The abundance of Profilicollis botulus was monitored in eider ducks for 3 years. No significant difference in P. botulus abundance was found between eiders taken alive and those collected dead from the shore line, or between adult males and adult females. Adult male eiders had a seasonal pattern of infection. Incubating female eiders lost their infection in almost all cases, suggesting that a seasonal pattern of infection must also occur in these birds. Eiders in their first winter had P. botulus abundances which were approximately 10 times that of adult eiders, but by the following summer the abundance had declined to that found in adults. Data are compared with previous studies undertaken on the Ythan estuary. Captive eiders were used to determine the developmental rate of female P. botulus and the percentage of administered cystacanths which established in the intestine. There was no evidence to suggest that male and female P. botulus have different life–spans.

Examination of the short-term interaction of the haemocytes and lysozyme of Galleria mellonella larvae with the entomogenous nematode Steinernema feltiae DD136, in vitro revealed that the nematodes did not reduce the adhesion of Bacillus subtilis or Xenorhabdus nematophilus subsp. nematophilus to larval granulocytes or plasmatocytes. There was no evidence of humoral, sheath or cellular encapsulation of S. feltiae in the haemolymph in vitro or in vivo. Compared with the phosphate-buffered saline-injected larvae the axenic nematodes did not alter the total or differential haemocyte counts during the initial 4 h of parasitism. The ability of the insect larvae to remove B. subtilis and X. nematophilus from the haemolymph was not influenced by axenic S. feltiae. The bacteria from the intestine of surface disinfected, monoxenically cultured S. feltiae elevated the larval total haemocyte counts and damaged the haemocytes. The activity of larval lysozyme was not influenced by axenic S. feltiae.

The influence of a chronic subclinicael infection of Trichostrongylus colubriformis, 2500 larvae/day for 12 weeks, on gastrointestinal motility and digesta flow was studied in 12 sheep supplied ad libitum with food and water. Motility was recorded by X-radiography and electromyography from chronically implanted electrodes;abomasal volume and outflow were estimated by dilution of CrEDTA; small intestinal transit time was estimated by passage of Phenol Red. The findings were compared with measurements made prior to infection at restricted food intake and reported separately. The first effects of infection were seen after 3–4 weeks. No animal developed diarrhoea, but food intake was progressively reduced. Small intestinal transit time, abomasal volume and half-time of marker dilution increased while abomasal outflow decreased during infection. These changes occurred both in absolute terms and when compared with values predicted from the observed level of food intake. As the animals became resistant to the parasites abomasal volume and digesta flow returned towards control values (weeks 10–12). The migrating myoelectric complex (MMC) was disrupted in only one sheep, and only transiently. In all sheep the frequency of the MMC was increased during infection and there was a progressive inhibition of abomasal, duodenal and jejunal motility. X-radiography showed there was prolonged pooling of digesta in the proximal small intestine which was cleared only at the phase of regular spiking activity. Two sheep given an anthelmintic drench recovered normal motility and clearance of digesta. It is concluded that subclinical infection of sheep with T. colubriformis alters the normal pattern of gastrointestinal motility in the absence of any diarrhoea, and causes inhibition of abomasal and proximal small intestinal motility and digesta flow. The increased frequency of MMCs helps to maintain digesta flow through the proximal small intestine.

Succinate dehydrogenase and fumarate reductase activities from a participate fraction of 4 isolates of the supposed ‘species’ of Trichinella, T. spiralis, T. pseudospiralis, T. nativa and T. nelsoni have been determined using spectrophotometric methods. The ‘in vitro’ effect of the anthelmintics thiabendazole, mebendazole and ivermectin on succinate dehydrogenase and fumarate reductase activities from the above isolates is also described. The significance of the results is discussed in the context of the controversy that surrounds speciation of the genus Trichinella.

Corynetoxins, the toxic glycolipids produced by Corynebacterium rathayi colonizing bacterial galls induced by the seed gall nematode Anguina agrostis in annual ryegrass (Loliurn rigidum), did not affect embryogenesis or larval development of A. agrostis although they did inhibit the rate of egg hatching. Corynetoxins were not toxic to several species of nematode which are parasites of roots nor to various stages of the free-living nematode Caenorhabditis elegana and they did not appear to influence the numbers of C. rathayi that became attached to the surface of the cuticle of infective larvae of A. agrostis.

The effect of mouse population density on the establishment, survival and fecundity of single cohorts of Heligmosomoides polygyrus was investigated. No significant relationship was found between host population density and the worm burden at post mortem. But, lower host population densities were associated with higher parasite fecundities and with higher overall mean daily faecal output. The results might be explained by a decrease in male hormone secretion or digestive disturbances associated with lower ingesta in the higher host population densities. Effects resulting from changes in immunological responses might also exist.

The fully embryonated egg of Notocotylus attenuatus is shown to contain a sporocyst, an opercular cord and apparently 2 cells which are situated outside the sporocyst. One of these cells is rich in glycogen whereas the other contains a variety of inclusions. These contents are indicative of a truncated life-cycle which omits the miracidium, an observation as yet unique among the Digenea.

An experiment using lysimeters suggested that the eggs of Taenia saginata and Ascaris lumbricoides survive for only a short time when applied to pasture in sewage sludge. However, a subsequent experiment which followed the survival of eggs throughout the soil profile demonstrated that some T. saginata eggs could still be found at 200 days on the soil surface, and that survival increased down the profile. Rainfall is shown to be able to wash eggs into the soil where they may be afforded protection from radiation and desiccation; this may have little epidemiological significance.

Rotylenchulus reniformis, Anguina agrostis and Meloidogyne javanica respond differently to gradients of chemical attractants. In chemotaxis assays performed on agarose plates, R. reniformis L2 larvae oriented their movement to several common inorganic salts, cyclic AMP and AMP, as well as to germinated host plant seeds. M. javanica L2 larvae were attracted to germinated seeds, but not to the salts tested, and A. agrostis dauer larvae were not strongly attracted to any of 12 different tested agents, including host root or shoot tips. Attraction of R. reniformis to salts was measured by comparing different pairwise combinations of ions at equivalent concentrations. The indicated order of attractiveness was: Cl− > Na+ > C2H3O2− > Mg2+, NH4+, SO42−. The least attractive salts, (NH4)2 SO4 and MgSO4, were weakly attractive at an orientation threshold of 1 mm, whereas the most attractive salt, MgCl2, was strongly attractive at a threshold of 0·2 mM Cl−. 3′, 5′ cyclic AMP was strongly attractive at a threshold of 0·05 mM, whereas 5′-AMP was a weak attractant. Some of these responses may affect the distribution of R. reniformis in its natural environment.

The sequential, quantitative histological analysis of adult Hyalomma anatolicum anatolicum feeding sites on rabbits showed that the cellular reactions at tick feeding sites change in character and magnitude with time after attachment, and differ considerably from primary infestation to tertiary infestation. Neutrophils (62–68%) followed by mononuclear cells (22–24%) were the major component of the cellular infiltrate throughout primary infestation. Eosinophils accounted for 10% of the cellular infiltrate at 24 h after attachment. Their proportions declined thereafter, forming 9% of the infiltrate at 72 h and 5% at 144 h. Basophil infiltration in most of the feeding lesions was noticed by 24 h, but always in low numbers. Despite a slight increase in absolute numbers the proportion of basophils fell from 3% at 24 h to 2– at 144 h. In contrast to primary infestation the cellular reactions on tertiary infestations were characterized by a significant increase in the numbers of basophils and eosinophils and marked degranulation of mast cells and basophils as early as 24 h after attachment. As the feeding advanced there was an increase in the mean proportions of basophils from 4% to 9% and mononuclear cells from 22% to 38%, and a decrease in the proportion of eosinophils from 21% to 9%. However, neutrophils (42–53%) remained the major component of the cellular infiltrate. There was no significant difference in the nature and sequence of cellular events in the feeding sites of male and female ticks, although the lesions produced by feeding males were 5–10 fold smaller than those of females. Mast cells, basophils and eosinophils appeared to be the major host cells involved in the resistance response, manifested by protracted feeding, reduced engorgement weight and poor egg laying. The mechanisms by which these cells might interact to mediate resistance are suggested and discussed.

According to the World Health Organization the global estimate of malaria is over 200 million infections, the majority of which are caused by the most life-threatening species, Plasmodium falciparum (Report of the Steering Committees of the Scientific Working Groups on Malaria, World Health Organization, June 1983). The causative agent of the disease, the malarial parasite, requires two hosts: a blood-sucking mosquito and a blood-containing vertebrate. Commonly, infection of the vertebrate begins when an infected mosquito bites a suitable vertebrate and injects minute sporozoites into the bloodstream. Within 30 mm the introduced sporozoites leave the bloodstream and enter parenchymal cells of the liver (mammals) or endothelial cells (birds). In these sites the parasite undergoes asexual multiplication (= exo-erythrocytic schizogony) producing daughter progeny called merozoites. The exo-erythrocytic merozoites are released from the tissues into the circulation where they invade red blood cells. Within an erythrocyte the merozoite undergoes asexual multiplication (= erythrocytic schizogony) producing a substantial number of merozoites. The erythrocyte lyses, merozoites are released, and invasion of another erythrocyte may then take place. The synchronous rupture of the red cell and merozoite release is marked by the periodic fever–chill cycles so characteristic of the malarial infection. Some merozoites continue to reinvade other erythrocytes and multiply by asexual means, whereas others enter erythrocytes and differentiate into sexual stages, male or female gametocytes. When a suitable mosquito feeds on an infected vertebrate gametocytes are ingested and the sexual cycle of development is initiated. In the mosquito stomach the gametocytes transform into gametes, fertilization takes place, the resultant worm-like zygote penetrates the cells of the mosquito gut and comes to lie on the outer surface of the stomach. Here each zygote forms a cyst-like body, the oocyst, within which thousands of sporozoites are produced by asexual multiplication. When the swollen oocysts burst, sporozoites are freed and these make their way to the salivary gland. At the next blood feeding the mosquito injects the infective sporozoites and the life-cycle is completed.