 60 mg worm, also from a 7 or 8 worm infection, absorbed only 35µmoles/g dry weight/5 min. This change in the rate of absorption is, at least partly, thought to be due to changes in the relative surface area: weight ratio during growth of the worm.

The kinetic parameter, Kt glucose, increased from 1.1 mM for a 5 mg (dry weight) worm from a 7 or 8 worm infection to 2 mM for a 60 mg worm. This change in the functioning of the glucose transport system may indicate that there are two components of the glucose transport system – or two separate systems – one with a low Kt and one with a high Kt, the ratios of which change during worm growth.

The smaller the number of worms in an infection the greater the rate of glucose absorption. Using 8–day–old worms in a 6 mM glucose solution, 1 worm from a single worm infection absorbs 111 μmoles/g dry weight/5 min, 1 worm from a 7 or 8 worm infection absorbs 88 μmoles/g dry weight/5 min and 1 worm from a 45–50 worm infection absorbs 77 μmoles/g dry weight/5min. The significance of this is discussed with reference to the ‘crowding effect’ in tapeworms.

The activity patterns of the cercariae of Transversotrema patialense have been examined by monitoring the behaviour of individual larvae. Records of three different behavioural modes, namely active, tail–first swimming, passive dropping and resting periods were made separately. The age- and temperature–dependence of the activity patterns during the spontaneously active life of the cercariae were examined and estimates made of the absolute speeds of swimming and dropping. Through the temperature range 25–32° C, the spontaneously active life of cercariae declined from about 18 h to about 6 h. Within this interval, after an initial period of high activity rates, a gradual decline in activity followed. The decline was a result of a decreasing frequency of swimming events rather than any change in the durations of such events. The neural control and energetic significance of the cercarial activity patterns are discussed.

Chicks infected with the Weybridge strains of Eimeria maxima and E. acervulina were not protected by the normal levels of amprolium, but the sporulation of the oocysts was inhibited. With higher drug concentrations, fewer oocysts were produced. E. brunetti was not so markedly affected, although oocyst sporulation was reduced by the higher dosage levels. The effects were not enhanced by the inclusion of ethopabate.

With dinitolmide the phenomenon was not so marked, although oocyats of E. maxima and E. acervulina were reduced in numbers by the normal drug concentration and sporulation was reduced when this level was increased. Much higher drug levels were required to obtain these effects with E. brunetti. Monensin at 120 ppm affected neither oocyst numbers nor their sporulation in any of the species tested. The significance of the effects of anticoccidial drugs on gametogony and sporogony is discussed.

R. cesticillus was found to undergo a diurnal migration in both multiple and single worm infections of the fowl. This migration involved movement of both scoleces and strobilae and occurred in an anterior direction when the intestine was empty of food, and in a posterior direction when the intestine contained food. The relevance of the migration to the histological picture of the worm in situ is discussed and some possible explanations for the migration are suggested.

This study compares papillae distribution in seven microphallid cercariae of the genera Microphallus and Maritrema. Certain papillae or groups of papillae have generic, supra–generic or specific significance. Microphallidae are characterized by the absence of C I cycle and of dorsal P II and P III, the presence of one C II1 and one C II2, of four mediodorsal A I D papillae and of two horizontal papillae on the tail. The number and disposition of the papillae at the front of the body (peribuccal and anterodorsal A I D and St DL) and at the back (P cycles) have a generic significance. The number and disposition of the papillae in the middle of the body (A and M cycles) have a specific significance.

Eimeria acervulina var. diminuta was serially passaged 12 times in chicken embryos, but growth in cultured chick kidney cells was linmited to 2 generations of schizonts. After 7 embryo passages the sensitivities of E. acervulina var. diminuta and an embryo-adapted strain of E. acervulina var. mivati to the anticoccidial drugs amprolium, methyl parasites were sensitive to all the anticoccidials but E. acervulina var. diminuta was more sensitive to sulphaquinoxaline and amprolium. The chicken-maintained strain of E. acervulina var. diminuta was extremely sensitive to clopidol, sulphaquinoxaline and decoquinate. Electrphoretic analyses of several enzymes from E. acervulina var. diminuta revealed enzyme profiles with similarities and differences to the embryo-adapted strain of E. acervulina var. mivati.

Interference microscopy has been used to study the rate at which water enters and is lost from larval and adult stages of Ditylenchus dipsaci and D. myceliophagus. It is shown that the cuticle of the dry nematode, irrespective of stage, is completely permeable to water. In contrast, marked intra– and interspecific differences were found in the rate at which stages dry at 0 and 50% relative humidity. All stages of D. myceliophagus dry very rapidly: in this species, death, as a consequence of severe desiccation, appears to be linked to a lack of any marked ability to control water loss. For D. dipsaci, those stages known to survive desiccation will appear to be the slower dryers. In general, the “order of performance” in slowing the rate of drying is the same as the order previously found for survival of desiccation. Both the 4th– and, to a lesser extent, the 3rd–stage larvae of D. dipsaci show evidence of an intrinsic ability to control water loss.

An analysis of the drying curve for 4th–stage larvae of D. dipsaci supports the indications of interference photographs that the rate of drying is slowed by a decrease in permeability of the drying cuticle.

Vacuum desiccation studies further demonstrate the remarkable ability of the 4th–stage larva of D. dipsaci to control its rate of drying. The survival of 4th– and 3rd–stage larvae of D. dipsaci is diminished by very rapid drying, and the survival of other stages of this species and larval and adult stages of D. myceliophagus is precluded. The decrease in survival of the 4th–stage larvae of D. dipsaci is shown to be associated with a more rapid rate of water loss.

The vegetative and sporogonic stages of Unikaryon allocreadii sp. nov. and Nosema gigantica sp. nov., from the parenchyma of adult flukes, Allocreadium fasciatusi in the gut of the freshwater fish Aplocheilus melastigma from India, are described and figured. U. allocreadii, which is uninucleate throughout development and is disporoblastic, differs from U. legeri in that it occurs in adult flukes from a freshwater host. N. gigantica has diplokaryon nuclei, at least in the sporogonic stages, and is much larger than all other microsporidia in platyhelminths.

Hatching of the spores and patholgenicity are described and the mode of transmission to the flukes is discussed. Infected flukes, which are sluggish and opaque, are often displaced from the normal site of infection.

Primary immune expulsion of Trichuris muris was markedly delayed by concurrent infection with Nematospiroides dubius. Maximum delay of expulsion was dependent on size and timing of N. dubius infection relative to T. muris infection. In NIH mice infection with 400 N. dubius larvae immediately before or after T. muris infection was found to be most effective in suppressing expulsion. Infection on day 8 of T. muris infection, when mice are sensitized to T. muris, also impaired expulsion. From this evidence it is suggested that the larvae of N. dubius are immunosuppressive and that the efferent role of the immune response to T. muris is inhibited. The results are discussed in terms of non-specific immunosuppression and their relevance to the tropical disease situation is emphasized.

During the course of a field study of coccidiosis in turkeys, Eimeria oocysts were found which had much smaller dimensions than any previously recorded isolate from the turkey. These oocysts were purified by single oocyst infection of a turkey. The first oocysts (mean dimensions 16.15 ×14.75 μm) were recovered 103 h later. Inoculation of between 0·5 and 2.5 ×105 oocysts of this isolate caused severe effects on body weight gain. Cross-immunity studies showed the parasite to be a strain of E. meleagrimitis. Electrophoretic analyses of two enzymes showed that the strain could be differentiated from another strain of E. meleagrimitis. (Weybridge strain B).

The results show that strain variation occurs within the species E. meleagrimitis and extreme caution should be used in identifying species of Eimeria from the turkey by their oocyst characters.

The structure and staining properties of the epithelium of the midgut in Unionicola intermedia are described. Intracellular non-specific esterase, acid and alkaline phosphatase are present and confined to vacuoles. Extracellular enzymes are absent. Nymphal and adult stages of U. intermedia feed principally on the haemocytes (= amoebocytes) and mucus of their molluscan host, Anodonta anatina. Feulgen-positive material recorded from the lumen and midgut cells of the mites is believed to be derived from the nucleated haemocytes and to undergo intracellular digestion in the midgut cells. Starved mites show steadily decreasing amounts of Feulgen-positive material in the vacuoles. Haemocytes are present in large numbers below the site of attachment of the mites, their presence represents an inflammatory response, and the mite feeds on the products of this response. Large amounts of bound iron are present in the midgut cells but the origin and role of this is unknown.

The life-cycle of Theileria parva in the gut of the tick Rhipicephalus appendiculatus was investigated in Giemsa-stained smears and in wet preparations under the phase-contrast microscope. The different developmental stages of T. parva were seen in a large proportion of specially-selected R. appendiculatus tickes. After the intra-erythorcytic merozoites were engorged by the ticks during a blood meal, the following development was observed. (1) In the lumen of the gut of infected nymphs, spindle-shaped microgamonts developed out of the ring-forms. These broke up into several thread-like microgameters after nuclear division and development of thread-like cytoplasmic projections. The ring-froms developed into round-forms of 3–4 μm in diameter which are considered to be macrogametes. (2) From the 6th day after repletion, zygotes with a clear zone in the centre appeared in the epithelial cells of the tick's gut. A steady increase in size and a progressively denser cytoplasm were observed up to the 3rd day after moulting to adult ticks. (3) Subsequently a slightly angular, retort-like stage developed by invagination inside the rounded zygotes, and from the 5th day after moulting this stage developed further into a club-shaped kinete. The kinetes propelled themselves in the gut by active gliding movements.

Activated oncospheres of Taenia ovis were incubated for 24 h or 48 h at 37.5°C in Medium 858 alone or in Medium 858 enriched with 20% lamb serum or foetal calf serum. Antigens contained in the supernatant medium from these incubations were concentrated, emulsified in Freund's incomplete adjuvant and injected intramuscularly into lambs. These lambs developed a very high level of immunity to subsequent challenge infection with T. ovis eggs.

The rapid elimination of the intestinal phase of Trichinella spiralis in NIH mice is associated with progressive inflammation of the intestinal tract. The non-specific effects of this inflammation were studied in. mice concurrently infected with an unrelated parasite, Hymenolepis diminuta, which does not stimulate a visible inflammatory response but is also immunologically rejected by this strain of mice.

It was demonstrated that the rejection phase of T. spiralis infection had a marked effect upon the growth and survival of H. diminuta,. The cestode either failed to establish or to grow; if the worms were already strobilate when inflammation developed then destrobilation occurred. There was no cross–immunity between the parasites, nor was the interaction a direct consequence of inter–specific competition.

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 eosino-philic 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 ⅔ 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 imnruno-electrophoresis, 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.

This paper describes in vitro antibody dependent cytotoxicity against Trypanosoma cruzi epimastigotes by normal mouse splenic lymphocytes. Cytotoxicity was expressed as the percentage reduction in the number of motile parasites upon incubation with lymphocytes at 37 °C in a denned medium. Failure of the non-motile parasites to regain motility and their ensuring degeneration at 28 °C in liver infusion tryptose (LIT) medium confirmed loss of motility as a criterion of cytotoxicity. Incubation of T. cruzi at 37 °C for 18 h in a defined medium per se did not interfere with motility but was followed by a lag phase of the growth curve in LIT medium at 28 °C. The lag phase was prolonged for T. cruzi which had previously been incubated at 37 °C in the absence of cells.