In micro-Particle Image Velocimetry, the requirement of a large field-of-view often results in a large depth-of-correlation, i.e. large depth of the measurement volume. When the velocity varies substantially over the depth-of-correlation, special attention should be paid to a correct interpretation of the measured velocities. When a specialized microscope is needed to meet the requirements of a setup, the resulting more complex optical arrangements can have additional effects on the measurement results. In order to determine flow parameters such as the flow rate, it is sufficient to have a robust estimate of the maximum velocity when the flow is Poiseuille flow. In this paper, an interpretation of the results from particle image velocimetry measurements with low magnification in a round capillary is given for two types of microscopes: a conventional and a specialized microscope. The measured velocity appears to be lower than the maximum velocity, yet is still above the average velocity. The interpretation of the measured velocity differs for the two types of microscopes. The under-estimation of the maximum velocity obtained from the conventional microscope remains small (within 6%) for low-magnification measurements, while the under-estimation of the maximum velocity obtained from the specialized microscope increases up to 25% for a large depth-of-correlation. The images of the in- and out-of-focus particles turn out to play a crucial role in this difference between the two microscopes. Validation of the optical properties of a microscope is important, especially for specialized microscopes where particle images deviate substantially from the existing theory, and this theory is also used to derive the analytical expression for the depth-of-correlation. A procedure is recommended to obtain a correct interpretation of the measured velocity. This procedure is generally applicable, but mainly of importance for specialized microscopes.

The recognition of low molecular weight proteins by sera obtained during a single oral (primary) infection with 100 000 3rd-stage Cooperia oncophora larvae was studied in calves. Three groups of 6 or 7 calves were selected based on different egg excretion patterns. SDS-gel electrophoresis of adult Cooperia antigen under reducing conditions, followed by Western blotting, revealed that resistance of individual calves to C. oncophora might be related with antibody responses (42 days post infection) against at least 2 protein fragments (14–16 kDa and 27 kDa). The 14–16-kDa protein complex was bound, to some extent, by individual sera from all calves. The intensity of staining was negatively correlated with egg excretion on Day 42 p.i. Calves with high egg counts on Day 21 p.i. either did not or only weakly recognized the 27-kDa band. It has to be established whether the 14–16 kDa (or recombinant 14.2 kDa) provides a tool for immunodiagnostics and whether the 27-kDa fragment can help further unravel immune-mediated resistance to Cooperia.

The residual effect of a 0.2 mg kg-1 injectable formulation of moxidectin against lungworm and gastrointestinal nematodes in cattle was studied in a grazing experiment in the Netherlands. Five groups of four calves were grazed between May and October 1991 and one similar group was used as permanently housed control group for the evaluation of the development of immunity against lungworm by challenge infections with 5000 larvae of all six groups. The main parameter used to determine the residual effect for lungworm was faecal larval counts. Additional information was derived from pasture larval counts, enzyme-linked immunosorbent assay (ELISA), respiration frequency, coughing score and, particularly for evaluating development of immunity, worm counts. For gastrointestinal nematode infections faecal egg counts and larval differentiation of faecal cultures were the main parameters used. Pasture larval counts and an ELISA for Ostertagia and Cooperia were used as additional parameters. In three treated groups lungworm larvae (re)appeared in the faeces after 67, 95 and 119 days, respectively. This implies that a 100% residual effect did not last longer than 67-21 = 46 days. The treated group with patency starting on Day 95 was exposed to extremely high infection pressure and the ELISA indicated some host-parasite interactions from 2-4 weeks after treatment. Thus some interaction between moxidectin treatment and high infection pressure delayed the onset of patency in comparison to another treated group under much lower infection pressure. In all treated groups, including the one under high infection pressure, lungworm disease was prevented and the worm counts demonstrated development of immunity. In contrast, severe lungworm disease occurred in two control groups grazing together with the 'high infection pressure' treated group. The faecal egg counts and differentiation of larvae from faecal cultures demonstrated a 100% residual effect of at least 3 weeks and indicated a high residual effect of approximately 5 weeks against Ostertagia. Moxidectin suppressed Cooperia faecal egg counts for over 98% and the results indicated a more than 95% residual effect on faecal egg output during 2-3 weeks. The ELISA results were indicative for a delay of 2 weeks in the acquisition of gastrointestinal nematode infections following moxidectin treatment.

An experiment was done to study whether estimation of the herd infection level, by assessing Ostertagia antibodies in bulk milk samples can serve to predict the effect of anthelmintic treatment on milk production. Bulk milk samples were collected from 134 farms at monthly intervals on three occasions prior to the start of the study. The ELISA titres to Ostertagia found in October at the end of the grazing season served as a basis to select 16 and 18 farms as having high and low levels of parasitism respectively. Heifers and cows within each herd were ranked by expected calving date, paired and randomly allocated to be treated with ivermectin or a placebo. Records of milk production and composition were collected for all the trial animals. The response to treatment expressed as the 305 day corrected milk yield of anthelmintic treated animals minus that of placebo treated animals was not statistically significant and amounted to 78 kg for multiparous cows and 124 kg for heifers. For cows as well as heifers the response to treatment was larger in the high antibody level herds than in low antibody level herds, but these differences also lacked statistical significance.

In two experiments, groups of calves which had been exposed to different levels and patterns of infection with Ostertagia and Cooperia spp. in a simulated first grazing season (FGS), were followed throughout a natural second grazing season (SGS). Milk yields in the subsequent first lactation period were also recorded. The results suggest that although there had been differences in immune status among groups, which had been infected in the FGS, prior to the SGS, weight gain among these groups was not significantly different during the SGS. Apparently, resistance to the pathogenic effects of reinfection had developed more strongly and at lower levels of exposure to infection than resistance against establishment of larvae as shown after an experimental challenge. The groups of calves not infected during the FGS did gain less than all other groups during the SGS. Further, infection-induced differences in weight gain among the infected groups in the FGS appeared to be permanent, at least up to the end of the SGS. Finally, first lactation yield was positively correlated with body weight at calving. On average, approximately 10 kg less milk was produced for each kg of lower body weight at calving. With respect to the implications for preventive control strategies in the FGS, it is suggested that parasite control should not be applied beyond a level at which weight gain reduction is prevented.

The systemic antibody responses to adult Cooperia oncophora antigen were studied using sera obtained from calves during a 6-week period following a single oral infection with either 20,000 or 100,000 third-stage C. oncophora larvae. Dose dependent increasing titres of IgG binding complete adult Cooperia antigen were found in the sera of Cooperia-infected calves. SDS-gel electrophoresis under reducing conditions, followed by Western blotting, revealed that the increase of IgG binding Cooperia antigens could be attributed mainly to specific binding of IgG to a complex of 12-15 kDa protein fragments of Cooperia adult antigen. This protein may represent a Cooperia oncophora-specific component that can be used for serodiagnosis.

In two experiments groups of calves were exposed to different levels and patterns of infection with Ostertagia spp. and Cooperia spp. The experimental design simulated the stereotypic pattern of herbage infestation, including a normal or a delayed midsummer increase, under conditions of set-stocking. After this simulated 'first grazing season', calves were monitored throughout the subsequent winter housing period. No continuing negative effects of previous infection on growth performance were observed. Calves in all groups gained on average over 0.7 kg day(-1), irrespective of previous level of exposure. Differences between the experiments with respect to either level or pattern of infection during the preceding 'first grazing season' were all, to a greater or lesser extent, reflected in faecal egg counts, pepsinogen values, gastrin values and antibody titres against Cooperia spp. or Ostertagia spp. Depending on the time of sampling, pepsinogen values and antibody titres against Ostertagia spp. particularly were useful variables for assessing differences in levels of infection to which groups of calves had been exposed.

Characteristics of the humoral immune response of Cooperia oncophora-infected calves to low molecular weight antigens of C. oncophora were studied. Immunoblotting with sera obtained from calves 6 weeks after a single oral infection with 100,000 third-stage (L3) C. oncophora larvae revealed several corresponding antigenic fragments between adult worms and the fourth-stage (L4) larvae. No reactivity in the immune sera was found against the L3 stage. A previously defined complex of low molecular weight proteins (12-15 kDa) was found on both L4 and adult Cooperia stages, but not on the L3 stage. C. oncophora adults differed from the L4 larvae at the 31/32 and 37 kDa level. Several adult and L4 proteins were bound by biotinylated Concanavalin A, as was also true for L3 proteins. A 31/32 kDa glycoprotein of adult worms was recognised by a monoclonal antibody with specificity for phosphorylcholine. Using monoclonal antibodies in ELISA and Western blotting, the serum antibody response of C. oncophora-infected calves to adult worm antigen was almost entirely IgG1. Binding of the IgG1 antibodies was restricted to a complex of reduced 12-15 kDa protein(s) and a 27 kDa fragment of adult worms. The data suggest that the systemic humoral immune response of calves during a primary infection with C. oncophora consists mainly of an IgG1 response, and is directed to a non-glycosylated Cooperia protein (molecular weight estimated at 12-15 kDa under reducing conditions and 18 kDa under nonreducing conditions). This protein is probably present in both L4 larvae and adults. Since it was not bound by immune sera from calves mono-infected with several other nematodes, the 12-15 kDa protein complex may represent a Cooperia-specific component that can be used for serodiagnosis.

In two experiments, groups of calves were exposed to different levels and patterns of infection with Ostertagia spp. and Cooperia spp. The experimental design simulated the stereotypic pattern of herbage infestation, including both a normal and a delayed midsummer increase, under conditions of set-stocking. After this simulated ‘first grazing season’, calves were followed during the subsequent winter housing. At the end of that housing period some calves were collected with 100 000 L3 Cooperia spp. and 40 000 L3 Ostertagia spp. and slaughtered 23 days later. All previously infected calves were protected against the establishment of the challenge infection with Cooperia spp., but not against Ostertagia spp. For the latter a significant negative correlation was found between worm count and previous level of exposure to infection. During the simulated first grazing season, changes in the ratio of Cooperia to Ostertagia eggs in the faecal egg output and the genus-specific egg count were influenced by both the level of exposure and the timing of the midsummer increase. It is concluded that acquired immunity against both parasite genera develops depending on the level of exposure to infection during a first grazing season, and that delaying the midsummer increase results in a delay of the acquisition of an effective immunity as measured by faecal egg counts and the ratio of Cooperia to Ostertagia egg output.

In two experiments groups of calves were exposed to different levels and patterns of infection with Ostertagia spp. and Cooperia spp. The experimental design simulated the stereotypic pattern of herbage infestation, including a normal or a delayed midsummer increase, under conditions of set-stocking. The purpose of the experiments was to investigate the accuracy of egg counts, pepsinogen and gastrin values and antibody titres as estimators of the level of exposure to infection. Faecal egg counts significantly reflected levels of exposure during the first half of the simulated grazing season. Antibody titres and pepsinogen values reflected levels of exposure best during August and September, partly depending on the pattern and range of levels of exposure. Antibody titres against Cooperia spp. were particularly useful when levels of exposure to gastrointestinal nematode infection were low. Gastrin values were elevated only at high levels of exposure, which caused large weight gain reductions, in the later part of the simulated first grazing season. It is suggested that antibody titres and pepsinogen values can be used for prognostic diagnosis, indicating whether or not control measures should be taken. Both estimators of infection correlated significantly with the realised weight gain at the end of the simulated grazing season. Egg counts in the second month after the initial infection (turnout) also may be of significant value to support decisions concerning control measures. Comparisons with data from field trials and experiments conducted by others under various conditions suggested that the conclusions of the present experiments are also valid under field conditions. Furthermore, the results supported the conclusions drawn from previous field work, that levels of exposure are often very low on commercial farms in the Netherlands.

An experiment was carried out to study the build-up of infection and development of immunity against Dictyocalus viviparus infections in calves. Six groups of four calves were used. Groups 1-5 grazed on separate pastures and Group 6 served as a permanently housed control group. To stimulate 'low' and 'very low' overwintered pasture infectivity, Groups 1 and 2 were infected experimentally six times with ten and two larvae, respectively, during the first 3 weeks on pasture in May. From the middle of July, Groups 2-4 were experimentally infected six times in 3 weeks with 10, 10 and 100 larvae, respectively, to simulate 'low' and 'moderate' pasture contamination by carriers. Group 5 served as a non-infected pasture control group. After housing of Groups 1-5 in October, all calves were treated with oxfendazole and challenged with 5000 larvae of D. viviparus to evaluate the development of immunity.The results showed a similar population build-up of lungworm infections in Groups 1-4. After the beginning of patency, 24-35 days after primary infection, an increase in faecal larval counts occurred 31-35 days later as a result of re-infection. For Group 2, this was only true when the infections with a total of 12 larvae in May were ignored, as these did not result in patent infections. Faecal larval counts were highest in Group 4, which was the only group with mild signs of lungworm disease occurring in the re-infection period. The worm counts at necropsy showed the development of immunity in Groups 1-4 but not in Group 5. This is consistent with the fact that Group 5 did not develop patent lungworm infections throughout the grazing season.

For the evaluation of control strategies against, and economic impact of gastrointestinal nematode infection, the quantitative relationship between level of exposure to infection and growth performance is important. Available data in the literature are summarised. Based on questions derived from earlier work concerning the relationships between infection, growth performance and acquired immunity during the entire rearing period, two experiments were set up. In these experiments, groups of calves were exposed to different levels and patterns of infection with Ostertagia ostertagi and Cooperia oncophora. The experimental design simulated the stereotypic pattern of herbage infestation under conditions of set-stocking. A significant negative linear relationship between the level of exposure and growth performance was found (P < 0.001). The time sequences observed for body weight changes in response to infection and the magnitudes of the effects of infection on weight gain in both experiments suggested a good predictability of the relationship between infection and growth performance. By comparison, it is also suggested that in the Netherlands parasite control is excessive in the first grazing season. A more limited use of anthelmintic treatments is proposed.

Antibodies against Ostertagia spp., Cooperia spp. and Dictyocaulus viviparus were assessed in serum and individual milk samples of cows and in bulk milk samples from the refrigerating tank. Titres in milk samples were related to serum titres, but also influenced by milk yield, lactation stage and age of the cow. Correlation coefficients between serum and individual milk samples were highly significant, and varied from 0.42 to 0.56. Correlations between herd means of serum titres and herd means of individual milk titres varied from 0.41 to 0.61, and those between herd means of serum titres and means of bulk milk samples from 0.43 to 0.67. Finally, the correlations between herd means of individual milk samples and means of bulk milk samples varied from 0.52 to 0.82. This variation was dependent upon worm species and whether or not correction for milk yield was applied.The discrimination of herds was evaluated by the between/within herd ratio of variances. F values for all types of samples were highly significant, and at least as high for milk samples as for serum samples. If, as has been shown for serum samples, a positive relationship exists between the milk yield response to anthelmintic treatment and the mean herd litre of milk samples or bulk milk samples, assessment of these titres could offer a rational basis for treatment of dairy cows.

An experiment was carried out simultaneously in Glasgow and in Wageningen to investigate possible differences between the local strains of Ostertagia ostertagi and Cooperia oncophora. In each location calves of the local Friesian breed were infected with 100,000 larvae of either the Glasgow or Wageningen strain of O ostertagi or C oncophora. At both locations the calves received the same diet. The Glasgow strain of O ostertagi was more pathogenic than the Wageningen strain and a larger proportion of the worm burden was found in the abomasal mucosa. The number of ova per female was greater in the Wageningen strain. For C oncophora the Wageningen strain gave rise to higher worm burdens and longer worms. Differences were also present between locations. The British Friesians had higher worm burdens of C oncophora and the worms of this species were longer in this host. Compared with the Dutch Friesians the British calves had a higher proportion of O ostertagi in the mucosa. This experiment showed how difficult it is to compare data from the literature because of differences in parasite and host strains and laboratory techniques.

Gastrointestinal nematodes are an important cause of reduced production of meat, milk and wool in domestic livestock. It is generally believed that problems caused by these parasites have increased owing to the intensification of animal husbandry1–3 of resistance to anthelmintics, current research is focussed on alternative control strategies that do not rely on anthelmintics. Here, Bram Kloosterman, Henk Parmentier and Harm Ploeger review work on the genetic resistance of domestic ruminants to these nematodes and discuss the practicality of breeding programmes.